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Aussie Barb
Research Team
| Joined: | Thu Jul 22nd, 2004 |
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Posted: Sun May 22nd, 2005 02:40 |
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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)
____________________
Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| 24+ years not Dx| ABCofMP
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Meg Mangin R.N.
Research Team
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Posted: Thu May 26th, 2005 09:50 |
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 16:19 |
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 16:29 |
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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?
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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?
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 16:34 |
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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 05:33 by Meg Mangin R.N.
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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 17:02 |
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 17:07 |
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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?
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 17:31 |
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 17:33 |
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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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Meg Mangin R.N.
Research Team
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Posted: Sun May 29th, 2005 17:44 |
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| SARCOIDOSISlink< | | |
