Sarcoidosis or sarc is a multisystem disorder characterized by granuloma, ball-like encapsulations of phagocytic cells driven by microbes. Sarcoidosis is often called the “great masquerader” as there may be several atypical or nonspecific presentations – including not just the lungs but the brain, lymph glands, spleen, liver, skin and heart among others.1)

An infectious etiology of sarcoidosis has long been suspected. Today scientific evidence provides a strong, if not conclusive, link between infectious agents and sarcoidosis.2)

Sarcoidosis was the first disease treated by the Marshall Protocol.3) The FDA's Office of Orphan Products Development has conferred orphan drug status on several MP medications.

Evidence of infectious cause

Today scientific evidence provides a strong, if not conclusive, link between infectious agents and sarcoidosis.4)

History of conflicting results

An infectious etiology of sarcoidosis has long been suspected and investigated, sometimes with inconsistent results. For example, the histologic similarity of sarcoidosis to Mycobacterium tuberculosis (see discussion of granuloma below) infection led to the “extensive” evaluation of this organism as a possible etiologic factor.5) The findings have been mixed with some investigators finding evidence of M. tuberculosis6) 7) and some failing to confirm this work.8) 9) 10) 11) 12) In their 1996 review of mycobacteria's possible role in sarcoidosis, Zumla and James list 15 studies evaluating a mycobacterial cause of sarcoidosis, only three of which were negative.13)

There appear to several reasons why researchers have failed to definitively link microbes to sarcoidosis in all cases. For one, even today researchers adhere to the antiquated model of disease set forth by Koch's postulates namely that a pathogen must be: found in all cases of the disease examined, prepared and maintained in a pure culture, capable of producing the original infection, even after several generations in culture, and retrievable from an inoculated animal and cultured again. For all their lingering influence, Koch's postulates never anticipated the era of the human metagenome in which thousands of difficult or impossible-to-culture species of bacteria – rather than just one – contribute to a single disease state. Indeed, the notion of a single causative agent is not in keeping with the worldwide distribution of sarcoidosis.14) Koch's century-old ideas have held science back from understanding how chronic disease occurs because they make no provision for these facts.

Communities of microbes found in patients

The following types and species of bacteria have been found in patients with sarcoidosis, especially the granuloma:

  • L-form/cell wall deficient bacteria 15) 16) 17)
  • mycoplasma 18)
  • Borrelia burgdorferi 19) 20) 21) 22)
  • Mycobacterium, in general 23) 24); in one study 25) Mycobacterium was found in the majority of sarcoidosis patients
  • Mycobacterium avium 26)
  • Mycobacterium tuberculosis27) 28) 29) 30) 31)
  • Propionibacterium acnes32) 33)
  • Rickettsia helvetica34)

Mycobacterial and propionibacterial DNA have been found in the lymph nodes of Japanese and European patients with sarcoidosis.35)

Granuloma without necrosis in a lymph node of a person with sarcoidosis.


A granuloma is a ball of immune cells associated with various disease states including sarcoidosis, Crohn's, and tuberculosis. (Hence, the term “granulomatous diseases.”) The presence of noncaseating (no tissue death) granuloma of the lungs is the hallmark of sarcoidosis. In sarcoidosis, granuloma are most commonly found in the alveolar septa, the walls of bronchi, and the pulmonary arteries and veins.

At their core, granuloma contain cells from the innate immune system: macrophages and monocytes. Lymphocytes, which are a part of the adaptive or acquired immune system, tend to exist on the periphery or in latter stages of development.36) 37)

Granulomas may represent an extreme form of innate immune dysfunction.38) The macrophages and monocytes in granuloma are infected by intracellular pathogens such as Mycobacteria. When infected, the internal chemistry of innate immune cells is altered such that these cells no longer undergo apoptosis (programmed cell death).39) Significant differences in the expression of apoptosis-related genes were found in peripheral blood of patients with acute onset sarcoidosis.40)

Also, they cease to move towards chemical signals driving an immune response, instead aggregating in clumps. One other side effect of infected macrophages is the dysregulation of the Vitamin D Receptor, leading to the high levels of 1,25-D characteristic of chronic inflammatory diseases.

In a number of diseases such as tuberculosis, leprosy, histoplasmosis, cryptococcosis, blastomycosis, coccidioidomycosis and syphilis, the formation of a granuloma is widely considered to be an indication of infection.41) Even so, many researchers continue to assume that certain chronic diseases such as sarcoidosis and Crohn's disease are not caused by infection even though they present with granuloma which are similar to those found in diseases known to be infectious.

In fact, the presence of granuloma are entirely consistent with an infectious disease. For example, a Japanese team showed that one could use Propionibacterium acnes in mice to induce lung granuloma mimicking sarcoidosis.42) The distinction between infectious and “non-infectious” granulomatous diseases, may be further complicated by reports such as those by Warrier who reported a case of cutaneous sarcoidosis, the histology of which showed tuberculoid granuloma.43)

Some researchers have argued that, rather than be a host-protective structures formed to contain infection,44) granuloma may be exploited to expand and disseminate an infection. A Cell paper explains how Mycobacteria implicated in tuberculosis may recruit new macrophages to, nascent granulomas.45)

Other evidence

  • Difficulty distinguishing sarcoidosis from tuberculosis – Although they have identified a signature that distinguishes healthy individuals from sarcoidosis or tuberculosis patients, the biosignatures of both diseases are nevertheless very similar. Gupta et al. write that differential diagnosis between the two is “very challenging.”46) According to the Max Planck Institute, it is almost impossible to distinguish between tuberculosis and sarcoidosis with just a single signature. A set of different biosignatures is better suited for distinguishing in a first step between diseased and healthy individuals and, in a further step, between the specific diseases.
  • Disease appearing in scars – There are several case reports of sarcoidosis lesions forming within scars, which are especially susceptible to infection. That these granuloma often take long periods of time to be realized corresponds with the growth rate of the slow-growing chronic pathogens which the Marshall Pathogenesis implicates in chronic disease.47) According to one report, a patient developed sarcoid granuloma fully 50 years after his initial injury.48) Sorabee et al write49) that in addition to reactivation of scars obtained from previous wounds, scar sarcoidosis has been reported at the sites of previous intramuscular injections, blood donation venepuncture sites, scars of herpes zoster,50) sarcoidosis on ritual scarification,51) and at the sites of allergen extracts for desensitisation.52)
  • Transmission of disease through blood, bone marrow, organs or other tissues – Organs and tissue from sarcoidosis patients have been known to cause sarcoidosis in the transplanted recipients.53) 54) 55)
  • Disease prevalence of small communities in close contact – A number of studies of unrelated people shows that mere proximity seems to be enough to transmit chronic disease. A case-controlled study of residents of the Isle of Man found that 40 percent of people with sarcoidosis had been in contact with a person known to have the disease, compared with 1 to 2 percent of the control subjects.56) Another study reported three cases of sarcoidosis among ten firefighters who apprenticed together.57)
  • Familial aggregation of the same disease – A number of studies have shown that spouses have a greater chance of developing the same disease as their partners - a phenomenon that can best be explained if familial aggregation has an infectious cause. One study of sarcoidosis 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, an incidence 1,000 times greater than could be expected by chance.58) In an analysis of 706 patients and 10,862 first-degree relatives, the 2001 ACCESS study quantified the increased risk relatives of sarcoidosis have in acquiring the illness.59) According to the analysis, first-degree relatives of sarcoidosis patients have a 3.8 times greater risk of having sarcoidosis themselves, with siblings having the greatest risk.
  • Kveim reaction – The mKatG protein, a mycobacterial protein, was detected in sarcoidosis tissues and, when injected into sarcoidosis tissues has been shown to induce an adaptive immune response in a subgroup of patients with sarcoidosis.60)
If anything, patients with autoimmune disease are immunocompromised. A study of the prevalence of the key antimicrobial peptide showed that patients with sarcoidosis expressed it less than healthy subjects, and that sicker sarcoidosis patients expressed it least of all. Source: Kanchwala et al.

Autoimmune vs. immunosuppressed

Patients with autoimmune disease often show inconsistent signs of autoimmune reactivity.

Kanchwala et al. showed that patients with sarcoidosis expressed the antimicrobial peptide cathelicidin less than healthy subjects, and that sicker sarcoidosis patients expressed it least of all.61) Wiken et al. showed that there was a reduced TLR2 mRNA expression in patients with Lofgren's syndrome (a type of acute sarcoidosis).62) Note that TLR2 (which the Marshall Pathogenesis theorizes is downregulated in autoimmune disease states) is expressed by the VDR.

Tests and diagnosis

No definitive laboratory test diagnostic of sarcoidosis has been identified. For example, sarcoidosis is not diagnosed by the presence of certain antibodies as there usually are none.63)

In the absence of a single agreed upon etiologic agent, sarcoidosis often remains a diagnosis of exclusion, although a typical presentation may strongly suggest the diagnosis. The diagnosis of sarcoidosis is established when a compatible clinical and radiographic picture is supported by histologic evidence of noncaseating granulomas in affected tissues and exclusion of other granulomatous diseases (e.g. Crohn's) capable of producing a similar histologic or clinical picture. Note that sarcoidosis is sometimes confused with benign or malignant cancerous tumors.64) 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.

  • pulmonary (lung) function tests – many patients with sarcoidosis have extensive pulmonary fibrosis
    • gas transfer coefficient (DLco) – Gas-transfer ability of a patient's lungs
    • FEV1 – ???
  • angiotensin converting enzyme (ACE) – ACE is made by cells in the granulomas. However, ACE levels are not always elevated in those with the disease.
  • tuberculin skin test – The tuberculin tine test is the test administered most frequently to screen for tuberculosis, which like sarcoidosis, is a granulomatous disorder.
  • x-rays and CT scans – Several imaging technologies are used to show the hallmarks of sarcoidosis in lung tissue. A chest x-ray offers a single scan of the chest while a chest CT relies on x-ray radiation in higher doses than a standard x-ray but allows better pictures of the lung. A CT scan will use a contrast material, typically iodine, to provide superior image quality 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. These imaging technologies may show granulomas, which appear as a shadow, or enlarged lymph glands in the chest. A staging system is used to classify chest x-rays taken to detect sarcoidosis.
    • Stage 0 is a normal chest x-ray.
    • Stage 1 is a chest x-ray with enlarged lymph nodes but otherwise clear lungs.
    • Stage 2 is a chest x-ray with enlarged lymph nodes plus infiltrates (shadows) in the lungs.
    • Stage 3 is a chest x-ray that shows the infiltrates (shadows) are present but the lymph nodes are no longer seen.
    • Stage 4 shows scar tissue (fibrosis) in the lung tissue.

The MP medication olmesartan blocks formation of fibrotic tissue. However, given that the MP works through generating immunopathology, it would be expected that some sarcoidosis patients on the MP experience a temporary increase in signs of their disease. This would include temporary increases in the appearance of fibrotic tissue and size of lymph nodes a visible on an x-ray. Earlier in the course of therapy, patients 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.

Spontaneous remission

Its reputation for spontaneous remission not withstanding, chronic inflammatory diseases such as sarcoidosis never go away on their own. It’s not that patients with sarcoidosis don't experience periods where they might feel better. Unfortunately, these intervals are usually a sign that the immune system has become severely compromised. In sarcoidosis, symptom resolution tends to be temporary as evidence by the epidemiological research.

Management and treatment

The Marshall Protocol is a treatment for sarcoidosis. Other treatments (some of which are contraindicated) include the following.

Immunosuppressive medications

For many physicians, immunosuppressive medications are a first-line treatment for sarcoidosis. These drugs suppress the innate immune response, which provides some patients with temporary symptom palliation, because they reduce immunopathology, the bacterial die-off reaction.

  • corticosteroids – There are no studies which show that glucocoritcoids (corticosteroids) improve long-term prognosis in the treatment of illness. Van den Bosch and Grutters write65), “Remarkably, despite over 50 years of use, there is no proof of long-term (survival) benefit from corticosteroid treatment.” The 2003 NIH ACCESS study66), the largest and most ambitious to date, validates that these drugs are ineffective for sarcoidosis patients, even for a time period as short as two years. For even short periods of time, steroid use can become genuinely addictive. Research shows that any kind of short-term symptomatic improvement from corticosteroid use does not last, and that over the longer term, use of the drugs entales a litany of side effects. For their own safety, patients on the Marshall Protocol (MP) must wean off of them as opposed to discontinuing them outright.
  • TNF-alpha inhibitorsTumor necrosis factor-alpha or TNF-alpha is a cytokine critical for effective immune surveillance.67) TNF-alpha inhibitors, also known as TNF blockers, anti-TNF drugs or TNF-alpha antagonists, are drugs which interfere with the body's production of TNF-alpha.68) Anti-TNF drugs are expensive, ineffective at treating chronic disease and have a number of adverse effects such as increase risk of serious infection such as mycobacterial infection.69) 70)
  • inhalers, steroid – Steroid inhalers suppress the innate immune response and delay progress on the MP. MP patients taking steroid inhalers should work with their physicians to switch drugs such as a bronchiodilator inhaler.

Lung transplantation

In the face of end-stage pulmonary sarcoidosis, many pulmonologists advise patients to consider lung transplantation. While a number of patients with advanced forms of sarcoidosis (including many who need supplemental oxygen) have done well on the MP, lung transplantation for sarcoidosis is problematic for several reasons.

A lung transplant fails to address the underlying cause, and, as a result, disease reoccurrence is not uncommon. A Danish study showed that lungs implanted in sarcoid patients are reinfected with granulomas five months later (reinfection was determined to come from the recipient patient)71) while another study showed recurrent sarcoidosis occurred as late as 56 months after the procedure.72)

According to several observational studies, the median survival time of sarcoidosis patients after they receive a transplant has been reported to be about 4.7 years73) – about half that of other major transplanted organ recipients.

Finally, any quality of life during time following transplant is limit. To ward off tissue rejection and survive several years, patients must take a cocktail of anti-rejection and immunosuppressive drugs, classes of drugs which entale a number of side effects.

There are at least several patients who have chosen to do MP rather than be on a Transplant List.

Other treatments

  • inhalers, bronchiodilator – A bronchodilator is a substance that dilates the bronchi and bronchioles, decreasing airway resistance and thereby facilitating airflow. A bronchodilator is delivered either by Medicated Dose Inhalers (MDI) or Dry Powder Inhalers (DPI) may be useful to reduce shortness of breath (dyspnea). As opposed to steroid inhalers, which are immunosuppressive, it is okay and sometimes essential to use bronchodilators while on the MP. Note that some combination products including Seretide, Advair, and Symbicort contain both bronchiodilating and steroidal medications and are therefore contraindicated.
  • supplemental oxygen – Some patients with obstructive lung diseases have trouble getting enough oxygen by breathing normally. For these patients, a prescription for supplemental oxygen should be seriously considered. Supplemental oxygen may be useful or necessary in some cases even though it may be needed only for a few hours a day for a few months. Some patients may need oxygen when flying or at high altitude.
  • methotrexate – Methotrexate (MTX) and sulfasalazine are antimetabolite antibiotics with actions similar to Bactrim DS, an MP antibiotic. MP patients taking MTX or sulfasalazine must discontinue those medications.

Vitamin D metabolism

Under most normal conditions, serum levels of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25-D), are constant throughout the year (no variability due to sun exposure),74) but there is no such tight biochemical regulation in at least some chronic inflammatory diseases such as sarcoidosis. Patients with sarcoidosis tend to have high levels of 1,25-D. As the article Metabolism of vitamin D and the Vitamin D Receptor explains, these high levels may be a direct outcome of microbes' effect on slowing activity of the VDR. It is also an indication of innate immune dysfunction.

It is sometimes thought that the liver and kidney are the only sites for conversion of 25-D into 1,25-D, but this process happens outside those organs – not coincidentally, at the very sites where patients report symptoms of chronic disease. High levels of 1,25-D and the enzyme which leads to the production of 1,25-D, 1 α-hydroxylase, have been found at various locations where the human body needs a strong host defense.75) Zehnder et al found increased expression of the enzyme 1 α-hydroxylase – the enzyme which converts 25-D into 1,25-D – in the skin cells of sarcoidosis patients where sarcoidosis patients tend to have disease symptoms.76) They write:

In particular, the expression of 1α-OHase [1 α-hydroxylase] by activated macrophages and epidermal keratinocytes [skin cells] suggests a role for 1,25(OH)2D3 [1,25-D] as an immunomodulatory and/or antiproliferative hormone.

A number of studies have demonstrated that the level of the hormone 1,25-D rises in patients with certain chronic diseases. Kavathia et al. found that in patients with sarcoidosis, those with high serum levels of 1,25-D have more pronounced chronic treatment needs.77)

Calcium metabolism

Hypercalcemia (excess levels of calcium in the blood) and hypercalciuria (excessive urinary calcium excretion) are frequently associated with the granulomatous diseases. Prevalence data suggests that 30 to 50 percent of patients with sarcoidosis have hypercalciuria and 10 to 20 percent have hypercalcemia.78) 79) Until recently, some researchers suggested that these processes were caused by high levels of 1,25-D.80) 81) As a result, patients with granulomatous disease are widely cautioned to limit sunlight exposure and vitamin D ingestion – recommendations that are generally not offered to patients with other chronic inflammatory diseases. Even pro-vitamin D advocates such as Michael Holick, M.D. have issued such cautions for high-dose supplementation of vitamin D in granulomatous diseases.82)

However, according to the Marshall Pathogenesis, any essential discrepancy in calcium/VDR metabolism between the granulomatous and non-granulomatous diseases is limited. The prevalence data suggests as much. Not everyone who has sarcoidosis gets hypercalcemia, and a large number of patients with other diseases such as breast and lung cancers are at risk for the condition.83) Further, in many diseases for which hypercalcemia is not suspected, the condition tends to go underdiagnosed.

Consistent with its classically understood role in maintaining bone health, the Vitamin D Receptor does appear to play at least some direct role in calcium regulation: a 2010 paper showed that the VDR signals stem cells responsible for osteoblast (bone-building) activity.84) But, researchers have since emphasized the role of estrogens and the estrogen receptor in maintaining bone health.85) In a 2007 study in Cell, Nakamura and colleagues showed that, in a female mouse model, removing estrogen receptor alpha in osteoblasts demonstrated that estrogen directly induces osteoclast apoptosis.86) The loss of estrogen among women at menopause may play some role in this process, but it is too soon to say this relationship is causal. Nakamura's work was done in otherwise healthy mouse cells rather than in human cells – which may be infected by pathogens. If such cells were infected, supplementation with estrogen would not address the underlying disease process.

Incidence and prevalence

An analysis of the 2001 ACCESS study challenged the widely held stereotype that the American patients most often affected by sarcoidosis are African-Americans and under 40.87)

Commonly involved organs

Sarcoidosis can affect any organ, initially presenting with one or more of the following abnormalities (in order of frequency according to the 2001 ACCESS study, which used data collected by pulmonologists).88)

Lung (pulmonary)

  • alveolitis – Inflammation in sarcoidosis does cause fluid in the lungs. Alveolitis is inflammation of the tiny sac-like air spaces where the exchange of carbon dioxide and oxygen take place. When the alveoli are filled with fluid, there is less exchange of gases.
  • atalectasis – The lack of gas exchange within alveoli, due to alveolar collapse or fluid consolidation. It may affect part or all of one lung. It is a condition where the alveoli are deflated, as distinct from pulmonary consolidation.
  • bronchiectasis – A disease state defined by localized, irreversible dilation of part of the bronchial tree. It is classified as an obstructive lung disease, along with emphysema, bronchitis and cystic fibrosis.
  • crackles – Crackles, crepitations, or rales are the clicking, rattling, or crackling noises that may be made by one or both lungs of a human with a respiratory disease during inhalation.
  • diffuse interstitial lung disease – A group of lung disorders in which the deep lung tissues become swollen and scarred. Caused by swelling and scarring of the air sacs (alveoli) and their supporting structures (the interstitium). This leads to reduced levels of oxygen in the blood.
  • hyperinflation – 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 (registration required) discusses how supplemental oxygen facilitates lung emptying.
  • obstructive lung disease – It's a little-recognized fact that sarcoidosis can cause PFTs results to indicate obstructive lung disease (sarcoidosis is considered a restrictive lung disease). This is because chest lymph nodes may become so enlarged they compress airways and/or granulomas themselves may obstruct airways. This article explains the difference between restrictive and obstructive lung disease.
  • pulmonary fibrosis – Formation or development of fibrous connective tissue in the lungs. Also called scarring, the creation of collagen allows the body to encase pathogens which have been missed by the immune system. Symptoms of pulmonary fibrosis include shortness of breath, a chronic dry cough, and chest discomfort. The angiotensin blockade (put into place by olmesartan) inhibits the formation of new fibrotic tissue.
  • pulmonary hypertension – Abnormally high blood pressure in the in the pulmonary artery, which connects the heart to the lungs. It makes the right side of the heart need to work harder than normal. PH is common in sarcoidosis.89) 90) 91) 92)
One estimation of percentage of overt organ involvement in sarcoidosis. Occult involvement is in parentheses.93)

Managing respiratory symptoms

Patients at risk for respiratory problems should ask their physicians for a prescription for supplemental oxygen.

A variety of strategies that do not involve medication are available for patients who have uncomfortable respiratory symptoms including breathing exercises, getting more fluids, rest, and others. Also, patients have reported relief taking guaifenesin, using bronchodilator inhalers (steroid inhalers are contraindicated), and nebulizers. Supplemental oxygen may be useful or necessary in some cases even though it may be needed only for a few hours a day for a few months.

While it is certainly possible to contract an acute respiratory infection while on the Marshall Protocol, many symptoms of immunopathology mimic those of an acute respiratory infection. Early recognition and effective management of immunopathology are very important when a patient has respiratory symptoms. Any symptom that correlates with MP therapy may be due to immunopathology.

Emergency medical personnel should know that a patient is on the MP. The article Notice for health care providers provides information that emergency medical personnel need to know.

→

A cough can develop at any time in sarcoidosis. It can be related to anything from upper respiratory involvement and post-nasal drip to chest involvement or even triggered by exposure to dust, fungus, odors or fumes.

Belinda, MarshallProtocol.com

Skin (cutaneous sarcoidosis)

Cutaneous manifestations of sarcoidosis are common and varied, and one patient can have different types of sarcoid skin lesions at the same time. Because of its diverse skin manifestations, sarcoidosis is most frequently diagnosed by a dermatologist. When a patient with sarcoidosis presents with skin problems, physicians should be alert to sarcoidosis as likely the source of these problems.

Lupus pernio

Lupus pernio is not another disease, nor is it related to lupus. Lupus pernio is a chronic plaquelike hardening of the face, usually appearing with violet discoloration of the cheeks, lips, nose, and ears. It can erode into cartilage or bone. Lupus pernio lesions can be permanently disfiguring and cause a patient to feel embarrassed, particularly since they may be noticeable on facial areas so visible to the public.

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. Like some other cutaneous sarcoidosis lesions, lupus pernio can appear at sites of old scars or trauma94) as well as in the upper respiratory tract95) – both sites of which can be quite resistant to the standard immunosuppressive therapies. These lesions can occur when the nose, face or hands are exposed to cold or wind, so it's a good idea for patients with sacroidosis to keep these areas protected from wind and cold. Avoiding exposure to bright lights is also an important preventative measure. Lupus pernio is said to be the skin lesion most characteristic (a diagnostic indicator) of sarcoidosis96), but not all sarcoidosis patients have these skin lesions.

Erythema nodosum (subcutaneous nodules)

Erythema nodosum are raised red, tender nodular lesions, generally but not exclusively on the anterior surface of the lower part of the leg. These lesions do not represent granulomatous involvement of the skin. Rather, the histopathology is primarily that of a panniculitis (inflammation of the fatty layer under the skin), with cellular inflammation and edema of the deep dermis and subcutaneous tissue. The presence of erythema nodosum is commonly observed in other infectious diseases such as tuberculosis.97)

Eye (ocular sarcoidosis)

The reported frequency of ocular manifestations for sarcoidosis varies according to the source and group studied, but may be as high as 70%.98) In the eye, the common sites of involvement are the skin of eyelid, conjunctiva, uveal tract, retina, optic nerve and lacrimal gland.99) Common symptoms of ocular sarcoidosis include:

  • uveitis – Swelling and irritation of the uvea, the middle layer of the eye. Most common is anterior uveitis, however, over a quarter of patients will have inflammation at the posterior of the eye, including retinitis pars planitis. according to the Cleveland Clinic, “Complications of uveitis may include glaucoma, cataract, abnormal blood vessel growth, fluid within the retina and vision loss.”
  • Sjogren's (Sicca) – 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). Sjogren's is reportedly seen in about half of patients.
  • blurred vision
  • increased tearing
  • dry eyes – may require natural tears or other lubricants
  • conjunctiva100)

Some asymptomatic patients still have active inflammation. Initially asymptomatic patients with ocular sarcoidosis can eventually develop blindness. Therefore, it is recommended that all patients with sarcoidosis receive a dedicated ophthalmologic examination.

Columbia University researcher Emil Wirotsko identified cell wall deficient bacteria – which he described as “mollicute-like organisms” – in the vitreous fluid of sarcoidal eyes.101) He further showed that the introduction of these microbes into mouse model effectively reproduced the chronic inflammatory process and granuloma that are the hallmark of sarcoidosis.

Lymph nodes

A lymph node, also called a gland, is a small ball-shaped organ of the immune system, distributed widely throughout the body and linked by lymphatic vessels. Lymph nodes are garrisons of B, T, and other immune cells. Lymph nodes are found all through the body, and act as filters or traps for foreign particles.

Lymph nodes play a vital role in the body's ability to fight off microbes. During an infection, the lymph nodes can expand due to intense B-cell proliferation in the germinal centers, a condition commonly referred to as “swollen glands.” Lymphadenopathy refers to “disease of the lymph nodes.” It is, however, almost synonymously used with “swollen or enlarged lymph nodes.” Lymphadenopathy can occur anywhere there are lymph node, but especially the neck, armpits, groin, or chest. Enlarged or tender glands can often be detected by low-tech means: visually or by palpation. Lymph nodes deep in the groin or beneath the ribs in the chest can be monitored with imaging such as chest x-ray, CT or PET scan.

Like any sarcoidosis symptom, lymphadenopathy may flare with immunopathology, resulting in enlarged and/or tender lymph nodes. The increase in the size of lymph nodes is consistent with an immunostimulatory therapy such as the Marshall Protocol. However, in later stages of sarcoidosis the lymph nodes shrink as their functionality decreases. This may be because they become too damaged to function. It is not unusual for lymph nodes to be calcified in sarcoidosis patients.102)

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. Enlarged lymph noses can also result in bronchial obstructions.


Massage can increase lymphatic flow103) as can osteopathic manipulation.104) Patients seeking this kind of therapy should look for therapists competent in techniques to help the lymphatic system and familiar with the needs of patients with chronic illness.


Sarcoidosis of the liver is not uncommon.105) According to Richard W Goodgame, MD, “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.”

The angtiotensin receptor blocker olmesartan has been shown to reduce liver fibrosis106) and aid liver healing.107) Some patients with sarcoidosis of the liver are mistakenly told they have “fatty liver disease” or cirrhosis.


The reported frequency of splenomegaly, enlargement or inflammation of the spleen, in sarcoidosis has ranged from 1% to 40%.108)

Neurologic (neurosarcoidosis)

Neurosarcoidosis (sometimes shortened to neurosarcoid) refers to sarcoidosis involving the central nervous system (brain and spinal cord). It can have many manifestations, but abnormalities of the cranial nerves (a group of twelve nerves supplying the head and neck area) are the most common. It may develop acutely, subacutely, and chronically. Approximately 5-10% of people with sarcoidosis of other organs develop central nervous system involvement. Only 1% of people with sarcoidosis will have neurosarcoidosis alone without involvement of any other organs. Diagnosis can be difficult, with no test apart from biopsy being completely reliable.

Psychiatric problems occur in 20% of cases; many different disorders have been reported, e.g. depression and psychosis. Peripheral neuropathy has been reported in up to 15% of cases of neurosarcoidosis.109)

Managing neurological symptoms


According to a 2003 study of Dutch patients, 30% of people with sarcoidosis suffer from chest pain.110) A similar proportion of sarcoidosis patients were found to have cardiac involvement upon autopsy.111) A third paper found that perhaps 50% of sarcoidosis patients have cardiac involvement that is not diagnosed112).

While it is true that chest pain can be due to cardiac involvement,113) 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.

All sarcoidosis patients are cautioned to assume they may have unrecognized cardiac involvement and to control their level of immunopathology accordingly.

Managing cardiac symptoms

While a severe cardiac immunopathological reaction is rare, it has the potential to be life-threatening. Therefore, health care providers are cautioned to be on the alert for cardiac symptoms in all their patients. Also, patients with risk factors or legitimate cause for concern should know when seek medical attention.


  • Heerfordt's syndrome – also referred to as uveoparotid fever, Heerfordt-Mylius syndrome, Heerfordt-Waldenström syndrome, and Waldenström’s uveoparotitis, is a rare manifestation of sarcoidosis. The symptoms include inflammation of the eye (uveitis), swelling of the parotid gland, chronic fever, and in some cases, palsy of the facial nerves.
  • mouth – Symptoms of sarcoidosis involvement in the mouth include: sores on or swelling of the face, tongue, mouth, gums or inside the cheeks,114) 115) 116) 117) gingivitis,118) too much or more commonly too little saliva, 119) and gum disease and increased dental cavities. Biopsy of the mouth often leads to diagnosis.
  • nails – Onycholysis, the loosening of lifting of the nail, is common in sarcoidosis. Several researchers describe this manifestation.120) 121) 122)
  • sleep apnea – Sleep apnea is the temporary absence of breathing during sleep. Sarcoidosis patients have a higher incidence of sleep apnea than the general population.123) Sarcoidosis itself can cause obstuctive sleep apnea due to the fact that sarcoid inflammation and granulomas can obstruct upper airway passages. In addition, use of the common therapy for relieving sarcoidosis symptoms: Prednisone, which is a corticosteroid, usually results in significant weight gain – which itself contributes to sleep apnea.

Patient interviews

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Mirek Wozga


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Roy P.

sarcoidosis, rheumatoid arthritis

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Leesa Shanahan

sarcoidosis (Heerfordt's Syndrome), uveitis

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Shirley J. (Saj)


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Carole Morgan

sarcoidosis, fibromyalgia, chronic fatigue syndrome (CFS)

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

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Interviews of patients with other diseases are also available.

Patients experiences

I just returned from a wonderful family vacation in Disney World. I was so excited that I was able to walk and keep up with my family… mostly, anyway and didn't need a wheelchair! When we booked our trip 10 months ago, I was planning to reserve a wheelchair to access the monorail and keep up with my family. As the summer progressed and I was feeling better I was confident that I was able to walk up ramps, etc. and did! The other wonderful news I have is that I was able to fly round trip from Alaska to Florida keeping my oxygen saturation above 90% without supplemental oxygen! I had my approved POC with Doctor's prescription etc. if needed, but my saturation was good as was my heart rate between 55 bpm and 75 bpm! I am thrilled!

Sue Lyons, MarshallProtocol.com

It's been a long time since I posted and am ashamed of being so remiss. I do not go on the computer very often but I do read everyone's post especially if it has information that I want to know.

I have been on the MP for almost five years now and have seen a lot of improvement although I still have a good way to go. I am down to taking only benicar 40mg every six hours and feel that it is helping me a lot. Before MP I was on a lot of medications but most of the symptoms have been resolved.

My cholesterol has dropped to a reasonable level, blood pressure has dropped, bone density has improved. Before MP I was on so many medications for high blood pressure, osteoporosis, high cholesterol. I still have occasional dizziness and my hearing has become very poor, I cannot walk without a walker. I had another MRI in November last year and my doctor said that the tumor in my brain is still very small but it is benign and it is really of no significance so I was pleased about that.

I went in March and had a screening test and all the tests came back normal which is very encouraging.

I will try and post regularly as I have a little more time on my hands now.

Hester, MarshallProtocol.com

I am doing well. I completed phase three and right now I am on Benicar every six hours and max dose of zith every eight days as per Dr. Bleny's instruction. As I posted earlier, in January this year I had a chest x-ray which showed improvement. My sun tolerance has improved and my energy as well. My major problem at the moment is my knee. I think this will also go away with time.

Some of my blood markers are off:

  • Potassium 5.5 - range 3.3 - 5.1 mmol/L
  • Triglycerides - 2.9 - range <2.30 mmol/L

I am currently taking Soda Bicarb tablets every day.

Asif, MarshallProtocol.com

Read more

Notes and comments

smoking reduces risk

Am J Respir Crit Care Med. 2004 Apr 15;169(8):893-5.

Is smoking beneficial for granulomatous lung diseases?

Maier LA. Comment in: Am J Respir Crit Care Med. 2004 Jul 15;170(2):199-200; author reply 200. Am J Respir Crit Care Med. 2004 Oct 1;170(7):821; author reply 821. Comment on: Am J Respir Crit Care Med. 2004 Apr 15;169(8):903-9.

PMID: 15072982

The Etiologic Agent of SarcoidosisWhat If There Isn’t One?



Pulmonary sarcoidosis: atypical HRTC features and differential diagnostic problems.
Bottaro L, Calderan L, Dibilio D, Mosconi E, Maffessanti M
Radiol Med107p273-85(2004 Apr)
2) , 4) , 13) , 14)
Considering an infectious etiology of sarcoidosis.
Ezzie ME, Crouser ED
Clin Dermatol25p259-66(2007 May-Jun)
Sarcoidosis succumbs to antibiotics--implications for autoimmune disease.
Marshall TG, Marshall FE
Autoimmun Rev3p295-300(2004 Jun)
Detection of mycobacterial rRNA in sarcoidosis with liquid-phase hybridisation.
Mitchell IC, Turk JL, Mitchell DN
Lancet339p1015-7(1992 Apr 25)
A search for mycobacterial DNA in granulomatous tissues from patients with sarcoidosis using the polymerase chain reaction.
Bocart D, Lecossier D, De Lassence A, Valeyre D, Battesti JP, Hance AJ
Am Rev Respir Dis145p1142-8(1992 May)
Assessment of mycobacterial DNA in cells and tissues of mycobacterial and sarcoid lesions.
Richter E, Greinert U, Kirsten D, Rüsch-Gerdes S, Schlüter C, Duchrow M, Galle J, Magnussen H, Schlaak M, Flad HD, Gerdes J
Am J Respir Crit Care Med153p375-80(1996 Jan)
Absence of DNA from mycobacteria of the M. tuberculosis complex in sarcoidosis.
Vokurka M, Lecossier D, du Bois RM, Wallaert B, Kambouchner M, Tazi A, Hance AJ
Am J Respir Crit Care Med156p1000-3(1997 Sep)
Mycobacterium tuberculosis DNA in tissues affected by sarcoidosis.
Wilsher ML, Menzies RE, Croxson MC
Thorax53p871-4(1998 Oct)
Growth of acid fast L forms from the blood of patients with sarcoidosis.
Almenoff PL, Johnson A, Lesser M, Mattman LH
Thorax51p530-3(1996 May)
Pulmonary sarcoidosis: could mycoplasma-like organisms be a cause?
Johnson LA, Edsall JR, Austin JH, Ellis K
Sarcoidosis Vasc Diffuse Lung Dis13p38-42(1996 Mar)
[Borrelia burgdorferi may be the causal agent of sarcoidosis]
Hua B, Li QD, Wang FM
Zhonghua Nei Ke Za Zhi30p631-3, 659(1992 Oct)
[Spirochetes in the cheilits granulomatosa and sarcoidosis]
Liu HG
Zhonghua Yi Xue Za Zhi73p142-4, 189-90(1993 Mar)
Seroprevalence of anti-Borrelia antibodies among patients with confirmed sarcoidosis in a region of Japan where Lyme borreliosis is endemic.
Ishihara M, Ohno S, Ono H, Isogai E, Kimura K, Isogai H, Aoki K, Ishida T, Suzuki K, Kotake S, Hiraga Y
Graefes Arch Clin Exp Ophthalmol236p280-4(1998 Apr)
23) , 35)
Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis.
Eishi Y, Suga M, Ishige I, Kobayashi D, Yamada T, Takemura T, Takizawa T, Koike M, Kudoh S, Costabel U, Guzman J, Rizzato G, Gambacorta M, du Bois R, Nicholson AG, Sharma OP, Ando M
J Clin Microbiol40p198-204(2002 Jan)
Identification of mycobacterial DNA in cutaneous lesions of sarcoidosis.
Li N, Bajoghli A, Kubba A, Bhawan J
J Cutan Pathol26p271-8(1999 Jul)
Molecular analysis of sarcoidosis tissues for mycobacterium species DNA.
Drake WP, Pei Z, Pride DT, Collins RD, Cover TL, Blaser MJ
Emerg Infect Dis8p1334-41(2002 Nov)
Identification of Mycobacterium avium complex in sarcoidosis.
el-Zaatari FA, Naser SA, Markesich DC, Kalter DC, Engstand L, Graham DY
J Clin Microbiol34p2240-5(1996 Sep)
Cellular recognition of Mycobacterium tuberculosis ESAT-6 and KatG peptides in systemic sarcoidosis.
Drake WP, Dhason MS, Nadaf M, Shepherd BE, Vadivelu S, Hajizadeh R, Newman LS, Kalams SA
Infect Immun75p527-30(2007 Jan)
Mycobacterial antigens may be important in sarcoidosis pathogenesis.
Drake WP, Newman LS
Curr Opin Pulm Med12p359-63(2006 Sep)
High prevalence of Mycobacterium tuberculosis DNA in biopsies from sarcoidosis patients from Catalonia, Spain.
Fité E, Fernández-Figueras MT, Prats R, Vaquero M, Morera J
Mycobacterial DNA in recurrent sarcoidosis in the transplanted lung--a PCR-based study on four cases.
Klemen H, Husain AN, Cagle PT, Garrity ER, Popper HH
Virchows Arch436p365-9(2000 Apr)
Detection of M. tuberculosis DNA in sarcoidosis: correlation with T-cell response.
Grosser M, Luther T, Müller J, Schuppler M, Bickhardt J, Matthiessen W, Müller M
Lab Invest79p775-84(1999 Jul)
Propionibacterium acnes in granulomas of a patient with necrotising sarcoid granulomatosis.
Arai T, Inoue Y, Eishi Y, Yamamoto S, Sakatani M
Thorax63p90-1(2008 Jan)
The presence of Propionibacterium spp. in the vitreous fluid of uveitis patients with sarcoidosis.
Yasuhara T, Tada R, Nakano Y, Tei M, Mochida C, Kamei M, Kinoshita S
Acta Ophthalmol Scand83p364-9(2005 Jun)
Presence of Rickettsia helvetica in granulomatous tissue from patients with sarcoidosis.
Nilsson K, Påhlson C, Lukinius A, Eriksson L, Nilsson L, Lindquist O
J Infect Dis185p1128-38(2002 Apr 15)
Apoptosis in infectious disease: how bacteria interfere with the apoptotic apparatus.
Häcker G, Kirschnek S, Fischer SF
Med Microbiol Immunol195p11-9(2006 Mar)
Functional genomics in sarcoidosis--reduced or increased apoptosis?
Rutherford RM, Kehren J, Staedtler F, Chibout SD, Egan JJ, Tamm M, Gilmartin JJ, Brutsche MH
Swiss Med Wkly131p459-70(2001 Aug 11)
41) , 44)
The secret lives of the pathogenic mycobacteria.
Cosma CL, Sherman DR, Ramakrishnan L
Annu Rev Microbiol57p641-76(2003)
Experimental pulmonary granuloma mimicking sarcoidosis induced by Propionibacterium acnes in mice.
Iio K, Iio TU, Okui Y, Ichikawa H, Tanimoto Y, Miyahara N, Kanehiro A, Tanimoto M, Nakata Y, Kataoka M
Acta Med Okayama64p75-83(2010 Apr)
Cutaneous sarcoidosis with tuberculoid granuloma.
Warrier S, Muhammed Fassaludeen AS, Safia B
Indian J Dermatol Venereol Leprol68p300-1(2002 Sep-Oct)
Scar sarcoidosis: a case report and brief review.
Selim A, Ehrsam E, Atassi MB, Khachemoune A
Cutis78p418-22(2006 Dec)
Scar sarcoidosis with a 50-year interval between an accident and onset of lesions.
de Almeida HL, Fiss RC
Dermatol Online J14p18(2008 Nov 15)
Reactivation of old scars: inevitably sarcoid.
Sorabjee JS, Garje R
Postgrad Med J81p60-1(2005 Jan)
Post-herpes zoster scar sarcoidosis.
Corazza M, Bacilieri S, Strumìa R
Acta Derm Venereol79p95(1999 Jan)
Cutaneous sarcoidosis and tribal scarifications in West Africa.
Alabi GO, George AO
Int J Dermatol28p29-31(1989 Jan-Feb)
The development of scar sarcoidosis at the site of desensitization injections.
Healsmith MF, Hutchinson PE
Clin Exp Dermatol17p369-70(1992 Sep)
Donor-acquired sarcoidosis.
Padilla ML, Schilero GJ, Teirstein AS
Sarcoidosis Vasc Diffuse Lung Dis19p18-24(2002 Mar)
Possible transmission of sarcoidosis via allogeneic bone marrow transplantation.
Heyll A, Meckenstock G, Aul C, Söhngen D, Borchard F, Hadding U, Mödder U, Leschke M, Schneider W
Bone Marrow Transplant14p161-4(1994 Jul)
Granulomatous pneumonitis following bone marrow transplantation.
Sundar KM, Carveth HJ, Gosselin MV, Beatty PG, Colby TV, Hoidal JR
Bone Marrow Transplant28p627-30(2001 Sep)
Incidence and mortality of idiopathic pulmonary fibrosis and sarcoidosis in the UK.
Gribbin J, Hubbard RB, Le Jeune I, Smith CJ, West J, Tata LJ
Thorax61p980-5(2006 Nov)
Investigation of a unique time-space cluster of sarcoidosis in firefighters.
Kern DG, Neill MA, Wrenn DS, Varone JC
Am Rev Respir Dis148p974-80(1993 Oct)
Lesson learned from ACCESS (A Case Controlled Etiologic Study of Sarcoidosis).
Rossman MD, Kreider ME
Proc Am Thorac Soc4p453-6(2007 Aug 15)
59) , 88)
Familial aggregation of sarcoidosis. A case-control etiologic study of sarcoidosis (ACCESS).
Rybicki BA, Iannuzzi MC, Frederick MM, Thompson BW, Rossman MD, Bresnitz EA, Terrin ML, Moller DR, Barnard J, Baughman RP, DePalo L, Hunninghake G, Johns C, Judson MA, Knatterud GL, McLennan G, Newman LS, Rabin DL, Rose C, Teirstein AS, Weinberger SE, Yeager H, Cherniack R
Am J Respir Crit Care Med164p2085-91(2001 Dec 1)
Potential etiologic agents in sarcoidosis.
Moller DR
Proc Am Thorac Soc4p465-8(2007 Aug 15)
No evidence of altered alveolar macrophage polarization, but reduced expression of TLR2, in bronchoalveolar lavage cells in sarcoidosis.
Wikén M, Idali F, Al Hayja MA, Grunewald J, Eklund A, Wahlström J
Respir Res11p121(2010 Sep 2)
63) , 79)
Vitamin D, calcium, and sarcoidosis.
Sharma OP
Chest109p535-9(1996 Feb)
Sarcoidosis mimicking recurrent endometrial cancer.
Powell JL, Cunill ES, Gajewski WH, Novotny DB
Gynecol Oncol99p770-3(2005 Dec)
Corticosteroid treatment in sarcoidosis.
Grutters JC, van den Bosch JM
Eur Respir J28p627-36(2006 Sep)
Two year prognosis of sarcoidosis: the ACCESS experience.
Judson MA, Baughman RP, Thompson BW, Teirstein AS, Terrin ML, Rossman MD, Yeager H Jr, McLennan G, Bresnitz EA, DePalo L, Hunninghake G, Iannuzzi MC, Johns CJ, Moller DR, Newman LS, Rabin DL, Rose C, Rybicki BA, Weinberger SE, Knatterud GL, Cherniak R
Sarcoidosis Vasc Diffuse Lung Dis20p204-11(2003 Oct)
TNF blockade: an inflammatory issue.
Aggarwal BB, Shishodia S, Takada Y, Jackson-Bernitsas D, Ahn KS, Sethi G, Ichikawa H
Ernst Schering Res Found Workshopp161-86(2006)
Anti-tumour necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management.
Gardam MA, Keystone EC, Menzies R, Manners S, Skamene E, Long R, Vinh DC
Lancet Infect Dis3p148-55(2003 Mar)
Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells.
Milman N, Andersen CB, Burton CM, Iversen M
Eur Respir J26p549-52(2005 Sep)
Medium term results of lung transplantation for end stage pulmonary sarcoidosis.
Walker S, Mikhail G, Banner N, Partridge J, Khaghani A, Burke M, Yacoub M
Thorax53p281-4(1998 Apr)
Lung transplant outcomes in white and African American recipients: special focus on acute and chronic rejection.
Lingaraju R, Pochettino A, Blumenthal NP, Mendez J, Lee J, Christie JD, Kotloff RM, Ahya VN, Hadjiliadis D
J Heart Lung Transplant28p8-13(2009 Jan)
Seasonal variation of 1,25-dihydroxyvitamin D and its association with body mass index and age.
Moan J, Lagunova Z, Lindberg FA, Porojnicu AC
J Steroid Biochem Mol Biol113p217-21(2009 Feb)
Respiratory epithelial cells convert inactive vitamin D to its active form: potential effects on host defense.
Hansdottir S, Monick MM, Hinde SL, Lovan N, Look DC, Hunninghake GW
J Immunol181p7090-9(2008 Nov 15)
Extrarenal expression of 25-hydroxyvitamin d(3)-1 alpha-hydroxylase.
Zehnder D, Bland R, Williams MC, McNinch RW, Howie AJ, Stewart PM, Hewison M
J Clin Endocrinol Metab86p888-94(2001 Feb)
Elevated 1, 25-dihydroxyvitamin D levels are associated with protracted treatment in sarcoidosis.
Kavathia D, Buckley JD, Rao D, Rybicki B, Burke R
Respir Medp(2010 Jan 11)
Vitamin D metabolite-mediated hypercalcemia.
Adams JS
Endocrinol Metab Clin North Am18p765-78(1989 Sep)
Vitamin D deficiency.
Holick MF
N Engl J Med357p266-81(2007 Jul 19)
Mechanisms of cancer-induced hypercalcemia.
Rosol TJ, Capen CC
Lab Invest67p680-702(1992 Dec)
Importance of Vitamin D receptor for neuronal control of hematopoietic stem cell niche.
Kawamori Y, Katayama Y, Asada N, Minagawa K, Sato M, Okamura A, Shimoyama M, Nakagawa K, Okano T, Tanimoto M, Kato S, Matsui T
Bloodp(2010 Sep 2)
Estrogens maintain bone mass by regulating expression of genes controlling function and life span in mature osteoclasts.
Imai Y, Youn MY, Kondoh S, Nakamura T, Kouzmenko A, Matsumoto T, Takada I, Takaoka K, Kato S
Ann N Y Acad Sci1173 Suppl 1pE31-9(2009 Sep)
Estrogen prevents bone loss via estrogen receptor alpha and induction of Fas ligand in osteoclasts.
Nakamura T, Imai Y, Matsumoto T, Sato S, Takeuchi K, Igarashi K, Harada Y, Azuma Y, Krust A, Yamamoto Y, Nishina H, Takeda S, Takayanagi H, Metzger D, Kanno J, Takaoka K, Martin TJ, Chambon P, Kato S
Cell130p811-23(2007 Sep 7)
Clinical characteristics of patients in a case control study of sarcoidosis.
Baughman RP, Teirstein AS, Judson MA, Rossman MD, Yeager H Jr, Bresnitz EA, DePalo L, Hunninghake G, Iannuzzi MC, Johns CJ, McLennan G, Moller DR, Newman LS, Rabin DL, Rose C, Rybicki B, Weinberger SE, Terrin ML, Knatterud GL, Cherniak R
Am J Respir Crit Care Med164p1885-9(2001 Nov 15)
Pulmonary hypertension associated with sarcoidosis: mechanisms, haemodynamics and prognosis.
Nunes H, Humbert M, Capron F, Brauner M, Sitbon O, Battesti JP, Simonneau G, Valeyre D
Thorax61p68-74(2006 Jan)
Sudden death with clinically undiagnosed pulmonary hypertension.
Srigley JA, Pollanen MS
J Clin Forensic Med12p264-7(2005 Oct)
Pulmonary hypertension in advanced sarcoidosis: epidemiology and clinical characteristics.
Shorr AF, Helman DL, Davies DB, Nathan SD
Eur Respir J25p783-8(2005 May)
CT findings in severe thoracic sarcoidosis.
Hennebicque AS, Nunes H, Brillet PY, Moulahi H, Valeyre D, Brauner MW
Eur Radiol15p23-30(2005 Jan)
93) Carey, W. D., & Cleveland Clinic Foundation. 2010. Current clinical medicine. Philadelphia: Saunders Elsevier.
Lupus pernio following facial trauma.
Lewis FM, Harrington CI
Clin Exp Dermatol18p476-7(1993 Sep)
Sarcoidosis of the upper respiratory tract and its association with lupus pernio.
Neville E, Mills RG, Jash DK, Mackinnon DM, Carstairs LS, James DG
Thorax31p660-4(1976 Dec)
Lupus pernio in sarcoidosis: clinical features and treatment outcomes of 14 patients.
Yanardag H, Pamuk ON, Pamuk GE
J Clin Rheumatol9p72-6(2003 Apr)
Erythema nodosum: an experience of 10 years.
Mert A, Ozaras R, Tabak F, Pekmezci S, Demirkesen C, Ozturk R
Scand J Infect Dis36p424-7(2004)
Nunes H, Bouvry D, Soler P, Valeyre D
Orphanet J Rare Dis2p46(2007 Nov 19)
Lid swelling and diplopia as presenting features of orbital sarcoid.
Biswas J, Krishnakumar S, Raghavendran R, Mahesh L
Indian J Ophthalmol48p231-3(2000 Sep)
Scleritis associated with sarcoidosis.
Dursun D, Akova YA, Bilezikçi B
Ocul Immunol Inflamm12p143-8(2004 Jun)
Sarcoidosis associated uveitis. Parasitization of vitreous leucocytes by mollicute-like organisms.
Wirostko E, Johnson L, Wirostko B
Acta Ophthalmol (Copenh)67p415-24(1989 Aug)
The measurement of skin lymph flow by isotope clearance--reliability, reproducibility, injection dynamics, and the effect of massage.
Mortimer PS, Simmonds R, Rezvani M, Robbins M, Hopewell JW, Ryan TJ
J Invest Dermatol95p677-82(1990 Dec)
Increased lymphatic flow in the thoracic duct during manipulative intervention.
Knott EM, Tune JD, Stoll ST, Downey HF
J Am Osteopath Assoc105p447-56(2005 Oct)
Sarcoidosis of the liver.
James DG, Sherlock S
Sarcoidosis11p2-6(1994 Mar)
Angiotensin II activates I kappaB kinase phosphorylation of RelA at Ser 536 to promote myofibroblast survival and liver fibrosis.
Oakley F, Teoh V, Ching-A-Sue G, Bataller R, Colmenero J, Jonsson JR, Eliopoulos AG, Watson MR, Manas D, Mann DA
Gastroenterology136p2334-2344.e1(2009 Jun)
Splenomegaly in sarcoidosis: a report of 16 cases.
Salazar A, Mañá J, Corbella X, Albareda JM, Pujol R
Sarcoidosis12p131-4(1995 Sep)
Sarcoidosis of the nervous system.
Joseph FG, Scolding NJ
Pract Neurol7p234-44(2007 Aug)
Impact of pain in a Dutch sarcoidosis patient population.
Hoitsma E, De Vries J, van Santen-Hoeufft M, Faber CG, Drent M
Sarcoidosis Vasc Diffuse Lung Dis20p33-9(2003 Mar)
Screening for cardiac involvement in sarcoidosis?
Zimmer R
Postgrad Med112p12(2002 Sep)
Cardiac sarcoidosis with presentation of large left atrial mass.
Abrishami B, O'Connel C, Sharma O
Curr Opin Pulm Med10p397-400(2004 Sep)
Oral manifestations of sarcoidosis.
Blinder D, Yahatom R, Taicher S
Oral Surg Oral Med Oral Pathol Oral Radiol Endod83p458-61(1997 Apr)
[Cheilitis granulomatosa in a child]
Olivier V, Lacour JP, Castanet J, Perrin C, Ortonne JP
Arch Pediatr7p274-7(2000 Mar)
Sarcoidosis presenting as gingivitis.
Hayter JP, Robertson JM
Br Med J (Clin Res Ed)296p1504(1988 May 28)
[Sicca syndrome in sarcoidosis and involvement of the salivary and lacrymal glands]
Vasil'ev VI, Logvinenko OA, Simonova MV, Safonova TN, Radenska-Lopovok SG, Bozh'eva LA, Shornikova NS, Andrianov SG
Ter Arkh77p62-7(2005)
Nail dystrophy and bony involvement in chronic sarcoidosis.
Santoro F, Sloan SB
J Am Acad Dermatol60p1050-2(2009 Jun)
Sarcoidosis presenting as nail dystrophy.
Cohen PD, Lester RS
J Cutan Med Surg3p302-5(1999 Oct)
Sarcoidosis: nail dystrophy without underlying bone changes.
Wakelin SH, James MP
Cutis55p344-6(1995 Jun)
Sleep apnea in sarcoidosis.
Turner GA, Lower EE, Corser BC, Gunther KL, Baughman RP
Sarcoidosis Vasc Diffuse Lung Dis14p61-4(1997 Mar)
home/diseases/sarcoidosis.txt · Last modified: 08.02.2013 by drtrevormarshall
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