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  Vol. 135 No. 11, November 1999 TABLE OF CONTENTS
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Granuloma Annulare and Human Immunodeficiency Virus Infection

Jorge R. Toro, MD; Paul Chu, MD; Tien-Sze Ben Yen, MD, PhD; Philip E. LeBoit, MD

Arch Dermatol. 1999;135:1341-1346.

Objectives  To characterize human immunodeficiency virus (HIV)–associated granuloma annulare (GA) by clinical, microscopic, and molecular methods and to investigate the role of Epstein-Barr virus infection in the pathogenesis of GA.

Design  Patients were evaluated clinically, and biopsy specimens of lesional skin were examined by light microscopy. Polymerase chain reaction and in situ hybridization for Epstein-Barr virus were performed on 4 and 12 biopsy specimens, respectively.

Setting  Academic referral center.

Patients  Thirty-four consecutive HIV-positive patients who have a clinical and histological diagnosis of GA.

Outcome Measures  Clinical distribution of lesions, light-microscopic features, and the presence of Epstein-Barr virus DNA and RNA in biopsy specimens.

Results  Granuloma annulare was generalized in 20 patients and localized in 14. Twenty patients (59%) presented with acquired immunodeficiency syndrome. Unusual features were the presence of oral lesions in 1 patient, perforating lesions in 2 patients, and the coexistence of GA and Kaposi sarcoma in 1 biopsy specimen. Microscopic examination of 34 biopsy specimens showed a granulomatous pattern that was interstitial in 8, palisaded in 18, perforating in 2, and mixed interstitial and palisaded in 6. Special staining of all specimens was negative for organisms. Epstein-Barr virus infection was not detected by either polymerase chain reaction or in situ hybridization.

Conclusions  Generalized GA is the most common clinical pattern in HIV infection. Granuloma annulare associated with HIV can present at all stages of HIV infection, but it is slightly more common in patients with acquired immunodeficiency syndrome. Epstein-Barr virus is an unlikely causative agent of HIV-associated GA. Granuloma annulare may be a manifestation of increasing immune dysregulation.


From the Departments of Dermatology (Drs Toro and LeBoit) and Pathology (Drs Chu and Yen), University of California–San Francisco School of Medicine.


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