Gastric acid secretion in Chinese with particular reference to the dose of histamine required for maximal stimulation

Studies of basal and histamine-stimulated gastric acid secretion were performed in 42 controls, in 133 patients with duodenal ulceration, in 57 patients with gastric ulceration, in 13 patients with both duodenal and gastric ulceration, and in 20 patients with gastric carcinoma. All these subjects were Chinese. Statistical analysis of the results showed that all clinical groups differed from the controls in both basal and stimulated secretion. The mean basal acid output of Chinese controls and of patients with duodenal ulcer in most cases did not differ statistically when compared with western series. The basal secretion of Chinese patients with gastric ulceration, however, was statistically higher than in most of the western series. The histamine-stimulated response of Chinese controls and patients with duodenal ulcer was statistically much lower than in all western series with which they were compared. For Chinese patients with gastric ulcer, the stimulated responses were in some instances lower than and in others similar to results obtained in some western series. In contrast to most western reports, the basal and histamine-stimulated secretion in Chinese patients with gastric ulcer was significantly higher than in controls. In the Chinese controls and Chinese patients with peptic ulcers the response after histamine was generally lower than western reports. This was due to the inadequacy of the standard dose of histamine acid phosphate of 0.04 mg/kg body weight in Chinese subjects. A dose of 0.06 mg/kg body weight produced a significantly higher acid output. In the comparatively leaner Chinese subjects, therefore, a dose of histamine acid phosphate of 0.06 mg/kg is required for maximal stimulation of gastric acid secretion. This agrees well with the results of a similar study in Indian subjects.     

Gastric ulcers differ from duodenal ulcers evaluation of basal acid output

Patients with pyloric channel and prepyloric gastric ulcers are often considered to have an ulcer diathesis similar to patients with duodenal ulcers, while patients with more proximal gastric ulcers (ie, fundus, body, antrum) are excluded. To evaluate possible differences in basal acid outputs with regard to gastric ulcer location, basal acid outputs were determined by nasogastric suction in 80 patients with endoscopically documented benign active gastric ulcers. The results were compared to 65 normal subjects and 155 patients with endoscopically documented duodenal ulcers. There were no significant differences in basal acid outputs among the 80 patients with gastric ulcers with regard to location (ie, fundus-body, antrum, prepyloric, channel), and no significant differences compared to the 65 normal subjects. However, basal acid output for the 155 patients with duodenal ulcers was significantly different from the 80 patients with gastric ulcers (P<0.05) and the 65 normal subjects (P<0.05). Basal acid outputs tended to be higher and there was more gastric acid hypersecretion when gastric ulcers were located near the pylorus. However, irrespective of gastric ulcer location, basal acid outputs were higher in patients with duodenal ulcers. Seventy-one of the 80 patients with gastric ulcers were treated for eight weeks with standard doses of antisecretory medications, and endoscopic healing or nonhealing was documented. In 60 patients their gastric ulcers completely healed, while 11 patients had nonhealed gastric ulcers. There were no significant differences between the two groups with regard to gender, mean age, or basal acid output. The gastric acid secretory profiles determined in this study do not appear to support the view that prepyloric and pyloric channel gastric ulcers are similar to duodenal ulcers.     

Low acid output in Pima Indians

Duodenal ulcer has not been observed in full-heritage Pima Indians, while gastric cancer is relatively frequent. To investigate possible underlying factors for this phenomenon, we determined gastric acid output, gastric emptying rate, and plasma levels of gastrin, pepsinogen I, and pepsinogen II in apparently healthy Pima Indian and in Caucasian controls. The Pimas had significantly lower basal and stimulated outputs of gastric acid and higher fasting and postprandial plasma gastrin concentrations than the caucasians. Plasma pepsinogen I levels were similar in the two groups, but plasma pepsinogen II was significantly higher and the ratio of pepsinogen I to pepsinogen II was significantly lower in the Pima Indians. In addition, gastric emptying of an acaloric liqid meal was significantly delayed in the Pimas. The results suggest that the absence of duodenal ulcer in Pima Indians may be related to low gastric acid production and aslow rate of gastric emptying in this population. The associated findings of hypergastrinemia, hyperpepsinogenemia II, and a low ratio of pepsinogen I to pepsinogen II suggest that the hypochlorhydria may reflect an increased pervalence of chronic gastritis in full-heritage Pima Indians. This, in turn, could represent a risk factor for the development of gastric cancer in this population.Supported in part by research Contract 1-Am-6-2219 and grant AM 13233 from the National Institutes of Health, Bethesda, Maryland     

Gastric acid secretion in patients with typhoid fever.

Gastric secretory studies were carried out in the following groups of patients: group A, 30 Salmonella typhi positive enteric patients, group B, 15 non-enteric fever patients and group C, 20 healthy controls. Patients with typhoid were divided into two subgroups on the basis of the severity of the disease: group A1 (17) consisted of uncomplicated cases of enteric fever and group A2 (13) comprised of those who had associated complications. During convalescence both groups of typhoid patients showed significantly lower basal acid output (BAO) and maximal acid output (MAO) levels compared with controls and patients with non-enteric fever. Patients in group A2 had significantly lower MAO levels compared with group A1 but the BAO levels showed no such difference. In contrast BAO and MAO levels during convalescence in patients with non-enteric fever were similar to those in the control group. After two months, there was a significant increase in both the BAO and MAO levels in groups A1 and A2. The levels in group A2, however, remained significantly lower compared with group A1, controls and patients with non-enteric fever. Histologically, the gastric mucosa did not show any significant abnormality in either group of typhoid patients. The results suggest that depressed gastric secretion is the result of enteric infection and is related to the severity of the disease process.     

Gastric acid secretion in pancreatic disease.

Gastric acid secretion studies were carried out in 48 patients with pancreatic disease and in 20 control subjects. The mean basal and maximal outputs were lower in the patients than in control subjects. The present study indicates that such patients are not likely to suffer from gastric hypersecretion and peptic ulceration.     

Gastric secretion and basal gastrin concentration in bilharzial hepatic fibrosis.

Gastric secretion and fasting plasma gastrin levels were investigated in 26 patients with bilharzial hepatic fibrosis and 26 controls. The groups did not differ in their basal secretion. When stimulated by intravenous infusion of histamine the maximal acid output in patients with bilharzial hepatic fibrosis was significantly less than in the control group. This was unlikely to be a result of neutralisation by reflux of alkaline duodenal contents as the volumes of reflux were not different from control subjects, but was compatible with a true reduction in gastric secretion as assessed by two-component hypothesis. Neither the lowered gastric acidity nor the liver damage in patients with bilharzial hepatic fibrosis correlated with circulating gastrin. The fasting levels of plasma gastrin in these patients were not different from controls. As in other liver diseases the cause of diminished gastric secretion remains unclear.     

Adverse reactions to methyldopa with particular reference to hypotension.

Of 26,294 consecutive patients monitored in a comprehensive drug surveillance program, 1067 (4 per cent) received methyldopa for treatment of hypertension. Adverse reactions attributed to methyldopa were reported in 149 patients (14 per cent), the most frequent being hypotension. Life-threatening adverse effects were reported in nine patients (6 per cent of reactors)--the major problems being hypotension associated in several patients with signs of cardiac or cerebral ischemia. Hypotension attributed to methyldopa was more frequent in younger patients, in those with uremia, in lighter subjects, and in those receiving a high daily dose. Marked interaction between these factors was demonstrated and eightfold differences in the frequency of hypotension were observed in different sub-groups of methyldopa recipients. Adverse effects other than hypotension were reported infrequently and did not correlate well with the previously mentioned factors. The findings suggest that methyldopa therapy should be commenced cautiously in younger patients, in the non-obese, and in those with impairment of renal function as manifest by elevated blood urea nitrogen levels.