title: Etiology of pruritic papular eruption with HIV infection in Uganda.
abstract: BACKGROUND
  A frequent cause of human immunodeficiency virus (HIV)-related morbidity in sub-Saharan Africa is a commonly occurring, intensely pruritic skin rash. The resulting scars are disfiguring and stigmatizing. Despite the substantial prevalence of pruritic papular eruption (PPE) among HIV-infected Africans, the cause has been elusive.
  
  
  OBJECTIVE
  To determine the etiology of PPE occurring in HIV-infected individuals.
  
  
  METHODS
  Cross-sectional study of HIV-infected patients with active PPE from clinics in Uganda conducted from May 19 through June 6, 2003. Enrollment occurred in the month preceding May 19. Each participant was clinically examined by 2 dermatologists, had laboratory studies performed, was administered an epidemiologic questionnaire, and had a skin biopsy of a new lesion evaluated by a dermatopathologist.
  
  
  METHODS
  Histological characteristics of new pruritic lesions. Other assessments included CD4 cell count, eosinophil count, and physician-assessed rash severity.
  
  
  RESULTS
  Of 109 patients meeting inclusion criteria, 102 (93.6%) completed the study. The CD4 cell counts in this study population were generally low (median, 46/microL) and inversely related to increasing rash severity (median CD4 cell counts: 122 for mild, 41 for moderate, and 9 for severe; P<.001 for trend). Eighty-six patients (84%; 95% confidence interval, 77%-91%) had biopsy findings characteristic of arthropod bites. Patients with arthropod bites on biopsy had significantly higher peripheral eosinophil counts (median, 330 vs 180/microL; P = .02) and had a trend toward lower CD4 cell counts (median, 40 vs 99/microL; P = .07) than those without histological evidence of arthropod bites.
  
  
  CONCLUSIONS
  Pruritic papular eruption occurring in HIV-infected individuals may be a reaction to arthropod bites. We hypothesize that this condition reflects an altered and exaggerated immune response to arthropod antigens in a subset of susceptible HIV-infected patients.
authors.affiliation: Department of Dermatology and Institute for Health Policy Studies, University of California, San Francisco, School of Medicine, CA 94143-0363, USA. resneck@itsa.ucsf.edu
authors.forename: Jack S
authors.initials: JS
authors.lastname: Resneck
authors.forename: Marta
authors.initials: M
authors.lastname: Van Beek
authors.forename: Lisa
authors.initials: L
authors.lastname: Furmanski
authors.forename: Jessica
authors.initials: J
authors.lastname: Oyugi
authors.forename: Philip E
authors.initials: PE
authors.lastname: LeBoit
authors.forename: Elly
authors.initials: E
authors.lastname: Katabira
authors.forename: Fred
authors.initials: F
authors.lastname: Kambugu
authors.forename: Toby
authors.initials: T
authors.lastname: Maurer
authors.forename: Tim
authors.initials: T
authors.lastname: Berger
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Pletcher
authors.forename: Edward L
authors.initials: EL
authors.lastname: Machtinger
mesh_terms: D000328:Adult; D000818:Animals; D001181:Arthropods; D001706:Biopsy; D001733:Bites and Stings / Q000150:complications / Q000175:diagnosis / Q000276:immunology*; D018791:CD4 Lymphocyte Count; D003430:Cross-Sectional Studies; D004804:Eosinophils; D005076:Exanthema / Q000209:etiology* / Q000473:pathology; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000276:immunology*; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D011536:Prurigo / Q000209:etiology* / Q000473:pathology; D011537:Pruritus / Q000209:etiology / Q000473:pathology; D014454:Uganda