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In one thousand of 1500 examinees with nonulcerous dyspepsia the syndrome was due to chronic gastritis, duodenitis and gastroduodenitis, in five hundred of them it was attributed to probable dysfunction of the upper gastrointestinal tract. Morphological evidence of chronic gastritis activity is essential but not the only factor affecting the dyspepsia syndrome. Of importance are also motor dysfunctions: high intragastric and/or intraduodenal pressure, unbalance of intracavitary pressure parameters, gastroesophageal and duodenogastric refluxes. A significant contamination of antral mucosa with Helicobacter pylori aggravated dyspeptic manifestations.

The investigations of 43 duodenal ulcer cases in the patients whose ulcers failed to cicatrize after a 8-week treatment with almagel and vicalin or cimetidine monotherapy revealed the role of the hereditary load, smoking intensity, initial ulcer dimensions, the presence of antral erosions and a pronounced periulcerous duodenitis in the phenomenon of slow healing duodenal ulcer. There was no statistical difference between the values of the basal and pentagastrin-stimulated levels of hydrochloric acid secretion in the morning, partial alkaline gastric secretion, gastrinemia, the rate of evacuation of the gastric contents into the duodenum, the outcome of pancreatic bicarbonates in the sample with exogenic secretin in those whose ulcers cicatrized after a 6-week therapy and those who failed to be cured after being exposed to the same therapy during 8 weeks. The production of hydrochloric acid in the evening and the incidence of manifest duodenal reflux were significantly higher in the patients with slowly healing ulcer. They also had a decreased sensitivity to the intraduodenal inflow of the hydrochloric acid that resulted in the increase of endogenic secretin (stimulating the production of pancreatic bicarbonates and their transport into the duodenum). In case the combination treatment with almagel and vicalin failed, the therapy with gastrocepin or sucralfate was employed. A supplementary course of sucralfate helped to reach a complete healing of noncomplicated ulcers even in the patients in whom the preceding cimetidine treatment failed.

Toxic hepatitis developed but in one out of 127 peptic ulcer patients treated with cimetidine. In patients (n-142) treated with gastrozepine, no cases of toxic hepatitis were recorded. These anti-ulcer agents did not influence absorptive capacities of the liver or hepatic blood flow. Meanwhile microsomal exidase (antitoxic) function of hepatocytes noticeably declined as a result of cimetidine treatment in every 8th patient with peptic ulcer subjected to the continuous 5-week treatment with the drug and in every 5th patient given the treatment (maintenance included) for a longer time. In patients suffering from liver cirrhosis with secondary gastroduodenal ulcers or multiple erosions, the 5-week treatment either with almagel and platyphylline or gastrozepine provided approximately similar results and promoted ulcer and erosion healing in half the cases. Adjuvant 3-week therapy with sucralfate (venter) having cytoprotective properties led to the disappearance of gastroduodenal ulcers and erosions in 23 out of 26 patients, in whom the previous treatment was ineffective.

Altogether 78 patients were examined over time. They had erosive reflux esophagitis that complicated the course of duodenal ulcer (in 42 patients, hypersecretion of hydrochloric acid was the leading mechanism of the disease development) and chronic gastroduodenitis (36 persons manifested failure of the inferior sphincter of the esophagus with or without excess acid output). In patients with peptic ulcer exacerbation, the four-week treatment with cimetidine or gastrozepine compared very favourably with almagel and vicalin as regards the treatment efficacy. In chronic gastroduodenitis, the combination of almagel, vicalin and cerucal produced a therapeutic effect that did not yield to the effect of cimetidine or gastrozepine. In 1/5-2/5 of cases, erosive esophagitis was not amenable by the four-week treatment. In 17 out of 18 such patients, the two-week therapy with sucralfat (venter) resulted in the disappearance of esophagitis with multiple erosions. During 1-2 years, erosive reflux esophagitis recurred in 11 out of 34 patients with peptic ulcer and in 2 out of 17 suffering from chronic gastroduodenitis. In all the cases, the disease recurred in those patients who had not received systematic treatment with antisecretory and cytoprotector agents.

Fundal pH and pH of withdrawn gastric juice were measured under basal condition (with no stimulants used) in normal subjects and patients with chronic moderately severe and marked fundal gastritis and duodenal ulcer (altogether 96 examinees). Aspiration pH-metry with a tube designed by Ye. Yu. Linar was employed. Comparison of the results revealed statistically significant differences (the 'agreement criterion') in the pH values obtained by the compared methods. Low pH values were more frequent in intragastric fundal pH-metry, possibly at the expense of the presence of not only acid but of the antral-alkaline component in the withdrawn gastric juice. These differences should be taken into consideration in the clinical laboratory diagnosis.

Values of intraesophageal pH, basal fundal pH and hydrochloric acid debit were studied in 73 patients with exacerbation of peptic ulcer on the first days of exacerbation and 2-4 weeks after the initiation of therapy with various drugs. Gastrozepin and cimetidine in parallel with gastric acidity inhibition reduced regularly and considerably a degree of gastroesophageal reflux in the patients. The action of combined vicalin and almagel therapy was manifested later on and was less marked.