Pyoderma Gangrenosum Medication

  • Author: J Mark Jackson, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Apr 23, 2012
 

Medication Summary

Therapy with corticosteroids—such as the glucocorticoid prednisone—is often initially prescribed. An immunosuppressive agent is also sometimes initiated, either later or simultaneously; this is particularly the case in patients for whom high-dose, long-term therapy is anticipated. Some physicians select cyclosporine as the initial therapy. Other immunosuppressives used in treatment include azathioprine, mycophenolate, cyclophosphamide, chlorambucil, and tacrolimus.

The TNF inhibitors—which include thalidomide, etanercept, infliximab, adalimumab, and clofazimine—are showing promise in the treatment of pyoderma gangrenosum.

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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.

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Prednisone

 

Prednisone is considered the drug of choice. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. Methylprednisolone IV may be used in some patients.

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Immunosuppressants

Class Summary

These agents have immunomodulatory effects. Also, see the clinical guideline summary from the Guidelines for prescribing azathioprine in dermatology, from the British Association of Dermatologists.

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Cyclosporine (Sandimmune, Neoral, Gengraf)

 

Cyclosporine has been demonstrated to be helpful in a variety of skin disorders. An effective steroid-sparing agent, it has also been used as primary therapy in some patients.

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Azathioprine (Imuran, Azasan)

 

Azathioprine is another drug that may be effective as a steroid-sparing agent. It antagonizes purine metabolism and inhibits the synthesis of deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and proteins. Azathioprine may decrease the proliferation of immune cells, which results in lower autoimmune activity.

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Mycophenolate (CellCept, Myfortic)

 

Mycophenolate inhibits purine synthesis and the proliferation of human lymphocytes. It may be used as a steroid-sparing agent or as a primary agent in patients who do not respond to first-line agents.

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Cyclophosphamide

 

Cyclophosphamide is an alkylating agent that depresses B-cell and T-cell function. It is chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with the growth of normal and neoplastic cells.

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Chlorambucil (Leukeran)

 

Chlorambucil alkylates and cross-links strands of DNA, inhibiting DNA replication and RNA transcription. It is used as a primary or steroid-sparing agent.

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Tacrolimus (Prograf, Hecoria)

 

Tacrolimus suppresses humoral immunity (T-lymphocyte) activity.

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Blood Components

Class Summary

These agents are used to improve the clinical and immunologic aspects of the disease. They may decrease autoantibody production and increase solubilization and removal of immune complexes.

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IV immunoglobulins (Octagam, Hizentra, Gammagard, Gamunex)

 

IV immunoglobulin neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including interferon (INF)-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; and promotes remyelination. It may increase cerebrospinal fluid (CSF) IgG (10%).

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Immunomodulators

Class Summary

These agents have effects on the activity of the immune system.

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Thalidomide (Thalomid)

 

Thalidomide is an immunomodulatory agent that may suppress excessive production of TNF-alpha and may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration. In patients less than 50 kg (110 lb), start at the low end of the dose regimen.

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Ustekinumab (Stelara)

 

Ustekinumab is a human monoclonal antibody directed against IL-12 and IL-23, thereby interfering with T-cell differentiation and activation and subsequent cytokine cascades. It is indicated for moderate-to-severe plaque psoriasis and has been used successfully in pyoderma gangrenosum.

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Etanercept (Enbrel)

 

Etanercept is a soluble p75 TNF-receptor fusion protein (sTNFR-Ig). It inhibits TNF binding to cell surface receptors, thereby decreasing inflammatory and immune responses.

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Infliximab (Remicade)

 

Infliximab is a chimeric IgG1k monoclonal antibody that neutralizes the cytokine TNF-alpha and inhibits its binding to the TNF-alpha receptor. The drug reduces infiltration of inflammatory cells and TNF-alpha production in inflamed areas.

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Adalimumab (Humira)

 

Adalimumab is a TNF-alpha inhibitor. It is a fully human inhibitor of TNF-alpha that is administered by subcutaneous (SC) injection.

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Clofazimine (Lamprene)

 

Clofazimine inhibits mycobacterial growth, binding preferentially to mycobacterial DNA. It has antimicrobial properties, but its mechanism of action is unknown.

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Contributor Information and Disclosures
Author

J Mark Jackson, MD  Clinical Professor of Medicine/Dermatology, Division of Dermatology, University of Louisville School of Medicine

J Mark Jackson, MD is a member of the following medical societies: American Academy of Dermatology, American Acne and Rosacea Society, American Medical Association, Kentucky Medical Association, and Texas Medical Association

Disclosure: Abbott, Amgen, Centocor, Honoraria Speaking and teaching

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, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

David P Fivenson, MD Associate Director, St Joseph Mercy Hospital Dermatology Program, Ann Arbor, Michigan

David P Fivenson, MD is a member of the following medical societies: American Academy of Dermatology, Medical Dermatology Society, Michigan Dermatological Society, Michigan State Medical Society, Photomedicine Society, Society for Investigative Dermatology, and Wound Healing Society

Disclosure: Nothing to disclose.

Warren R Heymann, MD Head, Division of Dermatology, Professor, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey

Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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Classic, or typical, pyoderma gangrenosum. This patient did not have an associated disease, and the condition responded well to cyclosporine.
Atypical pyoderma gangrenosum.
Peristomal pyoderma gangrenosum.
Factitial ulceration on the scalp from chronic manipulation mimicking an ulceration of pyoderma gangrenosum.
 
 
 
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