Prophylaxis of Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis Using Temporary Pancreatic Stents Versus Rectal Nonsteroidal Anti-inflammatory Drugs: A Randomized Controlled Trial.

OBJECTIVES: Both pancreatic stenting and rectal nonsteroidal anti-inflammatory drugs (NSAIDs) prevent post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. The aim of the study was to compare post-ERCP pancreatitis (PEP) prophylaxis using pancreatic stents and/or rectal NSAIDs prospectively. METHODS: A total of 321 patients undergoing ERCP were studied. Each patient was randomly allocated to receive pancreatic stent placement (PS), 50 mg of rectal diclofenac (NSAID), or both (PS + NSAID) for PEP prophylaxis. The primary outcome was the occurrence rate of PEP, and secondary outcomes included the severity of PEP and serum pancreatic amylase and lipase levels on the day after ERCP. RESULTS: Five patients (PS: 2/101, NSAID: 1/106, PS + NSAID: 2/102) developed PEP, and the overall occurrence rate of PEP was 1.6% (5/309). The occurrence rates of PEP in the PS, NSAID, and PS + NSAID groups were statistically equivalent with an equivalent margin of 10%. The severity of PEP was mild in all 5 patients. Median serum pancreatic amylase and lipase levels in the NSAID group were significantly lower than those in the PS and PS + NSAID groups. CONCLUSIONS: Rectal administration of 50 mg of diclofenac may become a first-line therapy for PEP prophylaxis in our country.

Fulminant massive gas gangrene caused by Clostridium perfringens.

Clostridium perfringens (C.P) gas gangrene is one of the most fulminant infectious diseases. We encountered fulminant massive gas gangrene in a 56- year-old man with alcoholic liver cirrhosis. The patient died 14 hours after diagnosis of gas gangrene (54 hours after admission). Dramatic changes in abdominal CT imaging revealed development of a massive volume of gas in the intra-portal vein, retroperitoneum and abdominal subcutaneous tissue within 24 hours. We also proved C.P infection by immunohistological staining, leading to a diagnosis of C.P gas gangrene.

Association study of the effect of WFS1 polymorphisms on risk of type 2 diabetes in Japanese population.

Mutations of WFS1 gene cause Wolfram syndrome, which is a rare autosomal recessive disorder characterized by juvenile diabetes mellitus, optic atrophy, deafness and diabetes insipidus. The product encoded by WFS1 gene, wolframin, could be involved in ER stress response causing beta-cell loss through impaired cell cycle progression and increased apoptosis. Recently, polymorphisms in the WFS1 gene were strongly associated with type 2 diabetes in Caucasians. The aim of the present study was to examine whether the variants of WFS1 are associated with risk of type 2 diabetes in Japanese individuals. Four single nucleotide polymorphisms, rs6446482, rs12511742, rs1801208 (R456H) and rs734312 (H611R) were genotyped in a total of 536 diabetic patients and 398 nondiabetic control subjects. Among the four variants, rs12511742 showed a marginal association with susceptibility to type 2 diabetes (odds ratio = 1.32, 95% confidence interval = 1.02-1.71, P = 0.033). Carriers of the risk allele at rs12511742 exhibited lower pancreas beta-cell function (P = 0.017). However, this association disappeared after adjustment for sex, age and BMI (Adjusted P = 0.24). Although we found no evidence for a substantial effect of WFS1 polymorphisms on risk of type 2 diabetes or clinical characteristics of diabetic subjects in Japanese population, this gene is still a good candidate for a type 2 diabetes susceptibility gene, potentially, through impaired insulin secretion.