Stenosis of the gastroenterostomy after LRYGBP is an infrequent but serious problem, which results in considerable morbidity.
nized factors in cholesterol gallstone formation; bile which is Obese persons are at risk for cholesterol gallstones saturated with cholesterol is essential for crystals to form, because their bile is saturated with cholesterol. The risk nucleation factors can influence whether crystals form in satincreases during rapid weight loss by means of certain urated bile, and gallbladder stasis can allow crystal growth. very-low-calorie diets or gastric bypass surgery. GallObesity is associated with increased bile cholesterol secrestone risk factors during rapid weight loss include intion and saturation index. 6 Several studies suggest that bile creased bile cholesterol saturation index and gallbladsaturation index increases further during rapid weight der stasis. Obese subjects were randomized to one of two loss. 1,6,7 In one study, 10 subjects losing weight on a 1,000-low-calorie liquid diets for rapid weight loss: a 520-kcal kcal diet showed reduced output of all bile lipids, but 6 of the diet with less than 2 g fat/d, and a 900-kcal diet with 30 10 increased their bile saturation index. 6 On the other hand, g fat/d (including one 10-g fat meal to stimulate maximal several studies have reported decreased bile saturation index gallbladder emptying). Bile and blood lipids, saturation after 6 to 20 days of fasting. 8,9 Cholesterol may be mobilized index, leukocyte 3-hydroxy-3-methylglutaryl coenzyme from tissue stores to be secreted into bile during rapid weight A (HMG CoA) reductase activity, and ultrasonographic loss. 6 Decreased bile acid synthesis has also been detected gallbladder emptying were measured repeatedly during during diet-induced weight loss and fasting. 6,9,10 Thus, rapid dietary treatment. Both diets produced comparable weight loss may alter secretion of cholesterol and bile acids weight loss of 22%. Bile cholesterol saturation index inin a manner conducive to gallstone formation. creased during both diets (26%), but fell to 15% below Pro-and antinucleating proteins and mucins are described prediet level after weight loss. Compared with subjects' in gallbladder bile, and may predispose to gallstones. These maximal gallbladder emptying fraction of 66%, the 520-factors could change during rapid weight loss. Shortened kcal diet provided poor gallbladder emptying (35%), crystal nucleation time has been observed during very-lowwhereas the 10-g fat meal of the 900-kcal diet provided calorie liquid diets. 7 Mucin and calcium increased in gallbladmaximal emptying. Gallstones developed in four of six der bile of obese subjects forming gallstones after gastric by-520-kcal subjects and none of seven 900-kcal subjects (P pass. 11,12 Å .021), an unanticipated difference that resulted in preGallbladder emptying may also participate in gallstone formature study termination for ethical reasons. Blood lipmation. 13 Studies of meal-stimulated gallbladder emptying in ids and HMG CoA reductase activity in mononuclear leuobese subjects have given variable results. [14][15][16][17] We and others kocytes fell at week 8 durin...
Helicobacter pylori is a major cause of gastroduodenal injury, gastric cancer, and lymphoma, and, thus, there is great interest in its detection and eradication. Several detection methods are available, including histochemical and immunohistochemical stains. Application of these stains in clinical practice is heterogenous, to say the least. Although they were developed to enhance H. pylori detection, changing practice models, financial considerations, and a perceived need for rapid case turnaround have led to their widespread use in routine staining studies ordered reflexively on all gastric biopsies. Emerging data suggest that most of these stains are not needed to establish a diagnosis of H. pylori infection, and their added value when biopsies show minimal, or no, inflammation is not clear. In this manuscript, the Rodger C. Haggitt Gastrointestinal Pathology Society puts forth recommendations regarding ancillary stain usage for H. pylori detection based upon critical literature review and collective experience. Pathologists rarely, if ever, detect H. pylori in "normal" biopsies, but readily observe them in optimally stained hematoxylin and eosin sections from infected patients. Therefore, we suggest that use of ancillary stains is appropriate when biopsies show chronic, or chronic active, gastritis without detectable H. pylori in hematoxylin and eosin-stained sections, but performing them "up front" on all gastric biopsies is generally unnecessary. Application of these stains to nongastric biopsies and polyps is appropriate in an extremely limited set of circumstances. It is our hope that recommendations provided herein will provide helpful information to gastroenterologists, pathologists, and others involved in the evaluation of patients for possible H. pylori infection.
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