title: Granuloma annulare and human immunodeficiency virus infection.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  Academic referral center.
  
  
  METHODS
  Thirty-four consecutive HIV-positive patients who have a clinical and histological diagnosis of GA.
  
  
  METHODS
  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.
authors.affiliation: Department of Dermatology, University of California-San Francisco School of Medicine, 94115, USA.
authors.forename: J R
authors.initials: JR
authors.lastname: Toro
authors.forename: P
authors.initials: P
authors.lastname: Chu
authors.forename: T S
authors.initials: TS
authors.lastname: Yen
authors.forename: P E
authors.initials: PE
authors.lastname: LeBoit
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications; D000328:Adult; D001706:Biopsy; D003094:Collagen; D004396:Coloring Agents; D004279:DNA, Viral / Q000235:genetics; D020031:Epstein-Barr Virus Infections / Q000150:complications; D005260:Female; D016460:Granuloma Annulare / Q000150:complications* / Q000473:pathology / Q000821:virology; D015658:HIV Infections / Q000150:complications*; D004854:Herpesvirus 4, Human / Q000235:genetics; D006801:Humans; D017403:In Situ Hybridization; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000473:pathology; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000235:genetics; D012514:Sarcoma, Kaposi / Q000150:complications / Q000473:pathology; D012867:Skin / Q000473:pathology / Q000821:virology; D014412:Tumor Virus Infections / Q000150:complications
chemical_list: D004396:Coloring Agents; D004279:DNA, Viral; D012367:RNA, Viral; D003094:Collagen