Evaluation of antacid tablets and liquid in fasting and fed men and women.

In view of in vitro tests suggesting good performance of an experimental tablet formulation of an aluminum hydroxide-magnesium hydroxide antacid, a study was conducted to evaluate the efficacy in vivo. Twenty-three healthy men and women were enrolled in the study, which was carried out in two parts: fasting and postprandial. Eight of the volunteers failed to qualify because of repeated baseline pH greater than 2.5. In the 15 participants who qualified, the intragastric pH was monitored for up to 240 minutes after the administration of one or two experimental tablets, 5 or 10 ml of a commercially available liquid antacid, or placebo. In the fasting subjects (n = 10), the antacids rapidly increased the mean pH. One antacid tablet and 5 ml of liquid antacid yielded similar results, with mean peak pH values of 5.2 and 4.8 and durations above pH 3.5 of 25 and 40 minutes, respectively. When the doses were doubled, 10 ml of liquid produced a peak pH of 6.7 and maintained the pH above 3.5 for 40 minutes, whereas two tablets produced a peak pH of 4.8 and maintained pH above 3.5 for 15 minutes. In the fed subjects (n = 10), neither antacid formulation at either dose significantly raised intragastric pH. Further studies are needed to establish the optimal time for postprandial administration of antacids.

Enprostil reduces G-cell hyperplasia and hypergastrinemia in duodenal ulcer.

A 42-year-old man with a 26-year history of duodenal ulcer volunteered for a 24-hour intragastric pH monitoring study, at which time his fasting gastrin concentration was found to be elevated. Secretin injection decreased the serum gastrin concentration. When not on treatment his total gastrin, gastrin-17 (G-17), and gastrin-34 (G-34) response to a protein-containing breakfast was marked. Immunocytochemical staining of antral biopsies showed hyperplasia of gastrin-containing cells, more pronounced for G-17 than for G-34. Cimetidine or cimetidine plus pirenzepine increased 24-hour intragastric pH, whereas pirenzepine alone rendered the gastric contents more acidic, particularly overnight. The total serum gastrin concentrations increased after meals and were unaffected by cimetidine or pirenzepine; enprostil, however, reduced the postprandial increase in total gastrin, G-34, and G-17. After six weeks of treatment with enprostil, the number of cells containing G-17 and G-34 was reduced. The findings show that G-cell hyperplasia may occur in the presence of a normal fasting serum gastrin concentration; fasting serum gastrin concentrations may fluctuate widely over time; the food-stimulated increase in G-17 was greater than that for G-34, and is associated with more pronounced antral hyperplasia for G-17 and G-34; and enprostil blunts the postprandial increase in G-17, G-34, and total gastrin. These observations suggest that enprostil may reduce G-cell hyperplasia and hypergastrinemia.

A system of workload measurement for clinical dietitians.

Although the role of the clinical dietitian has undergone dramatic change in recent years, standards for staffing patterns that were developed in 1935 and often still in use. The need for workload measurement systems to quantify the daily activities performed by clinical dietitians led to the development of a new system at the University of Alberta Hospitals in 1984. The workload of clinical dietitians was divided into eight major categories and further divided into 60 activities. A one- or two-week study was conducted four times over an 18-month period. The results indicated that 44 to 54% of the dietitians' time was spent in activities involving direct patient care and team approach. The system has enabled this institution to quantify the workload of its clinical dietitians and may provide a vehicle to measure the impact of major changes on that workload. Since the system covers all possible activities of the clinical dietitian, it may be applicable for use in other institutions. In view of rising health care costs, hospitals must make greater efforts to improve the efficiency of their operations while maintaining the quality of health care services provided to patients. This issue, as it applies to clinical dietetics, was recently addressed by the Nutrition and Food Services Department at the University of Alberta Hospitals.

Synergistic interaction between an H2-receptor antagonist and enprostil on 24-hour intragastric pH, serum gastrin concentration, and tissue immunoperoxidase staining for gastrin, somatostatin, and serotonin in a patient with metastatic gastrinoma.

A 56-year-old woman newly diagnosed as having Zollinger-Ellison syndrome due to a metastatic gastrinoma underwent 24-hour intragastric pH monitoring, serum gastrin (total, G-17 and G-34) measurements, and immunoperoxidase staining of duodenal, antral, and gastric body biopsies for gastrin, somatostatin, and serotonin. Determinations were made while the patient was given different doses of ranitidine, enprostil (a synthetic orally administered prostaglandin E2), or ranitidine plus enprostil. Following are the findings from this single-patient study: Intragastric pH was persistently low but varied in response to food when the patient was given ranitidine. Immunocytochemical staining of antral biopsies obtained before the patient was treated revealed a reduced number of cells containing G-17 and G-34 but an increase in the antral somatostatin-containing D-cells. Treatment with 35 micrograms of enprostil BID plus 300 mg of ranitidine BID for two and 11 weeks was associated with an increased number of duodenal G-cells, a decrease in antral D-cells, and a decrease in the number of antral serotonin-containing cells. Enprostil in a dosage of 35 or 70 micrograms BID had no effect on intragastric pH, but when enprostil was given in combination with ranitidine, postprandial and nocturnal intragastric alkalinity was accentuated along with a return of duodenal and antral G-cells and a loss of the antral D-cell hyperplasia. Optimal pH control was achieved with 300 mg of ranitidine BID; more frequent dosing with ranitidine did not further increase intragastric pH. Both the total serum gastrin concentration and G-17 levels fluctuated in response to meals. The serum concentrations of total gastrin, G-17, and G-34 were reduced with enprostil and with ranitidine.