Anal carcinoma: Incidence and effect of cumulative infections

• Published in: AIDS (London) Vol. 18; no. 11; pp. 1561 - 1569
• Main Authors: SOBHANI, Iradj, WALKER, Francine, ROUDOT-THORAVAL, Francoise, ABRAMOWITZ, Laurent, JOHANET, Hubert, HENIN, Dominique, DELCHIER, Jean-Charles, SOULE, Jean-Claude
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 23-07-2004
• Subjects: Adult; AIDS/HIV; Anus Diseases - complications; Anus Neoplasms - virology; Biological and medical sciences; Condylomata Acuminata - complications; Cytomegalovirus; Dendritic Cells; Epstein-Barr virus; Female; Follow-Up Studies; Gastroenterology. Liver. Pancreas. Abdomen; HIV Infections - complications; Human immunodeficiency virus; Human papillomavirus; Human viral diseases; Humans; Immunohistochemistry; Infectious diseases; Logistic Models; Male; Medical sciences; Middle Aged; Neoplasm Invasiveness; Prospective Studies; Recurrence; Risk Factors; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tumors; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Mixed infection; Alphaherpesvirinae; Epstein Barr virus; Papovaviridae; Betaherpesvirinae; anal carcinoma; Human cytomegalovirus; Incidence; HPV; Papillomavirus; Prevention; Human papillomavirus; Spirochaetosis; Immunological investigation; Syphilis; Intestinal disease; Herpesvirus hominis; Benign neoplasm; Anorectal disease; Gammaherpesvirinae; Human; Immunopathology; Herpesviridae; Retroviridae; Anus carcinoma; AIDS; Malignant tumor; Immune deficiency; Lentivirus; Treponematosis; Anal canal; Infection; Virus; Sexually transmitted disease; HIV; Viral disease; Condyloma; Risk factor; Bacteriosis; Digestive diseases; Papilloma; Human immunodeficiency virus; dendritic cell
• ISSN: 0269-9370; 1473-5571
• DOI: 10.1097/01.aids.0000131335.15301.dd

Human papilloma virus (HPV) causes anal condyloma that is a risk factor for anal carcinoma. The incidence and mechanism of invasive anal carcinoma in patients with anal condyloma are prospectively determined.
From 1993 to 2002, 228 consecutive patients (164 HIV positive) with anal canal condylomas were included in the study, after curing of their lesions. They were asked to attend follow-up visits at 3- or 6-month intervals. We checked for anal co-infection with syphilis, gonococci, viruses (Epstein-Barr virus, cytomegalovirus, herpes simplex, HPV types), and quantified Langerhans' cells (LC) in anal mucosa at baseline and during follow up. We cured and analysed relapsed condylomas during follow up (3-112 months; median 26). Serum HIV loads and CD4 T-lymphocyte counts were determined at each visit and the densities of LC in consecutive specimens from patients with cancers were compared with that for a matched control group (n = 23).
Analysis of 199 patients showed high-grade dysplasia (HGD) in 13.6% of patients, more in HIV-positive (16%) than in HIV-negative (6%) patients at baseline. During follow up, 3.5% (7/199; six HIV positive) patients developed invasive carcinoma after 13-108 months and 112 (56%) patients relapsed condylomas. HIV and anal co-infection were identified as independent risk factors (P < 0.01) for HGD and cancer: odd ratio (95% confidence interval) of 9.4 (2.4-37.4) and 3.67 (0.95-14.2), respectively. LC densities in anal mucosa were lower in patients with invasive carcinoma than in controls.
The risk of invasive carcinoma in HPV-infected patients is increased by HIV and anal co-infection. Decreases in LC numbers in anal mucosa may favour this outcome.