BACKGROUND: The anal epithelium is subject to dysplastic change in patients with human immunodeficiency virus (HIV). We sought to determine if the duration of HIV disease or the patient's immune status were associated with the development of anal carcinoma. METHODS: HIV-positive patients diagnosed with anal neoplasms were reviewed. Statistical analysis was performed via an unpaired Student t test and the Fisher exact test. RESULTS: Fourteen patients were identified, 7 with anal intraepithelial neoplasms (group 1) and 7 with anal carcinoma (group 2). Human papillomavirus was detected in 100% of patients in group 1 and in 67% of patients in group 2. There was no significant difference in the level of immunosuppression as assessed by the CD4 counts (266.9 +/- 48.5 vs. 274.7 +/- 92.0 cell/c microl; P = .94) and viral loads (19,243 +/- 18,034 vs. 67,140 +/- 39,570 RNA/mL; P = .29) between groups 1 and 2, respectively. Group 2 had been HIV positive for a significantly longer period of time (12.6 +/- 2.3 y) compared with group 1 (5.9 +/- 2.0 y, P = .05). CONCLUSIONS: The most significant factor for the development of invasive anal carcinoma in patients with HIV is duration of disease. As a result of improved long-term survival secondary to new HIV therapy, anal invasive carcinoma will become an increasing problem.
BACKGROUND: The anal epithelium is subject to dysplastic change in patients with human immunodeficiency virus (HIV). We sought to determine if the duration of HIV disease or the patient's immune status were associated with the development of anal carcinoma. METHODS:HIV-positive patients diagnosed with anal neoplasms were reviewed. Statistical analysis was performed via an unpaired Student t test and the Fisher exact test. RESULTS: Fourteen patients were identified, 7 with anal intraepithelial neoplasms (group 1) and 7 with anal carcinoma (group 2). Human papillomavirus was detected in 100% of patients in group 1 and in 67% of patients in group 2. There was no significant difference in the level of immunosuppression as assessed by the CD4 counts (266.9 +/- 48.5 vs. 274.7 +/- 92.0 cell/c microl; P = .94) and viral loads (19,243 +/- 18,034 vs. 67,140 +/- 39,570 RNA/mL; P = .29) between groups 1 and 2, respectively. Group 2 had been HIV positive for a significantly longer period of time (12.6 +/- 2.3 y) compared with group 1 (5.9 +/- 2.0 y, P = .05). CONCLUSIONS: The most significant factor for the development of invasive anal carcinoma in patients with HIV is duration of disease. As a result of improved long-term survival secondary to new HIV therapy, anal invasive carcinoma will become an increasing problem.
Authors: Felix Aigner; Friedrich Conrad; Andreas Widschwendter; Robert Zangerle; Bettina Zelger; Alfred Haidenberger; Sebastian Roka; Kurt Heim; Reinhard Höpfl; Martin Klimpfinger; Yves Marcus Rigler; Hugo Bonatti; Johann Pfeifer; Andrea Maier; Reinhard Kirnbauer; Andreas Salat Journal: Wien Klin Wochenschr Date: 2008 Impact factor: 1.704
Authors: Nancy F Crum-Cianflone; Katherine Huppler Hullsiek; Vincent C Marconi; Anuradha Ganesan; Amy Weintrob; Robert V Barthel; Brian K Agan Journal: AIDS Date: 2010-02-20 Impact factor: 4.177