eMedicine Specialties > Rheumatology > Vasculitis

Wegener Granulomatosis: Treatment & Medication

Author: Patricia J Papadopoulos, MD, Fellow, Department of Rheumatology, Walter Reed Army Medical Center, Washington, DC
Coauthor(s): Robert John O'Brian, MD, Staff Rheumatologist, National Naval Medical Center
Contributor Information and Disclosures

Updated: Aug 4, 2009

Treatment

Medical Care

Untreated generalized or severe Wegener granulomatosis (WG) typically carries a dismal prognosis, with up to 90% of patients dying within 2 years, usually of respiratory or renal failure. Even nonrenal WG carries a mortality rate of up to 40%.9

Outcomes for this previously fatal disease improved dramatically with the introduction in the 1970s of cyclophosphamide, which is administered in combination with corticosteroids. Approximately 90% of patients with WG respond to cyclophosphamide, with approximately 75% experiencing complete remission. However, 30%-50% of those who respond experience at least one relapse, requiring another course of therapy. In general, limited disease does not require as aggressive therapy as does severe disease. Additionally, treatment recommendations are different for remission induction and remission maintenance.

Current treatment recommendations in WG depend on the severity and activity of disease. The European Vasculitis Study Group (EUVAS) recommends grading disease severity of the AAVs into the following 5 categories:18

  • Localized - Upper and/or lower respiratory tract disease without any other systemic involvement or constitutional symptoms
  • Early systemic - Any, without organ-threatening or life-threatening disease
  • Generalized - Renal or other organ-threatening disease, serum creatinine level less than 5.6 mg/dL
  • Severe - Renal or other vital-organ failure, serum creatinine level exceeding 5.6 mg/dL
  • Refractory - Progressive disease unresponsive to glucocorticoids and cyclophosphamide

Remission induction

Localized disease generally requires milder therapy and may respond to a single agent.

  • Single agents used in localized disease include corticosteroids, azathioprine, or methotrexate.19

Generalized or severe disease generally requires more aggressive therapy. A combination of cyclophosphamide (intravenous or oral) and glucocorticoids is recommended for induction of remission in generalized WG.18

  • Combination therapy with oral cyclophosphamide 2 mg/kg/d (maximum 200 mg/d) and prednisone 1 mg/kg/d has been used for induction of remission in AAV since introduced by Fauci et al the 1970s. Cyclophosphamide continues to be the treatment of choice, although, in recent years, emphasis has been placed on optimizing treatment by minimizing exposure to cyclophosphamide and seeking alternative comparable therapies.
  • Pulsed (intravenous) cyclophosphamide (15 mg/kg every 2 weeks for the first 3 pulses, then every 3 weeks for the next 3-6 pulses) is an alternative to daily oral cyclophosphamide and results in less cumulative exposure to cyclophosphamide and therefore fewer side effects. Pulsed cyclophosphamide has been shown to be as effective as daily oral cyclophosphamide in inducing remission.20 However, there was a trend toward higher relapse rates with pulsed cyclophosphamide later in the maintenance phase of treatment. Nonetheless, this study was not intended to detect a difference between the two groups; more studies are needed.18,20
  • Cyclophosphamide doses are reduced as needed for renal function and age.
  • Therapy is usually continued for 3-12 months following remission. The patient is then transitioned to a medication for maintenance of remission.
  • Prophylaxis against Pneumocystis jiroveci pneumonia should be instituted while patients are taking cyclophosphamide and corticosteroids (particularly high-dose corticosteroids). Typically, TMP-SMX 160/800 mg 3 times per week is used. If the patient has a sulfa allergy, dapsone 100 mg daily can be substituted.
  • Cyclophosphamide toxicity manifests as hemorrhagic cystitis (in 15%-43% of cases after oral treatment), bladder cancer (30-fold increased incidence as compared to controls), and opportunistic infections, typically occurring during cyclophosphamide-induced leukopenia. Patients receiving pulse cyclophosphamide should also be given oral or intravenous 2-mercaptoethanesulfonate sodium (Mesna), which binds to acrolein, the toxic metabolite of cyclophosphamide responsible for hemorrhagic cystitis. Mesna may also be beneficial in patients receiving continuous oral cyclophosphamide.

A combination of methotrexate (oral or subcutaneous) and glucocorticoids can be considered as a less-toxic alternative to cyclophosphamide for the induction of remission of non–organ-threatening or non–life-threatening WG.18

  • Methotrexate (20-25 mg/week, oral or subcutaneous) can be used in patients with less severe disease with normal renal function.
  • It may take longer to reach remission with methotrexate than with cyclophosphamide, but methotrexate has been shown to be equal to cyclophosphamide in terms of its capacity to induce remission.21
  • Daily folic acid 1 mg/d is recommended to lessen some of the adverse effects of methotrexate.

High-dose glucocorticoids are an important part of remission induction therapy in WG.18

  • Historically, corticosteroid monotherapy prolonged median survival in WG by only 7.5 months. There have been no clinical trials evaluating the role or dosing of glucocorticoids, but every clinical trial has used glucocorticoids in combination with other immunosuppressants. Thus, corticosteroids remain the cornerstone of treatment.
  • Glucocorticoids are usually given orally, but, if a rapid response is needed, such as in the case of rapidly progressive glomerulonephritis and/or alveolar hemorrhage, intravenous pulse methylprednisolone (0.5-1 g/d for 3 consecutive days) can be used in addition to oral prednisone.
  • Initial high-dose glucocorticoids (1 mg/kg/d) should be continued for at least 1 month. Doses should not be reduced to less than 15 mg/d within the first 3 months. The dose should then be slowly tapered to a maintenance dose of 10 mg/d or less during remission.18
  • Methods to prevent glucocorticoid-induced osteoporosis should be followed.

Plasma exchange should be considered in patients with rapidly progressive renal disease (serum creatinine level >5.65 mg/dL) in order to preserve renal function.18

  • Plasma exchange has not been shown to improve overall survival rates but has been associated with improved survival free of hemodialysis long-term.22,23
  • Plasma exchange is used with daily oral cyclophosphamide and glucocorticoids, usually pulse methylprednisolone.
  • Plasma exchange is theoretically helpful, as it should remove ANCAs.
  • Additionally, plasma exchange, along with aggressive immunotherapy, may be helpful in DAH.24

Remission maintenance

Remission maintenance should be continued for at least 18 months.

Agents that can be used in remission maintenance include azathioprine, methotrexate, and leflunomide.18

  • Long-term oral cyclophosphamide has been used for remission maintenance but results in significant toxicity, making it unattractive.
  • As shown by the CYCAZAREM trial, azathioprine (2 mg/kg/d) is safer and as effective as cyclophosphamide in maintaining remission.25
    • Azathioprine impairs leukocyte proliferation by inhibiting purine synthesis.
    • Azathioprine results in somewhat higher relapse rates than cyclophosphamide, especially if the patient is still PR3-ANCA–positive at the time of switch from cyclophosphamide to azathioprine.26,27
  • Methotrexate (20-25 mg per week, oral or subcutaneous) has been used for maintenance of remission if the serum creatinine level is less than 1.5 mg/dL. Methotrexate has been shown to be similar to azathioprine in terms of adverse effects, efficacy in maintaining remission, and rates of relapse.28
  • Leflunomide (20-30 mg daily) is as effective as methotrexate but it is associated with more adverse effects.29
    • Leflunomide targets T cells by inhibiting the mitochondrial enzyme dihydroorotate dehydrogenase and thus limits pyrimidine synthesis. It is used in the treatment of rheumatoid arthritis.
    • Leflunomide is metabolized by the liver and thus may be used in patients with renal insufficiency.

The glucocorticoid dose should be tapered to prednisone 10 mg/d (or less) during remission. The dose can be tapered gradually after 6-18 months depending on the patient’s response.

The addition of TMP-SMX (800/160 mg twice daily) to standard maintenance therapy may reduce the rate of relapse in WG.30


Alternative and/or promising therapies

  • Intravenous immunoglobulin (2 g/kg)
    • Intravenous immunoglobulin (IVIG) may be effective by interfering with ANCAs and thus inhibiting ANCA-mediated neutrophil activation.31
    • In a study of 22 patients with AAV given IVIG as an adjunct to immunosuppressants and/or glucocorticoids reported good results.32
  • Mycophenolate mofetil (2 g/d)
    • Mycophenolate mofetil (MMF) is a derivative of the fungus Penicillium stoloniferum that, similar to azathioprine, limits purine synthesis. MMF is primarily used for immunosuppression in transplant patients and suppresses both B and T cells.
    • Because of its favorable side-effect profile and clinical potency, MMF is being increasingly used in the management of systemic connective-tissue disorders.
    • MMF has been used in small series of refractory WG cases, for both induction and maintenance, with varying responses.33,34
    • MMF is used in combination with prednisone.
    • Clinical trials examining the use of MMF in AAVs are underway.
  • Tumor necrosis factor-α blockade
    • Etanercept is a dimeric, recombinant human fusion protein with two soluble p75 TNF-α receptors linked to the Fc region of human IgG1.
      • The initial pilot study showed good response when etanercept was added to standard therapy.35
      • The larger WGET subsequently assessed the efficacy of etanercept in the treatment of WG. Etanercept or placebo was added to standard therapy (corticosteroids plus cyclophosphamide or methotrexate) and found no improvement in the primary endpoint of sustained remission and found more solid cancers in the etanercept group. The WGET trial suggested etanercept does not improve AAV relapses and likely contributes to increased risk of infection and malignancy.36
    • Infliximab is a chimeric monoclonal antibody to TNF-α that consists of murine antigen recognition sites bound to human Fc regions. The results in various studies and/or case reports have been mixed; so it is not currently possible to comment on the efficacy of infliximab.37,38 The safety of infliximab therapy in patients with WG, similar to results in trials with etanercept, seems to be the limiting factor.39 Further studies are needed.
  • Rituximab
    • Rituximab is a chimeric monoclonal anti-CD20 IgG1 antibody that induces apoptosis of B cells, with the exception of plasma cells and pre-B cells. Infusion causes a 6-month depletion of circulating B cells and therefore may decrease production of autoantibodies such as ANCAs.
    • Clinical improvement or remission with rituximab has been described in the literature.40,41 It appears to be more effective in the vasculitic rather than the granulomatous phase, but recent small studies show good results even in limited disease.42,43 The most effective dosage has not yet been determined. There are concerns for the development of progressive multifocal leukoencephalopathy (PML) with its use. Overall, randomized controlled evidence is needed.13
    • Clinical trials examining the use of rituximab in AAV are underway.
  • 15-Desoxyspergualin (0.5 mg/kg/d subcutaneous or intravenous)
    • Synthetic derivative of spergualin, a protein from Bacillus laterosporus that is capable of preventing T- and B-cell maturation. It is licensed in Japan for recurrent kidney transplant rejection.
    • 15-Desoxyspergualin has been used with some success in refractory WG cases and in patients with contraindications to cytotoxic therapy.44,45
    • It may offer a safer alternative to cyclophosphamide for induction therapy but is not yet supported for routine clinical use.38
  • Antithymocyte globulin: These are polyclonal antibodies targeted against T-lymphocyte antigens. Infusion of antithymocyte globulin causes rapid deep depletion of T lymphocytes. It has been investigated for use in severe refractory WG.46 However, severe adverse effects may occur; thus, its use is not clinically supported.38,31
  • Anti-CD52 therapy (alemtuzumab): This is a humanized monoclonal antibody to CD52 with antilymphocyte activity. Its use in WG is considered experimental.47
  • Hematopoietic stem cell transplant: Evidence is limited.38

Surgical Care

The natural history of WG is such that inflammation may lead to tissue necrosis and damage to the nose, subglottic areas, trachea, and bronchi caused by fibrosis. Surgical intervention can be considered in these situations.

  • Saddle nose deformity can be surgically repaired by an otolaryngologist or plastic surgeon.
  • For subglottic stenosis, laser treatment, balloon dilatation, or resection of the stenotic area with reanastomosis may be performed.
  • Obstruction of the nasal lacrimal ducts can be corrected surgically.
  • Recurrent middle ear infections due to dysfunction of the eustachian tube can be treated by introducing ventilating tubes through the tympanic membranes.
  • Stenosis of major bronchi may be treated with dilatation or with silastic stents. Intralesional injections of corticosteroids may also be considered.
  • Renal transplant is an option in patients with renal failure. Glomerulonephritis usually does not affect the transplanted kidney.

Consultations

WG is a multisystem disease that requires a multidisciplinary approach to management, involving rheumatologists, pulmonologists, nephrologists, and otolaryngologists (ENT specialists).

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.


Prednisone (Sterapred)

Used as an immunosuppressant in the treatment of autoimmune disorders and vasculitis. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.

Adult

1-1.5 mg/kg PO daily initially; see Medical Care section for recommended taper

Pediatric

Not established

Risk of peptic ulcer disease is increased if concurrently taking aspirin or NSAIDs; coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infections; peptic ulcer disease; hepatic dysfunction; connective-tissue infections; fungal or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use


Methylprednisolone (Medrol, Solu-Medrol)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult

Severe or rapidly progressive disease: 1000 mg IV q24h for 3 d; switch to PO prednisone once stabilized

Pediatric

Pulse therapy: 15-30 mg/kg/dose over ≥30 min given q24h for 3 d

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications

Alkylating agents

These agents have improved the prognosis of Wegener granulomatosis (WG). Cyclophosphamide is initiated with corticosteroids but is continued for at least 3-12 months following disease remission.


Cyclophosphamide (Cytoxan)

Chemically related to nitrogen mustards. As an alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells. Complete blood cell counts should be checked every 2 weeks while taking this medication to monitor for bone marrow suppression.

Adult

PO: 2 mg/kg/d initially; maximum 200 mg/d
IV: 15 mg/kg (maximum 1.2 g) q2wk for first 3 pulses, followed by infusions q3wk for next 3-6 pulses

Pediatric

Not established

Concomitant use with barbiturates, phenytoin, or chloral hydrate increases metabolic rate of cyclophosphamide; allopurinol may increase risk of bleeding or infection and enhance myelosuppressive effects of cyclophosphamide; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones; chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity of cyclophosphamide; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function; regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis; increased risk of bladder and ureteral carcinoma; increased risk of lymphoma and leukemia

Immunosuppressive agents

These agents are useful in patients who experience significant adverse effects with cyclophosphamide induction therapy, as induction therapy in mild-to-moderate disease, and, most commonly, for maintenance of remission. It is generally started at a lower dose and gradually increased over time. Onset of effect generally takes several weeks; therefore, use in induction therapy of severe disease is not advised.


Azathioprine (Imuran)

Inhibits mitosis and cellular metabolism by antagonizing purine metabolism and inhibiting synthesis of DNA, RNA, and proteins. Effects may decrease proliferation of immune cells and result in lower autoimmune activity.

Adult

2 mg/kg/d PO as a single daily dose; not to exceed 200 mg/d

Pediatric

Not established

Toxicity increases with allopurinol; concurrent use with ACE inhibitors may induce severe leukopenia; may increase levels of methotrexate metabolites and decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Increases risk of neoplasia; caution with liver disease and renal impairment; hematologic toxicities may occur; GI disturbances (eg, nausea, vomiting, diarrhea, abdominal pain, pancreatitis) may occur; thiopurine methyltransferase (TPMT) enzyme activity should be checked before initiating treatment with azathioprine as patients with reduced TPMT activity are at increased risk for myelosuppression.


Methotrexate (Rheumatrex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust dose gradually to attain satisfactory response.

Adult

0.3 mg/kg/wk PO/SubQ usual dose; 15-25 mg/wk average dose

Pediatric

Not established

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral methotrexate; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity; folic acid or derivatives contained in some vitamins may decrease response; coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides (including TMP-SMX) may increase effects and toxicity; may increase plasma levels of thiopurines

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC counts qmo and liver and renal function q1-2 mo during therapy (monitor more frequently during initial dosing, dose adjustments, or during risk of elevated levels, eg, dehydration); can have toxic effects on hematologic, hepatic, GI, pulmonary, and neurologic systems; monitor liver test results; discontinue if significant drop in blood counts occurs; aspirin, NSAIDs, or low-dose steroids may be administered concomitantly (possibility of increased toxicity with NSAIDs, including salicylates, has not been tested)

Antibiotics

Cotrimoxazole is recommended for prophylaxis against P jiroveci pneumonia. It is continued as long as patient is on immunosuppressive therapy. Recent data show cotrimoxazole may be beneficial in decreasing relapses during maintenance therapy of WG.


Trimethoprim-sulfamethoxazole (Septra, Bactrim)

Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid, inhibiting folic acid synthesis. Results in inhibition of bacterial growth. Antibacterial activity of includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Adult

160 mg TMP, 800 mg SMX PO 3 times/wk

Pediatric

<2 months: Not recommended
>2 months: 150 mg/m2/d TMP PO divided q12h 7 days a week

May increase PT of warfarin; thus, monitor coagulation test results and adjust dose prn; increased serum levels of both dapsone and TMP may occur when medications are administered concomitantly; in elderly patients, incidence of thrombocytopenic purpura may increase when used concurrently with diuretics; hepatic clearance of phenytoin may be decreased and half-life prolonged; sulfonamides can displace methotrexate from plasma protein binding sites, thus increasing free methotrexate concentrations, which may potentiate methotrexate effects in bone marrow depression; hypoglycemic response of sulfonylureas may increase with coadministration of both medications; may decrease renal clearance of zidovudine, causing increase in zidovudine levels

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly patients, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMX; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation

More on Wegener Granulomatosis

Overview: Wegener Granulomatosis
Differential Diagnoses & Workup: Wegener Granulomatosis
Treatment & Medication: Wegener Granulomatosis
Follow-up: Wegener Granulomatosis
Multimedia: Wegener Granulomatosis
References
Further Reading
[ CLOSE WINDOW ]

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Keywords

Wegener granulomatosis, WG, Wegener's granulomatosis, Wegener's disease, Wegener disease, systemic vasculitis, systemic necrotizing angiitis, necrotizing glomerulonephritis, necrotizing granulomatous inflammation of the respiratory tract, rapidly progressive glomerulonephritis, ANCA-associated vasculitis, ANCA, AAV, PR3-ANCA, alveolar capillaritis, diffuse alveolar hemorrhage, pauci-immune complex, glomerulonephritis

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Contributor Information and Disclosures

Author

Patricia J Papadopoulos, MD, Fellow, Department of Rheumatology, Walter Reed Army Medical Center, Washington, DC
Patricia J Papadopoulos, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and American College of Rheumatology
Disclosure: Nothing to disclose.

Coauthor(s)

Robert John O'Brian, MD, Staff Rheumatologist, National Naval Medical Center
Robert John O'Brian, MD is a member of the following medical societies: American College of Rheumatology
Disclosure: Nothing to disclose.

Medical Editor

Robert E Wolf, MD, PhD, Professor Emeritus, Department of Medicine, Louisiana State University Health Sciences Center at Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Administration Medical Center of Shreveport
Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, and Society for Leukocyte Biology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn Allegheny Health System None Board membership

 
 
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