Endoscopic studies were performed to determine whether changes occurred in the duodenum related to portal hypertension in patients with liver cirrhosis. The total of 271 patients studied were subdivided into three groups: 83 patients with liver cirrhosis and portal hypertension, 53 with liver cirrhosis but no portal hypertension, and 135 controls. In the duodenum of cirrhotic patients with portal hypertension several changes were observed on endoscopy that were also present in the other two groups. Atrophy and vascular malformations, however, were present only in the duodenum of cirrhotic patients with portal hypertension, although in only a few patients and with statistical significance only for vascular malformations (p less than 0.01, phi = 0.21). Eleven percent of the patients had more than one endoscopic finding, but the associations of findings were without statistical significance. No statistically significant correlation was observed between the clinical severity of cirrhosis or the severity of esophageal varices and the endoscopic findings. Finally, there was no statistically significant difference between the histological findings of duodenitis in the three groups of patients.

A multicenter study that involved 15 Italian institutions was carried out to compare the efficacy and safety of famotidine 40 mg at bedtime, famotidine 20 mg b.i.d., famotidine 40 mg b.i.d., and ranitidine 150 mg b.i.d. in promoting the healing of acute duodenal ulcer. Two hundred and twenty-four patients with endoscopically proven duodenal ulcer were randomly allocated into four treatment groups. Efficacy results for the four groups were similar at weeks 2, 4, and 8 of therapy. At week 8, the percentage of patients healed in each group was as follows: 92% in the famotidine 40-mg bedtime group, 97% with 20 mg b.i.d., 93% with 40 mg b.i.d., and 90% with ranitidine 150 mg b.i.d. Day pain and night pain were markedly reduced in all four groups, antacid consumption fell considerably, and therapy was generally well tolerated. The adverse experiences evaluated by the investigator as possibly, probably, or definitely related to test medication were rare and moderate.

In 2436 duodenoscopies performed in 1979-1980, 142 cases of duodenal erosions were found. In 68% of the cases erosions were autonomous, while in the remaining 32% they were associated with peptic ulcer. Either autonomous or associated erosions were mainly present in males with prevalence of the 4th, 5th and 6th decades of life. Moreover, autumn and spring were the most common times of appearance. With respect to symptomatology, 125 cases complained of dyspepsia with a prevalence of ulcer-like symptoms in both autonomous and associated erosions: in the remaining 17 patients hematemesis and melena were the main symptoms. The intake of alcohol and of coffee, as well as the smoking habit did not reveal any particular pattern in these cases, while the association with recent consumption of potentially mucolytic drugs was frequent. In addition, the last 38 cases of autonomous duodenal erosions were studied from the anatomo-functional point of view, revealing the presence of normochlorhydria in 42%, hyperchlorhydria in 47% and hypochlorhydria in 11%: in contrast, fasting gastrinemia was always within normal limits. The histological evaluation of the fundic mucosa showed normal patterns in 71% of the cases, superficial gastritis in 18%, and preatrophic gastritis in 11%. The parietal index was normal in 42% of the cases, high in 47% and low in 11%. The results would seem to suggest that duodenal erosions should be included in the wide spectrum of peptic pathology.

Sclerotherapy of esophageal varices is an effective hemostatic treatment and may also prevent bleeding. In our study, we examined the effects of prophylactic sclerotherapy on esophageal motility in 15 patients with Child's A cirrhosis of the liver. All the patients underwent three manometric measurements, performed respectively before the sclerotherapy, 1 week after the eradication of varices, and 3 months later. The results of our study show that prophylactic sclerotherapy of esophageal varices does not significantly change the resting pressure and length of the lower esophageal sphincter. Neither the amplitude nor the duration of the postswallowing esophageal peristaltic waves is significantly influenced by sclerotherapy. However, sclerotherapy produces a significant increase in tertiary contractions in the distal esophagus, which could explain the onset of dysphagia among patients in whom postsclerotherapy stricture is not evident.

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