Changes in acid secretion over the years. A 30-year longitudinal study.

We studied the effect of aging on gastric acid secretion in 11 physicians who had augmented histamine tests while at medical school in 1962. One of them had a duodenal ulcer at the time. The augmented histamine test was repeated in 1991 and, in addition, upper gastrointestinal endoscopy was done to exclude peptic ulcer and to obtain biopsies for histologic analysis and assessment of Helicobacter pylori status. The mean basal acid output decreased from 7.3 to 1.9 mEq/hr during the 30-year period of follow-up (p < 0.001), and the mean maximum acid output decreased from 29.9 to 20.3 mEq/hr (p < 0.01). The maximum acid output data showed a profound decrease in 4 of the 11 participants, a lesser decrease in 4, and a minimal increase in the remaining 3. Histologic analysis suggested a greater likelihood of atrophic gastritis, H. pylori infection, or both in participants showing a pronounced decrease in acid secretion with aging.

Changes in nocturnal and peak acid outputs after duodenal ulcer healing with sucralfate or ranitidine.

Changes in basal and stimulated acid secretion after duodenal ulcer healing have been previously shown to be influenced by the nature of the treatment. This study aimed to determine possible changes in nocturnal acid secretion on duodenal ulcer healing in patients treated with sucralfate or ranitidine. Nocturnal acid output and peak acid output in response to pentagastrin stimulation were studied in 20 patients before and after duodenal ulcer healing with sucralfate (n = 9) or ranitidine (n = 11). Details regarding cigarette smoking were obtained from each subject. Median 10 hour nocturnal acid output fell significantly (p less than 0.05) from 82.4 (29.1-188.3) mmol (median range) to 45.2 (14.7-144.4) mmol after healing with sucralfate, and rose significantly (p less than 0.05) from 54.7 (16.8-74.3) mmol to 86.2 (11.7-118.1) mmol after ulcer healing with ranitidine. Peak acid output fell from 39.6 (22.0-52.8) mmol/hour to 27.8 (13.8-38.2) mmol/hour (p less than 0.01) after healing with sucralfate and was unchanged after healing with ranitidine. There was no correlation between smoking and nocturnal acid output. These results provide further evidence that acid secretion decreases with sucralfate healing and remains the same or may even increase after ranitidine healing.

Basal and maximum acid output after continuous overnight gastric aspiration.

Basal and maximum acid outputs were measured on two occasions in a group of 15 duodenal ulcer (DU) patients in remission. The initial study was carried out after a nocturnal acid collection, whereas the second was carried out in the conventional manner without preceding nocturnal aspiration. No difference in the basal acid output, concentration, or volume of secretion was found between the two study days. Maximum acid output on the other hand, was significantly (p less than 0.02) reduced from 30.9 (14.2-41.2) mmol/h, median (+range), to 23.7 (8.1-33.7) mmol/h after overnight aspiration. The reduction in maximum acid output was attributable to a fall in the volume of gastric secretion from 280 (170-371) ml to 230 (142-280) ml. No fall in acid concentration was seen. We conclude that overnight gastric aspiration does not affect basal gastric secretion, but reduces the maximum acid output as a result of a reduced secretory volume.

Acid secretory responses and parietal cell sensitivity following duodenal ulcer healing with omeprazole, sucralfate, and Maalox.

Acid secretory responses and parietal cell sensitivity (PCS) have been studied in 21 duodenal ulcer patients before and after successful treatment with omeprazole (n = 7), sucralfate (n = 7), or Maalox (n = 7). The second study was carried out 3 days after documented healing and withdrawal of treatment in the sucralfate- and Maalox-treated groups and 14 days after documented healing and withdrawal of treatment in the omeprazole-treated patients. Acid output (mmol/hour) was measured as basal secretion, and in response to 0.1 microgram/kg/hour pentagastrin (low-dose) and 6.0 micrograms/kg/hour pentagastrin (high-dose) stimulation. PCS was calculated as the ratio of low dose:high dose acid output (expressed as a percentage). Ulcer healing with sucralfate resulted in significant (p less than 0.05) decreases in low-dose acid output from 36.4% (13.2-51.0) (median [range]) to 8.4% (3.2-45.4) mmol/hour and PCS from 69.1% (44.9-91.4) to 22.0% (16.0-85.6), whereas no significant decreases in any of the measured parameters were noted following ulcer healing with Maalox. Ulcer healing with omeprazole resulted in significant (p less than 0.05) decreases in basal acid output from 6.3 (1.5-22.9) (median [range]) to 2.2 (0-6.9) mmol/hour, and low-dose acid output from 31.0 (6.0-58.0) to 23.0 (1.4-44.8) mmol/hour. These findings suggest that acid secretory responses following ulcer healing vary according to the therapeutic agent used.

Duodenal ulcer healing and acid secretory responses to modified sham feeding and pentagastrin stimulation.

The effect of duodenal ulcer healing on the acid secretory responses to modified sham feeding and maximal pentagastrin stimulation has been studied in 17 patients treated successfully with ranitidine (n = 9) and sucralfate (n = 8). Parietal cell sensitivity was calculated as the ratio of the modified sham feeding response to the peak pentagastrin response, expressed as a percentage. Ulcer healing after sucralfate therapy resulted in significant falls in modified sham feeding stimulated acid output (P less than 0.02), from 9.4 (1.8-17.0) (median + range) to 3.7 (0.2-9.4) mmol/h; in peak acid output (P less than 0.05) from 42.8 (23.0-61.4) to 27.7 (7.2-51.0) mmol/h; and in the parietal cell sensitivity (P less than 0.05) from 19.2 (4.4-42.6) to 14.3 (2.8-19.7)%. No significant falls in any of these parameters were noted following ulcer healing with ranitidine. Duodenal ulcer healing with sucralfate results in decreased acid secretory responses to vagal and pentagastrin stimulation.

Acid-secretory response and parietal cell sensitivity in patients with duodenal ulcer before and after treatment with sucralfate or ranitidine.

Patients with endoscopically proved duodenal ulcer were randomly assigned to treatment with either ranitidine 300 mg at bedtime or sucralfate 2 g twice daily for six weeks. Acid-secretory studies were performed before commencement and 60 to 84 hours after cessation of treatment and endoscopic healing was confirmed. Patients were randomly assigned to receive a constant infusion of secretory stimulant: either pentagastrin 0.1 and 6.0 micrograms/kg/hour or histamine acid phosphate 4.0 and 40 micrograms/kg/hour. Acid output in mmol/hour was measured for basal, low dose, and high dose output. Parietal cell sensitivity (PCS) was calculated as the ratio of low-dose acid output: high-dose acid output and expressed as a percentage. Values before and after treatment were compared and significance of differences was determined using the Student paired t test. There was an apparent decrease in basal acid output, low-dose acid output, high-dose acid output, and PCS with ulcer healing, regardless of treatment or stimulant used. Basal acid output, low-dose acid output, high-dose acid output, and PCS were significantly lower in the sucralfate-treated group, but only high-dose acid output decreased significantly in the ranitidine-treated group. These differences may be relevant to early duodenal ulcer relapse in ranitidine-treated patients.

Predictors of acute relapse of Crohn's disease. A laboratory and clinical study.

Relapses of Crohn's disease appear to be almost random. If these attacks could be reliably predicted, it might be possible to abort them with early treatment. In order to identify laboratory and clinical parameters that would predict an acute relapse, patients who had been assessed clinically in the three months prior to an attack were studied. Published clinical indices as well as variety of laboratory parameters were measured. The clinical indices and the serum C-reactive protein, orosomucoid, alpha 1-antitrypsin, and iron were increased at the time of the attack as compared to three months earlier, while only the clinical indices, orosomucoid and alpha 1-antitrypsin increased between three months and one month prior to the attack. There was a poor correlation of the parameters to each other. Further prospective studies are needed to determine the specificity of the suggested indices in predicting acute relapses of Crohn's disease.

Vitamin A therapy in patients with Crohn's disease.

Vitamin A therapy has been claimed in isolated reports to be of benefit to patients with Crohn's disease. To investigate this further, 86 patients were entered into a long-term double-blind study of vitamin A, 50,000 U twice daily, as compared with placebo. After a mean of 14.1 mo of treatment there was no significant difference between the groups as measured by a variety of activity indices (including the National Cooperative Crohn's Disease Activity Index), the number of acute attacks, and the surgical rate. No toxic effects of vitamin A were observed during the study. In this study vitamin A has not been shown to be of benefit to patients with Crohn's disease who are in remission.

In vitro enzyme activity of commercially available pancreatic enzyme extracts.

An in vitro study was performed to measure the enzyme activity in commerically available preparations of pancreatic enzyme extracts. Particular attention was paid to lipase content, because lipase deficiency is the most clinically relevant enzyme deficiency. Individual preparations varied greatly with regard to enzyme content, and Cotazym and Viokase proved the most effective preparations of those tested.