Discoid Lupus Erythematosus Medication

  • Author: Jeffrey P Callen, MD; Chief Editor: William D James, MD   more...
 
Updated: Dec 15, 2011
 

Medication Summary

Hydroxychloroquine and chloroquine phosphate have shown beneficial effects in treating discoid lupus erythematosus (DLE). Alternative therapies, anecdotal reports, and small, open-label trials (as reported by Callen[28] ) suggest that the following agents may be useful in some patients:

  • Dapsone
  • Auranofin
  • Quinacrine
  • Thalidomide
  • Isotretinoin[29]
  • Acitretin
  • Azathioprine
  • Mycophenolate mofetil
  • Phenytoin
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Antimalarial agents

Class Summary

Antimalarial agents may have immunomodulatory properties. Hydroxychloroquine is the drug of choice when a systemic agent is needed for discoid lupus erythematosus (DLE). Chloroquine is second-line therapy. Quinacrine may be added to either hydroxychloroquine or chloroquine.[17] The antimalarial drugs might also prevent the development of SLE in patients with DLE, and they might decrease the risk of cardiovascular disease.[18, 19]

Hydroxychloroquine (Plaquenil)

 

Hydroxychloroquine is used for the treatment of DLE and SLE. It inhibits chemotaxis of eosinophils and 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.

Chloroquine (Aralen)

 

Chloroquine inhibits chemotaxis of eosinophils and locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions.

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Leprostatic agents

Class Summary

Leprostatic agents may modulate the immune system.

Dapsone

 

Dapsone's mechanism of action is similar to that of sulfonamides, in which competitive antagonists of para-aminobenzoic acid (PABA) prevent the formation of folic acid, inhibiting bacterial growth. The anti-inflammatory action may relate to suppression of neutrophil function by inhibition of the halide-myeloperoxidase system.

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Gold compounds

Class Summary

Gold compounds have proven effective in the treatment of inflammation with autoimmune etiology.

Auranofin (Ridaura)

 

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

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Immunomodulators

Class Summary

Immunomodulators affect factors that regulate the immune system.

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. Methotrexate is extensively used to treat cancer, rheumatoid arthritis, and psoriasis and is employed as a steroid-sparing agent in various autoimmune conditions.

Thalidomide (Thalomid)

 

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

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, which results in lower autoimmune activity.

Mycophenolate (CellCept, Myfortic)

 

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

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Corticosteroids

Class Summary

Corticosteroids are anti-inflammatory agents that suppress the immune system at several levels, including through the inhibition of inflammatory cells and the production of antibodies.

Triamcinolone (Kenalog-10)

 

Triamcinolone can be administered intralesionally in a concentration of 3-5 mg/mL. The amounts injected should be recorded. Systemic adverse effects are uncommon with low doses. Atrophy is possible and is dose dependent.

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Retinoids

Class Summary

Retinoids have the ability to regulate cell proliferation and the immune system.

Acitretin (Soriatane)

 

Acitretin is a retinoic acid analog 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, Sotret, Amnesteem)

 

Isotretinoin is a synthetic 13-cis isomer of naturally occurring tretinoin (trans -retinoic acid). Both agents are structurally related to vitamin A. 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.

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Contributor Information and Disclosures
Author

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

Specialty Editor Board

Craig A Elmets, MD  Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Palomar Medical Technologies Stock None; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor; UpToDate Salary Employment; Biogen Grant/research funds Independent contractor; Clinuvel Independent contractor; Covan Basilea Pharmaceutical Grant/research funds Independent contractor; ISDIN None Consulting; TenX BIopharma Grant/research funds Independent contractor

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Julia R Nunley, MD  Professor, Program Director, Dermatology Residency, Department of Dermatology, Virginia Commonwealth University Medical Center

Julia R Nunley, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Society of Nephrology, International Society of Nephrology, Medical Dermatology Society, Medical Society of Virginia, National Kidney Foundation, Phi Beta Kappa, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD  Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

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

Disclosure: Elsevier Royalty Other

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Discoid lupus erythematosus on the face.
Chronic scarred lesion of discoid lupus erythematosus.
Lesions of discoid lupus erythematosus in the conchal bowl demonstrate patulous follicles with follicular plugging.
Palmar lesions of discoid lupus erythematosus.
Scarring alopecia of discoid lupus erythematosus.
Widespread scarring alopecia.
Hypertrophic lesions of lupus erythematosus on the dorsal hands. Characteristic lesions were observed elsewhere.
 
 
 
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