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Biomedical subjects

Laurent Abramowitz

Publications and source records attributed to Laurent Abramowitz.

6 recordsLinked to original sources
PubMed2004

Anal carcinoma: incidence and effect of cumulative infections.

INTRODUCTION: 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. PATIENTS AND METHODS: 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). RESULTS: 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. CONCLUSION: 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.

Adult↗
PubMed2002

Anal fissure and thrombosed external hemorrhoids before and after delivery.

PURPOSE: Thrombosed external hemorrhoids and anal fissures are common and are responsible for severe discomfort during childbirth. However, the real incidence of these lesions is unknown. The aim of our study was to evaluate their incidence and the risk factors for these lesions during childbirth. METHODS: A prospective study with proctologic examination during the last 3 months of pregnancy and after delivery (within 2 months) was performed in 165 consecutive pregnant females. RESULTS: Fifteen females (9.1 percent) with anal lesions (13 thrombosed external hemorrhoids and 2 anal fissures) were observed during pregnancy. Fifty-eight females (35.2 percent) with anal lesions (33 thrombosed external hemorrhoids and 25 anal fissures) were observed during the postpartum period. Ninety-one percent of thrombosed external hemorrhoids were observed during the first day after delivery, whereas anal fissures were distributed, with no peak, over the two months after delivery. The 2 independent risk factors for anal lesions (among obstetric, baby's, and mother's information) were dyschezia, with a 5.7 odds ratio (95 percent confidence interval, 2.7-12), and late delivery, with a 1.4 odds ratio (95 percent confidence interval, 1.05-1.9). Furthermore, many thrombosed external hemorrhoids were observed after superficial perineal tears and heavier babies (P < 0.05). Only 1 of the 33 patients with thrombosed external hemorrhoids who were observed underwent a cesarean section. CONCLUSION: One third of females have thrombosed external hemorrhoids or anal fissures in the postpartum period. The most important risk factor is dyschezia. Traumatic delivery appears to be associated with thrombosed external hemorrhoids.

Adult↗
PubMed2002

Effect of anal epidermoid cancer-related viruses on the dendritic (Langerhans') cells of the human anal mucosa.

PURPOSE: The incidence of anal cancer is high in patients with anal condyloma. HIV increases this risk. We analyzed anal mucosa from normal individuals and individuals with condyloma. EXPERIMENTAL DESIGN: Normal anal mucosa from 155 consecutively recruited patients (102 HIV-positive and 53 HIV-negative) with anal condyloma was compared with that obtained from 30 HIV-negative patients after hemorrhoid surgery (controls). Langerhans' cells (LCs), T lymphocytes, and viruses [EBV, cytomegalovirus, herpes simplex virus 1, and human papillomavirus (HPV) types] in anal mucosa and HIV load and CD4 T-lymphocyte counts in the serum were characterized. RESULTS: None of the control individuals had anal squamous intraepithelial lesion or HPV versus 19 HIV-positive and 4 HIV-negative patients with anal condyloma (P = 0.07). The number of LCs/mm in anal tissue was significantly higher in HIV-negative patients with condylomata (median, 30; range, 2-130) than in HIV-positive patients (median, 15; range, 0-100) or in controls (median, 17; range, 4-35). In HIV-negative individuals, the occurrence of condylomata was linked with a higher number of LCs. Significant differences were observed between HIV-positive and HIV-negative patients with anal condylomata:number of LCs/mm anal tissue, oncogenic HPV (26% versus 8%), other current infections (35.6% versus 5%), being male (93% versus 74%). Multivariate regression analysis found HIV as the only risk factor for a decrease in the number of LCs (odds ratio, 6; 95% confidence interval, 2.28-16.1; P < 0.001) and the serum HIV load (odds ratio, 4.9; 95% confidence interval, 1.1-21.4 log/ml; P < 0.03) but not the serum CD4 T-lymphocyte rate as a predictive risk factor for having <17 LCs/mm tissue. CONCLUSION: HPV increases the number of LCs in anal mucosa in HIV-negative individuals. HIV alters anal dendritic cells, likely leading to an increase in anal cancer risk.

Adolescent↗