Sarcoidosis

A basic explanation of sarcoidosis from Wikipedia

http://jcm.asm.org/cgi/reprint/34/9/2240.pdf

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2383887 Look at the conclusions ConclusionThe most interesting finding in this study was the demonstration that molecular analysis of sarcoidosis granulomas for microbial virulence factors can lead to identification of target antigens. The responses detected closely parallel prior reports of immune recognition of secreted proteins in mycobacterial infections [17,26]. A dual analysis for microbial nucleic acids and immune responses increases the sensitivity for detecting microbial virulence factors in idiopathic diseases, providing complementary mechanisms.

The use of Minocycline in Sarcoidosis:

Ohtsuka S, Yanadori A, Tabata H, Yamakage A, Yamazaki S. Sarcoidosis with giant parotomegaly. Cutis. 2001 Sep;68(3):199-200. PMID: 11579785 [PubMed - indexed for MEDLINE]

This case showed improvement with Minocycline in another non-caseating granulomatous disorder;

Olivier V, Lacour JP, Castanet J, Perrin C, Ortonne JP. [Cheilitis granulomatosa in a child] Arch Pediatr. 2000 Mar;7(3):274-7. French. PMID: 10761605 [PubMed - indexed for MEDLINE]

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), inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. 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-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol., 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.

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.

See Hypervitaminosis D

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.

~Signs and symptoms of vitamin D intoxication

See also: “Facial paralysis in children”¹

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 “Facial Paralysis in Children”²

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.

Trevor Marshall, PhD*

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 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. 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 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).

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”³
• “Facial Swelling and Systemic Sarcoidosis”⁴
  
• “Oral manifestations of sarcoidosis”⁵
  
• “Granulomatous cheilitis (lip swelling) can lead to a sarcoidosis diagnosis”⁶
  

- gingivitis⁷ 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”⁸

- 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.

Dysphonia

• “Acute reversible dysphagia and dysphonia as initial manifestations of sarcoidosis”⁹

Since sarcoidosis causes a dysregulation of Hormone D (1,25-dihydroxyvitamin DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.), 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

Conjunctiva¹⁰

A patient with sarcoidosis diagnosed by biopsy of scleral nodules¹¹

Wirostko papers on eye disease

In the eye, the lacrimal gland¹² is a common area of manifestation for sarcoidosis. Its function is to 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.

Sarcoidosis itself can cause cataracts, because sarcoid inflammation of the eye can result in a cataract.

See Eye inflammation

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.

Eye inflammation (uveitis) is described by the Cleveland Clinic here. It says, “Complications of uveitis may include glaucoma, cataract, abnormal blood vessel growth, fluid within the retina and vision loss.”

Sarcoidosis can result in abdominal lymphadenopathy¹³. 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.

Nose and sinuses¹⁴

Sinonasal sarcoidosis¹⁵

Central Nervous System (Yes, they sometimes want a brain tissue biopsy which isn't necessary)¹⁶

Muscle¹⁷

Maxillary Involvement¹⁸

Renal¹⁹

Pancreas²⁰

Splenomegaly (Enlarged Spleen)²¹

Anemia See Anemia and Th1 DiseaseAny of the chronic inflammatory diseases caused by bacterial pathogens.

There is limited and controversial evidence that changes in the expression of cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. 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 cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. 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

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 Mental and neurological symptoms

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 sarcoidosis²²

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 corticosteroidA first-line treatment for a number of diseases. Corticosteroids work by slowing the innate immune response. This provides some patients with temporary symptom palliation but exacerbates the disease over the long-term by allowing chronic pathogens to proliferate., usually results in significant weight gain. Obesity has been related to sleep apnea and weight reduction can result in some symptomatic relief.

Extrapulmonary sarcoidosis primarily diagnosed in the liver²³

Asymptomatic organ involvement is quite common in sarcoidosis. An article from Medscape Gastroenterology 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 liver²⁴

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 sarcoidosis with presentation of large left atrial mass²⁵

Chest pain is, in fact, a common symptom endured by sarcoidosis patients, substantiated by reports such as “Impact of pain in a Dutch sarcoidosis patient population”²⁶, 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 diagnosed²⁷. Cardiac sarc can cause chest pain.

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 prognosis²⁸

Sudden death with clinically undiagnosed pulmonary hypertension²⁹

Pulmonary hypertension in advanced sarcoidosis: epidemiology and clinical characteristics³⁰

CT findings in severe thoracic sarcoidosis³¹

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.”

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 trauma³².

Lupus pernio lesions, like other sarcoid manifestations in the upper respiratory tract³³, can be quite resistant to the standard immunosuppressive therapies.

Lupus pernio is said to be the skin lesion most characteristic (a diagnostic indicator) of sarcoidosis³⁴, 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

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 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 are some photos 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.

Alan Cantwell, MD (dermatologist) wrote a paper on the skin in Th1.

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 Marshall, PhD*

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.

Sarcoidosis is a multi-systemic disease that can be confused with benign or malignant tumors³⁵.

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 Inflammation causes cancer

Question: 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.

Here is an alternative perspective on the ACCESS study data (saying race was not a big issue).

Trevor Marshall, PhD*

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.

Trevor Marshall, PhD*

The only effective treatment for sarcoidosis is the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis..

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 the first report from the 2005 American Thoracic Society Conference, 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.

You will note that our Autoimmunity Research FoundationNon-profit foundation dedicated to exploring a pathogenesis and therapy for chronic disease. is responsible for 2 out of the total 5 :):)

Trevor Marshall, PhD*

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 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

A variety of different kinds of evidence supports the contention that sarcoidosis is caused by bacterial infection:

• Donor transmissionAn incident in which an infectious disease is transmitted.: Bacteria is transmitted via bodily fluids and tissues including heart³⁶, bone marrow³⁷³⁸ and stem cell transplantation³⁹. There is even a term for it: “donor-acquired sarcoidosis.” According to the study Donor-acquired sarcoidosis indicates infectious origin⁴⁰, “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].”

• Presence of bacteria in patients with sarcoidosis especially in the granuloma – the following types and species of bacteria have been found in patients with sarcoidosis:
  • L-formDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria./cell wall deficient bacteria ^{41 42 43}
  • mycoplasma ⁴⁴
  • Borrelia burgdorferi ^{45 46 47 48}
  • Mycobacterium, in general ^{49 50}; in one study ⁵¹ Mycobacterium was found in the majority of sarcoidosis patients
  • Mycobacterium avium ⁵²
  • Mycobacterium tuberculosis^{53 54 55 56 57}
  • Propionibacterium acnes^{58 59}
  • Rickettsia helvetica⁶⁰
• Familial aggregation – One study⁶¹ found that among the 215 study participants who had been diagnosed with sarcoidosis, there were five husband-and-wife couples that both had the disease. Yet sarcoidosis is such a rare disease that statistically speaking there should have been none. They also noted that the risk for sarcoidosis increased nearly five-fold in parents and siblings with the disease. Another study⁶² reported three cases of sarcoidosis among ten firefighters who apprenticed together.

A Case-Control Etiologic Study of Sarcoidosis (ACCESS)

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 aggregationOccurrence of a given trait shared by members of a family (or community) that cannot be readily accounted for by chance. 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 families⁶³

A sarcoidosis genetic linkage consortium: the sarcoidosis genetic analysis (SAGA) study⁶⁴

~Belinda Fenter

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.

In a large study involving 10,862 first- and 17,047 second-degree relatives of 706 sarcoidosis case-control pairs (Risk of Sarcoidosis for First- and Second-Degree Relatives), 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.

How does Th1 inflammation develop? What is successive infection?

Am I contagious?

Will re-infection occur if my partner or family members are not treated?

The only thing that can cause the granuloma of sarcoidosis is the intraphagocytic microbiotaThe bacterial community which causes chronic diseases - one which almost certainly includes multiple species and bacterial forms. of antibiotic-resistant bacterial pathogens.

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 Medicine and 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”.

• 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? ⁶⁵ 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.

• In 2001, Dubois,et al, published an article, Sarcoidosis: genes and microbsoil or seed?⁶⁶, 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”.

• A landmark Swedish study from 2002, Presence of Rickettsia Helvetica in Granulomatous Tissue of Patients With Sarcoidosis⁶⁷, 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.”

• Lida Mattman's study Growth of Acid Fast L Forms From the Blood of Patients With Sarcoidosis⁶⁸, was published in Thorax and reports that various Cell Wall Deficient bacteria were found in 95% of sarcoid biopsy samples.

• 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 Response⁶⁹, found Mycobacteria in 64% of tissue samples.

• D.R. Moller from Johns Hopkins University School of Medicine, concludes in his paper titled What causes sarcoidosis?⁷⁰ 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.
3. 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

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.

There is an excellent Canadian Radio show on which the World's leading scientists were interviewed regarding Cell Wall Deficient mycoplasma. Although it is pretty long (two hours) you will find it an amazing eye-opener. Here is the link to it.

Trevor Marshall, PhD*

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.

~Friedrich Flachsbart, MD.

Initiating treatment with antibiotics to provide a therapeutic probeA brief trial of the Marshall Protocol to see if it will generate an immunopathological response. The "gold standard" for testing whether a patient is a good candidate for the MP. (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 Cantwell, MD

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 Marshall, PhD*

The presence of detectable bacteria in the spinal fluid is common. Indeed, Emil Wirostko (whose group took those wonderful photos of the bacteria) was convinced that stem cells become infected at an early stage of Th1 disease, and that is why it spreads so evenly throughout the body.

Trevor Marshall, PhD*

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 containing species info:

Molecular Analysis of Sarcoidosis Tissues for Mycobacterium Species DNA

Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis⁷¹

Seroprevalence of anti-Borrelia antibodies among patients with confirmed sarcoidosis in a region of Japan where Lyme borreliosis is endemic⁷²

Trevor Marshall, PhD*

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. See Molecular analysis of sarcoidosis tissues for mycobacterium species DNA⁷³

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.

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 Marshall, PhD*

Other studies citing a bacterial cause for sarcoidosis:

• Antibacterial Therapy Induces Remission in Sarcoidosis Authors: Trevor G Marshall, PhD, Belinda J. Fenter, and Frances E Marshall, GradDipPharm, RPh
• Chlamydophila bacteria prevalent in Sarcoidosis patients
• Experimental Skin Sarcoidosis In A Doctor Volunteer proves pathogenic cause of sarcoidosis
• More recent studies from PubMed showing a microbial pathogenesis for sarcoidosis
• Evidence that all chronic diseases are caused by bacterial infection

Can I donate blood, organs, tissue or bone marrow if I have a Th1 inflammatory disease?

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.

One of Lida Mattman's slides in Chicago shows L-formsDifficult-to-culture bacteria that lack a cell wall and are not detectable by traditional culturing processes. Sometimes referred to as cell wall deficient bacteria. 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 Marshall, PhD*

I just saw this letter in CHEST online this morning. I thought you might be interested: Leukoreduction of transfusions and blood stream infections

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 Marshall, PhD*

Sarcoidosis has been transmitted to organ recipients from organ donors. It's in the bone marrow and stem cells.

Transmission of sarcoidosis via cardiac transplantation⁷⁴

Possible transmission of sarcoidosis via allogeneic bone marrow transplantation⁷⁵

Donor-acquired sarcoidosis⁷⁶

Granulomatous pneumonitis following bone marrow transplantation⁷⁷

Pulmonary sarcoidosis following stem cell transplantation: is it more than a chance occurrence?⁷⁸

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 sites⁷⁹

Cutaneous sarcoidosis in blood donation venepuncture sites⁸⁰

~Belinda Fenter

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 sarcoidosis⁸¹

Opportunistic infections and sarcoidosis⁸²

Sensitive differential detection of genetically related mycobacterial pathogens in archival material⁸³

Identification of Mycobacterium avium complex in sarcoidosis⁸⁴

Disseminated cutaneous Mycobacterium avium-intracellulare resembling sarcoidosis⁸⁵

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
Liver-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

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

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.

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.

Trevor Marshall, PhD*

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.

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 remissionTheory that diseases go away of their own accord. to pop up.”
Spontaneous remission

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.”
Sarcoidosis Mythology⁸⁶

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 the Marshall Protocol study site 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 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.

~Janet Foutin

Mac Attacked by Rare Disease

Feb 10, 2005: America, Bernie Mac is battling a nasty condition.

The 46-year-old star of Fox's The Bernie Mac Show announced Thursday that he has sarcoidosis, a rare and sometimes life-threatening autoimmune disease that causes inflammation of the body's tissues, most frequently in the lungs.

Mac, who first made the disclosure via Star magazine's Website, issued a statement through his publicist saying he was first diagnosed with sarcoidosis in his 20s.

“I've had sarcoidosis since 1983, and it has not altered or limited my lifestyle,” Mac says. “No one knows where sarcoidosis comes from or where it starts, and there's no known cause for this condition that effects primarily minorities.”

Last summer Mac's health became an issue when he was hospitalized after completing work on Ocean's Twelve. Filming on the fourth season of The Bernie Mac Show was subsequently delayed.

Initially, a Fox rep said Mac was merely taking a self-imposed hiatus because he was suffering from exhaustion, brought on by a heavy work schedule that included his TV show and the Ocean's Eleven sequel, along with the baseball film Mr. 3000 and the upcoming Guess Who, the racially flipped update of the 1967 drama Guess Who's Coming to Dinner, in which he plays a dad upset his daughter wants to marry a white guy. The network later said Mac was suffering from pneumonia.

But now, his spokesperson tells Star that Mac “had double pneumonia which weakened his lungs and his entire immune system, and the sarcoidosis symptoms became pronounced.”

The disease can prove fatal in about in about five percent of cases and is cited as the cause of death for football great Reggie White last December. Hall of Fame basketball player Bill Russell also suffers from the disorder.

Mac's publicist, Matt Labov, is quick to point out that sarcoidosis is a “treatable illness and not deadly.” In his statement, Mac says, “I still walk, play basketball and do normal things…Since sarcoidosis hasn't slowed me down, then it shouldn't be a concern for others.”

The Chicago native says he has visited several sarcoidosis patients at La Rabida Hospital in Chicago.

“I'll be devoting my summer to creating the Bernie Mac Foundation. Through my ongoing and private efforts, I'm organizing a golf tournament in Chicago, and the proceeds will be given to different sarcoidosis organizations. I hope to announce further details about this soon.”

Fox, meanwhile, says that since a healthy Mac has returned, there have been no further interruptions to filming his sitcom, which airs Fridays at 8 p.m. ET/PT. Production is complete on about half of its 22 scheduled episodes.

“Mac's publicist, Matt Labov, is quick to point out that sarcoidosis is a “treatable illness and not deadly.”

~Bridget Byrne, Eonline

It would seem to me that as many sarcoidosis patients as possible need to write to this gentleman, and let him know the truth about what Bernie's future is really going to look like

Trevor Marshall, PhD*

Sadly, Bernie Mac passed away August 9, 2008. His publicist attributes his demise to complications from pneumonia.

See this interesting article in Bacteriality: Bernie Mac didn’t have to die - pervasive misconceptions about sarcoidosis Author: Amy Proal

~Margo

Bernie Mac's final curtain call

Aug 11, 2008: BERNIE Mac, television and movie star, died yesterday aged 50.

Mac, who starred in the casino heist caper Ocean's Eleven and gained a Peabody Award for his sitcom, The Bernie Mac Show, died in Chicago from complications due to pneumonia, publicist Danica Smith said.

The comedian suffered from sarcoidosis, an inflammatory lung disease.

Mac's brand of comedy landed him in trouble when he was heckled during an appearance last month at a fundraiser for Democratic presidential candidate Barack Obama.

But despite controversy, in his words, Mac was always a performer.

“Wherever I am, I have to play,” he said in 2002. “I have to put on a good show.”

~AP

Corticosteroids

Cardiac sarcoidosis underlies idiopathic dilated cardiomyopathy⁸⁷

Cardiac sarcoidosis is frequently overlooked or misdiagnosed as idiopathic dilated cardiomyopathy (DCM), primarily because of difficulties in its diagnosis.

Lung involvement may be misdiagnosed as a “respiratory infection.” It has to be differentiated from “pneumonia” (see A case of pulmonary sarcoidosis with usual interstitial pneumonia-like lesions distributed predominantly in the lower lung fields⁸⁸
and lots of other conditions (Sarcoidosis masquerading as eosinophilic pneumonia⁸⁹)

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 immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed..

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 Marshall, PhD*

Lung diffusion testing Illustration of DLco test

The overall accuracy of the FVC for restriction is about 60%. How accurate is spirometry at predicting restrictive pulmonary impairment?⁹⁰ Full text here
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.

~www.spirxpert.com

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.

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.

This resource says that crackles are sometimes found in sarcoidosis. And interstitial lung disease is listed here as one reason for crackles.

Crackles (Rales) are discontinuous, non-musical, 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 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. Clinical bronchiectasis complicating pulmonary sarcoidosis: case series of seven patients⁹¹

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. 1) Since antibiotics are used to treat bronchiectastis, and
2. 2) there isn't a singular well-defined treatment for bronchiectasis,
3. 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 Fenter

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.

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. This Medscape article discusses how supplemental oxygen facilitates lung emptying.

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 Fenter

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. The pattern and distribution of calcified mediastinal lymph nodes in sarcoidosis and tuberculosis: a CT study⁹²

FAQ My lymph nodes are growing. Is this normal? Should I be concerned about cancer?

Photos of sarcoidosis gross pathology

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:

Assessing lung function & Improvements in pulmonary function tests

Pulmonary Function Tests (PFTs)

Pulomonary hypertension may develop as a result of sarcoidosis.

Pulmonary hypertension associated with sarcoidosis: mechanisms, hemodynamics and prognosis⁹³

Sudden death with clinically undiagnosed pulmonary hypertension⁹⁴

Pulmonary hypertension in advanced sarcoidosis: epidemiology and clinical characteristics⁹⁵

CT findings in severe thoracic sarcoidosis⁹⁶

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.

~Dr. Gary Kaiser, microbiology professor at the Community College of Baltimore County

In tuberculosis, for example, a macrophage can usually engulf the tuberculosis bacterium, but then apparently the bacterium has a means for preventing its 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.

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.

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.” 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
• Do people with Th1 inflammatory disease have a genetic defect?
  
• Inside the Cell (a tutorial)
  
• How the Immune System Works
  
• Innate and Acquired Immunity
  
• Immunology Syllabus
  
• Inner Life of the Cell video
  
• How Your Immune System Works

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. :)

ps: I would be happy to discuss these issues with Doc, if he calls me.

Trevor Marshall, PhD*

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. Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells⁹⁷

Take a look at 36 years of my own chest 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…

Trevor Marshall, PhD*

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 Marshall Protocol 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.

~Belinda Fenter

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
• Sarcoidosis and Remission
• 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 Marshall, PhD*

Question: 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.

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 :X But the lungs will function well despite the fibrotic scar tissue and any small calcifications.

Trevor Marshall, PhD*

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 Marshall, PhD*

What degree of healing is possible with the MP?

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.

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.

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.⁹⁸

You will note that our Autoimmunity Research Foundation is responsible for 2 out of the total 5.

Trevor Marshall, PhD*

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.

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

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. We also have an annotated copy of the full-text.

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 Marshall, PhD*

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.”

Pulmonary Reviews.com article by two of the ACCESS authors

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.

~Trends in pulmonary and critical care medicine, Vol. 7, No. 4 April 2002

Aug 14, 2003: 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 predict the need for therapy, the level of disability, or the prognosis IN AN INDIVIDUAL 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.

Sept 3, 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…especially the X-ray staging system.

Oct 30, 2003: Please realize that I personally think that this whole stage system is antiquated and offers very little today. It was developed prior to 1960 when there were no CT scans and we knew much much less about sarcoidosis.

~Marc Judson, MD

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.

Apr 30, 2002: 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.⁹⁹ 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.¹⁰⁰

Most importantly, we now know that 1,25 dihdroxyvitamin D3 is secreted by the inflammatory macrophages that make up granuloma.¹⁰¹ 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.¹⁰²

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.¹⁰³

Trevor Marshall, PhD*

Sarcoidosis patients must avoid ingested Vitamin D

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. Nowadays 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 DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. ) 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

Gene Johnson

sarcoidosis, bladder cancer

Read the interview

Chris Eastlund

diabetes, sarcoidosis, irritable bowel syndrome

Read the interview

Freddie Ash

sarcoidosis of the heart, coronary artery disease, atrial fibrillation

Read the interview

Sherry Cook

sarcoidosis, cat scratch fever, restless leg syndrome

Read the interview

Mirek Wozga

sarcoidosis

Read the interview

Guss Wilkinson

sarcoidosis, psoriasis, insomnia, kidney stones

Read the interview

Roy P.

sarcoidosis, rheumatoid arthritis

Read the interview

Leesa Shanahan

sarcoidosis (Hedfort Syndrome), uveitis

Read the interview

Shirley J. (Saj)

sarcoidosis

Read the interview

Carole Morgan

sarcoidosis, fibromyalgia, chronic fatigue syndrome (CFS)

Read the interview

Jane Taylor-Aoki

neurosarcoidosis, systemic sarcoidosis; spasticity, myasthenia, CNS dysfunction, joint pain, pulmonary, splenic and cardiac involvement

Read the interview

Interviews of patients with other diseases are also available.