Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lower esophageal sphincter pressure, basal gastric pH, fasting plasma gastrin, and plasma concentrations of estrone, estradiol, and progesterone were measured in pregnant volunteers at 12, 24, and 36 weeks of gestation, and again at 1 to 4 weeks postpartum. In addition, basal and pentagastrin-stimulated acid secretory responses at each time were measured. No differences in basal gastric pH, basal, and peak acid outputs were observed during pregnancy when compared to the postpartum values. In contrast, lower esophageal sphincter pressure was reduced at all times during pregnancy, reaching a nadir at 36 weeks. Postpartum lower esophageal pressures were normal. As expected, plasma concentrations of progesterone and both estrogens increased progressively during pregnancy. These data are consistent with earlier studies in women ingesting oral contraceptives. Moreover, they provide support for the thesis that the progressive increase in plasma progesterone alone or in combination with estrogens that occurs during pregnancy is responsible for the reduction of lower esophageal sphincter pressure which allows esophageal reflux to occur with the resultant development of symptomatic heartburn.
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PMID:Heartburn of pregnancy. 1 50

Lower esophageal sphincter pressure (LESP) was measured in 10 biopsy-proved cirrhotics with esophageal varices and tense ascites before and after diuresis to evaluate of ascites might play in the development of variceal bleeding. In the 10 cirrhotic men studied, basal LESP was 30.9 +/- 1.7 mm Hg before and 22.7 +/- 1.3 mm Hg (P less than 0.01) after a diuresis which resulted in a mean 12-kg weight loss. LESP responses to abdominal compression were also evaluated. The change in LESP in response to a standard degree of abdominal compression was greater in the presence of ascites (8.5 +/- 0.4) than in its absence (6.3 +/- 0.4) (P less than 0.01). Basal gastric pH and fasting plasma gastrin concentrations did not differ during the two testing periods. Based on these data and the rarity with which cirrhotic patients with ascites complain of heartburn, it is concluded that reflux esophagitis caused by failure of the lower esophageal sphincter to remain competent is unlikely to be a significant etiological factor in the development of variceal bleeding.
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PMID:Lower esophageal sphincter pressure in cirrhotic men with ascites: before and after diuresis. 1 65

To determine the effect of estrogenic and progesteronic activity on lower esophageal sphincter (LES) circular muscle, studies were performed on 20 adult opossums. Does-response curves on circular smooth muscle strips from the LES were constructed for gastrin and acetylcholine alone, and with 17beta-estradiol and/or progesterone added. Each female hormone significantly decreased the maximal LES muscle responses to gastrin and acetylcholine. A combination of 17beta-estradiol and progesterone abolished the response to gastrin. In contrast, the male sex hormone, dihydrotestosterone, had no effect. In conclusion, administration of estrogen and progesteron, but not dihydrotestosterone, in vitro reduced LES muscle responses to gastrin and acetylcholine. These studies suggest that the female sex hormones can alter LES function and potentially may be of importance in the pathogenesis of heartburn of pregnancy.
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PMID:Inhibition of lower esophageal sphincter circular muscle by female sex hormones. 62 38

Lower oesophageal sphincter pressure and fasting plasma gastrin and progesterone were measured in 31 women in the last trimester of pregnancy and in 10 healthy female control subjects. Eighteen of the pregnant women suffered from heartburn but 13 did not. All of the control subjects and 10 women from each of the two pregnant groups were tested for gastro--oesophageal reflux by direct measurement of intraluminal pH. The mean barrier pressure of the lower oesophageal sphincter was lower in both groups of pregnant women than in the controls (P less than 0-05) and the mean barrier pressure of the women with heartburn was lower than that of the pregnant women without heartburn, though this difference did not reach statistical significance. Eight of 10 of the pregnant women with heartburn had moderate or severe reflux, and3 of 10 of the pregnant women without heartburn also had moderate or severe reflux. Most women who reflux have heartburn, nevertheless, some asymptomatic women also reflux, and therefore all pregnant women must be considerered at risk from Mendelson's syndrome if subjected to a general anaesthetic for an emergency obstetric procedure.
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PMID:Gastro--oesophageal reflux in late pregnancy. 87 Nov 99

Lower esophageal sphincter pressure, basal gastric pH, and fasting plasma gastrin were measured sequentially in female volunteers who were using oral contraceptives. No difference in basal gastric pH or fasting plasma gastrin was observed during any of the three selected periods studied. Lower esophageal sphincter pressure was the same during menses (20.8 +/- 1.7) when the volunteers took no medication during the phase of the cycle when the volunteers were ingesting ethinylestradiol (18.3 +/- 1.7). Lower esophageal sphincter pressure decreased significantly (P less than 0.01) to 9.4 +/- 1.2 during the phase of the cycle when the volunteer took the progestation agent, dimethisterone, as well as ethinylestradiol. It is therefore proposed that the progessive rise in plasma progesterone alone or in combination with estrogens that occurs during the course of pregnancy might be responsible for the increased incidence of symptomatic heartburn in pregnant women.
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PMID:Lower esophageal sphincter pressure in women using sequential oral contraceptives. 93 83

Current concepts in physiology and pathophysiology of lower esophageal sphincteric mechanism are reviewed. With recent advances in manometric method for more accurate in-vivo human studies combined with in-vivo and in-vitro studies in animal models, there is much information regarding function of this sphincter. Three components of sphincter control have been identified: specialized circular smooth muscle at esophagogastric junction, autonomic nervous system, and probable physiology effects of gastrointestinal hormones, particularly gastrin. Clinical syndromes of sphincteric dysfunction have been identified relative to these three controlling elements. Foods and drugs that adversely effect sphincter pressure have been identified and indicate that anticholinergic agents, fatty foods, chocolate, alcohol, and cigarette smoking may have a harmful effect on a patient with heartburn. Drugs that increase the antireflux sphincter barrier have been studied. Clinical effectiveness of antacids and bethanechol in therapy of heartburn is supported by controlled treatment trials. Research continues on other medications producing increases in sphincter pressure.
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PMID:The lower esophageal sphincter. Physiologic and clinical aspects. 123 15

Secretion of gastric acid and volume, serum gastrin concentration, and ambulatory 24-hr esophageal pH monitoring were evaluated prospectively in 12 patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) undergoing treatment for refractory chronic long-standing pyrosis. Treatment lasted six months and consisted of three months of ranitidine (mean 2150 mg/day, range 1200-3000 mg/day), followed by three months of omeprazole (mean 33 mg/day, range 20-60 mg/day). Both ranitidine and omeprazole significantly reduced gastric acid output (P less than 0.001) and gastric volume output (P less than 0.001) compared to a basal evaluation and resulted in complete disappearance of pyrosis. Total reflux time (percent 24 hr intraesophageal pH less than 4) was significantly reduced by ranitidine (P less than 0.02) and omeprazole (P less than 0.001) compared to basal evaluation; however, the effects of omeprazole were significantly greater than ranitidine (P less than 0.05). Omeprazole caused a significant increase in serum gastrin concentration compared to both basal and ranitidine (P less than 0.05). Endoscopically documented erosive esophagitis was present in nine of the 12 patients, and seven of the 12 patients had Barrett's epithelium. All 12 patients had complete resolution of pyrosis and healed esophagitis by six months, but no significant endoscopic regression was observed in the extent of Barrett's epithelium. No side effects occurred with these high doses of ranitidine or omeprazole. These results indicate that high-dose ranitidine and omeprazole are effective therapy for refractory gastroesophageal reflux disease. However, with omeprazole, total reflux times are reduced more than with ranitidine, often into the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of omeprazole and ranitidine in treatment of refractory gastroesophageal reflux disease in patients with gastric acid hypersecretion. 158 94

Ninety-eight patients (26 females), who presented with erosive and/or ulcerative oesophagitis, despite at least a 3-month period of treatment with standard doses of cimetidine (greater than or equal to 1200 mg daily) or ranitidine (greater than or equal to 300 mg daily), were included in a double-blind, randomized trial to compare omeprazole (40 mg o.m.) with a high dose of ranitidine (300 mg b.d.). The treatment was given for 4-12 weeks; endoscopy assessment and laboratory screening were performed on entry to the trial and thereafter every fourth week. Endoscopic healing was defined as complete epithelialization of all macroscopic erosions or ulcers in the squamous epithelium. An 'intention-to-treat' analysis of the clinical data revealed omeprazole to be superior to ranitidine: 63% of those patients who were given omeprazole were healed endoscopically after a 4-week period of treatment, compared with only 17% of those given ranitidine. This difference in healing rate persisted during the 12-week study period (90% vs 47% after 12 weeks; P less than 0.0001). Reflux symptoms were more rapidly and completely relieved with omeprazole: heartburn resolved completely in 86% of patients treated with omeprazole for 4 weeks compared with 32% in the ranitidine group (P less than 0.0001). The mean basal gastrin concentrations increased only in those given omeprazole from 18.9 pmol/L at pre-entry to a mean value of 31.7 pmol/L on the last day of omeprazole administration. In ranitidine-treated patients no significant increase in basal gastrin concentration was observed. Both drugs were well tolerated with few adverse events, which were mainly mild and transient. These results demonstrate the superiority of omeprazole over a high dose of ranitidine in the treatment of resistant reflux oesophagitis.
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PMID:Omeprazole or high-dose ranitidine in the treatment of patients with reflux oesophagitis not responding to 'standard doses' of H2-receptor antagonists. 198 21

A 51 year-old woman with vomitus, intermittent epigastric pain and heartburn had chronic sideropenic anemia. Gastroscopy revealed a subcardial, submucosal tumor. The tumor was removed totally by endoscopic polypectomy. Histologically it was identified as a carcinoid. The endocrinologic examination showed hypergastrinemia caused by chronic atrophic gastritis. The association of this gastric carcinoid with chronic atrophic gastritis type A, hypergastrinemia, hyperplasia of the gastrin-producing antral cells and micronodular hyperplasia of endocrine cells in the gastric fundus, confirms the hypothesis about the pathogenesis of these extremely rare gastric tumors.
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PMID:[Gastric carcinoid in chronic atrophic gastritis with hypergastrinemia]. 203 30

In 42 patients (25 men, 17 women, mean age 62 years) with severe erosive or ulcerative oesophagitis not responding to H2-receptor antagonist treatment over at least 3 months and ineligible for surgery, omeprazole was administered at an initial dose of 40 mg/day, subsequently reduced to 20 mg after healing of the lesions. Patients had monthly clinical, endoscopic, histological and laboratory assessment over the healing period, then were reevaluated 3-monthly over one year, then 6-monthly, during the maintenance treatment. Stages of oesophagitis were based on the Savary-Miller classification, modified for stage I (erosions must be present). With 40 mg omeprazole, healing was observed in 71%, 83% and 90% of the patients after 1, 2 and 3 months of treatment, respectively. After one month of treatment, a complete healing was less frequently observed in patients with stage IV oesophagitis pre-trial (55%) than in the patients with stages I, II and III pre-trial (90%) (p less than 0.05). Ninety per cent of the patients healed at one month were asymptomatic whereas 50% of the patients with incomplete healing still had symptoms, most often dysphagia, rarely heartburn. Maintenance treatment with 20 mg was sufficient in most patients, with a probability of remaining healed of 69% from 9 to 24 months after starting this dosage. In 9 patients with Barrett's oesophagus, the lengths of the circumferential metaplasia were found to be reduced after one year of treatment compared to pre-trial lengths (p less than 0.005). There was no further significant reduction of length after 2 years of treatment. Fasting gastrin was increased in most of the patients, although great inter-patient variability was observed; 50% of the patients had levels not exceeding 5 times the upper limit of normal. There was no consistent increase of enterochromaffin-like cell density in 29 patients investigated up to nearly 2 years of omeprazole administration. The treatment was well tolerated. By inducing a profound and sustained inhibition of acid secretion, as confirmed by pH monitoring, omeprazole promotes healing of the lesions of severe oesophagitis and prevents recurrence of lesions and symptoms. Omeprazole is therefore a valuable treatment for patients ineligible for surgery, particularly in the elderly.
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PMID:Omeprazole in the treatment of patients with severe reflux oesophagitis not responding to H2-receptor antagonists and ineligible for surgery. 213 May 87


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