eMedicine Specialties > Dermatology > Connective Tissue Diseases

Lupus Erythematosus, Discoid: Differential Diagnoses & Workup

Author: Jeffrey P Callen, MD, Professor of Medicine, Chief, Division of Dermatology, University of Louisville School of Medicine
Contributor Information and Disclosures

Updated: Apr 14, 2009

Differential Diagnoses

Actinic Keratosis
Psoriasis, Plaque
Dermatomyositis
Rosacea
Granuloma Annulare
Sarcoidosis
Granuloma Faciale
Squamous Cell Carcinoma
Keratoacanthoma
Syphilis
Lichen Planus
Warts, Nongenital
Lupus Erythematosus, Subacute Cutaneous

Workup

Laboratory Studies

  • Serologic testing
    • Some patients with discoid lupus erythematosus (DLE) (approximately 20%) manifest a positive antinuclear antibody (ANA) when tested with human substrates. HEp-2 cells currently are the most common substrate used in commercial laboratories.
    • Anti-Ro (SS-A) autoantibodies are present in approximately 1-3% of patients.
    • Antinative DNA (double-stranded or nDNA) or anti-Sm antibodies usually reflect SLE, and they may occur in some patients (<5%).
  • Other laboratory findings
    • Cytopenias may be present.
    • Elevated sedimentation rate may occur in some patients.
    • Rheumatoid factor may be positive.
    • Complement levels may be depressed.
    • Urinalysis may reflect the presence of renal involvement with proteinuria.

Other Tests

  • Immunopathology
    • Deposition of immunoglobulin and/or complement at the dermal-epidermal junction is a characteristic feature of LE referred to in most texts and articles. Tissue may be examined from skin lesions (lesional) or normal skin (nonlesional). Nonlesional biopsies may be from exposed or nonexposed surfaces. Testing of nonlesional, nonexposed skin is termed the lupus band test (LBT).
    • The use and interpretation of these tests varies according to the biopsy site. Approximately 90% of patients with discoid lupus erythematosus manifest a positive direct immunofluorescence (DIF) test on lesional skin; however, the presence of immunoreactants in the basement membrane zone of lesional skin is not specific for lupus and can be seen in a variety of inflammatory skin diseases. Older lesions or very early lesions may be more likely to be negative on immunofluorescence microscopy. Only patients with SLE have a positive LBT, defined as the presence of multiple immunoreactants in the basement membrane zone. LBTs are neither sensitive nor specific and mostly have been replaced by advances in serologic testing.

Histologic Findings

The characteristic histopathologic alterations observed in discoid lupus erythematosus include vacuolar alteration of the basal cell layer, thickening of the basement membrane, follicular plugging, hyperkeratosis, atrophy of the epidermis, incontinence of pigment, and inflammatory cell infiltrate (usually lymphocytic) in a perivascular, periappendiceal, and subepidermal location. Often, an abundance of mucin is seen within the dermis. The histopathologic features differ depending upon the type and age of the lesion.

More on Lupus Erythematosus, Discoid

Overview: Lupus Erythematosus, Discoid
Differential Diagnoses & Workup: Lupus Erythematosus, Discoid
Treatment & Medication: Lupus Erythematosus, Discoid
Follow-up: Lupus Erythematosus, Discoid
Multimedia: Lupus Erythematosus, Discoid
References

References

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  2. Lehmann P, Holzle E, Kind P, Goerz G, Plewig G. Experimental reproduction of skin lesions in lupus erythematosus by UVA and UVB radiation. J Am Acad Dermatol. Feb 1990;22(2 Pt 1):181-7. [Medline].

  3. Parish LC, Kennedy RJ, Hurley J. Palmar lesions in lupus erythematosus. Arch Dermatol. Sep 1967;96(3):273-6. [Medline].

  4. Spann CR, Callen JP, Klein JB, Kulick KB. Clinical, serologic and immunogenetic studies in patients with chronic cutaneous (discoid) lupus erythematosus who have verrucous and/or hypertrophic skin lesions. J Rheumatol. Feb 1988;15(2):256-61. [Medline].

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  23. Callen JP, Fowler JF, Kulick KB. Serologic and clinical features of patients with discoid lupus erythematosus: relationship of antibodies to single-stranded deoxyribonucleic acid and of other antinuclear antibody subsets to clinical manifestations. J Am Acad Dermatol. Nov 1985;13(5 Pt 1):748-55. [Medline].

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Further Reading

Keywords

chronic cutaneous lupus erythematosus, discoid lupus erythematosus

Contributor Information and Disclosures

Author

Jeffrey P Callen, MD, Professor of Medicine, 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 Honoraria Consulting; Centocor Honoraria Consulting; Genetech Honoraria Consulting; Celgene Honoraria Consulting

Medical Editor

Craig A Elmets, MD, Director of Dermatology, Departments of Dermatology, Pathology, and Environmental Health Sciences; Professor, The Kirklin Clinic, University of Alabama at Birmingham
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; Merck Consulting fee Independent contractor; Tronox Consulting fee Independent contractor; Amgen Consulting fee Review panel membership; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment

Pharmacy Editor

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
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.

Managing Editor

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: Johnson and Johnson stock holder dividends; Amgen stock holder dividends; Forest Lab, Inc stock holder dividends; Galaxo Smith Klein stock holder dividends; Covidien stock holder dividends; Novartis Grant/research funds Consulting; Biolex  sub-investigator

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

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; american college of physicians Honoraria Other

 
 
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