PURPOSE: Although anorectal disease is common in human immunodeficiency virus-positive patients, little is known about the type and anatomic distribution of anal fistulas in this patient group. The aim of this study was to compare anatomic characteristics of anal fistulas in human immunodeficiency virus-positive patients with those in human immunodeficiency virus-negative patients by use of a retrospective chart review. METHODS: The charts of 146 male patients younger than 50 years with an anal fistula were reviewed. Incomplete fistulas referred to those tracts arising from an internal opening into either a blind sinus or an undrained abscess cavity. RESULTS: There were 60 human immunodeficiency virus-positive patients and 86 human immunodeficiency virus-negative patients. Mean age of the human immunodeficiency virus-positive patient group was 37 years vs. 40 years for the human immunodeficiency virus-negative patient group. Thirty-one human immunodeficiency virus-positive patients (52 percent) were classified as having AIDS, and the remaining 29 patients (48 percent) were asymptomatic. Mean T helper cell count in the human immunodeficiency virus-positive patient group was 277 cells per microliter. Fistulous tracts were intersphincteric (n = 56), transsphincteric (n = 41), suprasphincteric (n = 2), and incomplete (n = 47). Incomplete fistulas were identified in 33 (55 percent) human immunodeficiency virus-positive patients vs. 14 (16 percent) human immunodeficiency virus-negative patients (P < 0.001). Of the 47 incomplete fistulas, 37 (79 percent) were found in association with an abscess cavity. All ten patients with an incomplete fistula into a blind sinus were human immunodeficiency virus-positive. The incidence of an incomplete fistula without an abscess was significantly higher in the human immunodeficiency virus-positive patient group (17 percent) compared with the human immunodeficiency virus-negative patient group (0 percent; P < 0.001). CONCLUSIONS: Anal fistulas in HIV-positive patients arise from the dentate line in similar locations to human immunodeficiency virus negative patients. However, human immunodeficiency virus-positive patients were more likely to have incomplete anal fistulas than human immunodeficiency virus-negative patients. Furthermore, human immunodeficiency virus-positive patients are predisposed to incomplete fistulas leading into a blind sinus.
PURPOSE: Although anorectal disease is common in human immunodeficiency virus-positive patients, little is known about the type and anatomic distribution of anal fistulas in this patient group. The aim of this study was to compare anatomic characteristics of anal fistulas in human immunodeficiency virus-positive patients with those in human immunodeficiency virus-negative patients by use of a retrospective chart review. METHODS: The charts of 146 male patients younger than 50 years with an anal fistula were reviewed. Incomplete fistulas referred to those tracts arising from an internal opening into either a blind sinus or an undrained abscess cavity. RESULTS: There were 60 human immunodeficiency virus-positive patients and 86 human immunodeficiency virus-negative patients. Mean age of the human immunodeficiency virus-positive patient group was 37 years vs. 40 years for the human immunodeficiency virus-negative patient group. Thirty-one human immunodeficiency virus-positive patients (52 percent) were classified as having AIDS, and the remaining 29 patients (48 percent) were asymptomatic. Mean T helper cell count in the human immunodeficiency virus-positive patient group was 277 cells per microliter. Fistulous tracts were intersphincteric (n = 56), transsphincteric (n = 41), suprasphincteric (n = 2), and incomplete (n = 47). Incomplete fistulas were identified in 33 (55 percent) human immunodeficiency virus-positive patients vs. 14 (16 percent) human immunodeficiency virus-negative patients (P < 0.001). Of the 47 incomplete fistulas, 37 (79 percent) were found in association with an abscess cavity. All ten patients with an incomplete fistula into a blind sinus were human immunodeficiency virus-positive. The incidence of an incomplete fistula without an abscess was significantly higher in the human immunodeficiency virus-positive patient group (17 percent) compared with the human immunodeficiency virus-negative patient group (0 percent; P < 0.001). CONCLUSIONS: Anal fistulas in HIV-positive patients arise from the dentate line in similar locations to human immunodeficiency virus negative patients. However, human immunodeficiency virus-positive patients were more likely to have incomplete anal fistulas than human immunodeficiency virus-negative patients. Furthermore, human immunodeficiency virus-positive patients are predisposed to incomplete fistulas leading into a blind sinus.