Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.

Gastric emptying, mouth-to-cecum transit, and whole-gut transit of a solid-liquid meal were measured in 46 chronic alcoholics and in 30 control subjects by using scintigraphic techniques, hydrogen breath test, and stool markers. In the alcoholics various parameters such as ethanol consumption, gastrointestinal symptoms, and alcoholic neuropathy were determined and related to gastrointestinal transit times. Although there was no significant overall difference of gastric emptying, abnormally delayed gastric emptying was detected in 23.9% of the alcoholics but no control subject (P less than 0.005). Mouth-to-cecum transit was significantly prolonged in the alcoholics (P less than 0.001) with 14 alcoholics (37.8%) disclosing delayed mouth-to-cecum transit. No significant differences between both groups were detected concerning whole gut transit. In the alcoholics there was a significant correlation of dyspeptic symptoms with delayed gastric emptying (P less than 0.006), and alcoholics with diarrhea had an accelerated mouth-to-cecum transit as compared to those without diarrhea (P less than 0.05). Neither the presence of autonomic or peripheral neuropathy nor the presence of liver cirrhosis or ascites was significantly related to gastrointestinal transit times. However, the daily ethanol ingestion significantly correlated with gastric emptying (P less than 0.005). It is concluded, therefore, that in chronic alcoholics the small intestine and the stomach are most likely to be affected by gastrointestinal transit disorders and that these transit abnormalities are potentially related to toxic damage of gastrointestinal smooth muscle.

A comprehensive prospective ultrasonographic study was performed in 93 patients to investigate gallbladder wall thickness and gallbladder volumes in various nonbiliary disease states. Without changes in gallbladder volume, mean gallbladder wall thickness was significantly increased (p less than 0.01) in patients with liver cirrhosis, viral hepatitis, chronic congestive heart failure, hypoalbuminemia, and chronic renal failure (p less than 0.05) but not in patients with diabetes mellitus (n = 14) as compared to a control group. The present study confirms that a variety of nonbiliary disorders are associated with significant thickening of gallbladder walls and that this finding is not caused by incomplete gallbladder contraction.