Gastrointestinal stromal tumors in northeastern iran: 46 cases during 2003-2012

Gastrointestinal stromal tumors [GIST] are the most common mesenchymal tumors of the gastrointestinal [GI] tract. They are usually C-kit positive and seen slightly more common in men. These tumors are seen in the GI tract from the esophagus to the anus with occasional invasion or metastasis. In this retrospective study, we evaluated the prevalence of c-kit positive stromal tumors of the GI tract based on age, site of involvement, size of tumor, local invasion, and Immunohistochemical markers. The study was conducted in Mashhad University of Medical Sciences in Iran during 2003-2012. Of the total 46 patients, 18 [39.1%] were men and 28 [60.9%] were women with a mean age of 58.07 years [range: 18-93]. Common sites of tumor were stomach, small intestine, esophagus and rectum, respectively. The number of mitoses per 50 HPF varied between zero and 160 mitoses. Overall, 23 cases had 5 mitoses 50/HPF [50%] and 23 tumors expressed <5 mitoses/50 HPF [50%]. Local invasion and metastasis were observed in seven cases with extension to liver, pancreas, pregastric tissue, omentum, mesentery and appendix. Positive reaction for CD34, SI00, actin and desmin was seen in 47.8%, 13%, 21.7%, and 4.3% of the patients, respectively. Most patients were women. The prevalence of tumors in the esophagus was higher than the rectum. Invasion and metastasis did not correlate with mitotic rate, site and size of tumor. We suggest evaluation of genetic, racial and geographical or other unknown risk factors

Prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis

Pancreatitis is the most common and important complication of endoscopic retrograde cholangiopancreatography [ERCP]. Several risk factors play a role in the formation and progression of pancreatitis. These risk factors may be related to the patient, procedure or operator. All of these risk factors should be considered and should be lowered as far as possible with attention to pathogenesis of the development of post-ERCP pancreatitis. The pathogenesis include sphincter spasm, infection, contrast toxicity and pancreatic secretion that induce the activation of proteolytic enzymes and inflammatory processes. Some methods and pharmacologic agents assessed for the prevention of pathway in the pathogenesis to decrease post-ERCP pancreatitis