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Morphea Medication

  • Author: Jennifer V Nguyen, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Nov 18, 2015
 

Medication Summary

In general, therapy aimed at reducing inflammatory activity in early disease is more successful than attempts to decrease sclerosis in well-established lesions. The approach to treatment of the various subtypes of morphea is described in Medical Care. Note that phototherapy represents another important modality.

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Corticosteroids

Class Summary

These agents reduce inflammation and suppress collagen synthesis.

Triamcinolone topical (Kenalog Orabase, Kenalog topical, Pediaderm TA)

 

Triamcinolone is a medium-potency corticosteroid that reduces inflammation and may prevent progression of sclerosis.

Clobetasol propionate 0.05% cream or ointment (Temovate)

 

Clobetasol propionate is a superpotent topical corticosteroid that reduces inflammation and may prevent progression of sclerosis.

Prednisone (Deltasone, Orasone)

 

Prednisone reduces inflammation and prevents the progression of sclerosis. Systemic corticosteroid therapy (often used in combination with MTX; see below) is appropriate for patients with active inflammatory disease that is widespread, severe, and/or potentially disfiguring/disabling.

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Vitamin D analogs

Class Summary

These agents inhibit fibroblast activity and TGF-beta production and have anti-inflammatory effects.

Calcipotriene 0.005% ointment (Dovonex)

 

Calcipotriene is a synthetic vitamin D-3 analog that can lead to softening of morphea lesions.

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Antirheumatic agents

Class Summary

These agents can reduce inflammation associated with morphea.

Methotrexate (Rheumatrex, Trexall)

 

Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA and RNA synthesis in lymphocytes and other immune cells. This and other mechanisms lead to an anti-inflammatory effect, which is reflected in reduced levels of circulating cytokines such as IL-2, IL-6, and IL-8 (indicators of disease activity) in morphea patients. Response is often delayed until 1-3 months after initiation of therapy.

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Immunosuppressant Agent

Tacrolimus ointment (Protopic)

 

The mechanism of action of tacrolimus is not known. It reduces itching and inflammation by suppressing the release of cytokines from T cells. It also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, it may inhibit release of preformed mediators from skin mast cells and basophils and down-regulate the expression of FCeRI on Langerhans cells. It can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids. It is available as an ointment in concentrations of 0.03 and 0.1%. It is indicated only after other treatment options have failed.

Mycophenolate

 

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

Two formulations are available and are not interchangeable. The original formulation, mycophenolate mofetil (MMF, Cellcept) is a prodrug that once hydrolyzed in vivo, releases the active moiety mycophenolic acid. A newer formulation, mycophenolic acid (MPA, Myfortic) is an enteric-coated product that delivers the active moiety.

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Contributor Information and Disclosures
Author

Jennifer V Nguyen, MD Assistant Professor of Dermatology, Department of Dermatology, Hospital of the University of Pennsylvania

Disclosure: Nothing to disclose.

Coauthor(s)

Victoria P Werth, MD Professor of Dermatology and Medicine, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, Philadelphia Veterans Affairs Medical Center

Victoria P Werth, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American College of Rheumatology, Phi Beta Kappa, Society for Investigative Dermatology, Medical Dermatology Society

Disclosure: Nothing to disclose.

Nicole Fett, MD Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Nicole Fett, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American Medical Association, Women's Dermatologic Society, Medical Dermatology Society

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 Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Acknowledgements

Kendra G Bergstrom, MD Staff Physician, Ronald O Perelman Department of Dermatology, New York University School of Medicine

Kendra G Bergstrom is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Peter Fritsch, MD Chair, Department of Dermatology and Venereology, University of Innsbruck, Austria

Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Michael Girardi, MD Program Director, Assistant Professor, Department of Dermatology, Yale University School of Medicine

Disclosure: Nothing to disclose.

Julie V Schaffer, MD Assistant Professor, Departments of Dermatology and Pediatrics, New York University School of Medicine

Disclosure: Nothing to disclose.

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Inflammatory plaque-type morphea on the abdomen, characterized by induration, erythema, and a surrounding lilac ring.
A hyperpigmented band of linear morphea involving the left part of the trunk and thigh.
Linear atrophic depression of an en coup de sabre lesion on the right side of the forehead and the frontal part of the scalp.
Deep morphea involving the left lower extremity, with thickened, taut, bound-down skin.
Histopathology of mature scleroderma; full-thickness sclerosis of the dermis. Photomicrograph courtesy of Dirk Elston, MD.
 
 
 
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