The giant diverticulum was dissected from the transverse colon and a 10 cm small bowel learn more resection 30 cm from the duodeno-jejunal

flexure was performed with a side to side stapled anastamosis. The patient made an unremarkable recovery and was discharged on the sixth post operative day. Jejunal diverticulosis has an incidence of 1.3–4.6% on autopsy and 0.42% in radiological studies of the small bowel. It is usually asymptomatic and found in the sixth or seventh decade of life. It is thought that the diverticula originate due to bowel hypermotility or dyskinesia leading to increased intraluminal pressure. Major complications include diverticulitis, perforation, haemorrhage and enterolith formation. De novo enterolith formation within proximal small bowel is thought to be caused by stasis within

Selleckchem MK 2206 the diverticula and precipitation of bile salts within its alkaline environment. These are commonly radioopaque, making pre-operative diagnosis difficult. A well reported complication of enterolith formation within diverticula is small bowel obstruction, where surgical treatment may involve milking the stone distally in to the caecum to allow it to pass naturally and small bowel enterotomy. Jejunal diverticulosis is probably not as uncommon as previously thought. With an increasingly ageing population, it is should MCE公司 be a differential diagnosis considered in the management of

abdominal pain. “
“See Article on Page 455 ALT, alanine aminotransferase; CK-18, cytokeratin 18; ELISA, enzyme-linked immunoassay; M65ED, M65 EpiDeath; NAFL, nonalcoholic fatty liver; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis. To optimize the outcomes of patients with liver disease, physicians and researchers need better noninvasive tests for reliably detecting subclinical liver injuries and monitoring the progression/regression of liver damage. Joka et al.1 report exciting evidence showing that such tests are being perfected. The new assays quantify cytokeratin 18 (CK-18), an epithelial cytoskeletal protein that is released into the blood when hepatocytes die. CK-18 is a substrate for caspases that are activated during apoptosis. Fragmented CK-18 accumulates in apoptosing cells and then is released into the blood.1 Because many liver injuries increase hepatocyte apoptosis, an enzyme-linked immunoassay (ELISA) for detecting caspase-cleaved CK-18 was developed with M30, an antibody that recognizes a specific caspase-cleaved CK-18 epitope.1 Several groups have examined the ability of the M30 ELISA to detect subclinical liver disease and measure disease severity, and there has been much focus on patients with fatty liver disease and particularly nonalcoholic fatty liver disease (NAFLD).