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Acute Cutaneous Lupus Erythematosus (ACLE) Medication

  • Author: Ivan D Camacho, MD; Chief Editor: William D James, MD  more...
Updated: Nov 12, 2015

Medication Summary

As previously mentioned, systemic corticosteroids usually are the mainstay of therapy for systemic disease. Skin changes tend to respond in tandem with the systemic response to treatment.

Adjuvant therapy for systemic disease can be provided with azathioprine, cyclophosphamide, and thalidomide. Hydroxychloroquine, administered as first-line therapy to most patients with systemic disease, has particularly beneficial effects on skin lesions. Intravenous IgG has become important in controlling recalcitrant disease.[12]



Class Summary

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



Prednisone is a glucocorticoid (adrenocortical steroid) that is absorbed easily into the gastrointestinal (GI) tract. An immunosuppressant, it is used for the treatment of autoimmune disorders. Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN)-cell activity. It stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production.



Class Summary

These agents are used for immunosuppression and, ultimately, disease control.

Azathioprine (Imuran, Azasan)


Azathioprine antagonizes purine metabolism and inhibits the synthesis of DNA, ribonucleic acid (RNA), and proteins. It may decrease the proliferation of immune cells, in that way lowering autoimmune activity. For dermatomyositis/polymyositis, respiratory and muscular symptoms respond, but skin lesion response has not been consistent.

Azathioprine is slow acting, with its therapeutic effect not being seen for 6-8 weeks. Metabolites accumulate slowly, and maximal immunosuppression is not reached until after 8-12 weeks. The drug is available in 25-, 50-, 75-, and 100-mg tablets or in a 100-mg vial.



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

Thalidomide (Thalomid)


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

Hydroxychloroquine (Plaquenil)


This agent inhibits chemotaxis of eosinophils and the locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Immune globulin IV (Gammagard, Gamunex, Octagam, Gammaplex )


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


Monoclonal Antibody

Class Summary

These drugs restore the potential to minimize self-immunity. Monoclonal antibodies can induce cytotoxicity after binding to specific antigens that may regulate cell cycle initiation. This then results in the inhibition of cell growth and differentiation.

Rituximab (Rituxan)


Rituximab is a murine/human chimeric anti-CD20 monoclonal antibody. CD20 is expressed early in pre ̶ B cell development. Binding induces complement-dependent B-cell cytotoxicity along with antibody-dependent cellular toxicity. Rituximab is a murine/human chimeric anti-CD20 monoclonal antibody, US FDA approved for the treatment of refractory low-grade or follicular non-Hodgkin lymphoma and severe rheumatoid arthritis. It is available as an injectable solution of 10 mg/mL.

Contributor Information and Disclosures

Ivan D Camacho, MD Dermatologist, Private Practice; Voluntary Assistant Professor of Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine

Ivan D Camacho, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Florida Medical Association, International Society of Dermatology, Women's Dermatologic 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.


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; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

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Relationship of acute cutaneous lupus erythematosus (ACLE) to systemic disease. LE is lupus erythematosus. CCLE is chronic cutaneous lupus erythematosus. SCLE is subacute cutaneous lupus erythematosus.
Erythema involving the malar area, forehead, and neck. Note sparing of some of the creases.
Toxic epidermal necrolysis–like eruption.
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