1). Descriptive baseline characteristics by presence or absence of anal condylomata are shown

in Table 1. The most relevant differences between patients were that a higher percentage of patients with condylomata click here had a history of STIs (46%) and were MSM (84%) compared with patients without condylomata (27% had a history of STIs and 71% were MSM). Accordingly, the percentage of patients practising RAI was also higher in patients with anal condylomata than in those without them (76% vs. 58%, respectively). The overall prevalence of anal condylomata in HIV-infected men was 25% (157 of 640; 95% CI 21–28%). According to sexual behaviour, the prevalence was 28% (132 of 473) in MSM and 15% (25 of 167) in heterosexual HIV-infected men (OR 2.2; 95% CI 1.4–3.5). Condylomatous anal lesions were located in the internal region in 111 of 157 patients (71%), in the perianal area in 13 of 157 patients (8%) Selleckchem Navitoclax and in both locations in 33 of 157 patients (21%) (Fig. 1). The overall prevalence of anal canal HPV infection was 73% (469 of 640; 95% CI 70–77%). The prevalence in patients with anal condylomata was 92% (145 of 157; 95% CI 86–96%) [95.5% (126 of 132) for MSM and 76% (19 of 25) for heterosexuals; χ2 = 11.3; P = 0.001] and that in patients without anal condylomata was 67% (324

of 483; 95% CI 63–71%) [80% (273 of 341) for MSM and 36% (51 of 142) for heterosexuals; χ2 = 88.5; P < 0.001] (with/without anal condylomata, P < 0.001). Moreover,

the prevalence of LR HPV genotypes (63% vs. 19%, respectively; P < 0.001) and that of HR HPV genotypes (83% vs. 62%, respectively; P < 0.001) were considerably higher in the anal canals of HIV-infected men with condylomatous lesions than in those without (Table 2). A higher prevalence of presenting any HPV genotype in the anal canal was associated with having anal condylomata (adjusted OR 8.5; 95% CI 3.2–22). The overall prevalence of single HPV genotype infection was 23% (146 of 640; 95% Paclitaxel CI 20–26%). Similar prevalences of single HPV genotype infection were observed in patients with and without condylomata [18% vs. 24%, respectively; unadjusted OR 0.7; 95% CI 0.4–1.1: in those with condylomata, 14% (19 of 132) for MSM and 36% (nine of 25) for heterosexuals (χ2 = 6.69; P = 0.008); in those without condylomata, 26% (88 of 341) for MSM and 21% (30 of 142) for heterosexuals (χ2 = 1.19; P = 0.275)]. By contrast, the prevalence of HPV infection involving at least two genotypes differed by condylomata status, and this difference was statistically significant: 75% (117 of 157; 95% CI 70–81%) for patients with condylomata [81% (107 of 132) for MSM and 40% (10 of 25) for heterosexuals; χ2 = 18.6; P < 0.001] and 43% (206 of 483; 95% CI 38–47%) for those without condylomata [54% (185 of 341) for MSM and 15% (21 of 142) for heterosexuals; χ2 = 63.8; P < 0.001] (with/without condylomata, adjusted OR 4.0; 95% CI 2.2–7.1).