ObjectiveTo determine the variation in number, size, and symptoms in patients with polypoid lesions of the gallbladder. Summary Background DataA polypoid lesion is any elevated lesion of the gallbladder mucosa. Several studies have been reported in patients undergoing cholecystectomy, but little information exits regarding the natural history of these lesions in nonoperated patients. MethodsA total of 111 patients with ultrasound diagnosis of polypoid lesions smaller than 10 mm were followed up by clinical evaluation and ultrasonography. Twenty-seven patients underwent cholecystectomy. ResultsThere was no difference in terms of gender. Nearly 80% of the lesions were smaller than 5 mm; they were single in 74%. In nonoperated patients, 50% remained of similar size at the late follow-up, 26.5% increased in number and size, and 23.5% shrank or disappeared. Among the operated patients, 70% corresponded to cholesterol polyps. None of the patients developed symptoms of biliary disease or gallstones or adenocarcinoma. ConclusionsUltrasound is useful in the follow-up of patients with polypoid lesions of the gallbladder. Lesions smaller than 10 mm do not progress to malignancy or to development of stones, and none produced symptoms or complications of biliary disease.

In this study the location of the lower oesophageal sphincter measured by manometry and the location of the squamous columnar junction measured by endoscopy were determined in 109 healthy controls and 778 patients with different degrees of endoscopic oesophagitis. No significant differences in the prevalence and severity of the heartburn and regurgitation were observed when different degrees of oesophagitis were compared but dysphagia was more common and severe in patients with complicated Barrett's oesophagus (p

A prospective study was performed in 190 control subjects and in 236 patients with different degrees of endoscopic esophagitis in order to determine the prevalence of Helicobacter pylori infection at duodenal gastric and esophageal mucosa and its correlation with histological findings. All patients with pathologic gastroesophageal reflux had 24-h pH monitoring studies confirming the presence of acid reflux into the esophagus. Besides the endoscopic findings, biopsies were taken from the duodenal bulb, gastric antrum, gastric fundus and distal esophagus or at the specialized columnar epithelium in patients with Barrett's esophagus. Patients with pathological gastroesophageal reflux were divided into three groups: 55 with absence of endoscopic esophagitis (gastroesophageal reflux), 81 patients with erosive esophagitis and 100 patients with Barrett's esophagus. There was no H. pylori infection present at duodenal or esophageal mucosa or at the specialized columnar epithelium of the distal esophagus in any case. The prevalence of H. pylori infection at gastric antrum was similar in controls and in any group of patients with reflux disease (20-25% of H. pylori infection). No differences in age and sex distribution were seen. H. pylori infection at gastric fundus was very low (less than 5%). The presence of HP infections was correlated with the finding of chronic active superficial or athrophic gastritis while, in the absence of H. pylori infection, gastric mucosa was normal. In the presence of intestinal metaplasia, no H. pylori infection occurred. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic chronic gastroesophageal reflux, erosive esophagitis or Barrett's esophagus, and the presence of antral gastritis in patients with Barrett's esophagus is closely related to the presence of H. pylori infection, and probably not related to an increased duodenogastric reflux.

Histological changes in the Auerbach's plexuses of the oesophagus, stomach, jejunum, and colon were analysed in a prospective study in 34 patients with achalasia ofthe oesophagus. At the distal end of the oesophagus ganglia cells were absent in 91% of cases as well as in the middle third of the stomach (20%). The Auerbach's plexuses were normal in the jejunum and colon. The results of gastric acid secretion showed that the peak acid output was significantly lower in achalasia patients compared with controls (p<0-001). There was no correlation between the mean ganglion neuronal count in the gastric plexuses and the rate of gastric acid output (r=0.33). Gastric emptying of solids was also evaluated, but there was no correlation between gastric emptying and the mean ganglion neuronal count in the gastric Auerbach's plexuses. The rate of gastric emptying of solids was similar in controls and patients with achalasia. These studies suggest that denervation of the oesophagus in patients with achalasia, which is a constant finding in several previous reports may extend beyond the oesophagus to the stomach in nearly half the cases.

Gastric capacity can increase late after sleeve gastrectomy even after performing a narrow gastric tubulization. It is very important to measure objectively residual gastric volume after sleeve gastrectomy and its eventual increase in order to determine the late clinical results and to indicate eventual strategy for retreatment.

In patients with achalasia submitted to esophagomyotomy and Dor's antireflux procedure, there is a progressive clinical deterioration of initially good results if a very long follow-up is performed (23 years after surgery), mainly due to an increase in pathologic acid reflux disease and the development of short- or long-segment Barrett esophagus.

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