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Biomedical subjects

J I Isenberg

Publications and source records attributed to J I Isenberg.

At least 91 records · Page 5Linked to original sources
PubMed1983

Healing of benign gastric ulcer with low-dose antacid or cimetidine. A double-blind, randomized, placebo-controlled trial.

We conducted a 12-week, double-blind, randomized, placebo-controlled trial to determine whether cimetidine (300 mg with meals and at bedtime) or a convenient, liquid aluminum-magnesium antacid regimen (15 ml one hour after meals and at bedtime) would expedite healing or relief of symptoms in patients with benign gastric ulcer. Of the 101 patients who completed the trial according to protocol, 32 received the antacid, 36 cimetidine, and 33 placebo. At 4, 8, and 12 weeks after entry, ulcers had healed in a larger percentage of patients treated with cimetidine than of those treated with placebo: 53, 86, and 89 per cent of the cimetidine group versus 26, 58, and 70 per cent of the placebo group (P = 0.02, 0.01, 0.05), respectively. Healing at the three intervals had occurred in 38, 70, and 84 per cent, respectively, of the antacid-treated patients. Neither cimetidine nor antacid was more effective than placebo in relieving symptoms. The presence or absence of symptoms during the fourth and eighth treatment weeks was a poor predictor of the presence of absence of an ulcer crater. We conclude that cimetidine significantly hastens the healing of benign gastric ulcer.

Adult↗
PubMed1983

Comparison of the serial dilution indicator and intragastric titration methods for measurement of meal-stimulated gastric acid secretion in man.

Two in vivo methods that permit quantitation of gastric acid secretion immediately after the meal are currently in use: intragastric titration and the serial dilution indicator method. During intragastric titration, intragastric pH is artificially maintained at 5.5 to 7 by the continuous addition of alkali to the gastric contents, while during serial dilution the intragastric pH is permitted to seek its natural pH. This study compared gastric acid secretion and serum gastrin in response to a liquid protein meal measured by both techniques in 10 subjects. Mean (+/- SE) 3-hr acid outputs were almost identical (53.6 +/- 6.0 mmol/3 hr with intragastric titration and 52.0 +/- 8.5 mmol/3 hr with serial dilution indicator). Furthermore, 30 min secretory responses in individual subjects were highly correlated (r = 0.98 +/- 0.01, P less than 0.001). Also, in spite of intragastric pH being less than 1.5 by 90 min after the meal during the serial dilution method, total integrated serum gastrin concentrations after the meal were similar (intragastric titration = 20.6 +/- 7.3 ng min/ml versus serial dilution indicator = 23.5 +/- 9.8 ng min/ml) and individual 30-min gastrins during the two separate tests were highly correlated (r = 0.80 +/- 0.06, P less than 0.01). It is concluded that both meal-stimulated gastric acid secretion and serum gastrin concentrations as measured by intragastric titration and by the serial dilution indicator method produced similar results.

Dietary Proteins↗
PubMed1983

Midazolam, a new more potent benzodiazepine, compared with diazepam: a randomized, double-blind study of preendoscopic sedatives.

Midazolam is a new imidazobenzodiazepine. It is more potent and has a shorter duration of action than diazepam. Forty patients undergoing upper gastrointestinal endoscopy for the first time were randomized to receive either diazepam or midazolam as the preendoscopic sedative agent. Both the patient and the endoscopist were blinded regarding the treatment group. Vital signs were monitored before, during, and after induction. Questionnaires were used to assess patient recall of the procedure, as well as endoscopist and patient satisfaction. Recovery from sedation was assessed using the Treiger test (i.e., connecting a series of sequential points with a line). Twenty-four hours and 1 to 2 weeks later, follow-up was obtained on all patients to evaluate for any delayed adverse effects. When compared to diazepam, midazolam was more potent and decreased induction time by more than 2.5 min (p less than 0.001). Recovery time and endoscopist and patient satisfaction were similar (p greater than 0.1), but patient recall was significantly less in the midazolam group (p less than 0.01). Fewer adverse reactions (e.g., thrombophlebitis) were noted with midazolam; however, the magnitude of the difference was not statistically significant. Hemodynamic parameters were also similar. It is concluded that midazolam is a safe, effective, and promptly acting sedative for upper gastrointestinal endoscopy. Compared to diazepam it was significantly more potent, faster acting, and associated with greater amnesia.

Adolescent↗
PubMed1983

Intravenous infusion of L-isomers of phenylalanine and tryptophan stimulate gastric acid secretion at physiologic plasma concentrations in normal subjects and after parietal cell vagotomy.

To determine whether intravenous infusion of individual amino acids stimulated gastric acid secretion in man, graded doses of phenylalanine, tryptophan, glycine, alanine, histidine, and NaCl control were infused on separate days in nine healthy subjects. Intravenous infusion of phenylalanine and tryptophan significantly stimulated gastric acid secretion to 50 and 52%, respectively, of the acid secretory response to intragastric peptone. Intravenous alanine and histidine were without effect, whereas glycine produced a slight response. Serum gastrin concentrations did not significantly change during intravenous amino acid infusion, except in response to 0.1 M phenylalanine. However, the increase in serum gastrin occurred 2 h after acid secretion had significantly increased in response to the 0.025 M phenylalanine infusion. Plasma amino acid concentrations were measured during intravenous amino acid infusion and in response to a steak meal in five of the subjects. At a time when acid secretion was significantly increased during intravenous infusion of phenylalanine and tryptophan, plasma amino acids were similar to, or less than, that observed after the steak meal, suggesting that circulating levels of these three amino acids have a physiologic effect on gastric secretion in man. Intravenous infusion of a combination of graded doses of phenylalanine plus a continuous infusion of 0.01 M tryptophan shifted the dose-response curve to the left and resulted in a significantly greater response than to either amino acid alone. In five subjects with parietal cell vagotomy, intravenous phenylalanine and tryptophan stimulated acid secretion, whereas histidine was without effect, similar to normal subjects. These studies indicate that intravenous infusion of small amounts of phenylalanine (0.025 M, 3.1 mmol/h) and tryptophan (0.01 M, 1.25 mmol/h) stimulated gastric acid secretion at plasma concentrations similar to those observed after a steak meal, suggesting a physiologic role for circulating levels of these amino acids on gastric acid secretion. Because acid secretion increased at a time when serum gastrin was unchanged and since there was no correlation between changes in serum gastrin and acid secretion, the responses to phenylalanine and tryptophan are probably mediated by a nongastrin-related mechanism(s). Since both phenylalanine and tryptophan stimulated secretion in vagotomized subjects, the response is vagally independent. These observations suggest that circulating levels of these two amino acids have either a direct or indirect effect on or near the human parietal cell.

Amino Acids↗
PubMed1983

Wine and five percent ethanol are potent stimulants of gastric acid secretion in humans.

Previous studies reported that intragastric ethanol was not a stimulus of gastric acid secretion in humans. The effect of 240 ml of 5%, 10%, and 20% ethanol (vol/vol), equicaloric-equiosmolar control solutions, white wine (12% ethanol), bourbon whiskey (1:4 dilution with water, 10% ethanol), and water on gastric acid secretion and serum gastrin concentrations were evaluated in 8 healthy subjects. Also, to stimulate the before-meal cocktail, white wine, whiskey, or water was administered 30 min before a 50-g liquid protein meal. Five percent ethanol and white wine significantly (p less than 0.01) increased basal secretion to 58% and 82%, respectively, of the peak pentagastrin response (24.2 +/- 1.6 mmol/h). After each of the 5%, 10%, and 20% ethanol solutions, 3-h acid outputs were significantly greater than their respective equicaloric-equiosmolar controls, but only the responses to 5% and 10% ethanol were significantly greater than water alone. Total 3-h responses to white wine, 5% ethanol, and 10% whiskey, respectively, were 5, 4.5, and 2 times greater than water (p less than 0.05). Although serum gastrin was not altered by any of the ethanol solutions or bourbon whiskey, white wine significantly increases serum gastrin concentration, similar to the 50-g protein meal. These results indicate that 5% ethanol and 10% bourbon whiskey increase gastric acid secretion by a mechanism other than gastrin release. White wine markedly stimulates both an increase in acid secretion and serum gastrin concentration. The constituent(s) in wine responsible for the marked acid secretory and gastrin response is unknown.

Adult↗
PubMed1982

Rapid gastric emptying in duodenal ulcer patients.

Isosmotic liquid peptone meals adjusted to pH 7, 3, and 1.5 were instilled on separate days into the stomachs of 8 duodenal ulcer patients and 7 healthy controls. Using a marker-dilution method, duodenal acid load (DAL) was measured as the amount of unbuffered hydrogen ions delivered to the duodenum per unit time. Gastric emptying was measured as the total volume of gastric contents, including meal plus gastric secretion, passing through the pylorus per unit time (VPP). Mean pentagastrin-stimulated acid output was significantly different between the two groups. However, after all three tests meals, mean DAL was significantly greater in duodenal ulcer than in normal subjects in both hours of the test, and VPP was significantly greater in ulcer than in normal subjects in the first 40 min. In both groups, following peptone meals of pH 7 and 3, the volume of gastric contents delivered through the pylorus decreased as the amount of free hydrogen ions entering the duodenum increased, but a given load of acid was less effective in slowing emptying duodenal ulcer patients than in controls. These studies indicate that duodenal ulcer patients empty liquid meals more rapidly than do normal subjects, independent of the initial pH of the meals, and that, in addition, acid inhibition of gastric emptying is defective in duodenal ulcer.

Adult↗
PubMed1982

Most patients with active symptomatic duodenal ulcers fail to develop ulcer-type pain in response to gastroduodenal acidification.

The most frequent symptom of duodenal ulcer is epigastric pain. However, the pathogenesis of duodenal ulcer pain is not established, although it is often attributed to duodenal acidification. The purpose of this study was to determine whether or not gastroduodenal acidification with either 400 ml of pH 1 citric acid or pH 0.85 hydrochloric acid resulted in ulcer-type pain in patients with endoscopically documented active symptomatic duodenal ulcer under doubled-blind randomized conditions. Thirteen consecutive male duodenal ulcer patients with daytime and nocturnal epigastric pain were studied before beginning medical therapy; five with citric acid or sodium citrate at pH's 1, 3, and 7, and eight with hydrochloric acid at pH 0.85 and pH 7 sodium citrate. Ten normal subjects served as controls. Four of the five symptomatic duodenal ulcer patients failed to have pain with the pH 1 citric acid, while one developed pain. Five of the eight patients tested with 0.15 mM hydrochloric acid had no pain. Of the three who developed pain with hydrochloric acid, two had endoscopic evidence of esophagitis (one developed retrosternal pain and one both retrosternal and epigastric pain), and one had the sensation of epigastric "fullness" with both the pH 0.85 and pH 7 solutions. There were no significant differences (p greater than 0.1) between the responses of the duodenal ulcer and normal subjects nor within the duodenal ulcer group in response to the pH 0.85 or 1.0 solutions versus the pH 7 solution. In summary, gastric acidification equivalent to 80 mmol/hour failed to induce pain in most patients with active symptomatic duodenal ulcer. These observations suggest that duodenal ulcer pain is largely unrelated to duodenal acidification.

Adult↗
PubMed1982

Treatment of hemorrhagic gastritis with 15(R)-15 methyl prostaglandin E2: report of a case.

A 19-yr-old male developed severe hemorrhagic gastritis following three abdominal operations. Treatment with intravenous cimetidine and hourly antacids to maintain his gastric pH above 5 failed to affect gastrointestinal bleeding. Also, peripheral venous vasopressin, propantheline bromide, and glucagon were without effect. Total gastrectomy was considered to control his bleeding. However, since a number of prostaglandin analogs prevent gastric lesions produced by many noxious agents (e.g., aspirin, alcohol, strong acid or alkali, etc.) in animals and humans, the patient was treated with 50 micrograms of 15(R)-15 methyl prostaglandin E2 intragastrically every 6 h for 10 days. To epimerize the 15(R) form to the more active 15(S) form, 50-100 ml of 50-mN HCl was placed into the patient's stomach immediately before each dose. Bleeding ceased within 24 h of the onset of 15(R)-15 methyl prostaglandin E2 therapy and did not recur. The prompt response to 15(R)-15 methyl prostaglandin E2 in combination with hourly antacids in this patient with persistent and severe hemorrhagic gastritis suggests a therapeutic effect and the need for a prospective double-blind clinical trial.

Abdomen↗
PubMed1982

Patient acceptance and effectiveness of a balanced lavage solution (Golytely) versus the standard preparation for colonoscopy.

An oral electrolyte solution containing 125 mM/L sodium, 10 mM/L potassium, 80 mM/L sulfate, 20 mM/L bicarbonate, and 80 mM/L of polyethylene glycol, and associated with little water or electrolyte absorption from the gut was recently described in this journal. To determine the efficacy of this solution (Golytely) for colonoscopy, 20 consecutive patients were randomized to either a standard colonoscopy prep or Golytely. Both preps resulted in a feces-free colon, allowing colonoscopy to the cecum in most cases. Although Golytely produced mild cramps (3 of 12) and transient fullness (6 of 12 vs. 0 of 8 with standard prep, p less than 0.02), 11 of 12 were willing to repeat Golytely vs. 3 of 8 with the standard prep (p less than 0.02). It is concluded that Golytely is an effective prep for colonoscopy and well tolerated by patients. It is especially useful for those requiring repeated examinations because of patient acceptance and efficacy.

Adult↗
PubMed1981

Gastric acid and gastrin response to decaffeinated coffee and a peptone meal.

We compared five graded doses of decaffeinated coffee and a widely used protein test meal (Bacto-peptone) as stimulants of acid secretion (intragastric titration) and gastrin release (radioimmunoassay) in eight healthy men. In each subject, for both acid and gastrin, the sums of the responses to all five doses were greater to decaffeinated coffee than to peptone. The mean +/- SE peak acid output in millimoles per hour was 18.5 +/- 2.9 to decaffeinated coffee and 14.7 +/- 2.7 to peptone, representing 70% and 55%, respectively, of the peak acid output to pentagastrin. The mean +/- SEM peak increment over basal rate in serum gastrin in picograms per milliliter was 84.8 +/- 4.4 to decaffeinated coffee and 44.8 +/- 2.1 to peptone. At equal concentrations, decaffeinated coffee was a more potent stimulant of acid secretion and of gastrin release than peptone. The ingredient(s) of decaffeinated coffee that accounts for its high potency in stimulating acid secretion and gastrin release has not been identified.

Adult↗
PubMed1981

Peptic ulcer.

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Anti-Ulcer Agents↗
PubMed1981

Effect of oral and intravenous 16,16-dimethyl prostaglandin E2 in duodenal ulcer and Zollinger-Ellison syndrome patients.

Oral 16,16-dimethyl prostaglandin E2 is a potent inhibitor of meal-stimulated gastric acid secretion and gastrin release in humans. Experiments were performed in 5 patients with inactive duodenal ulcer to determine the effect of graded doses of intravenous 16,16-dimethyl PGE2 on meal-stimulated gastric acid secretion and gastrin release to demonstrate whether it is necessary for 16-16-dimethyl PGE2 to come into direct luminal contact with the oxyntic and antral gland portions of the stomach to produce its inhibitory effects. All doses of 16,16-dimethyl PGE2, between 0.01 and 0.1 microgram/kg i.v. and between 0.01 and 1.0 microgram/kg orally produced significant postprandial inhibitory effects on both gastric acid secretion and gastrin release as compared with saline control. 0.1 microgram/kg of intravenous of 1 microgram/kg of oral 16,16-dimethyl PGE2 inhibited meal-stimulated acid secretion and gastrin by 80-90%. In 6 unoperated Zollinger-Ellison syndrome patients, 1 microgram/kg of oral 16,16-dimethyl PGE2 significantly inhibited fasting gastric acid hypersecretion by approximately 85% without significantly altering serum gastrin. Each of the oral doses of 16,16-dimethyl PGE2 (0.01-1 microgram/kg) were without untoward effect, as were intravenous doses of 0.01-01 microgram/kg. Maximal inhibition of acid secretion was found with 0.1 microgram/kg 16,16-dimethyl PGE2 i.v. as compared with 1.0 microgram/kg orally. Since 16,16-dimethyl PGE2, whether given orally or intravenously, is a potent inhibitor of both gastric acid secretion and meal-stimulated gastrin release, without apparent untoward side effects, clinical trials with 16,16-dimethyl PGE2 are indicated in patients with acid peptic disease.

16,16-Dimethylprostaglandin E2↗
PubMed1980

Gastric acid secretion is abnormally sensitive to endogenous gastrin released after peptone test meals in duodenal ulcer patients.

We studied 25 duodenal ulcer patients and 14 age- and sex-matched normal controls to determine whether gastric acid secretion in duodenal ulcer patients is abnormally sensitive to stimulation by gastrin endogenously released in response to meals. Acid response to saline and to 0.5, 1.0, 2.0, 4.0, and 8.0% peptone infused into the stomach was measured by 30 min intragastric titration. Total serum gastrin (G-total) and serum heptadecapeptide gastrin (G17), fasting and 30 min after each test meal, were measured by specific radioimmunoassays. In 19 ulcer patients and 11 normal subjects (controls), acid response to graded doses (11, 33, 100, and 300 pmol kg(-1) h(-1)) of G17-I were also measured. Mean acid output in response to each dose of peptone was significantly higher in duodenal ulcer patients than in the controls. Gastrin levels in ulcer patients and controls were not significantly different. Within individual patients and controls, both G-total and G17 were significantly correlated with meal-stimulated acid output regardless of whether the absolute, basal-corrected, or distention-corrected values for acid output were examined (median r ranged from 0.82 to 0.94, P < 0.001). From the individual regression lines, the gastrin concentrations corresponding to half of the highest observed meal-stimulated acid response (D(50m)) were calculated. Mean D(50m) for G-total and G17 were significantly lower in duodenal ulcer patients than in controls both in the overall group and in pairs of ulcer patients and controls matched on the basis of highest observed meal-stimulated acid responses, or on the basis of maximal acid output in response to synthetic human G17. The dose of exogenously administered G17 required for half maximal G17 acid response mean D(50g), was significantly less in patients than in control subjects. In both ulcer and control subjects, D(50g) correlated significantly with D(50m). This and the significant correlation between meal-stimulated G17 and acid response strongly suggest that the endogenously released gastrin was responsible for most, if not all, of the postpeptone acid output.We conclude that after peptone test meals, gastric acid secretion in duodenal ulcer patients was abnormally sensitive to stimulation by endogenously released gastrin.

Adult↗