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Behçet’s disease

What is Behçet’s disease?

Behçet’s disease (or Behçet’s syndrome) is a chronic inflammatory disease that affects multiple organ systems, some but not all of which are from vasculitis. Oral ulcers (aphthous ulcers or “canker sores”) are seen in almost all patients, and genital ulcers in many. Eye inflammation (uveitis or iritis) is both common and potentially serious. Arthritis and skin disease (which commonly resembles either acne or a painful inflammatory nodule referred to as erythema nodosum) are common and bothersome symptoms. Less commonly, Behçet’s disease can involve the intestines, the brain, and large arteries (with risk of aneurysm) or veins (with risk of blood clots).

Who gets Behçet’s disease?

Behçet’s disease is most commonly diagnosed in young adults of both sexes. In most ethnic groups, Behçet’s is a rare disease, but it is much more common in persons of Turkish ancestry in particular, and is also relatively common in other areas of the Middle East, Central Asia, Korea, and Japan.

What causes Behçet’s disease?

The cause of Behçet’s disease is not known, but genetic background plays an important role. A gene called HLA-B51 has been associated with Behçet’s disease in multiple ethnic groups and has a far greater influence than any other gene. Close relatives of patients with Behçet’s disease are at increased risk of develop the disease themselves (compared to the general population), but the likelihood remains small.

How is Behçet’s disease diagnosed?

There is no blood test or imaging test to diagnose Behçet’s disease. The disease is diagnosed based on the clinical syndrome, which almost always includes oral ulcers, and some combination of genital ulcers, uveitis, or typical skin lesions. Frequent episodes of oral ulcers are common in the general population and are not sufficient to make the diagnosis of Behçet’s disease. Other diseases can resemble Behçet’s disease, so it is important for physicians to consider and “rule out” other causes.

What is the treatment for Behçet’s disease?

Because the severity of Behçet’s disease varies widely, the aggressiveness of treatment varies widely as well. Oral and genital ulcers, skin disease, and arthritis do not always require treatment, but colchicine (a non-immune-suppressive drug) is often used, and prednisone is sometimes needed if symptoms are disabling. Mild cases of uveitis can be treated with prescription eyedrops, but severe cases require high doses of prednisone and/or other immune-suppressive drugs. Immune-suppressive drugs such as azathioprine, cyclosporine, anti-TNF drugs (infliximab, etanercept, and others), and cyclophosphamide are used for severe eye disease, brain disease, gastrointestinal disease, and large artery or large vein disease, and for patients with other symptoms severe enough to require high doses of prednisone.

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Central nervous system (CNS) vasculitis

What is CNS vasculitis?

Central nervous system (CNS) vasculitis refers to vasculitis in the brain. The condition can be primary, with manifestations of vasculitis limited to the brain, or secondary, with brain involvement with a systemic form of vasculitis such as polyarteritis nodosa (PAN), granulomatosis with polyangiitis (Wegener’s), or others. The most typical symptoms of either primary or secondary CNS vasculitis include headache and cognitive dysfunction but may also include any of the following: seizure, stroke and coma.

Who gets CNS vasculitis?

Primary CNS vasculitis is extremely rare (less than 1-2 persons per million people per year. Men and women of all ages can get the disease although it is slightly more frequent in middle-aged men (45-65). Five to 15 percent of patients with PAN and granulomatosis with polyangiitis (Wegener’s) will get central nervous system manifestations (secondary vasculitis).

What causes CNS vasculitis?

The cause of primary CNS vasculitis is unknown as are the causes of the diseases associated with secondary CNS vasculitis.

How is CNS vasculitis diagnosed?

Since primary CNS vasculitis is so rare, a high index of suspicion is required to make the diagnosis. Mimickers must be ruled out, including drug use (ephedrine, cocaine, etc), migraine, infections and someunusual malignancies. A combination of tests, including magnetic resonance imaging (MRI), cerebral angiography and spinal fluid examination (spinal tap) may help. In many cases, a brain biopsy is the only way to confirm the diagnosis.

What is the treatment for CNS vasculitis?

Depending on the clinical manifestations and extent of the disease, patients with CNS vasculitis will usually require treatment with corticosteroids combined with immunosuppressive agents, such as cyclophosphamide or azathioprine, for a period varying between 6 and 12 months.

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Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) (CSS)

What is Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)?

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) (CSS), also known as “allergic granulomatosis”, is a rare form of vasculitis which, like Granulomatosis with polyangiitis (Wegener's) (GPA) and microscopic polyangiitis, affects small and medium-sized vessels. Most patients with Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) have asthma, nasal and sinus allergies. Patients which CSS often have unusually high numbers of eosinophils, a type of while blood cell in their blood. Asthma, as well as the presence of eosinophils are common and by themselves are not enough to base the diagnosis of CSS on. Other problems caused by CSS include lung infiltrates, rashes, peripheral nervous system disease, abdominal pain, kidney, and cardiac disease.

Who gets eosinophilic granulomatosis with polyangiitis (Churg-Strauss)?

CSS affects people of all ages and both sexes.

What causes eosinophilic granulomatosis with polyangiitis (Churg-Strauss)?

The cause of CSS is not known.

How is eosinophilic granulomatosis with polyangiitis (Churg-Strauss) diagnosed?

CSS is diagnosed on the basis of a combination of symptoms and abnormal laboratory tests including an ANCA test as well as biopsy of affected tissues.

How is eosinophilic granulomatosis with polyangiitis (Churg-Strauss) treated?

Treatment of eosinophilic granulomatosis with polyangiitis (Churg-Strauss) usually includes a combination of glucocorticoids and an immunosuppressive drug such as cyclophosphamide, methotrexate, or azathioprine. If diagnosed early, treatment can bring about early remission and prevent organ failure. It is important to understand that the asthma patients with CSS are treated in the same way as other patients with asthma. Worsening of asthma in patients with CSS does not necessarily mean that the CSS is active in other organs. Unfortunately, while remission of symptoms is usually achieved, the relapse rate remains high.

Is asthma part of vasculitis?

Not exactly. Even though asthma is present in almost all patients with eosinophilic granulomatosis with polyangiitis (Churg-Strauss) and corticosteroids represent the cornerstone treatment for both conditions, asthma it is not part of the vasculitis. In eosinophilic granulomatosis with polyangiitis (Churg-Strauss) asthma is more to be considered as an underlying predisposing condition, and it usually persists even after effective treatment for vasculitis.

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Drug-induced vasculitis

What is drug-induced dasculitis (DIV)?

DIV is a form of vasculitis that affects small blood vessels. The disease can affect many parts of the body but especially involves the skin, causing rash. A skin biopsy may show blood vessel inflammation termed leukocytoclastic vasculitis. Some patients can have inflammation in other organs, including nerve involvement. Systemic manifestations can include fever, weight loss and joint pain.

Who gets DIV?

Drug-induced vasculitis occurs in men and women of all races.

What causes DIV?

A variety of medications have been linked to drug-induced vasculitis. Commonly reported associations are with minocycline, an antibiotic used to treat acne, and propylthiouracil, a drug for hyperthyroidism. A variety of other drugs can cause leukocytoclastic vasculitis.

How is DIV diagnosed?

The diagnosis depends initially on the medical history and physical examination. A skin biopsy is commonly performed, showing leukocytoclastic vasculitis.

What is the treatment for DIV?

Treatment depends on the extent of involvement by vasculitis. For patients with only skin involvement, discontinuation of the causative medication is all that may be needed. Some patients will require corticosteroids to control more bother symptoms. Rarely immunosuppressive agents will be required.

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Giant cell (temporal) arteritis (GCA)

What is giant cell arteritis?

Giant cell arteritis (GCA), also known as “temporal arteritis” or “cranial arteritis”, is a form of vasculitis affecting medium and large sized blood vessels, especially those of the aorta and arteries going from the aorta to the arms, legs and the head. GCA most frequently affects the arteries in the head, leading to narrowing and sometimes to complete blockage of the blood vessel. This results in the surrounding tissues being deprived of an adequate blood supply. When GCA involves the arteries that supply blood to the eyes, blindness in one or both eyes may develop suddenly. Along with visual changes, the most common symptoms in GCA include headaches, pain in the jaw or tongue muscles when eating or talking, tenderness of the scalp, fevers, and arthritis, particularly pain and stiffness of the shoulders and hips. This pain and stiffness of the shoulders and hips is called polymyalgia rheumatica. Polymyalgia rheumatica can occur without giant cell arteritis.

Who gets giant cell arteritis?

Although still a relatively rare disease, GCA is one of the most common types of vasculitis. GCA only affects people older than 50 years of age and especially those older than 65. Women are somewhat more likely to get the disease than men.

What causes giant cell arteritis?

The cause of GCA is unknown.

How is giant cell arteritis diagnosed?

The diagnosis of GCA depends on both clinical signs and symptoms and a combination of laboratory tests and tissue biopsy. At the time of diagnosis, most patients (90%) with GCA have an elevated erythrocyte sedimentation rate (ESR or “sed rate”), a non-specific blood marker of inflammation, and many patients have anemia. Biopsy of the temporal artery, located above and front of the ear, is a simple and relatively safe procedure that does not usually require staying in a hospital, is the most reliable method of diagnosing GCA. Some patients with negative biopsies can still have the disease.

How is Giant Cell Arteritis treated?

Treatment with glucocorticoids should begin as soon as the diagnosis is assumed to be likely. Glucocorticoids are often started even before a biopsy is performed to help prevent blindness or other problems. Glucocorticoids are given in high doses for several months and then slowly reduced. Many experts also prescribe a low-dose aspirin each day for patients with GCA. There are no other drugs, including the chemotherapy and other drugs which affect the immune system which are clearly proven to be of benefit in the treatment of GCA. Polymyalgia rheumatica without GCA is treated with doses of glucocorticoids lower than those used for treating GCA. The average duration of treatment is between two and three years, but this varied considerably for individual patients.

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Granulomatosis with polyangiitis (Wegener's) (GPA)

What is Granulomatosis with polyangiitis (Wegener's) (GPA)?

Granulomatosis with polyangiitis (Wegener's) (GPA) is a rare form of vasculitis mainly involving small and medium-sized blood vessels. The disease can affect most parts of the body. It commonly affects the sinuses, nose, throat, lungs, ears, eyes, kidneys, skin, joints, brain and other parts of the nervous system. Not every one with GPA is affected in the same way. Some patients have mild disease, while others may have severe damage to these organs which can be life-threatening.

Who gets granulomatosis with polyangiitis (Wegener's) (GPA)?

Granulomatosis with polyangiitis (Wegener's) (GPA) occurs in both men and women and can affect children and adults. Although Caucasians are affected more often, people all over the world can get GPA.

What causes granulomatosis with polyangiitis (Wegener's) (GPA)?

Wegener's granulomatosis is thought to be an auto-immune disease for which there is no known cause.

How is granulomatosis with polyangiitis (Wegener's) (GPA) diagnosed?

The diagnosis of GPA is made by combining clinical features with laboratory tests (including tests for ANCA) and biopsy of affected tissues.

What is the treatment for granulomatosis with polyangiitis (Wegener's) (GPA)?

Treatment of GPA usually includes a combination of glucocorticoids and an immunosuppressive drug such as cyclophosphamide, methotrexate, or azathioprine. If diagnosed promptly, treatment can bring about early remission and prevent organ failure. It is a chronic disease, and although remission of symptoms is usually achieved, the relapse rate remains high.

What is "granulomatosis with polyangiitis?"

Granulomatosis with polyangiitis (GPA) is a new term introduced to replace the name Wegener’s granulomatosis. As the term is being adopted, the terminology “granulomatosis with polyangiitis (Wegener’s)” has been proposed.

What is the difference between limited and severe granulomatosis with polyangiitis (Wegener’s)?

Not all patients with granulomatosis with polyangiitis (GPA) have similar disease. The term “limited” GPA was introduced in 1966 and was originally defined as GPA that did not involve the kidney. Unfortunately, this term has often been misinterpreted. “Limited” GPA is not equivalent to non-severe GPA as there are people who meet the definition of “limited” disease who may have very severe disease and people who do not meet the definition of limited GPA whose disease may be quite mild. Because of this, the term “limited” GPA is best avoided. It is far more helpful to view this disease in terms of the location of organ involvement and the degree of severity of the disease in each of these locations.

What are anti-GBM antibodies and what do they have to do with my vasculitis?

Anti-GBM antibodies are antibodies directed against glomerular basement membranes. Patients with anti-GBM disease (Goodpasture’s syndrome) will present with involvement of lungs and kidneys, so-called pulmonary-renal syndrome. This can include bleeding in the lungs (hemoptysis) that can lead to respiratory failure and bleeding in the kidney (hematuria) that can lead to rapidly progressive loss of kidney function. Goodpasture syndrome has to be considered in patients who are thought to have ANCA-related vasculitidies (granulomatosis with polyangiitis and microscopic polyangiitis) as those diseases can also present with pulmonary-renal syndrome. Measuring anti-GBM antibodies and ANCA in these patients will usually help distinguish the two conditions although there are rare cases of patients with both ANCA and anti-GBM antibodies

What is the difference between ANCA and ANA?

Both are blood tests used by doctors to help in the diagnosis of autoimmune disease. Antineutrophil cytoplasmic antibody (ANCA) is blood test commonly elevated in patients with diseases such granulomatosis with polyangiitis, microscopic polyangiitis, and Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss). Antinuclear antibody (ANA) is a blood test most often elevated in patients with systemic lupus erythematosus (“lupus”), Sjogren syndrome, scleroderma, and other types of autoimmune diseases.

Can you still be diagnosed with granulomatosis with polyangiitis (GPA, Wegener’s) if the ANCA is negative?

Yes. Although ANCA is elevated in a majority of patients with granulomatosis with polyangiitis (Wegener’s) it is not detectable in all patients and is not necessary to make the diagnosis.

What are the chances of recovering lost hearing in a patient with granulomatosis with polyangiitis (GPA, Wegener’s)?

Hearing can be transiently decreased in patients with GPA with acute otitis, because of the presence of liquid in the inner ear(s), which will regress under appropriate treatment. However, when the inner ear damage is severe, because of prolonged or multiple recurrences of otitis, and/or when the auditory nerve(s) are involved by inflammation or compression, the hearing loss can be permanent.

Can a saddle nose deformity be repaired?

Yes, a saddle nose deformity can be repaired as long as the underlying vasculitis is not active. This would require consultation with a surgeon, often times an ear nose and throat (ENT) specialist who could discuss this option with you.

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Henoch-Schonlein purpura (HSP)

What is Henoch-Schonlein purpura?

Henoch-Schonlein purpura (HSP) is a form of vasculitis (vessel inflammation) which affects small blood vessels. Often times HSP starts out as a rash on the legs which is purplish and raised. It may cause joint aches. Serious complications like involvement of the intestines and the kidney can also occur.

Who gets Henoch-Schonlein purpura?

Henoch-Schonlein purpura most often affects children but it can occur at any age.

What causes Henoch-Schonlein purpura?

The exact cause of this disease is unknown but is related to your immune system. People may have a cold (upper respiratory infection) or a gastrointestinal illness just before they develop the disease. However, no virus or other infection has been identified as a cause of the disorder.

How is Henoch-Schonlein purpura diagnosed?

The diagnosis is based on your symptoms and examination findings. Your doctor will run some blood tests to look for inflammation, evaluate kidney function and rule out other forms of vasculitis. A urine sample will be needed to evaluate for kidney involvement. A biopsy from the skin or kidney may be needed.

What is the treatment for Henoch-Schonlein purpura?

Often times no treatment may be needed and the disease can resolve on its own. Sometimes if there is kidney or gut involvement, prednisone may be started.

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Kawasaki disease

What is Kawasaki disease?

Kawasaki is a form of vasculitis that affects medium-sized blood vessels but it can affect multiple parts of the body including rashes, cracked lips, reddened tongue, and fever. A major concern is inflammation of the coronary arteries that can lead to heart attack.

Who gets Kawasaki disease?

It is mainly a disease of children and rarely affects adults

What causes Kawasaki disease?

The cause of the disease is unknown. It is thought to be an autoimmune cause.

How is Kawasaki disease diagnosed?

The disease is suspected mainly by having the constellation of symptoms of fever, cracked lips, reddened tongue, and fever and feeling unwell. There is no one test for Kawasaki but it is important to have blood work to ensure other diseases such as infections are not causing these symptoms. An echocardiogram is important to assess the coronary arteries and make sure there is not inflammation of those arteries.

What is the treatment for Kawasaki disease?

Corticorsteroids and intravenous immunoglobulin are given to prevent coronary artery damage. Aspirin is also an important part of the treatment

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Microscopic polyangiitis (MPA)

What is microscopic polyangiitis?

Microscopic polyangiitis (MPA) is a rare form of vasculitis which mainly affects small and medium-sized blood vessels. The disease commonly affects the lungs, kidneys, skin, ears, and nervous system but can affect most parts of the body including the eyes, joints, and brain. Severe damage to these organs can occur. Involvement and severity varies widely from patient to patient, from mild to life-threatening.

Who gets microscopic polyangiitis?

MPA can affect children and adults and occurs in both men and women. Although caucasians are affected more often, people all over the world can get MPA.

What causes microscopic polyangiitis?

Microscopic polyangiitis is thought to be an auto-immune disease for which there is no known cause.

How is Microscopic polyangiitis diagnosed?

The diagnosis of MPA made by combining clinical features with laboratory tests (including tests for ANCA) and tissue biopsies.

What is the treatment of microscopic polyangiitis?

Like granulomatosis with polyangiitis (Wegener's) (GPA), treatment of MPA usually includes a combination of glucocorticoids and an immunosuppressive drug such as cyclophosphamide, methotrexate, or azathioprine. If diagnosed early, treatment can bring about early remission and prevent organ failure. It can be a chronic disease. While remission of symptoms is usually achieved, the relapse rate remains high.

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Polyarteritis nodosa (PAN)

What is Polyarteritis nodosa?

Polyarteritis nodosa (PAN) is a very rare form of vasculitis involving predominantly medium-sized blood vessels. Inflammation of the blood vessels may cause segments of vessels to weaken and stretch, resulting in an aneurysm (weakening of the vessel wall). Inflammation of the vessel wall can also lead to thickening and subsequent partial blockage (stenosis) or complete blockage (occlusion) of the artery. These aneurysms and blockages can result in the surrounding tissues being deprived of an adequate blood supply. The disease commonly affects the intestines, kidneys, skin, and peripheral nervous system but can affect most parts of the body. As is true of other forms of vasculitis, how PAN affects the body differs widely from patient to patient.

What causes polyarteritis nodosa?

PAN is thought to be an auto-immune disease for which there is no known cause in most cases. There is an important known association between infection with hepatitis B or hepatitis C viruses and development of PAN. However, only a small fraction of patients infected with these viruses develop PAN.

How is polyarteritis nodosa diagnosed?

The diagnosis of PAN is made by combining clinical features with the results of angiograms and tissue biopsies.

How is polyarteritis nodosa treated?

Treatment of PAN almost always involves use of glucocorticoids in high doses that are slowly reduced over many months. Often an immunosuppressive drug such as cyclophosphamide, methotrexate, or azathioprine, is added to the glucocorticoid therapy. If diagnosed early, treatment can bring about early remission and prevent organ failure. Unfortunately, while remission is usually achieved, relapses do occur.

What is the difference between systemic polyarteritis nodosa (PAN) and cutaneous PAN?

Polyarteritis nodosa (PAN) is a vasculitis affecting medium-sized blood vessel. In patients with "cutaneous polyarteritis nodosa", the findings of the disease are localized to the skin (purpura or subcutaneous nodules), but also sometimes the peripheral nerve(s) of the same limb (causing weakness and/or numbness). Patients with systemic polyarteritis nodosa have involvement of other organs, including the gastrointestinal tract, heart and/or kidney. The systemic form is therefore usually most severe and requires stronger treatment.

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Takayasu's arteritis (TAK)

What is Takayasu’s arteritis?

Takayasu’s arteritis (TAK) is a rare form of vasculitis affecting medium and large sized blood vessels, primarily of the aorta (the main blood vessel that leaves the heart) and its large branches going to the arms, abdominal organs, legs and the head. As with other forms of vasculitis, inflammation of the large blood vessels may cause segments of vessels to weaken and stretch, resulting in an aneurysm (weakening of the vessel wall) or, more commonly, the inflammation of the vessel wall leads to thickening and subsequent partial blockage (stenosis) or complete blockage (occlusion) of the artery. These blockages can result in the surrounding tissues being deprived of an adequate blood supply which causes mild to very severe problems including claudication (cramping) in the arms and legs, kidney damage with severe hypertension, strokes, or heart attacks. Many other symptoms and problems can be seen in TAK including joint pains, fevers, fatigue, and others.

Who gets Takayasu’s arteritis?

Takayasu's arteritis generally first strikes people when they are young (teens, 20s or 30s), is much more common in women than men, and is more common in Asia. However, the disease is seen all over the world and most patients with Takayasu's arteritis in non-Asian countries are not of Asian ancestry.

What causes Takayasu’s arteritis?

The cause of Takayasu’s arteritis is unknown.

How is Takayasu’s arteritis diagnosed?

The diagnosis of TAK is based on a combination of symptoms and laboratory tests. These usually include angiography, a study of the blood flow in arteries. The angiogram can be done with dye injected into the arteries, by MRI, or by CT scan. The study shows the characteristic changes of blockage and widening of the arteries affected by TAK. Physical examination of patients with TAK often demonstrates reduced blood pressure readings in the arms with blockages and reduced pulses (hence another name of the disease is “Pulseless Disease”).

How is Takayasu’s arteritis treated?

Treatment of TAK almost always involves use of glucocorticoids in high doses that are slowly reduced over many months. Often an immunosuppressive drug such as cyclophosphamide, methotrexate, and azathioprine, is added to the glucocorticoids. If diagnosed early, treatment can bring about early remission and prevent organ failure. Unfortunately, while remission is usually achieved, relapses occur frequently and TAK is often a chronic problem.

What is the difference between Takayasu’s and giant cell arteritis?

The key difference between Takayasu’s arteritis (TA) and giant cell arteritis (GCA) is the age of the patients affected by the disorders. Takayasu’s arteritis affects younger patients, generally less than 40 years of age, while giant cell arteritis affects older patients, generally over 50 years of age.

Both Takayasu’s arteritis and giant cell arteritis affect large arteries, but the typical initial manifestations of the two diseases are also usually different. Patients with giant cell arteritis typically present with headaches affecting the temples, scalp tenderness, jaw pain and fatigue with chewing, shoulder or hip pain and stiffness, and/or sudden changes in vision (temporary or permanent blindness or partial vision loss). Patients with Takayasu’s arteritis usually do not have these symptoms but may have arm or leg pain with use, or chest pain, or be found to have no pulse in an arm or leg. However, many clinical findings may be similar between the two diseases, including the presence of constitutional symptoms (fatigue, fevers, chills, malaise, weight loss), muscle and joint pains, stroke-like symptoms, diminished or absent pulses, asymmetric blood pressures, and narrowed or blocked primary branches of the aorta found on imaging studies.

Giant cell arteritis is usually diagnosed by a temporal artery biopsy, whereas Takayasu’s arteritis is not, since the temporal artery is not classically affected in TA. Diagnosis of Takayasu’s arteritis is usually made by imaging studies of arteries such as angiography.

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Other Types of Vasculitis

There are many different forms of vasculitis, and the VCRC is focusing on studying six different types: granulomatosis with polyangiitis (Wegener's) (GPA) (WG), microscopic polyangiitis (MPA), eosinophilic granulomatosis with polyangiitis (Churg-Strauss) (CSS), polyarteritis nodosa (PAN), Takayasu’s arteritis (TAK), and giant cell arteritis (GCA). Although it is not possible to study each individual type of vasculitis separately with limited resources, our hope is that information learned in studying several types of vasculitis will be beneficial for understanding and treating other types of vasculitis as well.

If you wish to learn about other forms of vasculitis that are not discussed on this website, please visit the Vasculitis Foundation at www.vasculitisfoundation.org.