Johns Hopkins Vasculitis Center

Home / Search for "search.html/whatis/cryoglobulinemia.html/treatments/methotrexate.html"

Search Results for: search.html/whatis/cryoglobulinemia.html/treatments/methotrexate.html

Giant Cell Arteritis

Description

Giant cell arteritis (GCA) is the most common form of vasculitis that occurs in adults. Almost all patients who develop giant cell arteritis are over the age of 50. GCA commonly causes headaches, joint pain, facial pain, fever, and difficulties with vision, and sometimes permanent visual loss in one or both eyes. Because the disease is relatively uncommon and because the disease can cause so many different symptoms, the diagnosis of GCA can be difficult to make. With appropriate therapy, GCA is an eminently treatable, controllable, and often curable disease. The disease used to be called “temporal arteritis” because the temporal arteries, which course along the sides of the head just in front of the ears (to the temples) can become inflamed. However, we also know that other blood vessels, namely the aorta and its branches, can also become inflammed. The term “giant cell arteritis” is often used because when one looks at biopsies of inflamed temporal arteries under a microscope, one often sees large or “giant” cells.

Who gets Giant Cell Arteritis?

GCA is a disease of older people. The average age at onset is 72, and almost all people with the disease are over the age of 50. Women are afflicted with the disease 2 to 3 times more commonly than men. The disease can occur in every racial group but is most common in people of Scandinavian descent.

Classic Symptoms of Giant Cell Arteritis

The most common symptoms of GCA are headache, pain in the shoulders and hips (called polymyalgia rheumatica), pain in the jaw after chewing (called jaw claudication), fever, and blurred vision. Other symptoms can include tenderness of scalp (it hurts to comb the hair), cough, throat pain, tongue pain, weight loss, depression, stroke, or pain in the arms during exercise. Some patients have many of these symptoms; others have only a few. Blindness — the most feared complication — can develop if the disease is not treated in a timely fashion.

What Causes Giant Cell Arteritis?

We do not know. We do know that aging has something to do with the disease. And we know that the body’s immune system attacks and inflames the arteries. But we do not know why the immune system attack occurs when and where it does.

How is Giant Cell Arteritis Diagnosed?

The diagnosis is made by doing a biopsy of the temporal artery. Using a local numbing medication (the same one used by a dentist), the doctor can remove a small part of the temporal artery from under the scalp and look at it under the microscope for evidence of inflammation. A temporal artery biopsy is almost always safe, causes very little pain, and often leaves little or no scar. An example of this is pictured below

There are blood tests that help the doctor decide who is likely to have GCA. Almost everyone with the condition has an elevated erythrocyte sedimentation rate (also called “sed rate”). The sed rate measures how fast a patient’s red blood cells settle when placed in a small tube. In inflammatory conditions, red blood cells settle more quickly than in non–inflammatory states. In addition, most patients with GCA have a slight–anemia, or low red blood cell count. Other conditions can also cause a high sed rate or anemia, so the final diagnosis depends on a temporal artery biopsy.

A few patients with GCA do not have positive biopsies. We now know that GCA does not affect every part of every temporal artery but can “skip” around. When one biopsy is negative, biopsying the temporal artery on the other side can lead to the diagnosis.

Treatment and Course of Giant Cell Arteritis

GCA requires treatment with prednisone, a type of corticosteroid. Typically, treatment begins with 40–60 mg of prednisone, taken by mouth each day. Most patients improve rapidly and dramatically on this dose, with improvement of most symptoms in 1–3 days. Unfortunately, if blindness has occurred as a symptom it is usually irreversible, which only emphasizes the importance of early detection and treatment.

Almost all patients experience side effects from prednisone. After the patient improves, the doctor gradually reduces the prednisone dose. The rate of tapering prednisone depends on how the patient feels, what the doctor finds on exam, and the results of blood tests, including the sedimentation rate. Although virtually all patients are able to reduce their prednisone dose, most require some amount of prednisone for 1–2 years. Longer treatment periods are not uncommon.

In medical terms, by David Hellmann, M.D.

A discussion of Giant Cell Arteritis written in medical terms by David Hellmann, M.D. (F.A.C.P.), Co-Director of the Johns Hopkins Vasculitis Center, for the Rheumatology Section of the Medical Knowledge Self-Assessment Program published and copyrighted by the American College of Physicians (Edition 11, 1998). The American College of Physicians has given us permission to make this information available to patients contacting our Website.

Giant cell arteritis is vasculitis of unknown cause that affects the elderly and is characterized by panarteritis of medium- to large-sized arteries, especially in the extracranial branches of the carotid artery. The average age of onset is 72 years, and women are affected two times as often as men. Irreversible blindness, the most commonly feared complication, results from necrosis of the posterior ciliary branch of the ophthalmic artery and is usually preventable by early diagnosis and corticosteroid treatment.

Giant cell arteritis can begin suddenly or gradually with nonspecific symptoms such as malaise, weight loss, depression, and fatigue or with the classic symptoms of headache, scalp tenderness, jaw claudication, visual changes, or polymyalgia rheumatica. Polymyalgia rheumatica which can occur with or without giant cell arteritis, is characterized by pain and stiffness of the hips and shoulders that worsens in the morning. About one third of patients resemble the preceding patient and present with atypical manifestations such as fever of unknown origin, respiratory symptoms (dry cough is most common), large vessel disease (causing Raynaud’s phenomenon, claudication, or thoracic aortic aneurysm), mononeuritis mutiplex, glossitis, or profound anemia. Although giant cell arteritis accounts for only 2% of all fever of unknown origin, it accounts for 16% of fever of unknown origin in patients over age 65 years and is often associated with rigors and sweats. Only half of patients have enlarged, nodular, or nonpulsatile temporal arteries: normal temporal arteries on physical examination do not exclude the diagnosis. Subclavian bruits, diminished pulses, aoritic regurgitation, or Raynaud’s phenomenon are found in patients with large vessel disease. Fundoscopic examination is normal in the first day or two after blindness develops. Almost all patients have a markedly elevated ESR, averaging about 100 mm/h. Very rarely, the ESR may be normal, especially in patients who are already taking prednisone for allergic or respiratory diseases. MOst patients have mild normochromic normocytic anemia, and 20% to 30% resemble the preceding patient in having mildly elevated serum alkaline phosphatase. The leukocyte count at presentation is usually normal, a point favoring giant cell arteritis over infection or malignancy.

Because blindness from giant cell arteritis is almost irreversible, treatment with 40 to 60 mg of prednisone should be started as soon as the diagnosis is suspected. Although immediate temporal artery biopsy has been preferred, one study suggests that biopsy remains positive within at least the first 2 weeks of corticosteroid therapy. Therapy should not be held pending biopsy. In patients with giant cell arteritis, arterial involvement is patchy: therfore, maximizing the chance of diagnosis requires obtaining a long (3 to 4 cm) segment and examining multiple sections. Positive biopsy specimens show infiltration of the vessel wall with mononuclear inflammatory cells and giant cells, intimal proliferation, and thrombosis. Unilateral biopsy specimens are positive in approximately 85% of patients, and bilateral biopsy specimens are positive in 95%. Patients dramatically improve within 24 to 72 hours of beginning therapy, and the ESR usually normalizes within 1 month. Thereafter, prednisone can be tapered slowly, although most patients require some prednisone for at least 9 months and often longer.

Treatment decisions should probably be based on the patient’s symptoms, the hemoglobin, the ESR: ESR alone should not dictate therapy. Because compression fractures develop in one third of patients, prevention and treatment of osteoporosis should be part of initail management. Methotrexate, azathioprine, and cyclophosphamide have been used in rare patients who do not respond to adequate prednisone. Long–term follow–up is required to detect late recurrences (including the late onset of thoracic aortic aneurysms with aortic regurgitation, congestive heart failure, and aortic dissection). Patients with polymyalgia rheumatica but no symptoms of giant cell arteritis above the neck (such as jaw claudication, headache and visual symptoms) do not need temporal artery biopsy and respond to low–dose prednisone (10 to 20 mg/d orally). Because polymyalgia rheumatica is a clinical diagnosis, other conditions such as hypothyroidism, amyloidosis, rheumatoid arthritis, and malignancy should be considered in the initial evaluation and reconsidered if the patient does not improve rapidly on prednisone.

Eosinophilic Granulomatosis with Polyangiitis, formerly Churg-Strauss Syndrome (EGPA)

First Description

Eosinophilic granulomatosis with polyangiitis (EGP), formerly known as the Churg-Strauss Syndrome , is a systemic vasculitis. This disease was first described in 1951 by Dr. Jacob Churg and Dr. Lotte Strauss as a syndrome consisting of “asthma, eosinophilia [an excessive number of eosinophils in the blood], fever, and accompanying vasculitis of various organ systems”. EGPA shares many of the clinical and pathological features of polyarteritis nodosa (“PAN”, another type of vasculitis) and granulomatosis with polyangiitis (GPA). However, Drs. Churg and Strauss discovered that the presence of granulomas as well as the abundance of eosinophils distinguished this disease from PAN and GPA.

Who gets EGPA (the “typical” patient)?

The typical patient with EGPA is a middle aged individual with a history of new-onset or newly-worsened asthma. The distribution of the disease among males and females is approximately equal.

Classic symptoms and signs of EGPA

Asthma is one of the cardinal features of EGPA. Asthma symptoms may begin long before the onset of vasculitis – e.g., many years before any other symptoms of EGPA arise, and long before the diagnosis of EGPA is made. Other early symptoms/signs include nasal polyps and allergic rhinitis.

The next phase of the disease is often marked by eosinophilia, the finding of an excessive number of eosinophils in the blood or in tissues. An eosinophil is one subtypes of white blood cell. Normally, eosinophils comprise 5% or less of the total white blood cell count. In EGPA, the percentage of eosinophils may reach as high as 60%. In the picture below, the eosinophils are shown by the dark pink stain.

The third phase of the illness is a vasculitis, which involves the skin, lungs, nerves, kidneys, and other organs. Particular mention should be made of the frequent devastating involvement of the nerves (called mononeuritis multiplex), which produces severe tingling, numbess, shooting pains, and severe muscle wasting/power loss in the hands or feet. The list below contains the organs commonly involved by EGPA and the specific disease manifestation(s) in each organ.

Nose

  • Sinusitis, including allergic rhinitis
  • Nasal polyps

Lung

  • Pulmonary infiltrates (only one-third of all patients)
  • Bleeding into the lungs (occasionally)
  • Diffuse interstitial lung disease (rarely)

Skin

  • Rashes
  • Palpable purpura
  • Nodules (above or below the skin), often at sites of pressure, such as the elbows

Kidney

  • Glomerulonephritis (inflammation in the small units of the kidney that filter blood)
  • Hypertension

Gastrointestinal

  • Lesions (vasculitic) are occasionally found in the GI tract
  • Granuloma sometimes found in spleen

Heart

  • Vasculitis lesions in heart, can lead to congestive heart failure or a heart attack

Nerve

  • Peripheral nerve involvement including pain, numbness, or tingling in extremities (neuropathy/mononeuritis multiplex)

What causes EGPA?

The cause of EGPA is unknown but is probably multi-factorial. Genetics may play a small role in the disease, but EGPA is almost never seen in two members of the same family. Environmental factors such as exposure to industrial solvents may play a role in susceptibility to this disease, but this is largely speculative. Infections may be the inciting event(s), but to date there is no definitive evidence of this.

How is EGPA Diagnosed?

Among all of the vasculitides, asthma is a distinctive feature of EGPA alone. However, not all patients with asthma have vasculitis – only a tiny minority do, in fact. It is the specific combination of symptoms and signs, the pattern of organ involvement, and the presence of certain abnormal blood tests (eosinophilia, in particular) that help the doctor make the diagnosis. In addition to a detailed history and physical examination, blood tests, chest X-rays and other types of imaging studies, nerve conduction tests, and tissue biopsies (e.g., of lung, skin, or nerve) may be performed to help diagnose EGPA.

The following features are consistent with a diagnosis of GPA:

  1. asthma
  2. eosinophilia [>10% on differential WBC count]
  3. mononeuropathy
  4. transient pulmonary infiltrates on chest X-rays
  5. paranasal sinus abnormalities
  6. biopsy containing a blood vessel with extravascular eosinophils.

Treatment and Course of EGPA

EGPA usually responds to prednisone. Initially, high doses of oral prednisone are used in an attempt to get the disease into remission as quickly as possibly (e.g., using oral prednisone 40-60 mg/day). After the first month or so, this high dose of prednisone is gradually tapered down over the ensuing months. Other immunosuppressive drugs, such as azathioprine, cellcept, methotrexate, cyclophosphamide, or rituximab may be used in addition to prednisone. High doses of intravenous steroids (usually methylprednisolone) maybe useful for those patients with severe disease or for those who are unresponsive to the combination of oral prednisone used with other immunosuppressive medications.

Prior to the advent of prednisone, EGPA was often a fatal disease. The majority of patients died from rampant, uncontrolled disease. With present therapy, constitutional symptoms begin to resolve quite quickly, with gradual improvement in cardiac and renal function, as well as improvement in the pain that results from peripheral nerve involvement. The course of therapy can last for 1 to 2 years, although the length and type of treatment depend on the severity of disease and the organs involved. The patient’s response to treatment and the continuation of disease control during lowering of the prednisone dose are the primary determinants of how long therapy is continued. Laboratory monitoring of blood tests is very helpful in gauging the activity of disease. Some of the most useful laboratory tests are the erythrocyte sedimentation rate (ESR) and the eosinophil count.

Buerger’s Disease

First Description

This disease was first reported by Buerger in 1908, who described a disease in which the characteristic pathologic findings — acute inflammation and thrombosis (clotting) of arteries and veins — affected the hands and feet. Another name for Buerger’s Disease is thromboangiitis obliterans.

Who gets Buerger’s Disease (the “typical” patient)?

The classic Buerger’s Disease patient is a young male (e.g., 20–40 years old) who is a heavy cigarette smoker. More recently, however, a higher percentage of women and people over the age of 50 have been recognized to have this disease. Buerger’s disease is most common in the Orient, Southeast Asia, India and the Middle East, but appears to be rare among African–Americans.

Classic symptoms and signs of Buerger’s Disease

The initial symptoms of Buerger’s Disease often include claudication (pain induced by insufficient blood flow during exercise) in the feet and/or hands, or pain in these areas at rest. The pain typically begins in the extremities but may radiate to other (more central) parts of the body. Other signs and symptoms of this disease may include numbness and/or tingling in the limbs and Raynaud’s phenomenon (a condition in which the distal extremities — fingers, toes, hands, feet — turn white upon exposure to cold). Skin ulcerations and gangrene (pictured below) of the digits (fingers and toes) are common in Buerger’s disease. Pain may be very intense in the affected regions.

An angiogram demonstrating lack of blood flow to vessels of the hand (figure below). This decreased blood flow (“ischemia”) led to ulcers of the fingers and severe pain.

An abnormal result from an angiogram of the hand (figure below).

Despite the severity of ischemia (lack of blood flow) to the distal extremities that occurs in Buerger’s, the disease does not involve other organs, unlike many other forms of vasculitis. Even as ulcers and gangrene develop in the digits, organs such as the lung, kidneys, brain, and gastrointestinal (GI) tract remain unaffected. The reasons for the confinement to the extremities and sparing of other organs are not known.

What Causes Buerger’s Disease?

The association of Buerger’s Disease with tobacco use, particularly cigarette smoking, cannot be overemphasized. Most patients with Buerger’s are heavy smokers, but some cases occur in patients who smoke “moderately”; others have been reported in users of smokeless tobacco. It has been postulated that Buerger’s Disease is an “autoimmune” reaction (one in which the body’s immune system attacks the body’s own tissues) triggered by some constituent of tobacco.

Pictured below, are a patient’s fingertips that have developed gangrene. This is a very painful condition which sometimes requires amputation of the affected area.

How is Buerger’s diagnosed?

Buerger’s disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buerger’s Disease (for Buerger’s, there is only one treatment known to be effective: complete smoking cessation — see below).

Diseases with which Buerger’s Disease may be confused include atherosclerosis (build–up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynaud’s phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders of the blood, and others.

It should be noted that other substances, such as marijuana, have also been associated with a vasculitis similar to Buerger’s or polyarteritis nodosa that should be considered in the differential diagnosis.

Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buerger’s disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buerger’s. These findings include a “corkscrew” appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Angiograms may also show occlusions (blockages) or stenoses (narrowings) in multiple areas of both the arms and legs.

Pictured below on the left is a normal angiogram. On the right, is an abnormal angiogram of an arm demonstrating the classic “corkscrew” appearance of arteries to the hand. The changes are particularly apparent in the blood vessels in the lower right hand portion of the picture (the ulnar artery distribution).

In order to rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buerger’s), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram).

Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.

Treatment and Course of Buerger’s

It is essential that patients with Buerger’s disease stop smoking immediately and completely. This is the only treatment known to be effective in Buerger’s disease. Patients who continue to smoke are generally the ones who require amputation of fingers and toes.

Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as steroids have not been shown to be beneficial. Similarly, strategies of anticoagulation (thinning of the blood with aspirin or other agents to prevent clots) have not proven effective. The only way to prevent the progression of the disease is to abstain from all tobacco products.

Colchicine

What is colchicine?

Colchicine is an oral drug used in the treatment of some forms of cutaneous vasculitis. It is a very old medicine that is more frequently encountered in the treatment of gout.

How does colchicine work?

Colchicine seems to work by preventing immune cells from becoming fully activated.

How is colchicine given?

Colchicine is given as an oral pill at a dose of 0.6 mg either once or twice per day.

Side effects:

In contrast to most other vasculitis treatments, colchicine is not an immunosuppressant drug and does not cause any significant risk of infection.

Colchicine can cause gastrointestinal side effects and requires monitoring during its use. Some patients with kidney disease may not be able to safely take colchicine on a long-term basis.

Causes of Vasculitis

There are many different types of vasculitis, some with different causes than others.

Certain forms of vasculitis that can be due to infection where the microbe directly invades the vessel wall. Syphilis is one example of vasculitis that can be caused by infection in the blood vessel. Treating the infection is the main goal in managing this sort of vasculitis, which is not an autoimmune disease, but rather an infection.

Other infections can provoke the immune system into causing damage in blood vessels. Here, the infection is the trigger, but the immune system is the cause of the vascular damage. Viral hepatitis (B and C) are examples of this sort: some patients with Hepatitis B may develop polyarteritis nodosa, while some patients with Hepatitis C may develop cryoglobulinemic vasculitis.

Other types of vasculitis may be due to an ‘allergic‘-type reaction to medications. For example, certain blood pressure medications (hydralazine) or thyroid medications (propylthiouracil) can trigger ANCA associated vasculitis in some patients. Cocaine is an illicit drug that is linked to vasculitis and vascular damage.

However, the causes of most vasculitides are currently unknown. While we can identify some risk factors (such as older age in giant cell arteritis), we do not know the specific causes of these diseases. These forms of vasculitis of unknown cause are considered autoimmune diseases.

Under normal circumstances, our immune system serves to defend us from infection and other threats, such as cancers. In autoimmune diseases, the immune system generates a response not against a foreign threat, but against normal “self” tissues. This abnormal immune response against “self” tissues can result in a wide array of autoimmune diseases, including relatively common diseases (such as psoriasis or thyroid disease) as well as rare conditions (such as vasculitis).

In most cases, autoimmune diseases are believed to be due to an abnormal immune response that is generated in a susceptible person, and eventually leads to a cycle of ongoing inflammation in otherwise normal tissues where no infection or other identifiable threat is present. Some interaction between the immune system and the environment is thought necessary for this to occur, and a person’s genetic background likely places some individuals at higher risk than others.

A better understanding of the specific causes of these diseases would lead to improved means of diagnosing, treating, and even preventing these conditions. Uncovering the causes of vasculitis is a major goal of vasculitis research.

While we may not know the specific causes of the vasculitidies, we do have a basic understanding of the way that the immune system causes organ damage in these conditions. In all forms of vasculitis, activation of the immune system leads to the deposition of inflammatory cells and proteins in the walls of blood vessels. As this inflammation in blood vessels continues, the vessels become damaged and no longer serve their normal function of delivering blood to the organs that they supply. Consequently, the tissues downstream of these inflamed vessels are starved of oxygen and nutrients needed for normal function. At a basic level, this is a process similar to what occurs in a heart attack or a stroke – but instead of the cholesterol plaque that blocks a coronary artery in a heart attack, the immune system is responsible for blockage of blood vessels in vasculitis.

All information contained within the Johns Hopkins Vasculitis Center website is intended for educational purposes only. Visitors are encouraged to consult other sources and confirm the information contained within this site. Consumers should never disregard medical advice or delay in seeking it because of something they may have read on this website.

Linda’s Loop

contributed by Brenda Shilling

I have always known that chronic and life-threatening diseases can have a devastating effect on people’s lives. I’ve seen it happen to friends’ families and heard of it happening to friends of friends. But until 2002, the realities of such challenges were quite remote to me, as I had never felt a loved one struggle with a serious condition.

Linda Gray and her twin sister, Brenda Shilling.

In the spring of 2002, my identical twin, Linda, was diagnosed with neuropsychiatry lupus and central nervous system vasculitis. It was a scary time for all of us, particularly for Linda and her family. Like many lupus patients, Linda had been ill often and had many problems in the years leading up to her diagnosis. We were extremely thankful that The Johns Hopkins Vasculitis Center quickly identified what was wrong and started Linda on a treatment program.

In the months that followed, I watched my sister experience a multitude of emotions, including devastation over her diagnosis, fear for her future, and relief that she had finally found help. Although I know that not all lupus patients fare well, I learned that the treatment of lupus has come a long way over the years and I prayed that Linda would benefit from these advances. Her treatment was extremely challenging. However, during the hard realities of chemotherapy and steroids on Linda’s body, her spirit was amazing.

Despite knowing that family is extremely important during times like this and that frequent calls, letters, and visits to Linda were supportive, I slowly began to feel helpless. This was an unexpected emotion. I wanted to do more. I needed to do more. My sister was going through the most difficult time of her life, and I had do something more.

One morning in the late spring of 2003 I considered coordinating a bicycle ride to raise funds for The Johns Hopkins Vasculitis Center. Our sister, Liz, thought it was wonderful idea and wanted to help. We were driven by love for our sister and that was all the motivation we needed!

Linda Gray and her sister, Liz Adams.

We decided on a 50-mile ride – short enough to manage but long enough to sound good! We then mailed over 200 letters to friends and family asking for a financial gift to The Johns Hopkins Vasculitis Center in honor of our sister and others with her disease. We also distributed the letter to social and religious groups in which we are involved. Four of our friends asked if they could join us on the bike ride in a generous gesture of support. We even had t-shirts made!

Linda's Loop Participants

Participants in Linda’s Loop:

Left to Right: (Front Row, kneeling) Georgann Pattillo, Jan Rowe, Bill Schilling ; (Middle Row) Kevin Adams, Linda Moore, Liz Adams, Sue Schilling, Brenda Schilling, Betty Lamey, Patrick Pattillo, Leroy Lamey ; (Back Row) Chandler Burroughs, Steven Rowe, and Bill Schilling, Sr.

The night before the ride, we finished packing up drinks, snacks, and lunches and then headed home to get some sleep. Liz told me that she didn’t sleep a wink that night – neither did I! We were too excited.

The day finally arrived and everything went so well. It was such a wonderful day that I simply didn’t want it to end! Our family and friends came out to cheer us along. It felt great to have them there. But wow! The miles were more difficult than I expected. Although three riders finished far ahead, the remaining three of us dragged ourselves over the finish line some time later. We were quite the motley crew!

Hot, sweaty, hungry, but happy!

Response to our effort was overwhelming. My husband Bill teases that this was the only time I actually picked up the mail! Liz and I were moved by all the contributions. Some were from people who don’t know Linda but had read about the ride in the local paper. When we started planning we weren’t sure how much money we could raise. It was wonderful to have received just over $8,600 in contributions to vasculitis research!

Linda told me how much love she felt because of what we did for The Johns Hopkins Vasculitis Center. What more could I have asked of myself? We wanted to show Linda how proud we were of all she accomplished during her difficult treatment. We also wanted to say thank you to The Johns Hopkins Vasculitis Center for the wonderful work they do in caring for their patients everyday.

Hopefully we accomplished both.

All information contained within the Johns Hopkins Vasculitis Center website is intended for educational purposes only. Visitors are encouraged to consult other sources and confirm the information contained within this site. Consumers should never disregard medical advice or delay in seeking it because of something they may have read on this website.