[Canal anal carcinoma]. / Carcinomes du canal anal.

Canal anal carcinoma. Anal carcinomas are rare, but their incidence has increased in recent years. They are induced by the Human papillomas virus (mostly genotype 16). The prevalence is high among HIV-infected men who have sex with men (MSM) and primary prevention by vaccination against HPV is a source of hope in this population. Screening is based on the detection and treatment of precancerous lesions, called anal intra-epithelial neoplasia, which can be of low grade or high grade. It concerns a category of HIV-infected patients: MSM, history of condyloma or precancerous/cancerous lesions of the cervix. Treatment, based on a combination of simultaneous chemotherapy and radiation therapy, allows a complete response rate of 80%. In case of persistence or tumor recurrence, abdominoperineal resection remains the treatment of choice. Advanced diseases can benefit from highly effective chemotherapy combinations or even in the future, combination of chemotherapy and immunotherapy.

Carcinomes du canal anal. Les carcinomes anaux sont des tumeurs rares, dont l'incidence a augmenté durant les dernières années. Ils sont viro-induits par le human papillomavirus [HPV) [génotype 16 essentiellement]. La prévalence est élevée chez les hommes homosexuels infectés par le virus de l'immunodéficience humaine (VIH), dont la prévention primaire par vaccination anti-HPV constitue une source d'espoir. Le dépistage repose sur la détection et le traitement des lésions précancéreuses : néoplasies intraépithéliales anales qui peuvent être de bas grade ou de haut grade, chez une certaine catégorie de patients séropositifs pour le VIH : homme ayant des relations sexuelles avec les hommes, antécédents de condylome ou de lésion tumorale cervicale utérine. Le traitement, fondé sur une association de chimio- et de radiothérapie concomitantes permet une rémission complète dans 80 % des cas. En cas de persistance ou de récidive tumorale, l'amputation abdomino-pelvienne reste le traitement de choix. Les maladies avancées peuvent bénéficier de combinaisons de chimiothérapies très efficaces, voire dans le futur de combinaisons de chimiothérapie et d'immunothérapie.

Transmission of Hepatitis E Virus With Plasma Exchange in Kidney Transplant Recipients: A Retrospective Cohort Study.

BACKGROUND: After observing a case of plasma exchange-mediated hepatitis E virus (HEV) infection in a kidney transplant recipient, we investigated the relationship between plasma exchange and HEV infection after kidney transplantation. METHODS: A cohort of 263 patients who underwent kidney transplantation from January 1, 2011, through December 31, 2012, was screened for HEV markers, including anti-HEV IgG and IgM antibodies and HEV ribonucleic acid (RNA), on 3 consecutive blood samples: 1 before, 1 with a mean (standard deviation) of 9.5 (9) months, and 1 with a mean (standard deviation) of 18.2 (6.6) months after transplantation, respectively. Transfusional investigation was performed in patients with detectable HEV RNA. We explored the relationships between plasma exchange, posttransplantation transaminase elevation and HEV markers acquisition. RESULTS: Overall, 24 (9.1%) patients had acquired HEV markers on the first posttransplantation sample, including 2 patients with detectable HEV RNA, and 7 (2.3%) patients had long-term persistent HEV markers on the second posttransplantation sample, including 3 patients with detectable HEV RNA without detectable anti-HEV antibodies. Plasma exchange was an independent risk factor for the acquisition of posttransplantation and long-term persistent HEV markers. Pathogen-reduced plasma-borne transmission of HEV was demonstrated. Plasma exchange and long-term persistent HEV markers were risk factors of posttransplantation transaminase elevation. CONCLUSIONS: Plasma exchange, including with pathogen-reduced plasma, is a risk factor for posttransplantation HEV infection and transaminase elevation. Screening for HEV RNA should be carried out in kidney transplant recipients treated with plasma exchange.

Nab-paclitaxel plus gemcitabine for metastatic pancreatic adenocarcinoma after Folfirinox failure: an AGEO prospective multicentre cohort.

BACKGROUND: There is currently no standard second-line treatment for metastatic pancreatic adenocarcinoma (MPA), and progression-free survival is consistently <4 months in this setting. The aim of this study was to evaluate the efficacy and tolerability of Nab-paclitaxel plus gemcitabine (A+G) after Folfirinox failure in MPA. METHODS: From February 2013 to July 2014, all consecutive patients treated with A+G for histologically proven MPA after Folfirinox failure were prospectively enrolled in 12 French centres. A+G was delivered as described in the MPACT trial, until disease progression, patient refusal or unacceptable toxicity. RESULTS: Fifty-seven patients were treated with Nab-paclitaxel plus gemcitabine, for a median of 4 cycles (range 1-12). The disease control rate was 58%, with a 17.5% objective response rate. Median overall survival (OS) was 8.8 months (95% CI: 6.2-9.7) and median progression-free survival was 5.1 months (95% CI: 3.2-6.2). Since the start of first-line chemotherapy, median OS was 18 months (95% CI: 16-21). No toxic deaths occurred. Grade 3-4 toxicities were reported in 40% of patients, consisting of neutropenia (12.5%), neurotoxicity (12.5%), asthenia (9%) and thrombocytopenia (6.5%). CONCLUSIONS: A+G seems to be effective, with a manageable toxicity profile, after Folfirinox failure in patients with MPA.

Sustained response with gemcitabine plus Nab-paclitaxel after folfirinox failure in metastatic pancreatic cancer: report of an effective new strategy.

INTRODUCTION: Folfirinox has shown a benefit in terms of survival and quality of life in first line treatment of metastatic pancreatic cancer. However, efficacy of second line chemotherapy after folfirinox is still limited. Gemcitabine plus Nab-paclitaxel have been recently validated as first line treatment with an increased overall survival compared to gemcitabine. This combination has never been studied as second-line after folfirinox. CASE REPORT: A metastatic pancreatic cancer was diagnosed in a 60-year-old patient with a performance status of 0. After 10 cycles of folfirinox, and an initial objective response, we objectively noted progressive disease according to the RECIST 1.1 criteria together with an increased carbohydrate antigen 19-9. The multidisciplinary team decided to use gemcitabine plus Nab-paclitaxel as second line palliative chemotherapy. After 2 months, we obtained an objective response. After 6 months, this response was maintained with an acceptable tolerability. CONCLUSION: Gemcitabine plus Nab-paclitaxel, as second line palliative chemotherapy, after failure of folfirinox, could be a good strategy for patients with a performance status of 0 and 1. Obviously, this data has to be confirmed in larger patients series and in future comparative clinical studies.