Relation of gallbladder function and Helicobacter pylori infection to gastric mucosa inflammation in patients with symptomatic cholecystolithiasis

Background. Inflammatory alterations of the gastric mucosa are commonly caused by Helicobacter pylori (Hp) infection in patients with symptomatic gallstone disease. However, the additional pathogenetic role of an impaired gallbladder function leading to an increased alkaline duodenogastric reflux is controversially discussed. Aim:To investigate the relation of gallbladder function and Hp infection to gastric mucosa inflammation in patients with symptomatic gallstones prior to cholecystectomy. Patients: Seventy-three patients with symptomatic gallstones were studied by endoscopy and Hp testing. Methods: Gastritis classification was performed according to the updated Sydney System and gallbladder function was determined by total lipid concentration of gallbladder bile collected during mainly laparoscopic cholecystectomy. Results: Fifteen patients revealed no, 39 patients mild, and 19 moderate to marked gastritis. No significant differences for bile salts, phospholipids, cholesterol, or total lipids in gallbladder bile were found between these three groups of patients. However, while only 1 out of 54 (< 2%) patients with mild or no gastritis was found histologically positive for Hp, this infection could be detected in 14 (74%) out of 19 patients with moderate to marked gastritis. Conclusion: Moderate to marked gastric mucosa inflammation in gallstone patients is mainly caused by Hp infection, whereas gallbladder function is not related to the degree of gastritis. Thus, an increased alkaline duodenogastric reflux in gallstone patients seems to be of limited pathophysiological relevance. Copyright (c) 2006 S. Karger AG, Basel

Somatostatin in human pancreatic and gastric juice

Considerable amounts of IRS are secreted after secretin injection in human pancreatic juice collected during endoscopic retrograde cholangiopancreatography. The mean IRS levels in the pancreatic juice of non-diabetic patients were 79+/-10 (SE) pg/ml. The IRS levels in NIDDM were considerably higher, the mean value being 1635+/-313 (SE) pg/ml. The mean IRS level in IDDM were 312+/-151 (SE) pg/ml. In IDDM, those patients whose blood glucose levels were well controlled by insulin showed low pancreatic juice IRS ranging from non-detectable to 46 pg/ml. On the other hand, those with uncontrolled hyperglycemia showed IRS levels ranging from 452 to 1047 pg/ml. Gel-filtration profiles of IRS in pancreatic juice extracts were not consistent in all cases. Some showed IRS peaks eluting with SS14 and SS28, while others contained IRS species that were eluted in more retarded fractions. The retarded IRS fraction exhibited biological activity indistinguishable from that of SS14 as indexed using a quantitative cytochemical method.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24539/1/0000818.pd