Subacute Cutaneous Lupus Erythematosus (SCLE) Medication

  • Author: Janice Lin, MD, MPH; Chief Editor: William D James, MD  more...
Updated: Mar 07, 2016

Medication Summary

The basic therapy of skin disease uses sun-protection methods, such as sunscreens, sun-protective clothing, and alteration of exposure by decreasing activities during times of high intensity UV light. Topical corticosteroids are used and selected by the appropriate strength for the area of the body. Intralesional injection of triamcinolone acetonide is useful for individual recalcitrant lesions. Antimalarials are the mainstay of systemic therapy and are associated with lower rates of disease progression and lower risk of thrombovascular disease in patients with systemic lupus erythematosus (SLE).[39, 40]

Anecdotal reports or small, open-label trials, as reported by Callen, suggest that the following agents may be of use in some patients[29, 41, 42, 43, 44, 45, 46, 47] :

  • Thalidomide
  • Dapsone
  • Quinacrine combined with either hydroxychloroquine or chloroquine
  • Isotretinoin
  • Acitretin
  • Azathioprine
  • Methotrexate
  • Mycophenolate mofetil
  • Phenytoin
  • Auranofin
  • Clofazimine
  • Lenalidomide
  • Intravenous immunoglobulin
  • Rituximab


Class Summary

Antimalarials have immunomodulatory effects that may improve symptoms of the disease. Hydroxychloroquine is the drug of choice for systemic therapy of subacute cutaneous lupus erythematosus (SCLE). Chloroquine is second line. The lowest possible dose needed to control the patient’s disease should be used.

Hydroxychloroquine (Plaquenil)


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

Chloroquine (Aralen)


Chloroquine inhibits the effects of immune cells, impairing complement-dependent antigen-antibody reactions.


Leprostatic agents

Class Summary

Leprostatic agents may have immunomodulatory effects.



Dapsone's mechanism of action is similar to that of sulfonamides, with competitive antagonists of para-aminobenzoic acid (PABA) preventing the formation of folic acid, inhibiting bacterial growth.



Class Summary

Immunomodulators are effective in the treatment of diseases with autoimmune etiology.

Azathioprine (Azasan, Imuran)


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

Thalidomide (Thalomid)


Thalidomide may suppress the excessive production of tumor necrosis factor alpha (TNF-alpha), and it may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration.

If the patient weighs less than 50 kg (110 lb), start at the low end of the dose regimen. Thalidomide can cause severe, life-threatening birth defects and is contraindicated in pregnant women. It is also contraindicated in women of childbearing potential unless they are using 2 forms of reliable contraception and are complying with serial pregnancy testing while on therapy. In addition, thalidomide is contraindicated in sexually active men who are not using latex condoms as barrier contraception.

The drug is available only under a special, restricted distribution program called the STEPS (System for Thalidomide Education and Prescribing Safety) Program. Only prescribers and pharmacists registered with this program may prescribe and dispense thalidomide. For more information, contact the Celgene Corporation at 1-888-423-5436.

Mycophenolate (CellCept, Myfortic)


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

Methotrexate (Rheumatrex, Trexall)


Methotrexate reversibly inhibits dihydrofolate reductase; it limits the availability of 1-carbon fragments necessary for the synthesis of purines and the conversion of deoxyuridylate to thymidylate in the synthesis of DNA and cell reproduction. The drug is extensively used for cancer treatment, rheumatoid arthritis, and psoriasis and as a steroid-sparing agent in various autoimmune conditions.


Gold compounds

Class Summary

Gold compounds may regulate immune cell function.

Auranofin (Ridaura)


Gold is taken up by macrophages, which in turn inhibit phagocytosis and lysosomal membrane stabilization. It alters immunoglobulins, decreasing prostaglandin synthesis and lysosomal enzyme activity.



Class Summary

Retinoids play a role in cell growth and differentiation.

Acitretin (Soriatane)


Acitretin is a retinoic acid analogue similar to etretinate and isotretinoin. Etretinate is the main metabolite, and acitretin has demonstrated clinical effects close to those seen with etretinate. The mechanism of action is unknown.

Isotretinoin (Claravis, Amnesteem, Sotret)


Isotretinoin decreases sebaceous gland size and sebum production. It may inhibit sebaceous gland differentiation and abnormal keratinization.

A US Food and Drug Administration (FDA)–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to decrease the risk of pregnancy and unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

Contributor Information and Disclosures

Janice Lin, MD, MPH Clinical Instructor, Department of Immunology and Rheumatology, Stanford University School of Medicine

Janice Lin, MD, MPH is a member of the following medical societies: American College of Physicians, American College of Rheumatology, Medical Dermatology Society, Rheumatologic Dermatology Society

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, 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.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association

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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Early lesions of subacute cutaneous lupus erythematosus may simulate polymorphous light eruption.
Papulosquamous lesions of subacute cutaneous lupus erythematosus may simulate psoriasis.
Annular lesions of subacute cutaneous lupus erythematosus.
Tumid lupus erythematosus.
Neonatal lupus erythematosus.
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