Incidence of and risk factors for incisional hernia after abdominal surgery.

BACKGROUND: Few larger studies have estimated the incidence of incisional hernia (IH) after abdominal surgery. METHODS: Patients who had abdominal surgery between November 2009 and February 2011 were included in the study. The incidence rate and risk factors for IH were monitored for at least 180 days. RESULTS: A total of 4305 consecutive patients were registered. Of these, 378 were excluded because of failure to complete follow-up and 3927 patients were analysed. IH was diagnosed in 318 patients. The estimated incidence rates for IH were 5·2 per cent at 12 months and 10·3 per cent at 24 months. In multivariable analysis, wound classification III and IV (hazard ratio (HR) 2·26, 95 per cent confidence interval 1·52 to 3·35), body mass index of 25 kg/m(2) or higher (HR 1·76, 1·35 to 2·30), midline incision (HR 1·74, 1·28 to 2·38), incisional surgical-site infection (I-SSI) (HR 1·68, 1·24 to 2·28), preoperative chemotherapy (HR 1·61, 1·08 to 2·37), blood transfusion (HR 1·46, 1·04 to 2·05), increasing age by 10-year interval (HR 1·30, 1·16 to 1·45), female sex (HR 1·26, 1·01 to 1·59) and thickness of subcutaneous tissue for every 1-cm increase (HR 1·18, 1·03 to 1·35) were identified as independent risk factors. Compared with superficial I-SSI, deep I-SSI was more strongly associated with the development of IH. CONCLUSION: Although there are several risk factors for IH, reducing I-SSI is an important step in the prevention of IH. REGISTRATION NUMBER: UMIN000004723 (University Hospital Medical Information Network, http://www.umin.ac.jp/ctr/index.htm).

Rectal duplication cyst successfully treated by laparoscopic total mesorectal excision using the prolapsing technique.

Congenital alimentary tract duplication is a rare disease. It most frequently occurs in the ileum, with the rectum being the rarest site. Herein, we report a 38-year-old woman who was referred to our hospital because of severe anal pain. On digital examination, a smooth, round, rubbery mass was palpable; it was located 5 cm from the anal verge in the posterior rectal wall. A CT scan demonstrated a 5-cm cystic lesion located anterior to the sacrum that was displacing the rectum anteriorly. Spontaneous remission of the tumor was evident; however, after 5 months of follow-up, the patient experienced the same severe anal pain. MRI demonstrated a recurrent cystic lesion. To prevent further complications and to confirm or deny malignancy, laparoscopic total mesorectal excision using the prolapsing technique was performed. Pathologically, the cystic lesion was diagnosed as a rectal duplication cyst. This is the first report of a rectal duplication cyst successfully treated by laparoscopic total mesorectal excision.

Over-expression of polycomb group protein EZH2 relates to decreased expression of p16 INK4a in cholangiocarcinogenesis in hepatolithiasis.

Polycomb group protein EZH2 and Bmi1 are reportedly involved in the progression of malignant tumours. We examined the participation of EZH2 in multi-step cholangiocarcinogenesis in hepatolithiasis with respect to tumour suppressor gene p16 INK4a. We examined 20 hepatolithiatic livers with intrahepatic cholangiocarcinoma (ICC) and 10 histologically normal livers. Neoplastic biliary lesions were classified into biliary intraepithelial neoplasm (BilIN-1, 2 and 3) and invasive carcinoma. We selected 15 foci of invasive carcinoma, 8 BilIN-3 (carcinoma in situ), 12 BilIN-2 (high-grade dysplasia), 32 BilIN-1 (low-grade dysplasia) and 37 non-neoplastic biliary epithelia from these livers. Expression of p16 INK4a, EZH2 and Bmi1 were surveyed in these foci. P16 INK4a promoter methylation was examined in microdissected tissues. Taking advantage of two cell lines of CC (HuCTT-1 and TFK-1) and small interfering RNA (siRNA), the effects of the knockdown of EZH2 on p16 INK4a methylation of CC cells were examined. Expression of p16 INK4a, which was frequent in BilIN1, was decreased in BilIN-2/3 and invasive carcinoma, while EZH2 expression showed step-wise increase from BilIN-1, -2 and -3 to invasive carcinoma (p < 0.01). P16 INK4a promoter hypermethylation was related to aberrant expression of EZH2. The knockdown of EZH2 in cultured CC cells decreased p16 INK4a methylation and decreased binding of EZH2 to the p16 INK4a gene promoter. The latter suggested that direct binding of EZH2 is involved in the regulation of the p16 INK4a gene. Our data suggest that over-expression of EZH2 may induce hypermethylation of p16 INK4a promoter followed by decreased expression of p16 INK4a in the multi-step cholangiocarcinogenesis through intraepithelial neoplasm in hepatolithiasis.