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Cryoglobulinemia

The name literally means “cold antibody in the blood”, which refers to the chemical properties of the antibodies that cause this disease: cryoglobulins are antibodies that precipitate under cold conditions. Drug use is a prime risk factor for cryoglobulinemia because more than 90% of cases of cryoglobulinemic vasculitis are associated with hepatitis C infections. Hepatitis C is acquired by injection drug use (needle–sharing), tainted blood products, and (probably rarely), sexual transmission. Treatment of the underlying hepatitis may be an effective therapy for this type of vasculitis.

Pictured below is the hand from the same patient at different times. The image on the left is normal and the one on the right shows the patient in the midst of a flare of cryoglobuinemic vasculitis.

Pictured below is an electron micrograph of a kidney biopsy specimen from a patient with cryoglobulinemia.

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

A discussion of Cryoglobulinemia 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.

Cryoglobulins are immunoglobulins that precipitate in the cold and disolve on rewarming. Three types of cryoglobulins are distinguished based on whether the cryoglboulin is monoclonal and has rheumatoid factor activity. Knowing the type usually allows the physician to predict the clinical features; alternatively knowing the clinical features allows one to deduce the type of cryoglobulin. Type I is a monoclonal antibody that does not have rheumatoid factor activity. Most commonly, type I is associated with lymphoma, Waldenström’s macroglobulinemia, and multiple myeloma. Because type I cryoglobulins do not easily activate complement, patients with type I are asymptomatic until the level of cryoglobulinemia is sufficiently high to cause hyperviscosity syndrome. Both types II and III are rheumatoid factors — antibodies that bind to the Fc fragment of IgG. Therefore, both types are called mixed cryoglobulins. In type II, the rheumatoid factor is monoclonal, whereas in type III it is polyclonal. Type II is associated with lymphoproliferative diseases, and both types can occur in patients with rheumatic diseases and chronic infections. Cryoglobulinemia is said to be essential when there is no identifiable underlying disease. Type II and III cryoglobulinemia frequently presents as vasculitis, most commonly with recurrentlower extremity purpura, glomerulonephritis, and peripheral neuropathy.

It is now evident that most patients diagnosed with type II or type III mixed essential cryoglobulinemia have the disease as an immune response to chronic hepatitis C infection. The role of hepatitis C virus is suggested by finding that the cryoglobulins in these patients are enriched with anti–hepatitis C antibody and hepatitis C RNA. Moreover, antviral therapy can remit the disease in some patients.

Treatment depends on the type of cryoglobulin, underlying disease, and severity of symptoms. Cryoglobulinemia with severe hyperviscosity syndrome requires plasmapheresis and chemotherapy of the underlying malignancy. Some patients with cryoglobulinemia suffer from mild, recurrent crops of lower extremity purpura that require no specific therapy. More extensive vasculitis associated with autoimmune diseases or essential cryoglobulinemia may respond to prednisone, cyclophosphamide, or both. The most effective treatment for cryoglobulinemia associated with hepatitis C has not yet been determined. Brief use of prednisone followed by 6 months of interferon alfa has produced clinical and liver function test improvement, but relapse of liver disease and vasculitis often occurs when interferon alfa is stopped.

Microscopic Polyangiitis

First Description

The first description of a patient with the illness now known as microscopic polyangiitis (MPA) appeared in the European literature in the 1920s. The concept of this disease as a condition that is separate from polyarteritis nodosa (PAN) and other forms of vasculitis did not begin to take root in medical thinking, however, until the late 1940s. Even today, some confusing terms for MPA (e.g., “microscopic poly arteritis nodosa ” rather than “microscopic poly angiitis ”) persist in the medical literature. Confusion regarding the proper nomenclature of this disease led to references to “microscopic polyarteritis nodosa” and “hypersensitivity vasculitis” for many years. In 1994, The Chapel Hill Consensus Conference recognized MPA as its own entity, distinguishing it in a classification scheme clearly from PAN, granulomatosis with polyangiitis (GPA, formerly Wegener’s), cutaneous leukocytoclastic angiitis (CLA), and other diseases with which MPA has been confused with through the years.

Much of the explanation for the difficulty in separating MPA from other forms of vasculitis has stemmed from the numerous areas of overlap of MPA with other diseases. MPA, PAN, GPA, and CLA  and other disorders all share a variety of features but possess sufficient differences as to justify separate classifications.

Who gets Microscopic Polyangiitis? A typical patient

MPA can affect individuals from all ethnic backgrounds and any age group. In the United States, the typical MPA patient is a middle-aged white male or female, but many exceptions to this exist. The disease may occur in people of all ages, both genders, and all ethnic backgrounds.

Classic symptoms of Microscopic Polyangiitis

Many signs and symptoms are associated with MPA. This disease can affect many of the body’s organ systems including (but not limited to) the kidneys, nervous system (particularly the peripheral nerves, as opposed to the brain or spinal cord), skin, and lungs. In addition, generalized symptoms such as fever and weight loss are very common.

The FIVE most common clinical manifestations of MPA are:

  1. Kidney inflammation (~ 80% of patients).
  2. Weight loss (> 70%).
  3. Skin lesions (> 60%).
  4. Nerve damage (60%).
  5. Fevers (55%).

Kidney Inflammation

Inflammation in the kidneys, known as glomerulonephritis, causes blood and protein loss through the urine. This process can occur either slowly or very rapidly in the course of the disease. Patients with kidney inflammation may experience fatigue, shortness of breath, and swelling of the legs.

The image below is from a urinalysis of a patient with kidney inflammation. When MPA is active, red blood cells will form a clump or “cast” (bracketed in white) within the tubules of inflamed kidneys. These “casts” pass through the renal system and may be viewed under the microscope in a patient’s urine.

Constitutional Symptoms

Weight loss, fevers, fatigue, and malaise are part of a collection of complaints regarded as “constitutional” symptoms. Constitutional complaints are a common finding in patients with MPA, because the disorder is a systemic disease confining itself generally not to one specific organ system but rather broadly affecting a patient’s “constitution”.

Skin lesions

Skin lesions in MPA, as in other forms of vasculitis that involve the skin, can erupt on various areas of the body. The lesions tend to favor the “dependent” areas of the body, specifically the feet, lower legs and, in bed-ridden patients, the buttocks. The skin findings of cutaneous MPA include purplish bumps and spots pictured below (palpable purpura).

These areas range in size from several millimeters in diameter to coalescent lesions that are even larger. Skin findings in MPA may also include small flesh-colored bumps (papules); small-to-medium sized blisters (vesiculobullous lesions); or as small areas of bleeding under the nails that look like splinters (pictured below), hence the name splinter hemorrhages.

Peripheral nervous system

Damage to peripheral nerves (i.e., nerves to the hands and feet, arms and legs) results from inflammation of the blood vessels that supply the nerves with nutrients. Inflammation in these blood vessels deprives the nerves of their nutrients, leading to nerve infarction (tissue death). Multiple nerve involvement that is characteristic of vasculitis is known as “mononeuritis multiplex”. This condition is frequently associated with wrist or foot drop: the inability to extend the hand “backwards” at the wrist or to flex the foot upward toward the head at the ankle joint. If the condition is caused by nerve deterioration associated with vasculitis, unfortunately, surgery is not a treatment option due to the nerve infarcton (tissue death).

Neurologic symptoms resulting from peripheral nerve damage may also include numbness or tingling in the arm, hand, leg, or foot. Over time, muscle wasting (pictured below) that is secondary to the nerve damage may result from damage caused by vasculitis.

Pictured:

The hand on the left (the patient’s right hand) is normal, displaying normal muscle bulk of the areas between the fingers.  In contrast, the hand on the right (the patient’s left) shows wasting of the muscle in the web space between the thumb and first finger, leading to a hollowed-out, bowl-like appearance of that area.  The consequence of this muscle wasting is that the patient is unable to grasp objects between his thumb and fingers (i.e., has a weak pinch) and his hand grip is weak.

Lungs

Lung involvement can be a dramatic and life-threatening manifestation of MPA. When lung disease takes the form alveolar hemorrhage – bleeding from the small capillaries that are in contact with the lungs’ microscopic air sacs – the condition may quickly pose a threat to the patient’s respiratory status (and therefore to the patient’s life). Alveolar hemorrhage (pictured below), which is frequently heralded by the coughing up of blood, occurs in approximately 12% of patients with MPA .

Another common lung manifestation of MPA is the development of non-specific inflammatory infiltrates, identifiable on chext x-rays or computed tomography (CT scans) of the lung.

Eyes, Muscles, and Joints

Organs that also merit mention in discussions of MPA include the eyes, muscles, and joints. Intermittent irritation of the eye (resembling “pinkeye”) that is caused by either conjunctivitis or episcleritis may be an early disease manifestation or a sign of a disease flare. Occasionally other types of inflammation (e.g., uveitis) are also observed in MPA. Muscle or joint pains (known to clinicians as “myalgias” or “arthralgias”, respectively) are common complaints in MPA, generally accompanying the types of constitutional symptoms mentioned above. Arthritis (inflammation of the joints accompanied by swelling) can also be observed in MPA. Joint complaints in MPA and related forms of vasculitis tend to migrate from one joint to another – one day involving the left ankle, the next day the right wrist, the third day a shoulder, for example.

Forms of vasculitis similar to Microscopic Polyangiitis

The similarities and differences between MPA, GPA, and PAN are highlighted in the table below.

MPA GPA PAN
BLOOD VESSEL SIZE Small to Medium Small to Medium Medium
BLOOD VESSEL TYPE Arterioles to venules, And sometimes Arteries and veins Arterioles to venules, And sometimes Arteries and veins Muscular Arteries
GRANULOMATOUS INFLAMMATION NO YES NO
LUNG SYMPTOMS YES1 YES1 NO
GLOMERULONEPHRITIS YES YES NO
RENAL HYPERTENSION NO NO YES
MONONEURITIS MULTIPLEX COMMON OCCASIONAL COMMON
SKIN LESIONS YES2 YES2 YES2
GI SYMPTOMS NO NO YES3
EYE SYMPTOMS YES4 YES4 NO
ANCA-POSITIVITY 75% 65-90% NO
CONSTITUTIONALSYMPTOMS YES5 YES5 YES5
NECROTIZING TISSUE YES YES YES
MICROANEURYSMS RARELY RARELY TYPICAL

1 Pulmonary capillaritis in MPA and nodules or cavitary lesions in WG

2MPA can have small blood vessel skin lesions as mentioned above, similar to GPA or medium blood vessel lesions similar to PAN (livedo reticularis, nodules, ulcers, and digital gangrene)

3Stomach pain after meals

4MPA eye complications are typically milder than those of GPA, but serious

ocular problems including necrotizing scleritis can occur

5Constitutional symptoms include weight loss, fevers, joint and muscle aches, and malaise.

What Causes Microscopic Polyangiitis?

The cause of MPA is not known. However, enough is known about a few types of vasculitides that allow us to describe in general terms how MPA affects the body. MPA is clearly a disorder that is mediated by the immune system; the precise events leading to the immune system dysfunction (hyperactivity), however, remain unclear. Many elements of the immune system are involved in this process: neutrophils, macrophages, T and B lymphocytes, antibodies, and many, many others.

Because MPA is often associated with anti-neutrophil cytoplasmic antibodies (ANCA), antibodies directed against certain constituents of white blood cells (WBCs), the disease is often termed an “ANCA-associated vasculitis”, or AAV. ANCA, discovered in 1982, act against certain specific (and naturally occurring) enzymes in the body residing within the neutrophils and the macrophages, all of which are members of the WBC family. The result of the interactions of ANCA with their target proteins is an increase in the destruction of WBCs at the sites of disease and the release of white blood cell enzymes within blood vessel walls, causing the damage to blood vessels. In MPA, the ANCA are directed generally against to specific proteins: myeloperoxidase (MPO) and proteinase 3 (PR3).

How is Microscopic Polyangiitis diagnosed?

Blood is taken to detect any ANCA levels, if MPA is suspected. In addition, an erythrocyte sedimentation rate (ESR or “sed rate”) and C-reactive protein (CRP) are usually ordered. Both of these tests are elevated in many different types of inflammation and are not specific to MPA or any particular disease. The ESR and CRP, known as “acute phase reactants”, are often sensitive indicators of the presence of active disease. In and of themselves, however, elevations in acute phase reactants are not sufficient to justify additional treatment.

A carefully analyzed urine specimen should be obtained at the initial visit (and every follow-up visit!) to maintain vigilance for either the development or the progression of kidney involvement.

A computed tomography (CT) scan of the chest may also be performed to detect the presence of lung involvement. A tissue biopsy may be needed to make the diagnosis of MPA, and is taken from an organ that seems to be involved at the time. Sometimes an electromyography/nerve conduction (EMG/NCV) study may need to be done to identify a site for biopsy or to detect findings consistent with a mononeuritis multiplex (see classic symptoms section above). Tissues that might be biopsied are kidney, skin, nerve, muscle, and lung.

Pictured: a biopsy of the gastrocnemius muscle, performed in a 69 year–old man with microscopic polyangiitis. A blood vessel within the muscle shows an intense inflammatory infiltrate with destruction of the blood vessel wall, confirming the diagnosis of vasculitis.

Treatment and Course of Microscopic Polyangiitis

A steroid (usually prednisone) in combination with a cyclophosphamide (CYC) or rituximab is typically the first combination of medications to be prescribed.  After control of the disease – usually around 4 – 6 months of treatment maintenance therapy will be used to keep the disease in remission. This will vary between patients. Prednisone may be discontinued after approximately 6 months.

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.

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.

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.