Hypersensitivity Vasculitis Medication

  • Author: Mital Patel, MD; Chief Editor: William D James, MD  more...
 
Updated: May 03, 2016
 

Medication Summary

No standard therapeutic protocol exists for hypersensitivity vasculitis. In addition, few of the therapies currently used for this entity have been tested in controlled trials.

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Anti-inflammatories

Class Summary

These agents decrease inflammatory responses and systemically interfere with events leading to inflammation.

Colchicine

 

Colchicine has effects against neutrophils, which are involved in the pathogenesis of hypersensitivity vasculitis. Colchicine has been demonstrated to be steroid-sparing in open-label studies. The only double-blinded placebo-controlled trial failed to demonstrate its efficacy; however, several methodological errors occurred in this study. It is not FDA approved in children.

Dapsone (Avlosulfon)

 

Small open-label studies or single case reports have suggested that dapsone is effective in some patients with cutaneous vasculitis. Dapsone is used in hypersensitivity vasculitis not for its antimicrobial activity but for its modulatory effect on neutrophil activity.

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Corticosteroids

Class Summary

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

Prednisone (Deltasone)

 

Prednisone is indicated for vasculitis affecting internal organs (eg, kidneys, lungs, CNS). Patients with bullous skin lesions require corticosteroid therapy in order to prevent cutaneous ulceration.

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Cytotoxic/immunosuppressives

Class Summary

These agents inhibit cell growth and proliferation. Agents in this class possibly used in hypersensitivity vasculitis include cyclophosphamide, azathioprine, methotrexate, rituximab, and mycophenolate.

Cyclophosphamide (Cytoxan, Neosar)

 

Cyclophosphamide is useful in life-threatening cases of vasculitis. Patients with skin-limited disease generally should not be treated with this agent. It is useful in patients with granulomatosis with polyangiitis (formerly Wegener granulomatosis), polyarteritis nodosa, or eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome). Cyclophosphamide is an alkylating agent that depresses T- and B-cell function.

Azathioprine (Imuran)

 

Azathioprine antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins. It may decrease the proliferation of immune cells, which results in lower autoimmune activity.

Methotrexate (Folex, Rheumatrex)

 

Methotrexate inhibits 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) tranformylase, which leads to increased levels of adenosine. This increase in adenosine inhibits leukocyte accumulation, thereby decreasing inflammation. Methotrexate ameliorates symptoms of inflammation (eg, pain, swelling, stiffness). Adjust the dose gradually to attain a satisfactory response.

Rituximab (Rituxan)

 

Rituximab is a genetically engineered human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. It immunomodulates response against malignant cells.

Mycophenolate (CellCept)

 

Mycophenolate inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

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Contributor Information and Disclosures
Author

Mital Patel, MD Instructor of Dermatology, Harvard Medical School; Associate Physician, Assistant Program Director of Dermatology-Rheumatology Fellowship, Department of Dermatology, Brigham and Women’s Hospital

Mital Patel, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Womens Association, Dermatology Foundation, Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, Medical Dermatology Society, Rheumatologic Dermatology Society, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Ruth Ann Vleugels, MD, MPH Assistant Professor of Dermatology, Harvard Medical School; Associate Physician, Department of Dermatology, Brigham and Women's Hospital; Associate Physician, Department of Immunology and Allergy, Children's Hospital Boston

Ruth Ann Vleugels, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Rheumatology, American Medical Association, Society for Investigative Dermatology, Medical Dermatology Society, Dermatology Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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Hypersensitivity vasculitis.
Henoch-Schönlein purpura.
Histopathologic features of leukocytoclastic vasculitis.
Urticarial vasculitis. These lesions differ from routine hives by lasting longer (often >24 h), being less pruritic, and often resolving with a bruise or residual pigmentation.
Erythema elevatum diutinum, a rare cutaneous vasculitis.
 
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