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Aussie Barb Research Team 
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(filelink) Sarcoidosis and the Marshall Protocol The only effective treatment for sarcoidosis is the Marshall Protocol "Sarcoidosis kills. Your doctor is correct in that, but totally incorrect in representing that any (standard) treatment he can offer you will make any measurable difference in the rate of long-term decline. There are no studies showing that any of the treatments he is offering you will be effective. This is because he (and his pulmonologist colleagues) just do not understand the disease. .......... We know of around 300 sarcoid patients who are recovering on the MP. More than 50 of those have recovered beyond the point of relapse. There are hundreds more that we are not following. You need to understand that killing the bacteria is a CURE, not a therapy. The conventional treatments are *NOT* FDA approved. They have not even been checked by the FDA for safety. The prescription of Prednisone, Methotrexate, etc, for Sarcoidosis is ALL off-label. Please see First report from ATS, San Diego The FDA has never approved any drug for the treatment of Sarcoidosis. Prednisone was never approved, Methotrexate, Humira, NOTHING has ever approved by the FDA for the therapy of Sarcoidosis. FDA has designated several drugs which appear promising. This Foundation applied for, and received, designation by the FDA of Clindamycin and Minocycline in the treatment of Sarcoidosis. So now that you have found your caregivers are totally incorrect on one issue, are you prepared to look more closely at the other things they have told you? Here is the cumulative list of all drugs the FDA has designated might be suitable for Sarcodiosis. http://www.fda.gov/orphan/designat/alldes.rtf You will note that our Autoimmunity Research Foundation is responsible for 2 out of the total 5  Dr. Trevor Marshall, Ph.D. Myths Sarcoidosis experts continue to perpetuate many myths regarding this disease. This is the result of anecdotal misinformation which has gained credence by repetition. In other words, much of what sarcoidosis 'experts' proclaim about sarcoidosis is not substantiated by science or scientific study. The MP study site vs other sarc support groups This site tells you all about how sarc sufferers are getting better by following the Marshall Protocol, a treatment devised by a research scientist, Dr Trevor Marshall. There's a huge amount of information here - don't try to read it all at once! You can try the other sarc websites if you like, and listen to the despairing cries of those whose doctors have given them no hope, and no treatment but prednisone, which, as you've discovered, does no long-term good. Then come back here and sense the hopefulness and jubilation of those who know they're healing. The MP isn't easy, but it works, and you can look forward to better health now that you've found it. ~Julia For a basic explanation of sarcoidosis from Wikipedia, the free encyclopedia, see Sarcoidosis See also: What is the Marshall Protocol? The First Basic Questions Answered The Marshall Protocol -- simple explanations Why isn't the MP being used by more doctors? MP Phase One Guideline Papers for Physicians (scroll down for up-to-date, accurate information on Sarcoidosis) |
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[filelink] Pulmonary involvement Lung involvement may be misdiagnosed as a "respiratory infection" It has to be differentiated from "pneumonia" http://tinyurl.com/43hqr and lots of other conditions. http://tinyurl.com/58rjz DLco gas transfer factor test "The best test to show inflammation in pulmonary interstitial tissue is the DLco gas transfer factor test. The DLco is important because it recovers back to 'normal' during the MP, allowing sarcoidosis patients who were needing 24/7 oxygen to be able to discard the oxygen and still function reasonably well. Even if the fibrotic tissue remains, the sarcies recover lung capabilities based on FEV1 (muscle tone) and DLco (gas transfer) improvements. It my opinion that the biggest single factor in lung effectiveness is the ability of the lungs to transfer gases to and from the blood. This is measured by the DLco test. This capability is significantly reduced during active inflammation, and of course by immunopathology. The DLCO (diffusing lung capacity) test is usually given at the same time that other pulmonary function tests are given. It is not a self test - it's usually administered by a respiratory therapist in a facility such as a hospital, by a doctor's order. You inhale a single breath of a known quantity of carbon monoxide, then hold your breath, then exhale. This is all done with special equipment so the exhaled breath can be analyzed to determine the amount of carbon monoxide that was absorbed in the single breath. The results indicate how well oxygen passes from the lung's "air sacs" across to the blood." ...Trevor... Lung diffusion testing Illustration of DLco test Evaluating pulmonary function tests The overall accuracy of the FVC for restriction is about 60%.(Aaron SD, Dales RE, Cardinal P. How accurate is spirometry at predicting restrictive pulmonary impairment? Chest. 1999;115:869-873.) Based on this sort of accuracy, there is a wide a range of margin for errors. The PFT results are comparative; they are standardized for standing height, age and gender, and for ethnic group. This is called the predicted value. Predicted values can be selected by the user from amongst 16 sets for adults, and 13 sets of equations for children and adolescents. "In a healthy population there is great variation in spirometric values even after taking into account age, height, gender and ethnic group. This underlines the need for putting great emphasis on clinical data and the patient’s previous medical history in interpreting spirometric data. The best predicted value for a patient is the personal reference value, i.e. the value obtained in a clinically optimal period; such personal best values may reveal that values which were within the normal range are not the patient’s optimal values." http://www.spirxpert.com/welcome.htm Obstructive lung disease It's a little-recognized fact that sarcoidosis can cause PFTs results to indicate obstructive lung disease (sarcoidosis is considered a restrictive lung disease). This is because chest lymph nodes may become so enlarged they compress airways and/or granulomas themselves may obstruct airways. This article explains the difference between restrictive and obstructive lung disease. http://www.mayoclinic.com/invoke.cfm?id=AN00759 Alveolitis Inflammation in sarcoidosis does cause fluid in the lungs. Alveolitis is inflammation of the tiny sac-like air spaces where the exchange of carbon dioxide and oxygen take place. When the alveoli are filled with fluid, there is less exchange of gases. Crackles This resource says that crackles are sometimes found in sarcoidosis. http://www.chestjournal.org/cgi/content/abstract/73/3/333 And interstitial lung disease is listed here as one reason for crackles. i. Crackles (Rales) Crackles are discontinuous, nonmusical, brief sounds heard more commonly on inspiration. They can be classified as fine (high pitched, soft, very brief) or coarse (low pitched, louder, less brief). When listening to crackles, pay special attention to their loudness, pitch, duration, number, timing in the respiratory cycle, location, pattern from breath to breath, change after a cough or shift in position. Crackles may sometimes be normally heard at the anterior lung bases after a maximal expiration or after prolonged recumbency. The mechanical basis of crackles: Small airways open during inspiration and collapse during expiration causing the crackling sounds. Another explanation for crackles is that air bubbles through secreations or incompletely closed airways during expiration. Conditions: ARDS asthma bronchiectasis chronic bronchitis consolidation early CHF interstitial lung disease pulmonary edema Bronchiectasis Bronchiectasis is the abnormal widening of bronchi damaged by infection and the resulting inflammatory cytokines, or obstruction or traction. Sarcoidosis can result in bronchial obstructions from enlarged chest lymph nodes or granulomas. Traction bronchiectasis can occur when there is pulmonary fibrosis that distorts the airway. Since bronchiectasis can result in little 'pockets' where infections can take hold, one possibility you may want to discuss is perhaps bacteria cultured from a biopsy were secondary, opportunistic infections. If a decision is made to treat them, the primary goal remains to treat the primary cause of disease: sarcoidosis. You should be concerned if doctors are most concerned about bronchiectasis - seeing it as more threatening than the primary disease. So you may need to be prepared to dig in your heels to begin the MP, instead of palliative treatments (aimed to help you feel more comfortable) and because you will want to ward off recurring complications. -I have bronchiectasis - identified in my chest radiology - and I've done quite well on the MP! I've had no episodes of pneumonia, visits to the ER or anything like that. The rationale I used with my doc to convince him to try the MP initially was: 1) Since antibiotics are used to treat bronchiectastis, and 2) there isn't a singular well-defined treatment for bronchiectasis, 3) why not monitor a trial of the MP and see if it treats the sarcoidosis, which caused the bronchiectasis in the first place? We've never regretted the decision to use the MP. ~Belinda Atalectasis Atelectisis refers to collapse of a lung or a portion of one, due to incomplete filling with air. This usually occurs in association with some mechanical blockage of the airway which prevents new air from entering the lung. The air in the lung distal to the block is absorbed by the bloodstream leading to the collapse of the alveoli. Atelectasis can be caused by fibrosis. Sarcoidosis results in fibrosis and can also result in bronchial obstructions from enlarged chest lymph nodes or granulomas. Atelectasis is not a common occurance in sarcoidosis but it does happen. If you google 'atelectasis & sarcoidosis', you will find some cases studies and xrays. Hyperinflation A chest x-ray can give a general idea as to whether a patient is hyperinflating, as explained here. Dynamic hyperinflation, discussed here (you will need to register to read the article) occurs in COPD and other diseases. Pulmonary function tests may be used to give more information about this condition. Hyperinflation is sometimes called "air trapping" and may be helped by measures such as pursed lip breathing. Pursed lip breathing can help release air trapped in the lungs and can help relieve the feeling of shortness of breath, if it's due to hyperinflation. In some cases, supplemental oxygen might be useful in overcoming hyperinflation. The Medscape article discusses how supplemental oxygen facilitates lung emptying. ~Belinda Lymph nodes I personally wouldn't worry too much if lymph nodes are still swollen. Lymph nodes play a criticial role in removing bacteria, abnormal cells and other matter as part of the immune system. That means they are still working. ~Belinda Enlarged lymph nodes are usually a sign of infection and the way to treat is to treat the underlying cause when possible. ie MP is doing that. What happens in later stages of sarcoidosis is the lymph nodes shrink down; they stop doing their part. This may be because they become too damaged to function. It's not unusual for lymph nodes to be calcified in sarcoidosis patients. FAQ My lymph nodes are growing. Is this normal? Should I be concerned about cancer? Photos of sarcoidosis gross pathology Neurological inflammation can cause impairment of respiratory function and affect test results Breathing diffusion difficulties from neuro-muscular disease is a broad statement that could have many causes. Since Sarc is a restrictive disease when affecting the lungs, many times the expiratory phase is longer, making it difficult to exhale enough to register adequate numbers on their equipment. The reduced musculature effort could be translated to poor innervation which would be another way of saying the above. The words neuro muscular apply to all muscle as without innervation from the brain muscles would not work. ~VEZ R.N. See also: Improvement in pulmonary function tests Assessing lung function Pulmonary Function Tests (PFTs) |
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filelink Symptoms of sarcoidosis Many sarcoidosis patients experience symptoms long before they are correctly diagnosed, since their individual symptoms can sound vague (fatigue, for instance) and benign. Sarcoidosis is often misdiagnosed. Patients are often told they probably have cancer before they are correctly diagnosed, because the chest imaging in sarcoidosis looks similar to cancer and/or tuberculosis. One of the most frequent and universal symptoms of sarcoidosis is fatigue that is not relieved by sleep. Lack of concentration is one of the most frustrating symptoms, but neither of these is specific to sarcoidosis. They occur in other diseases. The relentless fatigue of sarcoidosis may be discounted by medical professionals because "everyone gets tired" and there is no good way to measure fatigue. The most common sarcoidosis symptoms listed by the Cleveland Clinic are: * Tender reddish bumps or patches on the skin * Red and teary eyes or blurred vision * Swollen and painful joints * Enlarged and tender lymph glands in the neck, armpits and groin. * Enlarged lymph glands in the chest and around the lungs * Nasal stuffiness and/or hoarse voice * Pain in the hands, feet or other bony areas * Kidney stone formation * Enlarged liver (or spleen) * Development of abnormal or missed beats (arrhythmias), inflammation of the covering of the heart (pericarditis) or heart failure * Nervous system effects, including hearing loss, meningitis, seizures or psychiatric disorders (for example, dementia, depression, psychosis) There are many other symptoms that may be due to sarcoidosis, because it can damage or alter the function of any body organ. Physicians like to have a tissue biopsy to diagnose sarcoidosis, and this is largely due to the fact that the common treatments for sarcoidosis are so fraught with side effects that biopsy proof is needed to justify their use. Biopsy is not always required, though, and now the serum D-metabolite tests are a good tool for measuring systemic inflammation. Sarcoidosis patients have a dysregulated vitamin D metabolism and produce excessive Hormone D, 1,25-D, in unregulated amounts due to activated macrophages. This can cause symptoms of Hypervitaminosis D (see the article below). Fatigue, sleepiness, and mood or mental changes can be due to hypervitaminosis D. We suggest you talk to your doctor about getting your D-metabolites measured. Get a copy of the lab test results and post them on our study website for help in understanding them. Sarcoidosis is often referred to as the "snowflake" disease because patients present with so many different symptoms. The clinical picture can be complicated by intermittent inflammation in many different organs. While the symptoms may vary from patient to patient, the underlying cause is the same. The disease is really very simple when you realize that sarcoidosis inflammation has only one cause: intracellular bacteria. The MP is designed to deal with all intra-phagocytic bacteria, regardless of the species. Hypervitaminosis-D Sarcoidosis results in abnormally high levels of dihydoxyvitamin-1,25-D, a powerful hormone which affects many other hormones. This diagram summarizes some of the key relationships between the body's hormones and 1,25-D. List of Hypervitaminosis-D symptoms "Signs of mild Vit D toxicity include hard stools, constipation, metallic taste, "weakness, headache, muscle pain, bone pain, somnolence (sleepiness), nausea, vomiting, dry mouth, constipation, polyuria, polydipsia, anorexia, weight loss, nocturia, conjunctivitis (calcific), pancreatitis, photophobia, rhinorrhea, pruritus, hyperthermia, decreased libido, elevated BUN, albuminuria, hypercholesterolemia, elevated SGOT and SGPT, ectopic calcification, nephrocalcinosis, hypertension, cardiac arrhythmias and rarely, overt psychosis" and facial paralysis." Bell's Palsy Bell's Palsy occurs as a result of the high levels of 1,25-dihydroxyvitamin-D which are associated with Lyme, and all the Th1 diseases. IMO, One of the earliest and best papers on the various issues is Muler H, et al: "Facial Paralysis in Children" Ann Otolaryngol Chir Cervicofac. 1975 May-Jun;92(4-5):229-34. PMID: 1217818 Unfortunately the paper is in French, but it is pretty easy to work through it with only High School French as a background. You can get it on Inter Library Loan. It also links Bell's palsy to the hypervitaminosis D of Tuberculosis. We see it in Sarcoidosis as well. Several patients have had their paralysis resolve as they worked down their bacterial load. Dr. Trevor G Marshall, PhD Granulomas Inflammation, including granulomas, seems to settle in injured tissues. Most of us have had some experience with that whether it was 'tennis elbow' or 'football shoulder' or carpal tunnel syndrome. Granulomas tend to make scar tissue pink. But intracellular bacteria also resides in noninjured tissues. Therefore, Th1 inflammation can and does occur in tissues that have not been injured. I'm sure there are many areas of your body that have never been injured that have sarcoidosis inflammation. Heerfordt's syndrome is the association of facial nerve palsy with anterior uveitis and parotid gland enlargement. It is caused by sarcoidosis. Sjogren's (sicca) syndrome Sjogren's and Sarcoidosis are both described in the standard literature as a collection of symptoms. Sjogren's is known to be related to diseases such as rheumatoid arthritis, sarcoidosis, lupus, scleroderma and polymyositis. Many Sarcoidosis patients manifest the same symptoms as described in Sjogren's syndrome (dry eyes and mouth, decreased tears and saliva, and resulting dental caries). Mouth Sarcoidosis can affect any organ, and the mouth is not exempt. We know sarcoidosis affects these areas because biopsy of these leads to diagnosis. Here, briefly, are some of the symptoms: - sores on or swelling of the face, tongue, mouth, gums or inside the cheeks Orofacial Manifestations and Systemic Sarcoidosis Facial Swelling and Systemic Sarcoidosis Oral manifestations of sarcoidosis. Granulomatous cheilitis (lip swelling) can lead to a sarcoidosis diagnosis - gingivitis is simply inflammation of the gums. Sarcoidosis is an inflammatory disease. - affected salivary glands can produce too much saliva or (more commonly) too little saliva Sarcoidosis with Involvement of the Salivary and Lacrimal Glands - too little saliva when inflammation impairs or blocks the function of the salivary glands can result in -gum disease and increased dental cavities. The term "xerostomia" means dryness of the mouth due to a decreased function of the salivary glands. It is not unusual for people with sarcoidosis or other Th1 disease to experience dysphagia, difficulty swallowing as a symptom. It is possible for dysphagia to begin abruptly, but you can be on the alert for alterations in the functioning of your throat and voice which would signal you might also have a problem if you ate at that time. The vocal cords must be able to close properly to avoid choking. Acute reversible dysphagia and dysphonia as initial manifestations of sarcoidosis. Dysphonia Dental Fractures Since sarcoidosis causes a dysregulation of Hormone D (1,25-dihydroxyvitamin D), a condition which causes calcium to be pulled from bones and teeth, the teeth can become weakened and susceptible to cracking easily. Sarcoidosis patients may experience multiple non-traumatic tooth fractures. Calcium pulled from bones and teeth is carried by the blood and deposited in soft tissues like the lungs, kidneys or dental pulp. Dental stones (pulp stones) can result from calcium deposits within the dental pulp. These may be found when root canal therapy is performed. See also: Dental Problems and Dental problems and sarcoidosis Eye Involvement See EYE INFLAMMATION The lacrimal glands In the eye, the lacrimal gland is a common area of manifestation for sarcoidosis. produce tears to moisten and protect the eyes. It's not unusual for sarcoid patients to have uncontrolled tearing of the eyes, dry eyes or blurry vision. Cataracts Sarcoidosis itself can cause cataracts, because sarcoid inflammation of the eye can result in a cataract. Uveitis Uveitis is a symptom, and has many identified causes and associations at this point. Some cases are widely accepted to be due to bacteria or viruses. Other cases are associated with “autoimmune diseases” like Crohns disease and rheumatic arthritis. Researchers found cell-wall deficient bacteria (sometimes called mollicute-like organisms) in the vitreous fluid of patients with sardoidosis, Crohn’s disease, ulcerative colitis, juvenile rheumatoid arthritis, etc. You can read about eye inflammation (uveitis)at this URL for the Cleveland Clinic: http://www.clevelandclinic.org/eye/patient_info/uveitis.asp It says, "Complications of uveitis may include glaucoma, cataract, abnormal blood vessel growth, fluid within the retina and vision loss." Conjunctiva http://tinyurl.com/55z7e A patient with sarcoidosis diagnosed by biopsy of scleral nodules. http://tinyurl.com/4mypt Wirostko papers on eye disease Lymphadenopathy Sarcoidosis can result in abdominal lymphadenopathy. Like any sarcoidosis symptom, lymphadenopathy may flare with Herxing, resulting in enlarged and/or tender lymph nodes. Muscle spasms and cramps often are worse at night. One explanation that was offered for this was an increase in lymphadic edema. Links to sarcoidosis in other organs: Nose and sinuses http://tinyurl.com/4wwsh Sinonasal sarcoidosis http://tinyurl.com/63ffa Central Nervous System (Yes, they sometimes want a brain tissue biopsy which isn't necessary) http://tinyurl.com/62zcb Muscle http://tinyurl.com/3wbbo Maxillary Involvement http://tinyurl.com/6jyqt Renal http://tinyurl.com/47z5f Pancreas http://tinyurl.com/57cdc Splenomegaly (Enlarged Spleen) http://tinyurl.com/3azaqd Anemia See Anemia and Th1 Disease Depression There is limited and controversial evidence that changes in the expression of cytokines and other molecules usually associated with immune function may be involved in the pathogenesis of depression. Cytokines are expressed in the brain, and during development they play important roles in normal brain embryogenesis. A recent study revealed that induction of increased cytokine activity was associated with depressed mood in normal volunteers (Duman et al 1997). Elevated IL-6 concentrations in plasma have been reported in depressed patients (Musselman et al 2001). Should further work confirm a relationship between cytokines and depression, medications directed at cytokines might represent novel antidepressants. See Depression Neuropathy One bacterial species which has shown an affinity to cluster around nerve fibres is Mycobacterium leprae. It is possible that this characteristic has been acquired by less pathogenic 'cousins' of that species, or that the species itself is one of the players in Th1 disease. See Will the MP treat paresthesia and neuropathy? Sleep apnea Th1 inflammation can cause dysfunction in any tissue of the body. The upper airway is often affected which could cause obstructive sleep apnea. In central sleep apnea, the airway is not blocked but the brain fails to signal the muscles to breathe due to instability in the respiratory control center. Central sleep apnea is usually observed in patients with central nervous system dysfunction, such as following a stroke or in patients with neuromusclular diseases like amyotrophic lateral sclerosis (which is a Th1 inflammatory disease). According to the following article, sarcoidosis patients have a higher incidence of sleep apnea than the general population. Sleep apnea in sarcoidosis Sarcoidosis Vasc Diffuse Lung Dis 1997, No. 14 (1), March 1997 Turner GA, Lower EE, Corser BC, Gunther KL, Baughman RP. see also sleep file link Liver involvement Extrapulmonary sarcoidosis primarily diagnosed in the liver. http://tinyurl.com/4ap64 Asymptomatic organ involvement is quite common in sarcoidosis. An article from Medscape Gastroenterology http://www.medscape.com/viewarticle/405532_4 says: "The prevalence of hepatic granulomas in sarcoidosis is 65%. In a study of 100 patients with hepatic sarcoidosis, the majority of patients were asymptomatic and had normal abdominal examinations. Abdominal pain and hepatosplenomegaly were seen in 15% and 8% of these patients, respectively. Much less common were features of chronic liver disease and cirrhosis." Sarcoidosis of the liver http://tinyurl.com/6ew3q Th1 inflammation commonly affects the liver, although it may be subclinical. Patients may be told they have "fatty liver disease" or cirrhosis. Angiotensin receptor blocking drugs are known to have organ-protective effects. An angiotensin II type 1 receptor antagonist, olmesartan medoxomil, improves experimental liver fibrosis by suppression of proliferation and collagen synthesis in activated hepatic stellate cells. Cardiac Involvement http://tinyurl.com/46l2g Chest pain is, in fact, a common symptom endured by sarcoidosis patients, substantiated by reports such as this one, http://tinyurl.com/4hg48, which found that about 30% of sarcoidosis patients suffer from chest pain. While it is true that chest pain can be due to cardiac involvement, it may simply be due to other problems brought on by sarcoidosis such as enlarged lymph nodes which can cause pressure, crowding and pain in the chest. 20 to 30 percent of sarcodiosis patients are found to have cardiac involvement upon autopsy. This is why we caution patients to assume they may have unrecognized cardiac involvement and to control their Herxing accordingly. This report found that perhaps 50% of sarcoidosis patients have cardiac involvement that is not diagnosed. Cardiac sarc can cause chest pain. Pulmonary Hypertension Pulomonary Hypertension is a severe condition that may develop as a result of sarcoidosis. PH is a form of high blood pressure in the pulmonary artery, which connects the heart to the lungs. Pulmonary hypertension associated with sarcoidosis: mechanisms, hemodynamics and prognosis. Thorax. 2005 Oct 14; [Epub ahead of print] PMID: 16227329 [PubMed - as supplied by publisher] http://tinyurl.com/d74hs Sudden death with clinically undiagnosed pulmonary hypertension. J Clin Forensic Med. 2005 Oct;12(5):264-7. Epub 2005 Mar 28. PMID: 16198969 [PubMed - in process] http://tinyurl.com/7pgqr Pulmonary hypertension in advanced sarcoidosis: epidemiology and clinical characteristics. Eur Respir J. 2005 May;25(5):783-8. PMID: 15863633 [PubMed - indexed for MEDLINE] http://tinyurl.com/dbmwn CT findings in severe thoracic sarcoidosis. Eur Radiol. 2005 Jan;15(1):23-30. Epub 2004 Sep 24. Review. PMID: 15449010 [PubMed - indexed for MEDLINE] http://tinyurl.com/8shc4 Cutaneous manifestatios of sarcoidosis Cutaneous manifestations of sarcoidosis are common and varied, and one patient can have different types of sarc skin lesions at the same time. Sarcoidosis is a systemic inflammatory disease, so be suspicious of sarcoidosis if you have a skin problem and you've already been diagnosed with sarcoidosis. The reason Sarcoidosis is called a "masquerader" is to alert physicians to be more suspicious in investigating skin lesions and rashes that generally indicate something else in normal (non-sarcoid) people. I guess you could say sarcoidosis is more than "skin deep." Cutaneous immunopathology The body of folks with systemic Th1 infection severe enough to cause sarcoid granuloma is going to exhibit wierd physical phenomena as it heals. These include spots on the skin which are often red. Although these manifestations can be scary but there is nothing we know which can help you get through the 'Herx' phase of this disease any faster than the slow, steady, bacterial killoff of the MP. Lupus pernio, first described by Ernest Besnier, is the most characteristic of all sarcoid lesions. Lupus Pernio is a skin manifestation of sarcoidosis. Lupus Pernio is not another disease (and is not related to lupus), it's simply a name for the red-to purplish lesions that can appear on the nose, face, ears or hands of sarcoidosis patients. These lesions can occur when the nose, face or hands are exposed to cold or wind, so it's a good idea for sarcies to keep these areas protected from wind and cold. Avoiding exposure to bright lights is also an important preventative measure. Sometimes lupus pernio lesions will have an appearance of small "beads" along their edge, especially if the sore is on the rim of the nose. If left untreated, lupus pernio lesions can be disfiguring and cause a patient to feel embarrassed, particularly since they may be noticeable on facial areas so visible to the public. Like some other cutaneous sarcoidosis lesions, lupus pernio can appear at sites of old scars or trauma. Lupus pernio lesions, like other sarcoid manifestations in the upper respiratory tract, can be quite resistant to the standard immunosuppressive therapies. Lupus pernio is said to be the skin lesion most characteristic (a diagnostic indicator) of sarcoidosis, but not all sarcoidosis patients have these skin lesions. -My experience with lupus pernio is that it flares with exposure to light plus cold and wind. I suspect you have still been having a good bit of cool wind and weather in your part of the world. You may need to keep your nose better protected. I know that's hard to do, so if nothing else, you can stay indoors during daytime as much as possible and wrap a scarf around your nose if it is cool or windy. Warning of the risk of scarring, whether on the skin or in the lungs, is a common tactic to pressure patients to use the treatment a physician prefers. Lupus pernio has a reputation for being difficult to treat. In reality, the doctor has no way to know whether you will scar. Certainly I sustained no scars from my winter bouts with lupus pernio. Within a month, you will probably have this lupus pernio flare behind you and you can deal more assertively with your doctor to reassure him you are on the correct treatment, MP. Continuing to take Benicar allows your immune system to work more efficiently and provides protection of organs. Prednisone injections will have a systemic effect, but less than if you took an oral dose. ~Belinda Skin rash I was diagnosed with sarcoidosis several years ago, after testing that included a tissue biopsy. Now I've had a skin rash biopsied and was told the result indicated no granulomas, so this can't be sarcoidosis. I think there is a mistake. This article by a practicing dermatologist explains that both "specific" and "non-specific" skin lesions are found in sarcoidosis, explaining, "Specific skin lesions are generally associated with chronic disease and demonstrate noncaseating granulomas in the dermis on histological examination. Nonspecific skin lesions are seen primarily with acute disease and noncaseating granulomas are absent." Erythema Nodosum is a common manifestation of acute sarcoidosis. Subcutaneous Nodules Subcutaneous nodular sarcoid lesions are sometimes called Darier-Roussy sarcoidosis, named for the French physicians Darier and Roussy who described these subcutaneous nodules in 1904. Here is a photo of skin tags. According to this source, alternate names for skin tags are: * Acrochordons * Papillomas * Soft fibromas * Pedunculated (this means they are on a stalk) * Filiform (this means they are thread-like) "Skin tags develop in both men and women as they grow older. They are skin coloured or darker and range in size from 1mm to 5cm. They are most often found in the skin folds (neck, armpits, groin). They tend to be more numerous in obese persons and in those with type 2 diabetes mellitus." Sarcoidosis manifests in a wide variety of skin lesions. You can find links to photos of cutaneous sarcoidosis on this SarcInfo thread. Here is a photo of sarc lesions around the eye. Some of the types of skin lesions encountered in sarcoidosis, and the other diseases these resemble are: Papules (little bumps) resembling Granulomatous rosacea Acne Benign appendageal tumors Plaques resembling Psoriasis Lichen planus Nummular eczema Discoid lupus erythematosus Granuloma annulare Cutaneous T-cell lymphoma Kaposi's sarcoma Secondary syphilis Lupus pernio resembling Scar Discoid lupus erythematosus (more info on lupus pernio can be found in a later post) Erythema nodosum resembling Cellulitis Furunculosis Other inflammatory panniculitis Sarcoid skin lesions can be painful, itchy, oozy or dry and peeling. They can also make your hair fall out. You can find more information and lots of pictures of skin sarcoidosis (to compare with your rashes) in the thread "Skin Sarc, What Does it Look Like?" or in the list later on in this thread. Sweat glands "Alan Cantwell, MD (dermatologist) wrote a paper on the skin in Th1. http://www.joimr.org/phorum/read.php?f=2&i=2&t=2 Alan told me that he always found bacteria in the sweat glands, that bacteria loved the skin, in all these diseases. That is in line with what I think we are seeing." ..Trevor.. Nails Onycholysis is the loosening (lifting) of the nail, starting at the border. Sarcoidosis can cause oncholysis. See: Derm Net NZ (with photos) and Internet Journal of Dermatology. If you click here, you will find a list of four PubMed-indexed articles about sarcoidosis nail disorders. Cancer Sarcoidosis is a multi-systemic disease that can be confused with benign or malignant tumors. Patients should make their doctors aware of any previous sarcoidosis diagnosis (even if only suspected) so sarcoidosis can be investigated as a possible cause of any lumps or tumors. See Cancer and Th1 inflammation |
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SARCOIDOSISlink REMISSION ...... It is a myth that sarcoidosis goes away on its own: NIH ACCESS study shows that Sarcoidosis does not go away Lessons Learned from the NIH ACCESS Study There were no spontaneous remissions in the placebo group of the NHLBI Trental study ....... from Dr Marshall: What causes Sarcoidosis to sometimes go into remission? is it possible? ...... MP.com thread Sarcoidosis and Remission FAQ: Does sarcoidosis go away on its own without treatment? ............. "Even though you may still be feeling terrible (while on the Marshall Protocol), a CT scan might well show that the lymph nodes are steadily shrinking. Granuloma shrink too, but not those which have been calcified or turned fibrotic. The body encases pathogens which have been missed by the immune system in collagen (fibrosis) commonly called 'scarring'. Angiotensin blockade inhibits the formation of new fibrotic tissue. The lungs also are really good at healing, even though they may be badly scarred from years of fibrosis. The PFTs usually improve, particularly the DLco, or gas diffusion capability." ..Trevor.. ==================== Lungs Q-I have calcified granuloma in my lungs which indicates old infection. I wanted to know if the MP will clear this up. I have not had any symptoms to indicate any herxheimer reaction in my lungs, but everywhere else that I have had active inflammation or infection, I am having herxheimer reactions. A-You will probably get Lung Herx when you get to phase 3. The bugs there are aerobic (they like oxygen) and more difficult to kill. I am not sure you want the calcified granuloma to clear up, as that may indicate that calcium is being absorbed into your bloodstream, which is not good for the bones  But the lungs will function well despite the fibrotic scar tissue and any small calcifications...Trevor.. ============================== "In sarc patients we find that those who have been aggressively treated (mostly with prednisone, cyclosporin, etc) do take longer to heal than those who have just tried to live with their symptoms." ..Trevor.. ================================== What degree of healing is possible with the MP? ================================================== Evaluating progress with chest xrays The ACCESS study showed that X-rays are not a good measure of disease, and Meg and I heard this verified as the current thinking when we attended the Cleveland Clinic's professional conference on Sarcoidosis last summer. Remember that symptoms get worse before they get better. X-rays picture lung inflammation and enlarged lymph nodes, which are symptoms. Since you had significant lung involvement, after about six months on the MP, it seems reasonable to me that your x-rays may seem a little worse or the same, rather than significantly improved.. because of the Herxheimer reaction. The impression from the radiology report is that you have only slightly more inflammation in your lungs, possible more adenopathy on the right side and stable adenopathy on the left side. All in all, it sounds pretty good. If your doctor is concerned, it may be that he still needs to get used to the concept of Herxheimer, which is very different from the effect of Prednisone, which may rapidly clear pulmonary imaging - yet allow and lead to disease progression. One possible explanation for the difference between the right and left sides is that there was originally more involvement on the right side, but I am only speculating. I know that there was a difference like this in my own case. My suggestion would be that you review your recent posts which discussed your improvement in symptoms, and rely on your assessment of symptoms to evaluate your progress. I believe that a frank evaluation of your progress along these lines will reassure both you and your physician. This is the point where your physician will really need to listen to your assessment of your symptoms because an improvement in lung imaging will probably not manifest for another 6-12 months. Belinda Fenter ===================================== Chest CT is a computed tomography scan of the chest and upper abdomen. It can be useful for diagnosing sarcoidosis. This scan relies on x-ray radiation in higher doses than a standard x-ray but allows better pictures of the lung. The patient lies very still on a gurney in the machine while a tube rotates around the chest to produce images. A contrast material may be used to provide superior image quality of some features, it is administered intravenously. The contrast material usually contains iodine. This may be pose a risk to patients who have renal insufficiency. Usual precautions are to drink plenty of water before and after a CT. Report of improved CT scan You are likely to see the most change in the gas transfer coefficient, the DLco, which most doctors don't measure because it can't be done with the simple office spirometer. |
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[filelink] Diagnosis You only need ONE positive biopsy to obtain a definitive diagnosis of sarcoidosis. If you have already had a biopsy, you do NOT need another. If your doctor is recommending a biopsy, please inform him/her that patients are recovering on the MP without the need of this invasive procedure that can have long-term consequences to the status of your lungs and your body will have to heal the damage caused by the biopsy. Please see: Explanation of biopsy You could go have a bronchoscopy with transbronchial biopsy done and the pathology might show granulomatous inflammation or even inflammation. The closest you will get to "seeing sarcoidosis" would be a pathology report saying the findings are consistent with sarcoidosis. There are risks in understaking this procedure, including possibility of a punctured lung or uncontrolled bleeding. It isn't necessary to undergo a Bronchoscopy with transbronchial biopsy or an invasive and risky open-lung biopsy for a proven diagnosis of sarcoidosis or expensive tests to locate inflamed tissues in order to prescribe the MP. A thoracotomy is major surgery that can take months to recover from and can leave you with permanent neurological pain. Dr Marshall wrote on having a biopsy for diagnosis?: "I am sorry to say the skeptics will never take you seriously. You see, pulmonologist folklore says that Sarcoidosis goes away on its own. So it is clear that you are one of the lucky 60% whose sarcoidosis has gone away without needing any treatment. That is why the Foundation has put so much effort into exposing these lies and myths, and trying to get the pulmos to cite the studies which show these statements are true. But they have not proven to be reasonable people, I am afraid. I think they are going to have to be dragged kicking and screaming into the 21st century. Don't put yourself out to prove anything. It really will not matter. We are not dealing with scientists, today's 'experts' are not interested in 'proof' or 'facts.'" Lung biopsies are risky See Allan Abrahams went into Wellington Hospital for what he thought would be a straightforward biopsy. Which details an adverse event: In 2003, Mr Abrahams was suffering from an unknown illness, later confirmed as sarcoidosis, which produces clumps of inflammatory cells in many organs. He was admitted to Wellington Hospital so surgeons could take a tissue sample. "I was supposed to be back at work in two days' time." But he began bleeding excessively during a mediastinotomy - a procedure in which a viewing tube is inserted into the chest. The surgeon could not see where the bleeding was coming from and the cut had to be extended. Alcohol iodine was applied to the wound and, when an electronic diathermy device was used, the iodine ignited. The fire was extinguished, but Mr Abrahams continued bleeding. The surgeon turned him on his side, opened his chest and managed to stop the bleeding and obtain the biopsy. Mr Abrahams was later told he had lost two litres of blood, and he ended up spending a week in hospital. ....when he woke up, his surgeon told him there had been "big flames" in the operating theatre. He had a burn mark on his chest, a result of his skin catching fire during surgery. -We were warned about having a lung biopsy done but we didn't really understand the MP stuff very well initially so went ahead and had it done. To this day, when my wife has herxheimer reaction, she sometimes feels the pain where she had the biopsy done because they pierced the lung back then. ~Ricco See Which diagnostic tests do I need? Granuloma are clumps of white cells-a sarcoid granuloma is less than 0.1mm (about 4 thousands of an inch) in diameter. They survive without a tissue-structure to support them, as the inflammatory Th1 reaction has progressed to the point where the phagocytes can exist in clumps on their own. Any disease where an extremely active bacterial infection is present can form granuloma. This includes Tuberculosis, and a number of the other common infections. But in your case (sarcoidosis) the granuloma were chronic (long lived) and their bacterial pathogenesis is more important than the label a Doctor might attach. Note that Lymphocytes are expelled to the periphery of granuloma - they play little or no part in the Th1 immune reaction. This observation was the fundamental step in comprehension which led me to an understanding of these Th1 diseases. ..Trevor.. Non-caseating granulomas There is some confusion about the use of the term "caseating." Caseation is what happens when necrosis changes what was once normal tissue so it looks "cheese-like" in appearance to the naked eye. (Think of Swiss cheese.) Basically, caseation is what you get when there is necrosis. A physician, Yale Rosen, M.D., who devoted his life to studying granuloma and granulomatous diseases explains, "The use of the terms "caseating" and "non-caseating" to describe the microscopic appearance of granulomas, although prevalent, is inappropriate since the term "caseous" applies only to the grossly visible cheese-like appearance that may be associated with necrotizing granulomas, necrotic neoplasms and other types of necrotic lesions. There is no typical microscopic appearance that corresponds to the gross appearance of caseation." You might be interested in knowing that necrosis can occur in sarcoidosis, although it is small and involves few of the granuloma. To sum it up, non-necrotizing (not dead/dying) is the best term to describe sarcoidosis granulomas viewed under the microscope and non-caseating (not cheese-like) is the best term to describe sarcoid tissue viewed with the naked eye. Sarcoidosis, or any Th1 disease with elevated 1,25-dihydroxyvitamin D (the D-hormone), can result in calcium being pulled from bones and deposited in soft tissues, resulting in calcification. The lymph nodes are and lungs are areas where calcification may be noted as a result of disease. ~Belinda Physicians like to have a tissue biopsy of usually non-necrotizing granulomatous inflammation to assist in diagnosing sarcoidosis, because the only way to diagnose the disease is by excluding other diseases that might possibly explain the symptoms. There is no one specific test that can be used to diagnose sarcoidosis. Blood tests are useful in diagnosing sarcoidosis; the two vitamin D metabolites, are some of the latest tests used. If symptoms involve tissues that are not easily biopsied (heart, liver, eye, joints for example), a presumptive diagnosis may be declared based on medical history and clinical signs such as symptoms and labwork. All biopsies are invasive and uncomfortable to some extent, even a simple skin biopsy. It isn't necessary to have a biopsy when you are already on the only treatment plan that will cure sarcoidosis, MP. Your D-metabolites results are definitive for extensive systemic inflammation. Pulmonologists are trained to verify sarcoidosis inflammation with a biopsy in order to justify using the standard medications which are often so toxic and have never cured anyone. Belinda Fenter had this to say about diagnosing sarcoidosis: "Naming a disease is sort of like "matching colors." Doctors try to get as close as they can to describe what they see, but (just like with colors) there can be disagreement about what the name is. Sometimes two names can describe the same or similar colors (or diseases). It's easy to differentiate shades from opposite sides of the color wheel. Only the color-blind would get confused there. On the other hand, people argue over similar color-names all the time. What my mother calls teal I call blue-green, and what I call a purple, my daughter insists is a shade of blue. You need to understand that any diagnosis that ends in "-itis" is indicating inflammation. The part of the diagnosis before "-itis" indicates where the inflammation is located. For example, "spondylitis is inflammation of the spondyles, which are joints in the backbone. Sarcoidosis is a disease that can result in inflammation in any part of the body. If you read my earlier answer... you will probably recognize that the symptoms associated with akylosing spondylitis are also symptoms of sarcoidosis, and there is "no known cause" of ankylosing spondylitis. It won't hurt to try the MP to see if it improves these symptoms that are very similar to sarcoidosis. It's a good idea to talk to your doctor about the similarity of these symptoms." Cardiac Sarcoidosis cardiac inflammation is very difficult to diagnose. It is only picked up by echo or MRI in its advanced stages. A biopsy of the heart is dangerous, often imprecise and unnecessary. Th1 inflammation in the heart is subclinical long before the damage it causes is detected by tests. A diagnosis of sarcoidosis heart involvement is usually based on symptoms which can include most heart symptoms, including but not limited to... chest pain, tachycardia, bradycardia, mitral valve prolapse, atrial fibrillation and premature beats. PET (Postitive Emission Tomography) Scan "In a PET (Positive Emission Tomography) scan, a radioactive marker is combined with a metabolite, usually glucose, and the degree of release of positron energy is supposed to be an indicator of the usage of glucose in that area. I wish more folks would be given PET scans rather than CT or MRI. PET is the best available imaging technology, and it images the metabolic activity within the body rather than just the shape of water-rich structures (organs and tissue), as MRI and CT scanning do. But the PET scanner is expensive, and many physicians don't like to believe what it tells them; that sarcoidosis is systemic. In about 1994 I visited Hamamatsu Photonics, in Japan, where they had been using some high-power computer modules I had designed. Their prototype PET scanner had its own building, including a cyclotron for making the radioactive 'sugar'. That was produced (by the cyclotron) in a room right adjacent to the scanner (and the patient). The computing power to image the weak particles emitted by the sugar as it was being metabolized inside the patient was really quite incredible, for the early 90's. PET is amazing technology. And it works. All imaging is imprecise and only a crude approximation of the inflammatory process. I think of it as a crutch for folks who are not able to visualize the progress of this disease by bloodwork alone - the same folks who failed to find either the pathogenesis or the cure." ..Trevor.. This article explains a bit more about PET scans and how they work. It states that this diagnostic tool is not specific for differentiating sarcoidosis or tuberculosis from cancerous tumors. In a PET scan, FDG may accumulate in non-neoplastic tissue such as new granulation tissue, areas of inflammation, and early post-op scarring. Gallium Scan "I have never really paid much attention to gallium scans. Most sarcoidosis patients have weakened kidneys, and I question the ethics of performing any test, such as a gallium scan, which is likely to hurt those weakened kidneys even more. Even though the coming of Ga67 scintillography has reduced the risk, there are safer alternatives available. For example, a PET scan. It gives better contrast (for systemic sarcoidosis) and is far less likely to make the patients sicker. Soluble Interleukin 2 Receptor (sIL2R) and 1,25-dihydroxyvitamin-D bloodwork tests are much cheaper, non-invasive, tests for Th1 inflammation, without causing any danger to the patient." Dr. Trevor Marshall Chronic fatigue "Nearly all sarcoidosis patients suffer from chronic fatigue, even if it is not clinically diagnosable as CFS. In Sarcoidosis the Th1 inflammation has gotten so energetic that the immune cells no longer need to gather in the inflamed tissue, they can actually form colonies (sometimes polyps) comprised solely of monocytes, macrophages and polymorphonuclear cells (collectively, phagocytes). They no longer need any tissue structure, but are self-sustaining colonies of phagocytes. These are called 'granuloma'. But the cause of all the Th1 diseases is Th1 inflammation, due to the intracellular bacterial pathogens. So it really doesn't matter what you want to call yourself. A doctor would say that if you have biopsy-proven granuloma then you probably have Tuberculosis. If you don't have TB, then maybe Sarcoidosis. It is more complex than that, but I am sure you get the picture. All I care about is how to get better. And it seems that for all the Th1 diseases the same approach works, regardless of the label we might place on the disease." ..Trevor.. Multiple diagnoses "If you get to know the disease sarcoidosis, arguably the most virulent of the inflammatory diseases because the phagocytes no longer need to gather in tissues, but can form colonies called 'granuloma', you will find folks who have been diagnosed with MS, Lupus, Crohn's, RA and a host of other ailments as they progressed to the sarcoid granuloma. All these diseases have a bacterial pathogenesis, with the species of bacteria and the genetic predispositions varying during the course of the diseases, and between individuals." ..Trevor.. Kveim test Anybody who knowlingly injects the ground-up spleens of dead sarcoidosis patients into a living human being, knowing full well that sarcoidosis has been proven to be communicated by transplanted lungs and other organs, needs to be hung, drawn and quartered. I have no sympathy whatsoever for the idiots who are promoting, and enriching their institution, using the Kveim test. They know that their own studies have shown the test is not 100% definitive, and also that Kveim is a very high risk procedure. Words fail me... ..Trevor.. See also What is the best way to assess lung function? Last edited on Fri Apr 11th, 2008 09:33 by Foundation Staff |
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SARCOIDOSISlink STAGING SYSTEM Dr. Marc Judson had this to say about staging sarcoidosis: "It is important to make several points about the staging system. First, is only a chest X-ray staging system. It tells you nothing about involvement of sarcoidosis outside of the lungs. Second, it is in general, a poor staging system. Most sarcoidosis experts do not use it because it's so poor. It has a few major problems. The first is that it's inaccurate. When you do much better views of the lungs by chest CT scans, you find out that the actual stage is different than what appears on chest X-ray. The next problem with the staging system is that it does not predicit the need for therapy, the level of disability, or the prognosis IN AN INDIVIDAL PATIENT with any good degree of accuracy. That is, if you had 100 patients with stage 1 disease and 100 with stage 2, the stage 1 would have better pulmonary function, less pulmonary symptoms, and a better prognosis. BUT many in the stage 2 group would have better pulmonary function, less pulmonary symptoms, and a better prognosis than in the stage 1 group...you can't tell what will happen to one specific patient. Probably the most useful part about the staging system is that patients with stage 4 generally have poor pulmonary function and have the worst prognosis. But I don't put too much weight on this staging system...it is antiquated and doesn't help me much at all." 14 August 2003 and on 3 September 2003 "you will learn that the ACE level and the stage of sarcoidosis give little information concerning who should be treated and the prognosis of the patient. They are both antiquated systems...especailly the X-ray staging system." and on 30 Oct 2003 "Please realize that I personally think that this whole stage system is antequated and offers very little today (please scroll down and see previous threads about the staging system). It was developed prior to 1960 when there were no CT scans and we knew much much less about sarcoidosis." |
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SARCOIDOSISlink ACE TEST Serum Angiotensin Converting Enzyme or S.A.C.E. ...... While serum ACE level is elevated in some sarcoidosis patients, not all sarcoidosis patients have elevated ACE levels. As a result, serum ACE is not a reliable diagnostic tool or measure of disease activity. The ACE level is less likely to be elevated in those with chronic sarcoidosis, for example. You can read a simple explanation of the ACE test and what it may indicate on Medline. The serum ACE test is a non-specific test used in helping diagnose sarcoidosis. The major problem is that it is unreliable -- in the sense that some people who are very ill with sarcoidosis do not *always* produce a high number on the ACE test. So the ACE test is not clinically reliable, either as a diagnostic tool, or to monitor how well a patient is doing. There are also genetic differences among individuals that affect the normal range of ACE, which confounds the problem. An elevated ACE test result *is* significant. If someone has an elevated ACE test, they should press on to understand why. The results of any blood test have to be considered in their clinical context. A high level of ACE is not meaningless. Angiotensive converting enzyme is only an enzyme, not the actual end-product that causes the body harm. The harmful end-product that causes damage is Angiotensin II, with ACE catalyzing the conversion of Angiotensin I to Angiotensin II. So a high level of ACE in the blood is an indication that there is a high conversion of Ang I to Ang II taking place. Many patients with serious Th1 inflammation have a normal ACE. ACE is an intermediate biochemical. It is a precursor to Angiotensin. It has no direct action in the inflammatory cycle other than to cause the release of quantities of Angiotensin II. That is probably why it is relatively insignificant in some patients; it depends on your Renin Angiotensin System activity level. See this article for a list of diseases with a high ACE level. ...... Why ACE sometimes elevates on the MP "The more your ACE is initially elevated, the more ACE is being generated in your inflammation, and the higher the ACE will go when the Angiotensin II receptors are blocked. We have had one report of ACE greater than 400. The serum ACE usually rises to quite high levels when you have an Angiotensin Receptor Blockade in place (eg with Benicar). This is because the inflamed tissue can't get any Angiotensin II binding at its receptors, so it puts out extra ACE to try and convert more Renin/A-1 into Angiotensin II (the Angiotensin-II level rises too). But even though all that Angiotensin II is manufactured, there are no receptors left for it to bind to, so it can do no harm. Note that ACE is not the same as Angiotensin II. They are different chemicals and have vastly different functions. Our paper "New Treatments Emerge..." describes the biochemistry as "the Angiotensin Hypothesis". Although put as a 'hypothesis' in that (old) paper, a Spanish group recently validated my etiology in-vitro and in rats." ...Trevor... =============== See also: Why has my ACE gone up since I started the MP? What do my lab tests mean? =================================== Q-Why do some patients with Th1 disease would have normal blood work for all tests other than 1,25D? My SED rate and CPK are normal. A-In sarcoid patients, the pathogens are so well secreted in the granuloma that the immune system does not touch them. There are no antibodies formed, and, since the pathogens delay apoptosis, the SED rate is almost always very low. When the MP antibiotics start killing the pathogens, then the SED rate shoots up, usually above the upper end of normal. I would expect the CRP to behave in the same way, as it is part of the body's reaction to infection, and so CRP would not be generated until the body can recognize that it is dealing with infective pathogens. This often doesn't happen until you start killing the pathogens, and the DNA fragments start to enter the bloodstream. ..Trevor.. |
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SARCOIDOSISlink Infectious etiology of sarcoidosis "The only thing that can cause the granuloma of Sarcoidosis is the intraphagocytic Microbiota of antibiotic-resistant bacterial pathogens." Dr. Trevor Marshall, Ph.D. There is a wealth of proof linking mycoplasma bacteria to sarcoidosis. There are many studies that have convinced me of the validity of the bacterial etiology. Here are just a few. I hope that you will share them with your doctor. The Center for Disease Control has published, in Emerging Infectious Diseases, a 2002 report from Vanderbilt University School of Medicineand Veterans Affairs Medical Center. It is titled Molecular Analysis of Sarcoidosis Tissues for Mycobacterium Species DNA. Their study "provide(s) evidence that one of a variety of Mycobacterium species, especially organisms M. tuberculosis, is found in most patients with sarcoidosis". http://www.cdc.gov/ncidod/EID/vol8no11/02-0318.htm R.M Du Bois, et al, of the Royal Brompton Hospital and Imperial College in London have written a Review titled Is There A Role For Microorganisms he Pathogenisis of Sarcoidosis? which was published in 2003 in the Journal of Internal Medicine. They concluded "that microbes are a likely trigger (but not as an infection) in a genetically predisposed individual and that this initial event culminates in the sarcoidosis granulomatous response. http://tinyurl.com/bdjdp In 2001, Dubois,et al, published an article, Sarcoidosis: genes and microbsoil or seed?, in the WASOG journal Sarcoidosis, that concludes "that one or more microbes behaving in a non-infectious fashion in a genetically predisposed individual trigger the sarcoidosis granulomatous response". http://tinyurl.com/8n7jo A landmark Swedish study from 2002, Presence of Rickettsia Helvetica in Granulomatous Tissue of Patients With Sarcoidosis, reports finding Rickettsia andious bacteria in 86% of tissue samples. They conclude "these results support the hypothesis that rickettsiae may contribute to a granulomatous process, as is seen in sarcoidosis." http://tinyurl.com/vahsu Lida Mattman's study Growth of Acid Fast L Forms From the Blood of Patients With Sarcoidosis, was published in Thorax and reports that various Cell Wall Deficient bacteria were found in 95% of sarcoid biopsy samples. http://tinyurl.com/akjs4 The 1999 German study by Grosser M, Luther T, Muller J, Schuppler M, Bickhardt J, Matthiessen W, Muller M., Detection of M. Tuberculosis DNA in Sarcoidosis: Correlation With T-cell Response, found Mycobacteria in 64% of tissue samples. http://tinyurl.com/ada4c D.R. Moller from Johns Hopkins University School of Medicine, concludes in his paper titled Treatment of Sarcoidosis- from a basic science point of view published in the Journal of Internal Medicine in 2003, "Given evidence for a genetic predisposition to sarcoidosis, these findings suggest that the etiology of systemic sarcidosis is linked to genetically determined enhanced Th1 immune responses to a limited number of microbial pathogens." In plain English Dr Moller says: 1. Sarcoidosis is caused by microbes and bacteria ("microbial pathogens") 2. The immune system response in sarcoidosis is a response to bacteria. It is a Th1 type reaction (which means is can be blocked with angiotensin receptor blocker medications) 4. It is accepted that there is a genetic predisposition to this immune reaction 5. Dr. Moller is limiting his observations to 'systemic' sarcoidosis http://tinyurl.com/d5g4b Live bacteria have been found, with significant frequency of occurrence, in sarcoid tissue. But they are of a variety called "Cell Wall Deficient" (CWD), or "L-Forms", or "Coccoid Forms". They have adapted with a resistance to the Penicillins, which attack bacterial cell walls. The bacteria that have been repeatedly and consistently found in sarcoid tissue do not have cell walls, they are much smaller, and very difficult to see in pathology unless special stains are used. can be cultured, but it usually takes several months for the culture to grow. They are consequently not usually identified during conventional lab testing. A description of which Pathology stains work best, and examples of CWD Coccoid forms (including photographs of cultures) are in the SarcInfo tutorial: "How a Pathologist can see Bacteria causing Sarcoidosis" http://www.sarcinfo.com/pathology.htm There is an excellent Canadian Radio show on which the World's leading scient were interviewed regarding Cell Wall Deficient mycoplasma. Although it is pretty long (two hours) you will find it an amazing eye-opener. The links to it are from URL http://sarcinfo.com/phorum/read.php?f=1&i=5320&t=5320 Bacteria in Sarcoidosis and a Rationale for Antibiotic Therapy in this Disease There is abundant evidence, some dating back to the 1930s and 1940s by various investigators (such as Gullberg, Hollstrom, Schaumann, and others) showing that bacteria, related to tuberculosis bacteria, are associated with sarcoidosis. This research has been largely ignored, prompting Moscovic to declare in 1982: "Had all the work and effort spent on proving a non-mycobacterial nature of the disease been channeled into pursuing these clues, the etiology of sarcoidosis may have long been clearly established and a more rational approach to diagnosis and treatment could by now have been developed. I would like to know why this early research has been ignored and why the latest studies documenting bacteria in sarcoidosis tissues are being denigrated. Scientists could spend another 100 years (while patients are dying) trying to identify each of the cell wall deficient bacteria that trigger the abnormal sarcoidosis immune system reaction in predisposed individuals. Luckily, it isn't necessary to know the identity of these offending organisms in order to eliminate them. Sarcoidosis provides a unique clue to the presence of mycoplasma in the cells of the immune system when a Jarisch-Herxheimer reaction is elicited with antibiotics. "Jarisch-Herxheimer is in fact the maximum of evidence possible in search of occult microbes." Dr. Friedrich Flachsbart, MD. Initiating treatment with antibiotics to provide a therapeutic probe (a time-honored medical technique) can verify the presence of these bacteria without expensive testing and validate the necessity of antibiotic treatment. I believe it's time to stop arguing about the cause of sarcoidosis and pursue this promising avenue of antibiotic therapy. It may not satisfy all of the scientific criteria but sarcoidosis patients don't care about that, they just want to get better. Alan Cantweill, M.D. Donor-Acquired Sarcoidosis Indicates Infectious Origin Sarcoidosis has developed in non-sarcoidosis transplant recipients who have recieved tissues or organs from donors who were not suspected or known to have active sarcoidosis. This article said, "We draw upon these cases to discuss etiologic considerations for sarcoidosis, and suggest that donor-acquired sarcoidosis strengthens the view that sarcoidosis is caused by a transmissible agent, perhaps of infectious origin. Since not all recipients of organs from donors with active sarcoidosis develop sarcoidosis, host factors also appear to be important in disease pathogenesis. Less credence is ultimately given to external or environmental factors" [as a cause of sarcoidosis]. Here are some of the reported cases: Transmission of sarcoidosis via cardiac transplantation. Possible transmission of sarcoidosis via allogeneic bone marrow transplantation. Antibacterial Therapy Induces Remission in Sarcoidosis Authors: Trevor G Marshall, PhD1, Belinda J. Fenter1, and Frances E Marshall, GradDipPharm, RPh2 See also: Cell Wall Deficient Bacteria and the Marshall Protocol Papers and Presentations for Physicians Studies Citing Bacterial Cause for Sarcoidosis All these diseases have a bacterial pathogenesis, with the species of bacteria and the genetic predispositions varying during the course of the diseases, and between individuals. "If you get to know the disease sarcoidosis, arguably the most virulent of the inflammatory diseases because the phagocytes no longer need to gather in tissues, but can form colonies called 'granuloma', you will find folks who have been diagnosed with MS, Lupus, Crohn's, RA and a host of other ailments as they progressed to the sarcoid granuloma. ..Trevor.. Experimental Skin Sarcoidosis In A Doctor Volunteer proves pathogenic cause of sarcoidosis. Bacteria in spinal fluid "The presence of detectable bacteria in the spinal fluid is common. Indeed, Emil Wirostko (whose group took those ownderful photos of the bacteria) was convinced that stem cells become infected at an early stage of Th1 disease, and that is why is spreads so evenly throughout the body." ..Trevor.. There are many species of CWD bacteria Many types of bacteria work together to cause sarcoidosis. Not all of them are necessarily present in any one patient. Here are some papers he can get species info from: http://www.cdc.gov/ncidod/EID/vol8no11/02-0318.htm http://tinyurl.com/anovw http://tinyurl.com/br7zp http://tinyurl.com/dybhe ..Trevor.. Mycobacteria isolated from a majority of sarcoidosis patients "Mycobacterium" is a species of bacteria which are very similar in many ways. Mycobacterium tuberculosis causes - you guessed it - TB. Mycobacterium leprae causes Leprosy. This species are very nasty little bugs indeed. Neverthless, very little is known about the members of the species other than M. tuberculosis. Yet they seem to be pretty ubiquitous, being isolated from a majority of sarcoidosis patients "Molecular analysis of sarcoidosis tissues for mycobacterium species DNA" http://tinyurl.com/4c8fh BCG vaccination against TB To state the significance of M. bovis...it is well documented to cause sarcoidosis when injected as the BCG vaccination against Tuberculosis. There are lots of studies from the 60's and 70's documenting this. Do a PubMed search. That is one of the reasons why BCG has fallen out of favor in the USA. Heavy metals do not cause Th1 inflammation "While there is no doubt that heavy metals cause the body's biochemistry to malfunction, and that metals are attracted to the active sites of inflammation, there is no reason to believe that the heavy metals actually cause the inflammation, even though they may help fuel it. An excellent example of this is Berylliosis, which, until recently, was thought to be an environmental disease. Now it is recognized as a Th1 disease. Early investigators found the beryllium in the inflamed tissue, and thought that beryllium caused the inflammation, but now those ideas are having to be entirely re-thought as we understand more and more of the human genome." ..Trevor.. |
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SARCOIDOSISlink Cutaneous anergy Cutaneous anergy In 1916, Boeck first described cutaneous anergy to tuberculin in patients with sarcoidosis. It was later on realized that this phenomenon was not limited to tuberculin alone, but that anergy to a variety of other skin tests-antigens such was also typical. In 1994, Kataria and Holter proposed a mechanism for the cutaneous anergy seen in sarcoidosis. At sites of granulomatous inflammation, there is a predominance of helper T lymphocytes, which proliferate and secrete large amounts of lymphokines, including interleukin (IL)-2, monocyte chemotactic factor (MCF) and migration inhibition factor (MIF). These lymphokines induce and amplify the immune response by enhancing T-lymphocyte proliferation as well as recruiting and retaining monocytes from the circulation. The lymphokines and monokines produced at sites of granulomatous inflammation have their highest concentration locally. Nevertheless, the protein molecules diffuse into blood, establishing a concentration gradient between the granulomatous inflammatory site and the remote site of the delayed type hypersensitivity (DTH) skin test. As a result, the traffic of T-helper lymphocytes and monocytes is preferentially directed towards site of granuloma formation. That leads to a preponderance of suppressor cells in the peripheral blood and competitively depletes the T-helper cells and monocytes available to sites of DTH. TB tests |
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SARCOIDOSISlink BLOODWORK Low white blood cell count "Th1 diseases are lymphopenic, which means a lack of T-cells. This is because the T-cells play only a minor role in Th1 disease. The bacteria inside the phagocytes directly activate the phagocytes, there is no need for any T-cell recognition of pathogens, and so the body down-regulates the number of T-cells it manufactures (hence the lymphopenia). The bacteria living inside your phagocytes cause the phagocytes to emit the Th1 cytokines without the need for Lymphocytes, Neutrophils, or indeed any other cells of the immune system, to be present. Some of the secreted cytokines cause down-regulation of Lymphocytes. In Sarcoidosis this causes the Lymphocytes to leave the area of highest inflammatory action (in the center of a granuloma) and migrate to the periphery. The down-regulation also reduces the number of Lymphocytes being generated from stem cells. In less intense Th1 inflammation, that does not form granuloma, the down-regulation of the T-cells is observable primarily by the down-regulation of the Lymphocytes. These Th1 diseases are therefore fundamentally Lymphopenic diseases. That is what your bloodwork shows. You can all expect your WBC count and the balance of monocyctes, lymphocytes, NK cells, and etc, to change a lot as the Th1 bacteria are killed. It is best not to get fixated on any expectation of "bad figures" and "good figures". If Doc gets too concerned about the numbers then, IMO, you should back off your antibiotic dose and take the therapy a bit slower." ..trevor.. Anemia The granuloma sequester Ferritin and iron, and the low assay is closely tied to the presence of inflammatory granuloma. Mild 'anemia' is expected in the Th1 diseases, as inflammatory macrophages accrete ferritin. Supplementation usually doesn't correct the 'anemia' and it feeds the inflammation. This article indicates that one of the potential *benefits* of the anemia of chronic disease is that bacteria are being starved of the iron essential for their proliferation. http://tinyurl.com/c95vv Bacterial pathogens, however, sequester iron from the host so it is available for their own use and reproduction. If we use iron supplements, we will provide iron not only for us (the host) but also for our parasitic pathogens -- who will in turn hoard the iron from us. http://tinyurl.com/4o847 The fatigue from chronic disease is a common symptom that will resolve if you stick with the protocol. It will gradually get better, but it may be one of your longer-lasting symptoms. The best thing is to persevere and treat the root cause of disease because once the bacteria are killed off, your iron will be available for your own body once again. Hemoglobin and serum ferritin are the most common ways to test for anemia. A new test called serum transferrin receptor is a good way to determine iron deficiency anemia because this test is not affected by inflammation. Triglycerides Elevated Triglycerides indicates (most probably) liver inflammation which will resolve during the MP. CRP "CR protein (CRP) is generated by the body to help it fight bacterial infection. This was in one of the papers presented at the recent Budapest conference. So it being high in Th1 disease and atherosclerosis is really no surprise Take a look at this abstract - it will change your view of CRP:" http://tinyurl.com/64cm5 In sarcoidosis patients, the CRP is part of the body's reaction to infection, but it would not be generated until the body can recognize that it is dealing with infective pathogens. This often doesn't happen until you start killing the pathogens with the MP, and the DNA fragments start to enter the bloodstream. ..trevor.. Many persons with Th1 inflammation have normal or low C-Reactive Protein. Our bodies respond to inflammation in a variety of ways depending on many factors. BUN "It is reasonable for BUN to be elevated, as the bacterial endotoxins cause Nitric Oxide (NO) to be generated in the inflamed tissues. It will almost certainly go higher once the antibiotics start to kill off the bacteria. Please ask Doc to call me if he is unduly worried about your kidney metabolites. ARBs are renoprotective, but the Th1 bacteria have to be killed off before Doc will see creatinine or BUN improve, I am afraid." ...Trevor... Creatinine and Potassium "These kidney function tests may increase to show inflammation which is to be expected with long-standing disease and the Herxheimer reaction. This article, Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what to do if the serum creatinine and/or serum potassium concentration rises, explains that long-term benefits have to be the focus when using ARBs. Alkaline phosphatase This article says, "In the serum of many patients with sarcoidosis, alkaline phosphatase activity is increased due to sarcoid liver involvement." There can be several reasons for an elevated alkaline phosphatase level. The basic Alkaline Phosphatase (ALP) test is explained here: http://www.nlm.nih.gov/medlineplus/ency/article/003470.htm When that basic ALP test is elevated, there is another test a doctor can order to measure the different forms of alkaline phosphatase present, to help analyze the problem. As Medline explains http://www.nlm.nih.gov/medlineplus/ency/article/003497.htm "Alkaline phosphatase is an enzyme in the blood, intestines, liver, and bone cells. Its chemical structure varies (called isoenzymes) depending on where it is produced. This makes it possible to determine where a problem has originated. When bones are growing, liver cells are damaged, or a biliary obstruction occurs, alkaline phosphatase levels rise considerably... The isoenzymes can reveal whether the increase is in "bone" ALP or "liver" ALP." ============================== See also: What do my lab tests mean? |
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SARCOIDOSISlink CALCIUM LEVELS "In 94% of sarc patients (approx) there is absolutely no connection between the 1,25-dihydroxyvitamin-D level and the serum calcium level. But Calcium is a pretty easy thing for Doctors to measure. So, in the other 6% of patients they see hypercalcemia (high serum calcium). They then are told to look at the 1,25-D and find it is often high. So they go away and assume that 1,25-D is solely assicated with calcium -WRONG - THEY ARE TOTALLY ABSOLUTELY WRONG It is this misconception that has kept the true cause of sarcoidosis hidden for so long. In 1949 The Royal College of Physicians was told that Sarc patients are hypersensitive to Vit D, and that the ones with the highest Vit D levels are the ones least likely to remit. Yet here we are, 54 years later, and Doctors still do not realize that 1,25-dihydroxyvitamin-D3 is one of the most important hormones in the body, and it drives the thyroid hormones, and a host of other body control systems. Many doctors, even so-called sarcoidosis experts, who may not have not cracked a textbook since medical school think that sarcoidosis causes people to absorb too much calcium in the gastrointestinal tract, and that can lead to too much calcium. They have a simplistic, inaccurate explanation of sarcoid's deranged calcium metabolism. They totally overlook/exclude the abnormal synthesis of 1,25-dihydroxyvitamin D by the activated macrophages that occurs in sarcoidosis and its effect on our bones. It's amazing that most doctors actually think that the complete story of sarcoid's abnormal calcium homeostasis is that it simply causes increased gut absorption of calcium, and that's all! Doctors without a proper understanding of Vitamin D biochemistry might think that sarcoid patients who try to discuss deranged vitamin D metabolism in sarcoidosis are a little strange, and erroneously believe it is impossible to have elevated vitamin D levels. If doctors were taught an old-fashioned understanding of calcium metabolism - that didn't include vitamin D metabolism or the role of 1,25-dihydroxyvitamin D in calcium metabolism - and they've never done further study of it, then we might as well be speaking Greek! This is simply a lack of education, and it indicates more realistically the amount of work to be done with doctors before there is widespread understanding of sarcoidosis. The (once) unknown is 1,25-dihydroxyvitamin D, and as this article explains, "The hormonal metabolite 1,25-dihydroxyvitamin D3 stimulates intestinal calcium absorption and "resorption of calcium and phosphates from bone..." There is so much more to 1,25-dihydroxyvitamin than digestive absorption of dietary calcium. Yet, that limited view is what led to vitamin D being added to all our milk in the USA. I can see now that it is a widely-held misconception. We have no choice but to be educators as well as patients." ..... "Blood may be drawn to test the level of 1,25 Dihydroxyvitamin D3 in your body at any doctor's office in the USA. This is the only test that can tell you if you are having this problem, although you need to have your 25 Hydroxyvitamin D measured at the same time, for comparison. It used to be thought that hypercalcaemia was the only result of excess Vitamin D, we now know it is far more complex than that. Many otherwise normocalcemic sarc patients have been suffering from kidney stones and calcium deposition into the soft tissue as a result of excess levels of this hormone in their tissue. We can only measure its level in the blood, which is still an approximation, but the best we can get." OSTEROPOROSIS .... "Excess amounts of 1,25 Dihydroxyvitamin D3 can result in bone resorption. This means that your bones and teeth can be absorbed into your blood stream and then be deposited into soft tissue, such as the lungs (and kidneys). Sarc patients should avoid all Vitamin D supplementation unless you have been tested to have normal values of the hormone. Here is an explanation for you to discuss with your doctors explaining why sarc patient's metabolism is different. As if the osteporotic side-effect of prednisone wasn't enough, we now learn that sarc patients may also have to contend with bone wastage due to the inflammatory biochemistry itself." ...Trevor... BMJ and Lancet recently published studies showing that Vit D and Calcium supplements do not strengthen bones: http://www.medicalnewstoday.com/medicalnews.php?newsid=23534 why sarcoidosis patients get hypercalcemia: There have been plenty of published reports such as this one. Elevated hormone D can cause symptoms even without hypercalcemia. Hyperhydration does lower the level of circulating calcium so thirst is a protective reaction. I would think that discussing Benicar and how ARBs are reno-protective (often used in CKD for this reason) would provide an opening so someone might be willing to write the prescriptions for you. See Uses of Benicar. ~ Belinda |
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SARCOIDOSISlink SUNLIGHT Sarcoidosis is a chronic progressive disease that is rarely diagnosed in its early stages. Someone who is exposed to excessive sunlight (such as on a vacation or moving to a sunnier climate) may have a symptom exacerbation that leads to a doctor visit and a diagnosis. This doesn't mean that the sunlight caused the saroidosis. It just made it more apparent. 4-30-02 "One of the topics that has often been too much of a "hot potato" to talk about is the extreme sensitivity of many sarc patients to sunlight, and the Vitamin D it produces in our skin. I am not talking about UVA or UVB or sunscreen or sunburn, I am talking about hormones being produced that play havoc with your body and mind. This is not a newly discovered phenomenon, it was detailed in 1950 by Scadding and in 1954 by Anderson. In 1968 a paper by Winnacker, et al, reported that sarc patients can be 20 times as sensitive to sunlight and dietary Vitamin D as the 'normal' population, in fact, only 9000 IU of Vitamin D was a toxic dose to some sarcoid patients, whereas 'normal' people could take in in 150,000 IU without a problem. Scadding (in 1950) reported that some sarc patients were intolerant to any dosage of Vitamin D at all... "25 hydroxyvitamin D" is produced as Sunlight strikes the skin. It is also produced after consuming Vit D from an artificial food source. This is then converted to 1,25 dihydroxyvitamin D3, the active Vit D hormone in our bodies. Most importantly, we now know that 1,25 dihdroxyvitamin D3 is secreted by the inflammatory macrophages that make up granuloma[/url]. It is a cytokine, and it has an essential task in maintaining the number of monocytes, which make up the macrophages, by catalysing the hematopoetic Stem Cells to produce monocytes. In the past I personally have stated that I believe it is a major cause of sarc relapses, and I have been ridiculed and pilloried for holding that opinion. However, the evidence is becoming overwhelming. Researchers are now starting to document and explain the hormone's key role in the formation of granulomas, and as an element of the immune system. So you will read more and more about this hormone as the research results come in. Meanwhile, The Canadian Lung Association has now joined National Jewish in warning sarc patients to stay out of the sun: "If you have sarcoidosis, it is best to avoid too much direct sunlight. Vitamin D sensitivity may occur with sarcoidosis, and excessive exposure to sunlight can result in increased calcium in the blood which may in turn produce kidney damage" It is almost impossible for most sarc patients to realize that exposure to sunlight is making them ill. This is because the time taken to generate monocytes and for the 1,25 dihydroxyvitamin D3 to clear your body, is a matter of days, not hours. If you are exposed on Monday you will still be suffering on Wednesday. Very difficult to correlate cause and effect. I have observed that sarc patient's eyes have to be shielded from bright light by wearing dark shades. 1,25 Dihydroxyvitamin D3 interacts with the cornea in ways which are yet to be fully explained." ..Trevor.. |
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SARCOIDOSISlink STANDARD TREATMENTS Prednisone Prednisone is used as a first line treatment because it ruthlessly suppresses the body's immune system. It stops the body from fighting the bacteria, and consequently reduces the inflammation the body produces during that fight. Prednisone stops the actions of a protein dimer called NuclearFactor-kappaB. This protein is essential to the immune system, to the body's response to other challenges (including hyperglycemia) and is vital for balance of bone generation. In the short term (a few months) your chest x-ray may "clear up" and your liver enzymes may drop. But you cannot shut down the body's immune response for very long. The bacteria multiply in the tissues without any hindrance once the Prednisone has shut down the body's immune reaction. At some time the sheer amount of toxin they are generating will become uncontrollable, even if the dose of Prednisone is continually increased. If the patient stops taking the Prednisone then their condition will relapse, to a state much worse than when they started on the steroid. The body has a complex mechanism for keeping the pathogenic bacteria out of the immune system. Prednisone destroys this mechanism, and bacteria can quickly invade the immune system while a person is using prednisone. It is clinically proven that 78% of patients relapse after trying to ease up their prednisone dose: Outcome in sarcoidosis-the relationship of relapse to corticosteroid therapy. Patients who never took prednisone end up healthier in the long run. Now we know why. Dr. Marc Judson, in his hypothesis on using corticosteroids to treat sarcoidosis, An Approach to the Treatment of Pulmonary Sarcoidosis with Corticosteroids, said, "Relapses occur in 20 to 50% of patients in whom corticosteroid therapy is discontinued." He recently noted on the MUSC forum that "prednisone does not cure the underlying disease." Prednisone will lead you down a path of increasing oral steroids and decreasing quality of life. This report states " Then there is also the possibility that corticosteroids prolong the course of the disease by delaying resolution,": Outcome in Sarcoidosis: the Relationship of Relapse to Corticosteroid Therapy Your doctor will be hard pressed to show you studies documenting the effectiveness of steroids in sarcoidosis because there are none. Here are some references that illustrate the reality of Prednisone therapy. National Jewish Jewish Hospital states in this article "The decision to initiate steroid therapy is further complicated by the knowledge that the treatment does not guarantee protection from pulmonary fibrosis and permanent functional impairment." According to this article from CHEST: Prednisone Improves Symptoms but not Lung Function in Sarcoidosis. "Prednisone is used only because there is nothing else for sarcoidosis. It makes the patient feel better (for a while), but doesn't improve lung function." And a 2002 JAMA article entitled Corticosteroid Therapy in Pulmonary Sarcoidosis: "There are no data to suggest that corticosteroid therapy alters long-term disease progression" Side effects are the least of prednisones problems. Steroids are addictive and when used long-term (as little as a month), they can destroy your hip bones and cause diabetes, cataracts, glaucoma, opportunistic infections and osteoporosis. This Johns Hopkins website describes and illustrates the many side effects of prednisone. This study, [Corticosteroid]http://tinyurl.com/qyt3w]Corticosteroid treatment in sarcoidosis[/URL], states: "Remarkably, despite >50yrs of use, there is no proof of long-term (survival) benefit fromcorticosteroid treatment. In addition, there are still no data regarding theoptimal dose and duration of corticosteroid or other immunosuppressive therapy." There is growing evidence that use of corticosteroids is linked to relapse in sarcoidosis. -As one author put it "It is remarkable how cortisone can get a seemingly hopeless patient on his feet again. Sometimes it is so effective that he can walk all the way to the autopsy table." Outcome in Sarcoidosis - the relationship of relapse to corticosteroid therapy http://www.chestjournal.org/cgi/reprint/111/3/623.pdf "We suggest.. that corticosteroid treatment itself, rather than the need for treatment, contributed to relapse... Although the answer to whether corticosteroid therapy prolongs the course of disease remains uncertain, the results of the present study add to the growing body of evidence suggest that this potential risk be considered in treatment decisions." Corticosteroids for Pulmonary Sarcoidosis (Chochrane Review) http://www.update-software.com/abstracts/ab001114.htm "Oral steroids improved the chest X-ray and a global score of CXR, symptoms and spirometry over 6-24 months., but there is little evidence of an improvement in lung function. There are no data beyond two years to indicate whether oral steroids have any modifying effect on long-term disease progression." Trevor Marshall wrote: The biggest study of Sarcoidosis in history, the NIH 6-year ACCESS study, found that there was no discernible improvement in 2 year outcome whether prednisone was used or not. See our summary at URL http://autoimmunityresearch.org/access-2yr.htm There is no study which shows that steroids improve long term prognosis but there are studies to show that relapse is certain when the immunosuppression is withdrawn http://tinyurl.com/66ahp Note the sentence in that last paper "Corticosteroids contribute to the prolongation of the disease by delaying resolution" "Prednisolone is a Vitamin D Receptor (VDR) antagonist. Now we know how Predisone works. And how it downregulates NuclearFactor-kappaB (which is generated by VDR)." ..Trevor.. Steroids will destroy your wife's joints (as well as her soul). Look for example, at this thread from 2002, four years ago, at SarcInfo http://sarcinfo.com/phorum/topic-1-1515-1515.html We don't talk about this basic stuff so much any more, it is taken as well-known. But clearly your wife needs to ask a heck of a lot more questions of her Doc about this wonder-drug (at least to her) called "Prednisone." There is a very good reason the NIH/NHLBI is now discouraging its long term use on sarcoidosis patients - it makes them much sicker in the long run. You might also review some of the forums populated by patients who have taken the road which seems so appealing to your wife right now. Two which come to mind are at http://tinyurl.com/f7lho http://tinyurl.com/fm7w8 It isn't any fun being hooked on soul-destroying drugs for the rest of your life, not to mention being totally dependent upon the whims of the pulmonologist prescribing them. ..Trevor.. Why steroids cause weight gain The acronym "Glucocorticoid" is explained here http://cancerweb.ncl.ac.uk/cgi-bin/omd?glucocorticoid Examples include: prednisolone, methylprednisolone, hydrocortisone, betamethasone and dexamethasone. However, the function of the receptor called the GCR is not fully known, as mice who are bred without it do not survive gestation. Additionally, some Glucocorticoids are now known to have greater affinity for the MCR (MineralCorticoid Receptor) than they have for the GCR. Just as nomenclature got it all wrong with 'Vitamin' D, so the nuclear receptor names do not uniquely define their function. As you surmise, any drug that affects PPAR-alpha, and, to a lesser extent, PPAR-gamma, can be expected to affect a patient's weight. Steroid injections: Steroid injections into arthritic hips offer questionable benefit, and by inducing immunosuppression they may actually put patients who later undergo total hip replacement at risk of infection. A retrospective matched cohort study of infections after arthroplasty in patients who had received a steroid injection and those who hadn't (40 in each group) showed that there had been five revisions in the injected group (four due to deep infection), but none in the matched group ( Journal of Bone and Joint Surgery 2005;87B: 454-7). Steroids are also given by injection, topically, nasally and via eye drops. The use of all these products is strongly discouraged because they are absorbed systemically and will, to some degree, inhibit the immune system. They can also cause adverse side effects. Occasionally they must be used on a short-term basis to ameliorate intolerable symptoms or dangerous inflammation. Please consult with your doctor to devise a plan to substitute other medication for symptom relief or to discontinue the use of the steroid product as soon as the acute inflammation is under control. Evidence Growing that Inhaled Steroids, Like Pills, Can Cause Bone Loss ...... Possible side effects from oral cortiocosteroids (prednisone) include: - increased risk of infection - fluid retention and increase in weight - thinning/softening of bones (osteoporosis) - diabetes - indigestion or worsening of peptic ulcer - changes in mood - impaired healing - stretch marks - skin thinning - bruising - increased facial hair - avascular necrosis - muscle weakness - eye cataracts These side effect are dose- and duration-dependent. Some of the questions you may ask your doctors are: 1. Whether you are suffering any of the above treatment-induced diseases or damage as a result of taking high-dose steroids. 2. Whether they are familar with reports that corticosteroids do not halt the advancement of sarcoidosis. 3. Whether they realize that withdrawal from corticosteroids causes relapse of sarcoid symptoms that may be worse than the original symptoms ....... When Weaning Prednisone: You may not realize that ANY symptoms are due to sarcoidosis inflammation. As the prednisone is weaned, you will experience withdrawal symptoms and an increase in inflammatory symptoms which will be similar to past disease symptoms but may also include new symptoms. If you are having more trouble breathing, or problems sleeping or increased fatigue and weakness, these are all symptoms that the inflammation is increasing due to the decrease in prednisone. Try to keep them manageable by decreasing the prednisone very slowly. We expect that you will not be feeling well but your symptoms should be tolerable enough so that you can continue with the weaning. Then, you will be able to really start zapping those intracellular bacteria. Last edited on Mon Apr 14th, 2008 13:09 by Foundation Staff |
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SARCOIDOSISlink STANDARD TREATMENTS Methotrexate (MTX) is used to treat diseases with rapid cell growth such as cancer and some 'autoimmune' diseases. "Methotrexate is an antibiotic. It has identical actions with Trimethoprim which combines with sulfa to make up Bactrim. Here are Course Notes from University of South Carolina which outline MTX's antibacterial actions. MTX is an anti-folate (actually it is an anti-dihydrofolate reductase (anti-DHFR)) which inhibits one stage in the formation of DNA. Thus any bacteria dwelling within a body which has MTX in the bloodstream will find it more difficult to replicate, and hopefully the bacteria will gradually die off. Bactrim (Sulfa/trimeth) not only blocks DHFR (with trimethoprim) but also blocks P-ABA with Sulfonamide. Here is a diagram showing the Folate biochemistry in more detail As you know, Bactrim is not a terribly effective antibiotic against the CWD of Sarc and RA (and Lupus and..etc), at least acting on its own. Neither is MTX especially effective (acting on its own). The interesting thing is that Folic Acid supplements are often given to ease the "side effects" of MTX. Folic Acid directly reduces the antibiotic action of both Trimethoprim and MTX. Sure, this may reduce pain from the 'herx', but wouldn't it be more sensible to just lower the dose of MTX and reduce the risk of liver damage. The antibiotic action of MTX is likely to increase the effect of herx with Benicar therapy, and that is why we say that you should wean off MTX before starting the Marshall Protocol." ...Trevor... Discontinuing methotrexate Benicar should be started only after MTX has been discontinued to avoid an intolerable Herxheimer reaction due to MTX's antibiotic action. It is not harmful to the body to discontinue MTX abruptly. This is in contrast to prednisone, where abruptly stopping can cause a number of serious problems, from rebound inflammation to an adrenal crisis as the body has to quickly begin producing adrenal hormone (which is suppressed by prednisone). People are advised to wean very slowly from prednisone. In conventional medical practice, people are advised to wean from methotrexate in an attempt to see at what dose their symptoms return. Sometimes, they are then advised to continue methotrexate at a lower dose. Some doctors think there is a risk of rebound inflammation from stopping methotrexate abruptly. Taking a few weeks to wean from MTX, while probably not necessary, is the cautious approach to avoid the symptoms of rebound inflammation. Some doctors say that the effects of MTX might linger for four to six weeks after stopping. This effect would be rebound inflammation. The Benicar blockade will reduce inflammation so it is not necessary to wait 4-6 weeks after discontinuing MTX to start Benicar. Last edited on Wed Feb 14th, 2007 04:04 by Foundation Staff |
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SARCOIDOSISlink STANDARD TREATMENTS Anti-TNF-a drugs Remicade (infliximab) Enbrel (etanercept) Trental (pentoxyfyllene) Humira (adatimumab) Cimzia (certolizumab thalidomide Sept. 4, 2008 WASHINGTON - The Food and Drug Administration ordered stronger warnings on four medications widely used to treat rheumatoid arthritis and other serious illnesses, saying they can raise the risk of possibly fatal fungal infections. The drugs Enbrel, Remicade, Humira and Cimzia work by suppressing the immune system to keep it from attacking the body. One problem with the anti-tumor necrosis factor alpha drugs, such as Remicade,is that tumor necrosis factor alpha (TNF-a) plays an essential role in keeping tuberculosis and similar diseases at bay, and suppressing it can reactivate or allow new TB infections. Here are two articles on this topic: Treatment with Remicade (Infliximab) is known to cause TB. Johns Hopkins Arthritis News 10/19/2001 http://tinyurl.com/4c6h7 A recent study says that TNF-a is essential to the proper expression of acquired specific resistance following infection with Mycobacterium tuberculosis: http://tinyurl.com/cg8d7 REMICADE (infliximab) This story from the AP wire about the new 'black box' warning (the highest level of warning for a medication) for Remicade is on the Johns Hopkins Center for Tuberculosis website: Remicade Takers to Get TB Tests [L. Neergaard, August 15, 2001]: WASHINGTON (AP) -- Rheumatoid arthritis patients must be tested for tuberculosis before they begin taking a treatment called Remicade, the drug maker and the government announced Wednesday. Patients using Remicade are at least four times more likely than average Americans to get active tuberculosis, the Food and Drug Administration estimates. The problem: Apparently the drug suppresses users' immune systems enough that if they unknowingly carry the TB germ, the respiratory illness can suddenly flare up. The warning is serious because untreated, TB can kill -- and it's also an airborne illness that these patients could spread to family and friends. Worldwide, 88 cases of tuberculosis have been reported among the estimated 170,000 people who have tried Remicade, FDA's Dr. Bill Schwieterman said Wednesday. Fifteen of those people died. Some 2 billion people worldwide are infected with TB and risk developing an active case of the disease. In the United States, TB cases dropped to a record low of 16,377 last year. But the illness is a continuing threat here, with increased foreign travel and immigration from countries where TB is common. Rheumatoid arthritis afflicts more than 2 million Americans when their immune systems go awry and attack their joints, causing severe swelling, pain and stiffness. Remicade is a bioengineered drug that roams patients' blood to sop up an immune system protein called tumor necrosis, a factor responsible for much of the swelling. But that immune suppression, so important in fighting rheumatoid arthritis, can leave users at a higher risk for serious infections. Remicade's label has long carried warnings about various infections, but it now will carry a boxed warning in bold type about the TB risk the strongest warning possible for a prescription drug. The warning doesn't say people should stop using Remicade. The risk of activating latent TB appears highest in the first three to six months of use, so doctors should carefully evaluate those patients, Schwieterman said. But before prescribing Remicade to a first- time user, doctors should test for TB -- it's a simple skin test -- and treat TB carriers, the FDA concluded. Manufacturer Centocor Inc. will send letters to thousands of doctors who prescribe Remicade, both for rheumatoid arthritis and the bowel ailment Crohn's disease, alerting them to the warning. A similar rheumatoid arthritis treatment called Enbrel also suppresses the immune system and carries warnings that users face the risk of serious infections. But so far, Enbrel users don't seem to face a special TB risk, Schwieterman said. http://www.hopkins-tb.org/news/8-13-2001.shtml But as the article below points out, TB skin tests on patients treated with immunospressants (routinely used on RApatients) are not reliable, because they result in false-negatives. And due to a phenomenon called cutaneous anergy,sarcoidosis patients may also have false negative TB skin tests even when not treated with immunosuppressants. Thus, the anti-TNF-a drugs can induce tuberculosisin a patient who unknowingly carries the TBbacteria.This is not too thrilling for someone who already has RA or sarcoidosis. Anti-tumor necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management. Lancet Infect Dis. 2003 Mar;3(3):148-55. Review. PMID: 12614731 [PubMed - indexed for MEDLINE] http://tinyurl.com/4ruzv The suggestion by some doctors to treat TB in a sarcoidosis patient so that he could then use Remicade is alarming. TB is treated with Rifampin which is extremely toxic: http://www.rxlist.com/cgi/generic2/rifampin_wcp.htm And Rifampin would create more mutant Cell Wall Deficient bacteria as it kills the TB. It is this CWD bacteria that trigger the sarcoidosis inflammation. As if TB weren't enough, Remicade can also cause an infection called mycobacterium avium: http://jcm.asm.org/cgi/reprint/34/9/2240.pdf These recent papers imply that suppressing TNF-alpha also seems to suppress the body's response to Cell Wall Deficient bacterial infection, allowing an infection to develop from within: A lupus-like syndrome associated with infliximab therapy. http://tinyurl.com/4yxub Sarcoid-related uveitis occurring during etanercept therapy. http://tinyurl.com/6bkfq Some people report an allergic response to Remicade. Here is a possible reason: The chimeric monoclonal antibody in Remicade is part human, part mouse. Exposed to purely mouse (murine) antibodies, human immune systems naturally develop human antibodies to the foreign mouse proteins, which can trigger an allergic-like response. So, they take parts of a mouse antibody and transplant to a human antibody using recombinant DNA technology, to make an antibody that is about 30% mouse and 70% human. Sounds pretty cool, this biotech stuff - until you realize that the 30% mouse portion of the chimeric antibodies can still elicit a response from the human immune system. Congestive heart failure exacerbation is a major side effect of Remicade use in patients with moderate to severe CHF. Keep in mind that many sarcoidosis patients do not know that they have cardiac involvement. "Centocor, Inc. would like to inform you of important new safety information for REMICADE® (infliximab). Upon review of preliminary results of its ongoing phase 2 trial in 150 patients with moderate to severe (NYHA class III-IV) congestive heart failure (CHF), higher incidences of mortality and hospitalization for worsening heart failure were seen in patients treated with REMICADE, especially those treated with the higher dose of 10 mg/kg. Seven of 101 patients treated with REMICADE died compared to no deaths among the 49 patients on placebo." http://tinyurl.com/4hehq "Revision of Package Insert to include a contraindication for patients with congestive heart failure, update the Warnings and Adverse Reactions sections, and update the patient information sheet" http://www.fda.gov/cder/biologics/biologics_table.htm The real problem is that TNF-alpha is the wrong target. This recentstudy from the Mayo Clinic was terminated early and concludes: “In patients with progressive stage II or III pulmonary sarcoidosis, etanercept (Enbrel) was frequently associated with early or late treatment failure. These data would not support the design of a large multicenter randomized trial comparing etanercept with conventional corticosteroid therapy.” http://tinyurl.com/6o8w8 Remicade costs $4600.00 PER MONTH for ONE IV treatment, with treatment expected to continue ongoing for a 'lifetime'. Each month about $1000 of the $4600 goes to pay the prescribing physician's clinical group, who provide the IV infusion, and any emergency care needed (for the (apparently) all-too-frequent anaphylaxis). So that means Remicade is regularly worth $20,000 per month to prescribing doctors and their clinical team. The New Jersey Citizen Action (NJCA), New Jersey's largest independent citizen watchdog, has filed a lawsuit to stop Remicade being promoted by promising doctors windfall profits when they prescribe the drug. Remicade does work, in that sarcoidosis patients have reported feeling much better for the first few months. It is then that the problems usually start. Personally, I don't think any drug which causes death as frequently as Remicade is worth paying $18,000 a year for. Minocycline will only cost you about $300 and promises far less excitement. Although there are studies reporting that Remicade slows Rheumatoid Arthritis, there is a 50% dropout rate: http://tinyurl.com/4scke It's understandable that drug companies will promote new drugs with large profit margins rather than new uses for old antibiotics with small profit margins.But we should be truly concerned about the outrageous costs and the risk-benefit ratio of anti-TNF-a drugs. The choice to use them or minocycline to treat Rheumatoid Arthritis is just one example that there are significantly less costly, yet effective drug options available. There are studies reporting that minocycline produces the same effect as Remicade, but at a fraction of the cost. The difference is that there are no pharmaceutical companies funding huge studies of minocycline. Here is one study, though, that indicates minocyclines effectiveness: Treatment of early seropositive rheumatoid arthritis with minocycline: four-year followup of a double-blind, placebo-controlled trial. Arthritis Rheum. 1999 Aug;42(8):1691-5. PMID: 10446869 [PubMed - indexed for MEDLINE] http://tinyurl.com/5w7ce The FDA issued a new warning regarding Infliximab (Remicade) on December 22, 2004. The new FDA warning is regarding severe hepatic reactions - including acute liver failure - in patients receiving Remicade. The FDA-ordered Dear Doctor Letter and label with new safety warning are available at the FDA website. You can read an abstract presented at the 2005 American Thoracic Society conference at this link. It concludes "Given the potential for adverse effects, use of IFX (Infliximab/Remicade) in this patient population should be confined to ongoing clinical trials" Infliximab is a biologic agent approved for marketing in the treatment of rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriatic arthritis and ankylosing spondylitis. The FDA has required warning letters and label changes due to the following adverse events in patients receiving infliximab: - the increased incidence of neoplasia and lymphoma http://tinyurl.com/lqq8m - hepatotoxicity and liver failure and http://tinyurl.com/n86v3 - serious opportunistic infections including tuberculosis and histoplasmosis. http://tinyurl.com/rx75w The half life of Remicade is 9.5 days. The excretion rate is unknown. If you are starting the Marshall Protocol, you may take Benicar to dampen inflammatory symptoms that may flare as Remicade leaves your system. Wait 3 weeks to begin minocycline so your body will be accustomed to the absence of Remicade's immunosuppression before you induce immunopathology with minocycline. TRENTAL (pentoxyfyllene) Trental may have a palliative effect which allows patients to reduce their dose of prednisone. But it does nothing to effect a cure as the following abstract reports: A Randomized Trial of Pentoxifylline in Pulmonary Sarcoidosis V.C. Manganiello, M.D.,Ph.D, M.K. Park, M.D., Ph, M. Stylianou, Ph.D., R. Litzenberger, R.N., K. Jackson, R.N., Y. Tsygansky, B.S., J. Moss, M.D., Ph, Bethesda, MD Steroid-sparing drugs which suppress inflammatory cytokines that are associated with the formation and maintenance of granulomas would be very useful therapeutics in management of sarcoidosis. In this regard, pentoxifylline (POF) has been reported to inhibit production of IL-2, IL-12, TNF-alpha and, in an open-label clinical study, to improve or stabilize pulmonary sarcoidosis. We therefore conducted a randomized, double-blinded, placebo-controlled trial to assess whether POF treatment would improve or stabilize pulmonary sarcoidosis, and be beneficial as an adjunct to corticosteroid therapy. In our study (NHLBI Protocol 99-H-0057), POF did not improve primary or secondary endpoints in patients with mild to moderate pulmonary sarcoidosis. Although recurrence of pulmonary sarcoidosis was not considered a formal endpoint, 5/13 POF-treated patients experienced disease recurrence versus 12/14 placebo-treated patients (P < 0.02). There were no spontaneous remissions in the placebo group. After 24 weeks, the mean prednisone dose for POF-treated patients was significantly lower than for placebo-controlled patients (P < 0.006). Adverse effects, primarily gastrointestinal, were reported in 11/13 POF-treated , but in no placebo-treated patients. Thus, although POF may have a corticosteroid-sparing effect in pulmonary sarcoidosis, with concentrations of drug used in this study, gastrointestinal side effects were commonly reported. You can read more about the anti-TNF-alpha drugs, which also include Trental (Pentoxifylline) and Humira (Adatimumab) at http://www.sarcinfo.com: "Warnings:Enbrel,Remicade,Pentoxyfylline,Thalidomide"on SarcInfo http://sarcinfo.com/phorum/read.php?f=1&i=3450&t=3450 Here's the latest article about TNF-alpha inhibitors, explaining that these drugs are designed to break down granulomas, which also breaks down the barrier that is one of the body's mechanisms to control pathogens. Immunosuppression related to collagen-vascular disease or its treatment. Proc Am Thorac Soc. 2005;2(5):456-60. PMID: 16322600 [PubMed - in process With the current standard medical treatment, the aim is to reduce granulomas by whatever means - not to bring about real recovery from disease symptoms. ~Belinda Infections warning upgraded in etanercept label (Enbrel) By Eleanor McDermid 21 March 2008 US Food and Drug Administration MedWire News: The US prescribing information for the psoriasis treatment etanercept now contains a boxed warning on the risk of infections in patients taking the drug. The warning has been strengthened from the previous bolded warning. The updated labelling "is similar to labelling for other medicines in the tumour necrosis factor (TNF) inhibitor class," notes a statement from Amgen and Wyeth Pharmaceuticals, the companies that manufacture and market etanercept (Enbrel). An increased infection rate is a theoretical risk associated with any immunosuppressive treatment. One of the main concerns is the risk of new or reactivated tuberculosis infection. The updated prescribing information includes statistics on the rate of tuberculosis infection seen in clinical studies of etanercept: about 0.01% in global studies involving more than 20,000 patients and 0.007% in more than 15,000 US and Canadian patients. Post-marketing data have shown incidences of tuberculosis infection with drugs targeting TNF, including etanercept. The boxed warning advises evaluating patients for tuberculosis risk factors and latent infection before they begin treatment with etanercept. It recommends treating latent infection to reduce the risk of tuberculosis reactivation during etanercept therapy. The warning also stresses that even patients who test negative for latent tuberculosis infection should be monitored for symptoms of the disease while they remain on etanercept. Etanercept treatment should be stopped in patients who develop a serious tuberculosis infection, the boxed warning states. The warning also notes that the risk of reactivated tuberculosis infection may be lower with etanercept than with monoclonal TNF blockers, however. Last edited on Fri Sep 5th, 2008 00:45 by Foundation Staff |
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filelink Standard Treatments Plaquenil "Plaquenil is hydroxychloroquine, an anti-malarial, anti-parasite drug with only very weak anti-inflammatory properties. Its use in Lupus and Sarcoidosis is historic, decades old. There are many anecdotal reports that Plaquenil has been effective in treating sarcoidosis. But nobody really seems to know why. It is sometimes useful against sarcoidosis microbes, somewhere under 10% of the time, reportedly. As for why doctors might think it is superior - you would have to ask them. I think you will find that most will not even admit to it being an antimicrobial. According to pulmonology folklore it is supposed to have some (unidentified) magic compound in it that suppresses the immune system. The flouroquinolones are not terribly effective against mycobacteria. See for example the rickettsia susceptibilities study at http://tinyurl.com/576az The full text shows the flouroquinolones are 1/20 as effective against the rickettsia as doxycycline. We don't use flouroquinolones on the MP because we have found that they produce litle or no Herxing in sarcoidosis patients and because their use over the long term raises some issues of bacterial resistance. Plaquenil has significant risk of side effects, you can about read them here: http://www.rxlist.com/cgi/generic/hquine_ad.htm At the dosage given to sarc patients it can cause loss of eyesight, and the FDA recommends frequent checking of a patient's eyes while they are on Plaquenil. There is an antibiotic, minocycline, which is more effective against the Cell Wall Deficient bacteria which drive the inflammation of Lupus and Sarcodiosis. But it needs to be given in a special dosage and combination. You can read about it at: http://www.sarcinfo.com/minocin.htm and the JAMA paper: http://archderm.ama-assn.org/cgi/content/abstract/137/1/69 Any antimicrobial/antibiotic that has has some effect in Sarc is worth trying - it is just that I would try some of the less drastic than Placquenil antibiotics first. There are several that are much safer. You will note that the FDA http://www.rxlist.com/cgi/generic/hquine_ids.htm gives the same advice - try other drugs first. My position on the safety of Plaquenil to treat these chronic Th1 diseases is primarily based on a "relative risk" doctrine. I know that COMPLETE recovery from these diseases is possible, and that it can be achieved with common antibiotics and an ARB blocker which have extremely good safety profiles, certainly they have significantly better safety profiles than the literature reports for Plaquenil in Lupus and Sarcoidosis." ...Trevor... Be aware that about 6% of patients on Plaquenil will lose their eyesight. This study ( http://tinyurl.com/ac84h ) wasn't the one coming up with a 6% figure, this study found that 20% of patients had to discontinue plaquenil therapy because of noticeable artifacts when their eyes were examined. There are lots of studies. There are too many people going blind solely because their physicians were too proud to admit defeat. ..Trevor.. Plaquenil and the MP Plaquenil is an antimicrobial which lingers in the system at least 50 days and cannot be taken while on the MP. Dr. Blaney reports he starts his patients on Benicar while they are waiting for Plaquenil to clear their system and has seen no adverse events. He prefers to wait a couple months before starting minocycline. |
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(filelink) Sarcoidosis is communicable Can I donate blood, organs, tissue or bone marrow if I have a Th1 inflammatory disease? (click here) You still have sarcoidosis because it doesn't go away on its own or without treating the underlying bacterial cause. Your blood contains bacteria that would be passed on to someone else. There are documented cases of sarcoidosis developing in patients who received tissue/organs from sarcoidosis patients. Dr Marshall wrote: One of Lida Mattman's slides in Chicago shows L-forms in supposedly sterile, whole Red-Cross blood. L-forms seem to survive all attempts at sterilization. Lida is certain that transfusion is one of the reasons that the chronic diseases have balloned to epidemic proportions over the last 50 years. Remember, the Red Cross blood transfusion service grew at the end of the second world war, and was not around during the first half of this century. Neither were beta-lactam antibiotics, Vitamin D supplementation, the Sun-worshipping ethos, and other factors which, IMO, have all contributed to the Th1 autoimmune diseases spiralling out of control. ..Trevor.. I just saw this letter in CHEST online this morning. I thought you might be interested "Leukoreduction of transfusions and blood stream infections" http://www.chestjournal.org/cgi/eletters/127/5/1722 They are advocating the removal of phagocytic cells from blood being transfused. Now the big question is - what could those phagocytes possibly have in them that might promote infection? -LOLOLOL ..Trevor.. =========================================================== Sarcoidosis has been transmitted to organ recipients from organ donors. It's in the bone marrow and stem cells. See below. Belinda Lancet published this case report in 1990: Transmission of sarcoidosis via cardiac transplantation. Burke W, Keogh A, Maloney P, Delprado W, Bryant D, Spratt P. Lancet Dec 22-29 1990; 336(8730):1579. PMID: 1979389 http://tinyurl.com/gdp7u Other cases: Heyll A, Meckenstock G, Aul C, Svhngen D, Borchard F, Hadding U, Mvdder U, et al. Possible transmission of sarcoidosis via allogeneic bone marrow transplantation. Bone Marrow Transplant 1994; 14:161-164. Padilla ML, Schilero GJ, Teirstein AS. Donor-acquired sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 2002;19:18-24. http://tinyurl.com/g7ck4 Granulomatous pneumonitis following bone marrow transplantation. Bone Marrow Transplant. 2001 Sep;28(6):627-30. PMID: 11607780 [PubMed - indexed for MEDLINE] http://tinyurl.com/fg77e Pulmonary sarcoidosis following stem cell transplantation: is it more than a chance occurrence? Chest. 2004 Aug;126(2):642-4. PMID: 15302757 [PubMed - indexed for MEDLINE] http://www.chestjournal.org/cgi/content/full/126/2/642 Another thing to consider is: there have been reported cases of sarcoidosis lesions at venipuncture sites (sorta like sarc eruptions in scars and tatoos). Cutaneous sarcoidosis in venepuncture sites. Br Med J. 1973 Mar 3;1(5852):547. No abstract available. PMID: 4692686 [PubMed - indexed for MEDLINE Hancock BW. Cutaneous sarcoidosis in blood donation venepuncture sites. Br Med J. 1972 Dec 23;4(842):706-8. No abstract available. PMID: 4646848 [PubMed - indexed for MEDLINE] =============================================== The recent ACCESS study, the largest study of sarcoidosis in the US sponsored by the National Institutes of Health, found that the risk for sarcoidosis among parents and siblings of sarcoidosis patients increased five-fold. The researchers also found familial aggregation was much more prominent in whites than African-American families, but an important risk factor in both races. Since so many physicians (and patients) are not aware of the results from the multi-center ACCESS study that followed newly-diagnosed patients for two years, we have a summary of findings from the ACCESS study in this brochure. No genetic factor has ever been identified to explain familial occurrences of sarcoidosis, although this has been studied - as noted below. Obviously, the alternative explanation is that family members share environmental bacterial exposure. [Familial sarcoidosis. Apropos of 22 families] A sarcoidosis genetic linkage consortium: the sarcoidosis genetic analysis (SAGA) study. Belinda How does Th1 inflammation develop? What is successive infection? |
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(filelink) OVERVIEW OF SIDE EFFECTS OF CORTICOSTEROID THERAPY includes topical, oral, inhaled and eye drop applications Adrenal Suppression and recovery of adrenal response after short-term, high-dose glucocorticoid treatment. Diagnosis and therapy of patients with adrenocortical insufficiency Adrenal insufficiency and diabetes mellitus secondary to the use of topical corticosteroids for cosmetic purpose. Brain Steroids and brain atrophy in multiple sclerosis. Corticosteroids: sculptors of the hippocampal formation. cognition, learning and memory Bone Current management of corticosteroid-induced osteoporosis: variations in awareness and management. Avascular bone necrosis. A complication of long-term corticosteroid therapy. 1965 article Malpractice and avascular necrosis: legal outcomes. Endocrine System [Endocrine consequences of corticotherapy. Weaning from long-term corticotherapy] Eyes Corticosteroids and glaucoma risk. Locally administered ocular corticosteroids: benefits and risks. Corticosteroid-induced cataracts. [Corticosteroid-induced glaucoma following treatment of the periorbital region] Females: Menstruation Disturbances [The most frequent complications during long-term corticotherapy] Gastrointestinal Hemorrhage [Immunosuppression--a tightrope walk between iatrogenic harm and therapy] Males: Decreased Testosterone Randomized placebo-controlled trial of androgen effects on muscle and bone in men requiring long-term systemic glucocorticoid treatment. Decreased testosterone levels in men with rheumatoid arthritis: effect of low dose prednisone therapy. Reduction of serum testosterone levels during chronic glucocorticoid therapy. Muscles Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle. Corticosteroid myopathy: a clinical and pathological study. Impact of physical training on the ultrastructure of midthigh muscle in normal subjects and in patients treated with glucocorticoids. [The effect of corticotherapy on respiratory muscles] [Clinical investigation of diaphragmatic function. Relationships with the biology of muscle] Skin Corticosteroid-induced atrophy and barrier impairment measured by non-invasive methods in human skin. |
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(filelink) RISKS OF CORTICOSTEROID USE IN CHILDREN Please read the Overview of Side Effects of Corticosteroid Therapy (the topic above) to understand the known side effects of this treatment in humans. Oral corticosteroids Allergic Reaction Steroid allergy: report of two cases. Appetite and Weight From emedicine: "All patients receiving pharmacologic glucocorticoid treatment develop Cushingoid features if exposed to a high enough dose for long enough (usually 1 mo or more). With the exception of abnormal growth, the signs of hypercortisolism are frequently subtler in pediatric patients than in adults. In children, the most common features that are observed include an increase in body weight due in part to an increase in appetite and a decrease in linear growth." Bone Children and the risk of fractures caused by oral corticosteroids. Growth Suppression Effect of corticoid therapy on growth hormone secretion. Treatment of glucocorticoid-induced growth suppression with growth hormone. National Cooperative Growth Study. More about Growth Suppression Pharmacy Update "In children, long-term treatment with oral corticosteroids can suppress growth." Article published in the NEJM in 2002 concluded that prolonged alternate day dosing in pre-pubescent boys with cystic fibrosis led to growth impairment that persisted after treatment was discontinued and significantly reduced the height obtained after 18 years of age. Eye Intraocular pressure profile of a child on a systemic corticosteroid. Psychological Effects Adverse psychological effects of corticosteroids in children and adolescents. The effects of corticosteroids on behavior in children with nephrotic syndrome. Reproductive System "In addition to changes in bone cells, glucocorticoids reduce the production of gonadal hormones through a number of mechanisms. Glucocorticoids have inhibitory effects on the pituitary gland and the gonads." From An Update on Glucocorticoid-Induced Osteoporosis Skin New aspects of the mechanism of corticosteroid-induced dermal atrophy. INHALED CORTICOSTEROIDS General Inhaled corticosteroids: past lessons and future issues. Inhaled corticosteroids are absorbed from the lungs into the systemic circulation, in which they can acutely decrease growth velocity in children, an effect that fortunately appears to be temporary and might have no effect on final adult height. In sufficient dosages, they also produce bone mineral loss leading to osteoporosis and might increase the risk of cataracts, glaucoma, skin atrophy, and vascular changes that increase the risk of ecchymoses. Effective evaluation of the severity and significance of these complications is challenging because highly sensitive tests do not reliably predict clinically significant events, and short-term observations do not predict long-term consequences. Also, compliance wanes with long-term treatment, and susceptibility to a particular adverse event can vary over time, even in the same individual, because of developmental or hormonal changes. Adrenal suppression Monitoring growth in asthmatic children treated with high dose inhaled glucocorticoids does not predict adrenal suppression. Inhaled steroids and the risk of adrenal suppression in children. Dental Use of asthma-drugs and risk of dental caries among 5 to 7 year old Danish children: a cohort study. Eyes Cataract and ocular hypertension in children on inhaled corticosteroid therapy. Growth Inhaled corticosteroid therapy for asthma in preschool children: growth issues. Skin Adverse skin reactions to inhaled corticosteroids. |
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SARCOIDOSISlink LUNG TRANSPLANT My doctor put me on the lung transplant list "Has your Doctor told you that the average survival of a sarcoidosis patient after a lung transplant is only 30 months? Very few live for 5 years. Has your physician told you that the quality of life during those 30 months is going to be pretty awful, as you will be on cocktails of anti-rejection and immuno-suppressive drugs? Has your doctor told you that the only way you will breathe comfortably again is with a transplant? Well, he is incorrect. There are recovered sarcies here who used to be on oxygen, and now no longer need it at all. It is probably a good time to talk with him about this, now, before it is too late. ..Trevor.. ps: I would be happy to discuss these issues with Doc, if he calls me." ============================== A new study from Denmark shows that lungs implanted in sarcoid patients are reinfected with granulomas five months later. Furthermore, sarcoidosis reinfection came from the recipient patient. http://tinyurl.com/75mjh ========================================== "Take a look at 36 years of my own chest xrays. http://sarcinfo.com/xrays/ You can see that I was stage 4 by 1978, and given 18 months to live. Luckily I figured out Vit D about 1986 and slowed the progression. However, you can see that the fibrosis (scarring) on my xrays (which I urge you to compare with your own) is stage 4++ You will also note that my heart has now shrunk back to a normal size... (it was enlarged through all those years of pulmonary hypertension) Now take a look at the conference DVDs and you can assess how much all that scarring slows me down these days - virtually not at all..." Dr. Trevor Marshall, PhD Belinda wrote: Lung transplantation for sarcoidosis has significant risks and according to this report the median survival for all the sarcoidosis patients who underwent transplantation was 14 months. You can read more about viability for sarcoidosis patients after lung transplantation on PubMed or on this thread at SarcInfo.com. Other patients with "end-stage" sarcoidosis have done well on the MP. If you watch the DVDs of our Chicago conference you will see and hear the story of one woman's recovery from "end-stage" sarcoidosis. You can also read the success stories on SarcInfo and here on the marshallprotocol forum. There are Members here who have chosen to do MP rather than be on the Transplant List. If I had to choose between a lung transplant or the MP, I would choose the MP because it relies on carefully selected, simple low-cost, low risk antibiotics to treat the chronic infection caused by pleomorphic bacteria, along with Benicar and lifestyle changes to control the runaway 1,25-D. I was able to get off oxygen (I was using 2 liters) and avoided what the pulomonologist believed was the impending collapse of my right middle lobe using the MP. Fibrosis and bronchiectasis were still visible on my last lung imaging, but I now walk six miles a day without dyspnea. You really need to think carefully about what you are willing to do/endure and how you are willing to live your life at this point. You have to realize that you get the final vote about your medical care; nothing goes without your approval, and you have a significant say in choice of treatment. I would only consider having a lung transplant after I had given the MP my all - like my life depended on it. Staying out of the sun and taking antibiotics and Benicar for a few years is a comparatively low-risk therapy for a disease that can be fatal. I had to fire my specialist and let my treating doctor know that I was "willing to risk dying from sarcoidosis" before I would accept the risks of the conventional treatment offered to me. If you have your mind made up, you should be able to get a physician to help you implement the MP. Last edited on Mon Oct 8th, 2007 01:22 by |
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Aussie Barb Research Team
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(filelink) ACCESS STUDY The NIH 6-year ACCESS study is the biggest study of Sarcoidosis in history. Because the PubMed abstracts supplied for public consumption do not tell the full truth as to what the ACCESS study actually found, the Autoimmunity Research Foundation has prepared and distributed a brochure highlighting the true ACCESS study findings. An electronic copy is at URL http://autoimmunityresearch.org/sarcoidosis.pdf We also have an annotated copy of the full-text online, at http://autoimmunityresearch.org/access-2yr.htm You have to understand that ACCESS did not confirm what was already set into the minds of the sarc pulmonologists, and they, therefore, want to forget all about that 'silly science stuff' as soon as possible, so that they can again get back to anecdotal misinformation which has gained credence by repetition and business as usual. ..Trevor.. One of the most expensive and revealing studies ever done on Sarcoidosis, ACCESS 2003, actually reversed the common misconception about Sarcoidosis remission. Sadly, most doctors treating the disease still labor under the remission myth that has been so oft repeated, even given the time for scientific data to get out to the industry. (Here it is 3 years later and the myth still persists.) Clinical parameters of FVC, FEV1, Scadding stage of chest radiograph, and dyspnea scale between ACCESS enrollment and the two-year follow-up: Table III: _____________FVC________FEV1_______CXR_______DYSPNEA IMPROVED........20.5% (44)...... 21.9% (47)..... 37.7% (81).....19.5% (42) UNCHANGED...57.7% (124)....56.7% (122)... 41.4% (89)......67.0% (144) WORSE..............11.6% (25)..... 11.2% (24)..... 16.3% (35)......13.5% (29) 2/3 of their study group saw no improvement Notice: FVC, FEV1, Scadding stage, and the dyspnea scale remained unchanged over the two-year period in the majority of the patients. Notice also: Even in the positive-sounding "improved" category for clinical markers, the percentages described were at best "improved." There is no column for remission because nobody went into remission. If nobody went into remission before 2 years, what about after 2 years?: "Therefore most patients with persistent disease at two years were unlikely to have resolution of Sarcoidosis." Finality detail worth noticing in the study: "end-stage pulmonary Sarcoidosis usually develops over one or two decades [17]" ............... Also read: Pulmonary Reviews.com Trends in pulmonary and critical care medicine, Vol. 7, No. 4 April 2002 ( http://www.pulmonaryreviews.com/apr02/view.html ), publication by two of the ACCESS authors to see their insights: "One analysis has proved what previous anecdotal reports only hinted at—that sarcoidosis aggregates in families.[1] It found that the risk for sarcoidosis was increased 4.5-fold in parents and siblings of patients with the disease, lead investigator Benjamin A. Rybicki, PhD, told PULMONARY REVIEWS. Familial aggregation was much more prominent in whites than in African-Americans, but an important risk factor in both races, added Dr. Rybicki, Senior Research Epidemiologist with the Henry Ford Health System in Detroit. "The second analysis revealed that the initial presentation of sarcoidosis varies by age, sex, and race.[2] This finding challenges the widely held stereotype that the patients most often affected are African-Americans and young adults, said lead investigator Robert P. Baughman, MD, Professor of Medicine at the University of Cincinnati." |
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(filelink) Pregnancy Pregnancy usually goes to term with no problems. You need to be aware that some of the drug therapies (methotrexate, anti-malarials, Thalidomide, etc. ) normally used for sarcoidosis are contraindicated in pregnancy. Oral corticosteroids increase the risk of cleft palate. We know that in pregnancy, the placenta manufactures 1,25-dihydroxyvitamin D, primarily in the second and third trimesters and the level of 1,25-D will soar. It is presumably produced to strengthen the immune system of the child, but it significantly overloads the immune system of mothers who are sufferers of sarcoidosis or other Th1 inflammatory diseases. This is in addition to the 1,25-D produced by the sarcoid activated macrophages. See Pregnancy increases 1,25-D Studies show that most women (not all) with sarcoidosis report that they feel better during pregnancy. This is probably due to suppression of the immune system by high 1,25-D, lack of bacteria killing and, therefore, no Herxheimer symptoms. A report about the mother's immune system response during pregnancy may help explain why women with sarcoidosis report feeling better when they are pregnant. Sarcoidosis involves a Th1-activated immune system response. This report explains that the NF-kappaB/IkappaB signaling pathway is down-regulated in T cells in pregnancy, shifting the immune system away from Th1 and toward a Th2 immune response. There are other factors to consider, especially vitamin D and sunlight exposure. We know that these play a role in activation of NF-kappaB and the Th1 immune response. High levels of 1,25-D can cause increased somnolence, fatigue and symptoms such as joint pain and breathing problems. The 1-25-D (calcitriol) levels increase throughout pregnancy in normal women. The level of 1,25-D is highest in the third trimester and falls soon after delivery in normal women. Relapse is common post-partum with symptoms often worse than before pregnancy. Your 1,25-D will come down after delivery. If that reduction allows your immune system to function better, you may experience an increase in symptoms due to the Herx reaction. This study reports that increased serum 1,25-D levels persist through lactation. ====================================== A healthy person will have 1,25-D manufactured by the placenta during pregnancy, but the manufacture of 1,25-D in the kidneys will be down-regulated to compensate. The kidneys of a person with advanced Th1 disease have usually lost the ability to adequately down-regulate the 1,25-D levels, as there is too much 1,25-D being manufactured in the inflammation, in the eyes, and in the skin. The interpretation of the 1,25-D data value during pregnancy will be more difficult. The 25-D levels may also be an aid to interpretation. Please be aware that ARBs (Benicar) and most of the Marshall Protocol antibiotics cannot be used during pregnancy and lactation. ===================================== If you are contemplating pregnancy, you should consult your doctor about taking care of your health and treating your inflammatory disease first. If you are already pregnant, you should do everything possible to keep the level of 1,25-D down. This means diligent avoidance of ingested Vitamin D and sunlight/bright lights exposure. Most sarcoidosis mothers do have healthy babies. This published article on pregnancy and sarcoidosis says, "If well managed, pregnancy in women with sarcoidosis is usually carried to term with no problem, excepting rare contraindications. There is no specific risk for the embryo-fetus. Fertility is unchanged. Pregnancy can be contraindicated in case of respiratory failure due to heart failure or central nervous system disorders. A vital capacity less than 100 ml or pulmonary hypertension contraindicate pregnancy. Pregnancy should be discouraged during a period of active disease progression., but pregnancy in itself does not aggravate sarcoidosis. A flare up 3 to 6 months after delivery is not unusual." Regarding cesarian section versus vaginal delivery, consider that sarcoidosis inflammation is known to have an affinity for scar tissue, You will have to decide if you want to postpone treating your sarcoidosis in order to nurse your baby. These bacteria multiply very slowly so you could base you decision on how well you feel. Can a pregnant woman be on the Marshall Protocol? Last edited on Sat Aug 25th, 2007 22:13 by Foundation Staff |
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(filelink) Familial Aggregation Familial Aggregation in Sarcoidosis A Case-Control Etiologic Study of Sarcoidosis (ACCESS) Am. J. Respir. Crit. Care Med., Volume 164, Number 11, December 2001, 2085-2091 Am I contagious? Will re-infection occur if my partner or family members are not treated? |
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(filelink) Cancer Diagnosis in Sarcoid Patients CANCER and Th1 inflammation |
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(filelink) Epidemiology I noticed in some reading that African Americans have almost 4 times the incidence of sarcoidosis as whites That data is largely erroneous. There is a group of sarcoidosis researchers who get their grants from studying Sarc as a minority disease, and they have a vested interest in see that it remains viewed as such. An alternative perspective on the ACCESS study data (saying race was not a big issue) can be found at http://www.pulmonaryreviews.com/apr02/view.html ..Trevor.. ...................................... Modern Scandinavians have a lot of fish in their diet. That puts them at a severe disadvantage by comparison with bacteria which have adapted to live in a high-vit-D environment. Sarcoidosis is a global disease. You just can't compare the incidence rates in poor countries with those in the first world. There are issues of service, and also of the poorer countries having bigger problems to worry about than reporting chronic disease. I deprecate all talk about differences between populations. When it all comes down to it, any differences are quite small, and tell us nothing about Th1 disease, or the impact of Th1 disease. Last edited on Sat Jan 28th, 2006 05:49 by Foundation Staff |
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(filelink) Studies reporting Mycobacterium Avium (MAC) as an opportunistic infection in sarcoidosis Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis. Author: Eishi Y, Suga M, Ishige I, Kobayashi D, Yamada T, Takemura T, Takizawa T, Koike M, Kudoh S, Costabel U, Guzman J, Rizzato G, Gambacorta M, du Bois, Nicholson AG, Sharma OP, Ando M Source: J Clin Microbiol, 40(1): 198-204 2002 Opportunistic infections and sarcoidosis[Article in French] Author: Girard N, Cottin V, Hot A, Etienne-Mastroianni B, Chidiac C, Cordier JF Source: Rev Mal Respir, 21(6 Pt 1): 1083-90 2004 Sensitive differential detection of genetically related mycobacterial pathogens in archival material. Author: Ikonomopoulos JA, Gorgoulis VG, Kastrinakis NG, Zacharatos PV, Kokotas SN, Evangelou K, Kotsinas AG, Tsakris AG, Manolis EN, Kittas CN Source: Am J Clin Pathol, 114(6): 940-50 2000 Detection of Mycobacterium avium complex in cerebrospinal fluid of a sarcoid patient by specific polymerase chain reaction assays. Author: el-Zaatari FA, Graham DY, Samuelsson K, Engstrand L Source: Scand J Infect Dis, 29(2): 202-4 1997 Disseminated cutaneous Mycobacterium avium-intracellulare resembling sarcoidosis. Author: Epps RE, el-Azhary RA, Hellinger WC, Winkelmann RK, Van Scoy RE Source: J Am Acad Dermatol, 33(3): 528-31 1995 |
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Chemotherapy (filelink) Chemotherapy usually brings to mind the drugs used to destroy rapidly growing cancerous tissue. On a very simplistic level, in the past, Th1 diseases like sarcoidosis have been considered to be caused by an "out of control" immune system so some physicians had concluded the same drugs used to stop cancerous cell growth may stop growth of immune cells and damage to major organs. Drugs used to treat cancer are usually not used on mild cases, but when prednisone doesn't stop aggressive sarcoidosis, physicians who don't know what causes sarcoidosis or what makes it worse may feel desperate to help a worsening patient. In those instances, chemotherapy can be "justified" with our current medical system. The misconception that sarcoidosis has a normal course a few months longer than chicken pox may result in a feeling of panic and gloom when it doesn't go away. Sadly, radiation therapy, even whole-brain radiation, has also been used in cases of aggressive sarcoidosis. Patients just don't have a clue beforehand that they may be headed in that direction. As more physicians become aware of the cause of sarcoidosis and the efficacy of the Marshall Protocol, no doubt attitudes and standard treatment will change Belinda Fenter |
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Sarcoidosis patients must avoid ingested Vitamin D avoidvitDlink It is true there is a lot of confusion about vitamin D. It's been that way ever since vitamin D -- which is not truly a vitamin -- was discovered in the 1900s. Vitamin D isn't really a vitamin because, by definition, a vitamin is a nutrient necessary for healthy life that cannot be obtained from any source other than food. Vitamin D is not a vitamin for two reasons: 1) Vitamin D is actually manufactured by the body, and this is by far the overwhelming major source for all humans. Vitamin D is manufactured by the body in response to light or sunshine. That is why it has long been called "the sunshine vitamin." It takes only a few minutes (10-15) minutes of sunshine on the forearm two or three times a week for a person to get all the vitamin D they need. Most people get lots more than that just from driving their car. 2) The end-product of vitamin D, the part put used by the body, is actually a hormone: Hormone D. The hormone was only discovered about 30 years ago, so some physicians may not have been thoroughly trained in the important role of Hormone D, which is much more important than food sources of vitamin D. Food sources of vitamin D beyond what the body manufactures and uses on its own are stored in fat cells, like other fat-soluble vitamins. Nowdays it is known that the immune and skin cells produce Hormone D without any help at all from the digestive system. People who have sarcoidosis produce Hormone D in unregulated amounts because sarcoidosis affects the immune cells, and excess production of Hormone D is one result. Research has shown that Hormone D helps granulomas to grow and proliferate, and there has not been any published research disputing that conclusion. Excessive amounts of Hormone D can make any person feel very ill, with symtoms including fatigue, drowsiness, pain, "brain fog," memory problems, insomnia, sensitivity to light, visual problems, tingling and numbness, headache and nausea. Including vitamin D foods or supplements in a daily routine will provide additional fuel to make more Hormone D. The warning that people with any granulomatous disease -- including sarcoidosis -- should avoid nutritional sources of vitamin D (including supplements) is found in many sources of published medical literature. Since people with sarcoidosis are producing so much Hormone D, their stores of the "vitamin D" used to make Hormone D are likely to measure low. That's because the vitamin D is being used at an abnormally rapid rate by the cells converting vitamin D into Hormone D. That is why it is important to have two blood tests done to determine what is going on. Both the vitamin D (25-hydroxyvitamin D) and Hormone D (1,25-dihydroxyvitamin D) must be tested to determine vitamin D status in people with sarcoidosis. Generally, unless a sarcie has been using vitamin D supplements or products, the vitamin D will be low (due to rapid conversion to Hormone D) and the Hormone D will be elevated. Levels of Hormone D generally have nothing to do with digestion or calcium levels. Some people with sarcoidosis do get elevated calcium, which is regulated by the parathyroid hormone. Years ago, it was thought that vitamin D alone regulated calcium. Now it is known that Hormone D has powerful and complicated effects on many body functions and cells, including the immune cells and the brain. Belinda Fenter |
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skinsarcimageslink Images of cutaneous sarcoidosis HAIR AND SCALP Hair Loss - Alopecia Caused by Sarcoidosis Hair Loss and Plaquelike Skin Lesions in sarcoidosis (click on Figures 1, 2 and 3 in the article) Scalp this is a man with a shaved head Scalp lesions may lead to diagnosis of sarcoid SARCOIDOSIS ON THE HEAD AND FACE Red Plaques on forehead Spots Darker than Flesh on the Face Swollen eyelids (Lacrimal gland swelling) Enlarged Lacrimal Gland Sarcoid Lesion In Lining of Eyelid Papules (discolored bumps) around the eyes Annular plaques on Face Cheek lesion Sarcoidosis on the nose - lupus pernio Sarcoidosis of the nose (Lupus pernio) Lupus Pernio in Sarc Lupus Pernio Arising from a Tattoo in Sarcoidosis Intranasal Inside the Nose Corner of the Mouth Inside Upper Lip On the Tongue Gingival Swelling Due to Sarcoidosis BACK AND TRUNK Upper Neck in Dark Skin Upper Back Back and flank Sarcoidosis on the back Multiple Large Plaques on the Back and Trunk Lived-red to brownish, deeply infiltrated and markedly elevated plaques of two years (Click on the Figure Numbers in the text) ARMS AND HANDS Sarcoidosis Lesions on the arm Sarcoidosis on the elbow Palmar erythema and hoarseness: an unusual clinical presentation of sarcoidosis Red Lesions, Pimple-like Skin -Colored Firm Plaques that appeared on hands, arms and legs due to Sarcoidosis LEGS and FEET Erythema Nodosum Erythema Nodosum Sarcoid Plaque on Knee Large Red Plaque Surrounded by Papules on lower leg Coarse, scaly skin Acquired Icthyosis CHILDREN Child first thought to have atopic dermatitis, diagnosed with sarcoidosis Several photos of sarcoidosis skin lesions on a 7-year old SARCOIDOSIS ERUPTION IN A SCAR Infiltration of scar PETECHIAE Pinpoint to pinhead-sized red dots (this image has an animation showing how these lesions don't blanch) that are a result of the rupture of capillaries IMAGE GROUPS A collection of photos of sarcoidosis Erythema Nodosum, papules, small nodules, raised plaques, lupus pernio and psoriasis-like lesions |
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Statins are contraindicated on the MP (statinlink) Myotonia associated with sarcoidosis: marked exacerbation with pravastatin. Clin Neuropharmacol. 1999 May-Jun;22(3):180-1. Riggs JE, Schochet SS Jr. Department of Neurology, West Virginia University School of Medicine, Morgantown 26506-9180, USA. A 37-year-old man with sarcoidosis developed severe electrical and clinical myotonia while taking pravastatin for hypercholesterolemia. Myotonia associated with sarcoidosis is rare. Pravastatin is associated with myotonia in animals. This case suggests that sarcoidosis and pravastatin, two entities not frequently associated with myotonia, may interact in a synergistic manner to produce severe clinical myotonia in humans. |
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Death from Sarcoidosis According to this 1997 report from the National Institute of Allergy and Infectious Disease, which is on file in the Library of Congress, "approximately one-fourth of the chronic sarcoidosis cases are dying due to respiratory failure, or other pulmonary dysfunctions." Belinda |
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Immunosuppressive and Cytotoxic Therapy for Pulmonary Sarcoidosis The Cochrane Database of Systematic Reviews recently published their review of the use of immunosuppressive and cytotoxic therapy for sarcoidosis and concluded there is: Not enough evidence that immune-suppressing drugs are beneficial in the treatment of pulmonary sarcoidosis "Sarcoidosis is a condition that can affect most of the organs in the body, including the lungs, heart, brain, bones, liver and skin. Patients who have severe disease or those who do not respond to treatment with steroids are often given powerful agents that suppress the immune system in an attempt to control the disease. However, these drugs have severe side effects. There is no evidence at the moment that the benefits of these drugs outweigh their side effects." The drugs reviewed included methotrexate, chloroquine and cyclosporin A. |
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Standard of Care (carefilelink) There is no "Standard of Care" in Sarcoidosis. The NIH/NHLBI just put out new guidelines which advises against the long-term use of steroids, and which mentions that antibiotics (Tetracycline) have been some use. It is at URL http://www.nhlbi.nih.gov/health/dci/Diseases/sarc/sar_treatments.html You should print a copy and send it to the Physician. Feel free to include a copy of this message. Note particularly the words "sometimes for a year or more." There is no concept that any patient should be on Prednisone for extended periods (beyond a year or so). An internal battle amongst the specialists has caused this text to change several times in the past 18 months (the Foundation was the instigator of many of those changes, and we have all the paperwork on file). They all know that Prednisone is not a long-term solution, and that it has significant side effects (count them) but it is all they have to hang their hat on. If the issue of "standard of care" is ever used to deny treatment, I would be happy to testify in an ethics hearing at the Hospital whose doctors are refusing to treat - testify that there is no standard of care, that there are no studies showing long-term efficacy of any sarcoid therapy (except ours). Mostly the physicians try to use a "concensus statement" as printed validation that a 'standard of care' exists, but the statement they use is old, and was not prepared through any NIH-accepted concensus process. I know that a similar ethics hearing was recently held at the NIH, and that the pulmos lost. I can disclose those details in camera, but not in public. I doubt they will find a pulmonologist with enough stupidity to try and paint an opposing picture, although some of these sarcoid specialists continue to confound me with their bluster and cover-up. Every one of them knows they bury their failures, yet they try to assuage their consciences by persuading themselves there was no other way. Sincerely, Trevor G Marshall, PhD, 31 March 2006 |
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WASOG politics (wasogfilelink) The pulmonology department at Cleveland Clinic knows about our research, but the sarcoidosis specialist there has apparently rejected it. You need to understand that for 5 years now, the sarcoid pulmonologists, as a group (they have an organization called WASOG) have done everything they could to throw hurdles into my path. You yourself will have to ask them their motivation for doing that. Pulmonary Hypertension resolves as folks recover with the MP, but you will have to find a physician who is prepared to help you survive, rather than just trying to prolong life (the specialists are still using the same ineffective treatment concepts which they have used for the entire last half of the 20th Century). It takes guts to go against current medical pragma, and a very cool head. Your choice of physician at this point is very important. ..Trevor.. ps: I myself was told I had 18 months to live. That was in 1978, so don't get too hung up on it. That prognosis was incorrect, just as just about all of the WASOG dogma about Sarcoidosis is incorrect. However, cardiac involvement is serious, and the treatments traditionally used for cardiac sarcoidosis make it very hard to survive for more than about 5 years beyond diagnosis (please ask your Doc about your specific survival prognosis). So that means you don't have a lot of time to sit and twiddle thumbs, if you value your life, and your family. |
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Sleep Apnea and Sarcoidosis (sleepfilelink) The business of diagnosing and treating sleep apnea has boomed over the past few years. Sleep apnea is the temporary absence of breathing during sleep. People with sarcoidosis or other Th-1 diseases are often diagnosed with disordered breathing (or sleep apnea). This diagnosis should not diminish concern about and focus on treating the primary disease: sarcoidosis. Sarcoidosis itself can cause obstuctive sleep apnea due to the fact that sarcoid inflammation and granulomas (which are tumors) can obstruct upper airway passages, causing . In addition, use of the common therapy for relieving sarcoidosis symptoms: prednisone, which is a corticosteroid, usually results in significant weight gain. Obesity has been related to sleep apnea and weight reduction can result in some symptomatic relief. |
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Disease Clusters and Husband/Wife Cases (familialLink) Clusters of the disease have been reported, leading to speculation about person-to-person transmission or a shared exposure to an environmental agent. There have been case reports of familial clustering of sarcoidosis as well as husband-wife disease. A case-control study of residents of the Isle of Man found that 40 percent of the persons with sarcoidosis had been in contact with a person known to have the disease, compared with 1 to 2 percent of the control subjects. Studies have also revealed seasonal clustering of cases in the winter and early spring... One study reported three cases of sarcoidosis among 57 firefighters who apprenticed together. In the Isle of Man study, 18.8 percent of the cases of sarcoidosis occurred in health care workers (mainly nurses), compared with an incidence of 4.2 percent in the control group. Risk of Sarcoidosis for First- and Second-Degree Relatives In a large study involving 10,862 first- and 17,047 second-degree relatives of 706 sarcoidosis case-control pairs, persons with the illness were almost five times more likely than controls to have a sibling or parent with a history of the disease. Writing in the first of two December issues of the American Thoracic Society peer-reviewed American Journal of Respiratory and Critical Care Medicine, Benjamin A. Rybicki, Ph.D., of the Department of Biostatistics and Research Epidemiology, Henry Ford Health System, Detroit, Michigan, along with 22 associates, reported that the odds of a first- or second-degree relative with a history of sarcoidosis being related to a disease case were 4.6 times greater than those of a control subject. |
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(filelink) Cautionary Warning for Members Who May Be Hospitalized It has come to the attention of the Autoimmunity Research Foundation that there is a serious problem concerning treatment received by seriously ill patients when they are hospitalized. Sarcoidosis Sarcoidosis patients are especially at risk.This may stem from the current attitude among pulmonologists who have deemed themselves sarcoidosis experts despite their dismal failure to find a cure. Current literature published by these specialists states that once a sarcoidosis patient’s respiratory function falls below 50%, there is little hope of recovery. This belief and the reluctance to acknowledge the success of the Marshall Protocol and the insistence on continuing to treat sarcoidosis with various immunosuppressants may lead to inadequate or detrimental treatment during hospitalization for a secondary illness or an apparent exacerbation of the disease. Immunosuppressants Because the average doctor knows little about sarcoidosis, patients in respiratory distress, may be given immunosuppressants inappropriately, even in the presence of an acute infection. Patients who are hospitalized may have no choice but to be treated by one of these sarcoidosis ‘experts’, either directly or by consultation. Misinformed doctors, believing that sarcoidosis is incurable, might consider the patient’s situation to be terminal and not support his/her efforts to overcome seemingly insurmountable odds. Therefore, it is necessary to warn all members with reduced respiratory function that hospitalization could be dangerous to their well-being. Risks of hospitalization for all patients Hospitalization exposes fragile patients to additional serious problems such as antibiotic-resistant secondary infections, emboli, medication side effects or other serious adverse events. Compromised patients may not be able to combat these complications. The following suggestions are meant to prevent the need for hospitalization and provide guidance should you find yourself in an emergency situation. -Do not minimize the seriousness of your illness to yourself or your family. -Follow the MP cautiously and slowly to avoid an exacerbation of symptoms that becomes so severe you feel you need to go to the ER or Urgent Care. -Ask the study site moderators for help as soon as you think you are having a problem. -Make sure a family member or friend knows how to access the study site should you be too ill to do so yourself. -Take all known precautions to avoid an acute infection. See My respiratory function is poor. How can I prevent an acute infection? -Ask your doctor about having a supple of oxygen on hand for an emergency situation. -If you do develop an upper respiratory infection (such bronchitis, pnuemonia, sinusitis, otitis media) that needs treatment with an antibiotic, insist on a culture and treatment with a fluoroquinoloe (such as Levaquin) until the culture is read so you can continue the Benicar blockade. See My doctor thinks I have an upper respiratory infection. What should I do? (Sinus infection, cold, flu, pneumonia, bronchitis) -Ask your MP doctor to alert his/her staff to fit you in at their clinic immediately if you should need to be seen by a doctor. -Ask your MP doctor to call Dr. Marshall for suggestions regarding your care if s/he isn’t sure what to do. Power of Attorney for Health Care Be sure any previously made advanced directive (living will or power of attorney for health care) is up to date and that your health care agent (designated decision-maker) is someone you deeply trust and who knows about the Marshall Protocol what your desires are in case you are unable to make them known. If you have not filled out POA papers for health care, your local clinic should have a simple form available (no lawyer is needed). Keep a copy on file with your doctor and one in your possession. If you find yourself at the ER or Urgent Care: -Ask the ER physician to call your MP doctor. -You have the right to refuse treatment to the extent permitted by law and to be informed of the consequences of your refusal. -You have the right to be involved in all aspects of your care, including treatment decisions. -If you are incapable, a member of your family or your designated decision-maker should be allowed to participate in these decisions. Make sure they are familiar with the MP guidelines. -Have someone with you who will be assertive enough to advocate for you. -Do not attempt to explain the Marshall Protocol, just advise ER staff of the meds you have been taking that were prescribed by your doctor. -The focus of treatment should be on stabilizing the acute problem with standard methods that will not compromize the MP and which will allow you to return home as soon as possible rather than be admitted to the hospital. -Question everything and ask your advocate to take notes. -If oxygen is not offered and you are short of breath, ask for it (assure the doctor oxygen is appropriate to treat sarcoidosis) -If you need an antibiotic, insist the doctor prescribe a fluoroquinolone (such as Levaquin) so you can go home and continue the Benicar blockade (you may need to discontinue MP antibiotics during the duration of treatment with a fluoroquinolone). See I need to take a different antibiotic for awhile. What should I do? -Refuse all steroids in any form (oral, IV, injected or inhaled). -Insist on increasing the Benicar blockade by taking 40mg orally every 3-4 hours and 20mg sublingually (under the tongue) with each oral dose. -You do not need the ER doctor’s permission to resume the MP when you return home. See Information for emergency personnel If hospitalization is suggested, you or your designated decision-maker should: -Ask for specific reasons why this is necessary. -Ask if you can receive the same care at home, perhaps utilizing a Home Care service while being supervised by your MP doctor. -Insist that the referring physician call your MP doctor or Dr Marshall before you agree to hospitalization. If you find yourself in the hospital, you and your designated decision-maker should know: -You have the right to refuse any treatment (you may have to sign a waiver). Ask to be allowed time to think it over before you agree to a treatment. -Insist that no one caring for you is allowed to consult a sarcoidosis expert or pulmonologist or any other health professional about your treatment without your (or your POA's) express written permission. You do not waive your right to privacy under HIPPA and no attempt should be made to bypass that right by hiding your identity. This will prevent doctors from consulting any 'expert' on sarcoidosis who is likely to tell them to discontinue the Marshall Protocol. -You have the right to know the identity, professional status and professional credentials of health care personnel, as well as the name of the health care provider primarily responsible for your care. -You have the right to receive an explanation regarding your diagnosis, treatment, medical procedures, and prognosis (what to expect), in terms you can understand. When it is not medically advisable to provide this information to you, it should be relayed to appropriate family members or your designated decision maker. -Have an assertive person (who will ask lots of pointed questions of everyone) to stay with you day and night if possible. -Your advocate/s should keep a diary of your hospital stay. -Insist your MP doctor be part of the consultative process. Ask if s/he has been consulted when any significant decision is made. -In the event that you cannot make decisions for yourself, your health care agent (Power of Attorney for heath care or POA) can advocate on your behalf. Make sure s/he is familiar with the Marshall Protocol guidelines. -Make sure the only sarcoidosis expert consulted is Dr. Marshall, Ph.D who has published papers describing both the cause of, and cure for, pulmonary, cardiac and neuro-sarcoidosis. In an emergency, he can be reached 24/7 at 805-492-3693 (PST). -Insist on being told when anybody outside the team of doctors you or your designated decision-maker have met is given a summary of the case, or consulted in any way. -Refuse all vitamin D supplementation......in food, IV fluids or tube feedings. Alert staff to any other food allergies. -Insist that your environment be altered to reduce lighting to 30 lux. -Treatment during hospitalization should be focused on stabilizing your acute disease exacerbation or infection. -Immunosuppressants such as corticosteroids (prednisone, solu-medrol, etc., Enbrel (etanercept) , Humira (adalimimab) and Remicade (infliximab) are not appropriate treatments for any patient. Doctors may insist it is the standard of treatment for a sarcoidosis patient. The success and increasing popularity of the Marshall Protocol is apparently threatening to the specialists who have exercised sole power in guiding the treatment of sarcoidosis patients. Sadly, it seems these specialists are looking for opportunities to demonstrate immunosuppression works, and the MP doesn't. Sarcoidosis patients are at high risk while this attitude prevails. The following paper will come in handy should you need to bring a doctor up-to-date with the newly documented ineffectiveness of immunosuppressive drugs in the therapy of sarcoidosis. The Cochrane Report http://tinyurl.com/yb8ond -You should refuse any 'standard treatment' for chronic sarcoidosis because this condition is being treated effectively by another physician. -It may be impossible to persuade a specialist to allow the Benicar blockade while hospitalized. -The goal should be to overcome the acute problem in order to be released from the hospital as soon as possible. -Make your wish to return home as soon as possible very clear. Ask for supportive home services to facilitate this. You may need 24/7 caregivers, oxygen, IVs, nebulizer, etc. -Demand to continue the Benicar blockade. -Refuse all antifungals. -If an antibiotic is ordered insist on a fluoroquinolone until a culture proves a different antibiotic is needed. See I need to take a different antibiotic for awhile. What should I do? -Know your HIPPA rights. Find out who is allowed to have access to your confidential medical information and how to get that information for your own use. -You have the right to voice concerns or complaints regarding your experience as a patient. You are entitled to information about the mechanism for the initiation, review, and resolution of any complaints or concerns. If necessary, contact the customer advocate, hospital ombudsman or social worker for help. Print out these documents and put them in a folder for easy reference. Take them with you if you go to the ER or Urgent Care. See also: See Information for emergency personnel Hints for MCS sufferers who may be hospitalized |
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Letter to the NIH from a long-time sarcoidosis sufferer (filelink) Hello, I'm Janet Foutin. I have Sarcoidosis. You might recognize it as the disease that killed Reggie White. Sarcoid death didn't just start or stop with him, either. That said, the NIH currently says that this is not a deadly disease, yet their own study shows that once you have it, it kills in 10 to 20 years. Yet this information is being hidden. The NIH is not telling the public the truth about this deadly disease. They are also doing their best to suppress the information that even low-cost antibiotics can effect a cure. Why? NIH FOR DUMMIES: If you read this information from the NIH for patients, you might be lead to believe this disease is no big deal (I did the math in parenthesis): 140,000 Americans suffer from Sarcoidosis. Most live a normal life. 60% (@84,000) recover on their own 30% (@42,000) permanent damage 10% (@14,000) serious damage that can be fatal A startling statement also posted on this slide show clearly contradicts findings in the NIH Access Study: "Fortunately, many patients with Sarcoidosis require no treatment. Symptoms are usually not disabling and tend to disappear on their own." (see reference for full online patient booklet below) Unfortunately, even the NIH ignored their own well-funded access study when they updated the slide show information this spring (see reference notes below). The expensive Access Study (2-year perspective of patients) indicates somewhat different outcomes for Sarcoidosis patients -- none of the patients showed remission, and most got worse! But you have to actually read the study and look at the data -- not the conclusions of the report to find that detail. (http://autoimmunityresearch.org/access-2yr.htm) FIND IT ON THE WEB Another very interesting phenomena is occurring, too. Sarcoidosis patients are finding and demanding health with the Marshall Protocol, which is based on science and research. More and more patients are getting it through word-of-mouth and the Web, and they are not daunted by detracters, either. Dr. Trevor Marshall, Ph.D. is a skilled bio-chemist that suffered years with Sarcoidosis, even with end stage lung conditions, but would not accept sickness and death for an answer. Building on research by other scientists like Dr. Lida Mattman (1998 Nobel Prize nominee) and understanding available prescription chemical processes in biological environs, he defined the "Marshall Protocol" to stop the disease process. Fully aware of technical publication requirements, he researched and published using ethical parameters. He now has willingly shared these findings --at no charge -- with Medical Doctors and their patients so others could achieve wellness, too. I, like hundreds of other Sarcoidosis patients, was tired of never getting any better or being fed drugs that do not cure but do cause serious side effects that had actually made my disease worse. I, like hundreds of other Sarcoidosis sufferers (that clearly were not getting any better or going into remission -- with/without traditional treatments), turned to the Web to find information that might lead to an end of my suffering. Fortunately, I found the Marshall Protocol, examined the evidence, took action, and am now enjoying the benefit if science at its best. Compared to the rosy picture the NIH paints for patients, Dr. Marshall is not afraid to write this: "Last year 73,000 discrete visitors looked at SarcInfo.com. Not one stopped by to say that their disease has gone away. Each month another 15,000 visitors drop by SarcInfo.com. I am still waiting for the first true case of spontaneous remission to pop up." http://tinyurl.com/ce2ek THE OTHER STORY The NIH distributes power. Many so-called Sarcoidosis centers that receive financial backing from the NIH want to squelch this protocol and have been actively working to discredit Dr. Marshall. The NIH still must take action on hundreds of letters from Sarcoid sufferers who flooded Dr. Zerhouni's email, fax and mail this spring with their testimony of the Marshall Protocol, and their call to accept science over "anecdotal misinformation which has gained credence by repetition." http://tinyurl.com/bp69b The NIH, NHLB and major Sarcoid center actions continue to dissuade and confuse well-meaning doctors with baseless criticisms of the Marshall Protocol. All this, while the majority of uniformed patients continue to suffer and die with outmoded but "accepted" treatments. I encourage you to please look into the facts, look at both sides of the argument and then look at those who have undergone the Marshall Protocol and are living healthy, happy lives after years of suffering. There is a great story and the potential to help speed the progress of truth to those who suffer with Th1 disease. EXAMINE THE MARSHALL PROTOCOL I suggest you also look at http://www.marshallprotocol.info to understand the Marshall Protocol. You will find the Marshall Protocol Phase I, links to peer-reviewed medical journal publications by Dr. Marshall, as well as the daily reports of those who are undergoing the Marshall Protocol at this time. You can even contact Dr. Marshall for an interview here: 805-492-3693 or at trevor.m@yarcrip.com. I highly recommend interviews with Meg Mangin, R.N. a member of the research team, and other medical professionals enjoying health from the Marshall Protocol. Nurses, doctors and others have a higher than expected infection rate with this disease, and some doctors are successfully treating themselves along with their patients with the MP. EXAMINE THE REST NIH information sites with a textbook historical content of Sarcoidosis are easily found in a variety of places. Of course, you should ask questions of the administration at the Cleveland Sarcoidosis Clinic, which hosted a recent national conference. The medical professionals sessions at that conference basically communicated to those in attendance that: -There is no cure -There is no tool to predict prognosis -Imaging (X-ray, CT) doesn't correlate with disease activity or severity -Conventional treatments seem effective at first, but they do not stop the patient's "deterioration" and demise -The main goal is to keep the patient at status quo for as long as possible with drugs and treatments that are known to do additional harm Their good news, though, was that the NIH has open avenues to access federal research funds for those who persist along these same lines of thought. By comparison, Dr. Marshall has a different perspective: -There is a cure -There is a method to identify the illness and current severity -Imaging is optional -It will stop the patient's "deterioration" and demise -Drugs and treatments are reasonable with low risk of side effects The bad news is, to date, Dr. Marshall's submissions to the NIH for funding have been denied and dismissed. THE PATIENT PERSPECTIVE You should also know that my experience is not unique. I had to go through a number of doctors before I even was diagnosed with this disease, as it pretends to be something else and may take years to discover using traditional clinical evaluation processes. When finally diagnosed in 1999, the predominant option was Prednisone. I quickly realized Prednisone (corticosteroid) was great for a short term quick fix to allow me to breath and walk, but long term it created more problems and actually did nothing to cure me. Doctors didn't tell me my disease could be fatal, either, they just gave me two slightly contradictory statements: it probably would go away by itself and I might need to be on prednisone for the rest of my life. But my disease didn't go away and as Prednisone caused many more problems, I self-weaned after 9 months. I didn't return to a doctor for five years in fear of having to take the drug again and hoped that the disease would go away on its own. The disease did not go away, though, and in February of 2005 when it was progressively getting worse, I took action to do something about it. Knowing the perils of Prednisone, I searched the Web in hopes of finding new information. From an MSN support chat board, I found http://www.sarcinfo.com (the earliest MP site). There I saw the disease accurately described, and found my symptoms clearly explained in simple, but well-founded truth based on science. I ordered the 2005 conference CDs and changed lifestyle habits to reduce my D exposure through food and light. That helped me to feel better over the next six months as I negotiated fruitlessly with my doctor (who eventually destroyed my hopes with mis-information from traditional sources, ordered only partial blood work, then told me my blood tests showed I was well). I finally found another MD that would treat me using the Marshall Protocol. |
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Why Does the Body Make Granulomas? (filelink) Dr. Gary Kaiser, microbiology professor at the Community College of Baltimore County, explains how and why the immune system produces granulomas: "The formation of granuloma in infections such as tuberculosis, leprosy, histoplasmosis, and coccidioidomycosis is a cytokine-mediated cellular response. Because macrophages have difficulty in removing the microbes that cause these infections, there is a continuous secretion of cytokines and chemokines that leads to an accumulation of densely packed macrophages around the microbes. The macrophages release fibrogenic cytokines such as TNF and IL-1 that lead to the formation of granulation tissue and scar tissue. The resulting mass is called a granuloma and is an attempt by the body to "wall-off" or localize the infection." In tuberculosis, for example, a macrophage can usually engulf the tuberculosis bacterium, but then apparently the bacterium has a means for preventing it own death. If the macrophage is not "activated" by paracrines from a specific immune response, the bacteria may remain alive for long periods within the macrophage. In this circumstance, other macrophages surround and wall off the infected macrophages, forming a type of chronic inflammation called a granuloma. What Goes Wrong? Macrophages are a type of white blood cell, assigned the duty of killing bacterial invaders. Macrophages are called phagocytes, or "eating cells." In fact, the word "macrophage" means they are the "big eaters" of the immune system. Take a look at the video clip on this web source by clicking on "time-lapse movie" to see how a white blood cell engulfs an enemy. This is what happens to bacterial invaders. In sarcoidosis, macrophages are highly activated, but not completely effective, so other macrophages surround and wall off the infected macrophages (the ones with bacteria inside them), joining together their cell material to form multi-nucleated giant cells with little or no dead material (necrosis) because the bacteria are still alive. Death for the Greater Good Macrophages have to die to kill the engulfed enemy bacteria and complete the phagocytic process. Otherwise, bacteria may be able to live and even replicate safely inside the macrophage and the human host will still be ill. This can be disastrous, considering that the life span of a macrophage may be months or even years. Even slowly-reproducing bacteria might establish a stronghold by living inside macrophages. Bacteria can continue living and replicating inside macrophages within granulomas. ABC Australia has a three-part series in their "Great Moments in Science" called "Apoptosis" in this link. It explains the natural process of cell death for the greater good and health of the host. Other Links and Resources: CELL WALL DEFICIENT BACTERIA AND THE MARSHALL PROTOCOL What is the basic definition of Th1 inflammation? Inside the Cell (a tutorial) Do people with Th1 inflammatory disease have a genetic defect? How the Immune System Works Innate and Acquired Immunity Immunology Syllabus Inner Life of the Cell video How Your Immune System Works |
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(filelink) Sarcoidosis can cause false positives in cancer tests Be aware that some of the tests used to identify cancer can be elevated in sarcoidosis, resulting in a "false positive." Sarcoidosis Associated With an Elevated Serum CA 125 Level American Journal of the Medical Sciences. 334(6):441-443, December 2007. Kalluri, Meena MD; Judson, Marc A. MD CA 125 is a glycoprotein expressed by a variety of tissues of mesothelial origin. It has classically been associated with ovarian carcinoma. It has also been reported to be elevated in certain granulomatous conditions. We describe a patient with sarcoidosis and an elevated serum CA 125 level and review the medical literature on this topic. Conclusions: Peritoneal sarcoidosis may "mimic" ovarian carcinoma in that it may present with peritoneal or abdominal findings and an elevated serum CA 125 level. |
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[filelink] Results of typical standard sarcoidosis treatment by a sarcoidosis 'expert' This message was recently posted on a sarcoidosis support message board. Bob Baughman is the best, or second best, Sarcoidosis specialist in the world (reputedly). This is how he treats the disease: ------------- Hi guys, I havae written in a while but I read daily.I'm in Ohio so I go to Dr.Baughman I went for a Ct scan of my chest on Friday and they put it on a CD and I gave it to him. I thought that's amazing.Take a chest x-ray and its on a Cd he said oh tahts your copy you can use it as a screensaver on your computer I told him I have prettier things on my computer. I'm an intresting case I've had sarc since 1992 but I moved to Ohio in 2001.I go for Remicade Iv therapy every four weeks and I have pulmnonary hypertension.The metroxtate, enbrel, humira, none of that works on me. But the $6,000 ventavis inhalation therapy that you take every two hours while wake does{thank God my husband has good insurance}the remicade helps my arthritis and sarc but now my veins are so thin and brittle I'm on coumadin and and a drug induced diabetes fro the prednisone,they want to install a port to draw blood from plus do another heart cath to check the pressures. I haven't had a heart cath in about a year the specialist I had argued me down that he didn't put me on coumadin and when I showed him the logbook where you record the minutes for the ventavis he wanted to know what it was?His nurse was trying to tell him he wouldn't listen,so I told him I might just be anumber to you but i'm somebody's wife,mother,sister,grandma,and I walked out.I got pulmonary hypertension from taking phen-Feb when I lived in Texas I thought if lost some weight it would help me to breathe better. I never suspected anything was wrong they always took my b/p and did EKG.So Dr.Baughman called me Friday said he got another cardiolgist to do the heart cath and they will do it the same time as the port and not to take the coumadin two days prior to the procedure because it would cause excessive bleeding. I'm on continous oxygen I have to go ofor a job interview Wed,I'm a paralegal graduated with tanker in 2004. I've only worked six months since I graduated the company lost there main client sometimes I feel as if I went to school for nothing. Rita |
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