Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomized, prospective, crossing-over clinico-pharmacological study was conducted on the tolerability by humans, of TISACID (Al-Mg-hydroxy-carbonate), a new antacid of up-to-date composition produced in Hungary. Even a relatively high dose of the preparation is tolerated by the human organism. During a 6-week continuous treatment neither subjective nor objective side-effects were observed. The tablet is immediately decomposed in the gastric juice, a considerable portion of it will permanently stick to the mucosa of the stomach and duodenum. Depending on the dose, it rapidly and permanently reduces the acidity of the gastric content and increases serum gastrin concentration only moderately and for a short time. Administered together with cimetidine, it promotes healing of duodenal ulcer and the cessation of complaints. It does not increase the aluminium and magnesium concentrations of the plasma not even on prolonged administration, and clinical symptoms and laboratory changes characterizing the phosphate depletion syndrome do not develop either. Based on the results, authors consider Tisacid a beneficial preparation as regards both effectivity and tolerability.
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PMID:Human tolerability and pharmacodynamic study of Tisacid tablet in duodenal ulcer patients. A prospective, randomized, self-controlled clinicopharmacological study. 307 55

In healthy human volunteers, a single oral dose of enprostil (35 micrograms) inhibited basal gastric acid output by a mean of 71 percent, pentagastrin-stimulated output by 46 percent, sham-meal-stimulated output by 48 percent, and histamine-stimulated output by 16 percent. In each case, there was a reduction in both the volume and acidity of the gastric juice. Pepsin output was unchanged. Although enprostil increased the gastric pH, it did not induce basal or post-prandial hypergastrinemia. In patients with hypergastrinemia secondary to achlorhydria, enprostil lowered the basal gastrin level and reduced or abolished the post-prandial gastrin rise in a dose-related fashion. Enprostil reduces basal and stimulated gastric acid secretion and inhibits gastrin release.
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PMID:Effect of a single oral dose of enprostil on gastric secretion and gastrin release. Studies in healthy volunteers and patients with pernicious anemia. 309 53

Hypochlorhydria induced by potent antisecretory drugs is followed by a marked elevation of serum gastrin levels which leads to changes in ECL cell density in rats. "Soft" antiulcer drugs like prostaglandins do not increase gastrin levels. Their use in peptic ulcer disease seems to be mainly limited by a relatively high incidence of diarrhea and abdominal cramps. Rioprostil is a new prostaglandin E1 analogue. We compared the potency and duration of action of rioprosil 600 micrograms nocte with 300 micrograms bid on human gastric secretion in a placebo-controlled double-blind study. We further evaluated the clinical effectiveness of rioprostil 600 micrograms nocte in the acute treatment of duodenal ulcer. Nocturnal gastric acidity (24:00 to 08:00) was inhibited from 54.5 +/- 1.7 mmol H+/L (placebo experiments; n =9) to 26.7 +/- 3.5 mmol H+/L (52%) by rioprostil 300 micrograms bid (p less than 0.05) and to 14.4 +/- 3.8 mmol H+/L (74%) by rioprostil 600 micrograms nocte (p less than 0.05). During the daytime (09:00 to 18:00), H+ activity was reduced by 33% and 15% respectively (n.s.). Two hundred and three patients with endoscopically proven duodenal ulcers were randomly allocated to treatment with either rioprostil 600 micrograms nocte or ranitidine 300 mg nocte for 4 weeks in a prospective double-blind study. The two groups were similar. After 2 and 4 weeks treatment respectively, about 55% and 85% of patients healed on rioprostil 600 micrograms nocte and 55% and 90% on ranitidine 300 mg nocte. There were no differences between the treatment groups in ulcer pain relief.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandins and peptic ulcer disease: nocturnal administration of rioprostil vs ranitidine in duodenal ulcer healing. 310 57

This study compares the prophylactic effects of two different diets and routes of feeding on restraint stress-induced gastric erosions in the rat. Thirty male Sprague-Dawley rats were food-deprived and immobilized for 24 hours using a steel wire mesh. A small silicone tube was placed into either the proximal jejunum or the stomach via a laparotomy. There were three groups of ten rats (five jejunum-fed, five stomach-fed), receiving infusions (50 ml/24 h) of: (A) normal saline; (B) free amino acids (Vivonex HN, Norwich Eaton Pharmaceuticals) (60 cal and 0.318 G nitrogen); or (C) a peptide diet, with the nitrogen source as lactalbumin hydrolysate, otherwise identical to B. Gastric acidity was measured every 4 hours. At 24 hours, blood was collected and serum gastrin levels determined. The animals were then sacrificed and the stomachs examined. The results were analyzed using one-way analysis of variance. Fewer gastric erosions and lower serum gastrin levels and gastric acidity were found in animals fed diets B and C, versus animals fed normal saline (p less than 0.05). There was no difference between groups B and C. Our results also show that enteral diets using the jejunal route are better than those using the gastric route in reducing the incidence of stress-induced gastric erosions in rats.
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PMID:Efficacy of enteral diets in the prevention of stress-induced gastric erosions in rats. 310 49

Misoprostol, a synthetic prostaglandin E1 analog, has been found to be safe and effective for the treatment of peptic ulcer disease. This brief overview summarizes the gastric antisecretory effects of misoprostol in healthy human subjects using randomized, double-blind, placebo-controlled studies. Misoprostol effectively and dose-dependently inhibited basal gastric acid secretion at single doses of 50, 100 and 200 mcg/subject. Furthermore, misoprostol effectively inhibited meal-, histamine-, coffee- and tetragastrin-stimulated gastric acid secretion. The inhibition of meal-stimulated gastric acid secretion was not a consequence of the reduction of serum gastrin. In addition, misoprostol inhibited nocturnal gastric acid secretion. In these studies, the titratable acidity, volume, acid output and pepsin activity were inhibited by misoprostol. The extent of the secretory inhibition achieved with the 200 mcg dose of misoprostol was comparable to that of cimetidine administered at a 300 mg dose. The duration of the gastric antisecretory actions was in the order of 3 to 5 hours. We conclude that misoprostol is a potent inhibitor of gastric acid secretion in man.
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PMID:Perspective on the gastric antisecretory effects of misoprostol in man. 312 77

To assess the effect of malnutrition on gastric acidity and gastric bacterial colonization, we studied 35 severely malnourished Bangladeshi children before (0 wk) and after (3 wk) they received nutritional rehabilitation for 3 wk. These results were compared with those obtained from a similarly examined group of 20 better-nourished Bangladeshi children. Gastric acid output, both basal and after betazole stimulation, was significantly lower in the malnourished group at 0 wk compared with the better-nourished children (p less than 0.01): basal 0.22 vs. 0.52 mEq HCl/h and stimulated 0.90 vs. 2.5 mEq HCl/h. Both the concentration of acid and the rate at which gastric juice was secreted were decreased in the malnourished group but serum gastrin levels were not significantly different. After 3 wk, the malnourished children had improved from 61% (+/- 9.0%; SD) to 81% (+/- 8.1%) of expected weight-for-height and were not significantly different than the better-nourished group (86% +/- 11%). Nevertheless, gastric acid concentration remained depressed in the 3-wk group, although the rate of gastric juice secretion equaled levels observed in the better-nourished group. None of the better-nourished children had detectable gram-negative bacterial colonization of their gastric juice. In contrast, 26 of 32 (81%) malnourished children at 0 wk were colonized--even after betazole stimulation, 11 of 33 (33%) gastric juice samples yielded viable organisms--suggesting that the decrease in gastric acid output greatly reduced the gastric acid barrier. Interestingly, only 9 of 20 (45%) better-nourished children had gastric juice with basal pH values below 4.0, suggesting that the gastric acid barrier may be an intermittent defense factor in Bangladeshi children.
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PMID:Decreased gastric acid secretion and bacterial colonization of the stomach in severely malnourished Bangladeshi children. 312 29

The effects of 40 mg oral famotidine at 2115 h on 24-h intragastric acidity and plasma gastrin concentration were measured in a double-blind placebo-controlled study in 10 healthy subjects. The subjects were studied on the 7th day of treatment with either famotidine or placebo. Famotidine, 40 mg at night, caused a pulse of decreased intragastric acidity during the night, with a longer-lasting elevation of plasma gastrin concentration. However, in the latter part of the day there was complete recovery from the antisecretory effects of the drug, with normal intragastric acidity and normal concentrations of plasma gastrin.
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PMID:The effects of famotidine, 40 mg at night, on 24-hour intragastric acidity and plasma gastrin concentration in healthy subjects. 328 19

Omeprazole in doses of 20, 40 or 60 mg dose-dependently inhibits basal acid secretion in young healthy subjects, with almost complete inhibition by 60 mg. Omeprazole has also been shown to dose-dependently inhibit vagally stimulated and meal stimulated acid secretion. Pentagastrin stimulated acid secretion is strongly inhibited by omeprazole for 4-5 hours, with moderate inhibition remaining 24 hours after a single dose. The plasma half-life of omeprazole, however, is about 50 minutes. The inhibitory effect accumulates over the first few days of repeated administration, and the effect continues for at least 24 hours after the last dose. A relatively high dose of intravenous omeprazole is required to keep the gastric pH above 4 over the 24-hour period. Both basal and postprandial serum gastrin concentrations have been observed to increase during omeprazole treatment. These changes, however, are probably secondary to a pronounced reduction of intragastric acidity which relieves acid inhibition of gastrin release from the antrum.
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PMID:Effect of omeprazole on gastric acid secretion in man. 346 Jan 64

In a series of 59 experiments on nine duodenal ulcer patients, 24-hour intragastric acidity was measured before, during and after treatment with daily oral omeprazole. Omeprazole, 10, 20, ro 30 mg/day for 1 week, caused a 37%, 90%, and 97% decrease respectively of 24-hour intragastric acidity. No further decrease of acidity was observed when the dose of omeprazole was doubled to 60 mg/day, or after a second week of treatment with 30 mg/day. One week after stopping treatment with omeprazole (14 doses), there was still a significant 26% decrease of 24-hour intragastric acidity, with full recovery 7 weeks later. Fasting plasma gastrin concentration was significantly elevated during treatment with all doses of omeprazole. The optimal dose of omeprazole is 30 mg/day for a maximal decrease of 24-hour intragastric acidity in duodenal ulcer patients.
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PMID:Twenty-four hour intragastric acidity during treatment with oral omeprazole. 346 Jan 65

In this double-blind cross-over study the effect of trimoprostil (trimethyldesoxyprostaglandin E2), an orally effective prostaglandin E2 analogue, on 24-h intragastric H+-activity, nocturnal acid output, nocturnal volume secretion and meal stimulated gastrin secretion was determined in 12 healthy male volunteers. On three different days the subjects received four times a day either placebo or 1.5 mg trimoprostil 30 min before or 30 min after meals. Trimoprostil administered before or after meals reduced 24-h intragastric acidity by 27.0 and 53.9%. Nocturnal acid output was inhibited by 32.7 and 55.6%. Nocturnal volume secretion and meal stimulated gastrin secretion remained unaffected. The study shows that the antisecretory activity is significantly increased when trimoprostil is given after meals.
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PMID:[Intragastric acidity under the prostaglandin E2 analog trimoprostil. Increased inhibitory effect through administration after meals]. 351 30


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