["Watermelon" in the stomach is an overlooked diagnosis. A treatable cause of gastrointestinal hemorrhage].
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Adult↗
Biomedical subjects
R Seensalu
Publications and source records attributed to R Seensalu.
Effects of omeprazole and amoxycillin on the human oral and gastrointestinal microflora in patients with Helicobacter pylori infection.
Fourteen patients with Helicobacter pylori infection were treated with omeprazole capsules 20 mg and amoxycillin capsules 1000 mg twice daily for 14 days and 14 patients with omeprazole capsules 20 mg and placebo twice daily for 14 days. Samples from saliva, dental plaque and faeces and biopsies from antrum and corpus were analysed in order to determine the ecological changes in the normal microflora. Several microorganisms were affected by both treatment regimens. Two patients were colonised with enterobacteria in the oral cavity and stomach during the omeprazole plus amoxycillin treatment. A general increase in the number of microorganisms from gastric mucosa was observed in both treatment groups. A selection of resistant enterobacteria and an increase in beta-lactamase production was observed in the faecal samples during the omeprazole plus amoxycillin treatment. Eradication of H. pylori in the omeprazole-amoxycillin group was 50% and in the omeprazole placebo group 0% four weeks after treatment. No viable H. pylori were cultivated in the saliva, dental plaque or faecal samples. Treatment with omeprazole 20 mg and amoxycillin 1000 mg twice daily for 14 days altered the normal microflora in the oral, gastric and intestinal tract and antibiotic resistant microorganisms increased in numbers in the intestinal microflora.
Adult↗
Adenocarcinoid of the liver arising within an area of hamartoma with predominant bile duct component.
Malignant transformation in bile duct hamartomas has been previously reported in very rare instances. Here, we describe a unique case of a neuroendocrine tumor of the liver arising within an area of unusually large hamartoma with predominant bile duct component, hitherto unreported and distinct from the conventional von Meyenburg complex. The tumor was apparently secreting gastrin and chromogranin, with associated gastrinoma syndrome over several years. The histologic picture was reminiscent of a moderately differentiated adenocarcinoid, with positive mucin staining in a signet ring pattern. Tumor cells showed positive staining for neuron-specific enolase, chromogranin A, gastrin, and serotonin. Staining for pancreatic hormone peptides was negative. Resection of the tumor was apparently curative, with complete resolution of the patient's symptoms.
Bile Duct Diseases↗
[Simple and painless for the patient with stomach ulcer. Blow and reveal the bacteria!].
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Breath Tests↗
Interphenotype differences in disposition and effect on gastrin levels of omeprazole--suitability of omeprazole as a probe for CYP2C19.
1. Fourteen healthy Swedish Caucasian subjects were given 20 mg of omeprazole orally each morning for 8 days. The subjects included five poor metabolisers (PM) of S-mephenytoin, four heterozygous extensive metabolisers (hetEM) and five subjects with a very rapid metabolism (rapidEM). 2. After the first dose, the relative mean areas under the plasma concentration vs time curve (AUC) of omeprazole in rapidEM, hetEM and PM were 1:3.7:20 (all different, P < 0.001). A similar relation was seen in the AUC(0,10 h) of the sulphone metabolite (1:3:12). Concentrations of hydroxyomeprazole were higher in EM than in PM confirming that the hydroxy, but not the sulphone metabolite, is formed by the S-mephenytoin hydroxylase (CYP2C19). After 8 days of treatment, the differences between groups were similar. 3. After both the first and the eighth doses, the omeprazole/hydroxyomeprazole plasma concentration ratio, determined 3 h after drug intake, correlated with the mephenytoin S/R ratio (rs = 0.94; P < 0.001; n = 14) suggesting that omeprazole might be used to phenotype for CYP2C19. 4. After the first dose of omeprazole, there was no difference in the AUC(0,10 h) of plasma gastrin between the three groups. From the first to the eighth dose, the AUC(0,10) of gastrin increased significantly in both hetEM and PM, while there was no change in the rapidEM. After the eighth dose, the AUC(0,10) of gastrin correlated significantly with the AUC of omeprazole in plasma (rs = 0.79; P < 0.01; n = 13).
2-Pyridinylmethylsulfinylbenzimidazoles↗
[Indications for therapy against Helicobacter pylori].
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Anti-Bacterial Agents↗
[Enteroscopy. A new method makes endoscopy of the entire small intestine possible].
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Endoscopes, Gastrointestinal↗
Effects of H1-receptor antagonists on 14C-aminopyrine accumulated in histamine-stimulated rabbit gastric glands.
After stimulation of gastric acid production there is a considerable delay before the acid starts to appear in the gastric lumen. The present study was carried out on isolated gastric glands to test the hypothesis that there may be a mechanism in the parietal cell that contributes to this delay by preventing emptying of the secretory canaliculi. Glands were incubated with 14C-aminopyrine and stimulated with histamine. After accumulation of 14C-aminopyrine various concentrations of H1-receptor antagonists were added. Clemastine, promethazine, and hydroxyzine effectively and cetirizine and tripelennamine less effectively decreased the accumulated 14C-aminopyrine content in a dose-dependent manner without significantly reducing the oxygen consumption. The H1-receptor antagonists influenced the 14C-aminopyrine content in another manner than H2-receptor antagonists. No effects were obtained by atropine or lidocaine, indicating that the elimination of 14C-aminopyrine is not an anticholinergic effect or due to membrane effects as exerted by local anesthetics. Stimulation of glands by further addition of histamine did not significantly stimulate the uptake of 14C-aminopyrine in the glands, whereas stimulation with db-cAMP produced an increase that was most pronounced when low concentrations of hydroxyzine had been used. It is suggested that H1-receptor antagonists do not inhibit stimulation of acid production in the secretory canaliculi. They may, however, interfere with a mechanism preventing acid from leaving the parietal cell. Such a mechanism may contribute to the delay in appearance of acid in the gastric lumen after stimulation of gastric acid production.
Aminopyrine↗
Effects of carbachol and gastrin on 14C-aminopyrine accumulated in rabbit gastric glands and cells.
The present study examines the possible existence of a mechanism regulating emptying of the secretory canaliculi content of the parietal cell and the possible effects of carbachol and gastrin on such a mechanism. In rabbit gastric glands stimulated with carbachol, 14C-aminopyrine accumulation reached a maximum after 15 min and then started to decrease. This decrease was not accompanied by a decrease in oxygen consumption, nor was any decrease of accumulated 14C-aminopyrine seen in dispersed gastric cells. In glands but not in cells stimulated with histamine together with 3-isobutyl-1-methylxanthine (IMX), carbachol induced a reduction in the accumulated 14C-aminopyrine content, whereas the effect of gastrin was less pronounced. The carbachol-induced reduction was counteracted by atropine but was not accompanied by a decrease in oxygen consumption. It is suggested that there exists a mechanism that controls the emptying of the secretory canaliculi content of the parietal cell, and that carbachol, in addition to stimulating acid production, also contributes to this emptying. Paracrine factors may be involved in this latter mechanism.
1-Methyl-3-isobutylxanthine↗
Economic costs of functional dyspepsia.
Dyspepsia is defined as chronic or recurrent symptoms believed to originate in the upper gastrointestinal tract. When routine investigation results in no identifiable explanation for those symptoms patients are labelled as having functional dyspepsia. In community-based surveys, approximately 30% of the otherwise apparently healthy population report dyspeptic symptoms and the majority are believed to have functional dyspepsia. Although only 1 in 4 or 5 patients make use of healthcare resources, this patient category is one of the largest in ambulatory care (1.6 to 5% of all consultations in general practice). The annual frequency of consultations for functional dyspepsia in Sweden has been estimated at 47 per 1000 population. In consequence of its high prevalence and associated absenteeism, the total costs of functional dyspepsia are considerable. In Sweden in 1981, the costs were estimated at $US55 000 per 1000 population ($US113 630 in 1991 dollars). The most cost-effective management strategy remains to be defined. Evidence is accumulating that the traditional 'wait-and-see' policy with initial empirical therapeutic trials without investigation may not be the most cost conserving strategy.
Absenteeism↗
Effects of omeprazole and ranitidine on plasma gastrin concentration and stomach gastrin content in rats.
Prolonged fasting and longer time between dosing and sampling reduced the plasma gastrin concentrations after omeprazole (80 mumol/kg x 2 for 14 days) treatment in male rats whereas the amounts of tissue gastrin were essentially unchanged during these initial experiments. After 28 days omeprazole (80 mumol/kg x 2) or ranitidine (375 mumol/kg x 4) that produced corresponding inhibition of acid secretion, increased the tissue gastrin content by 114 and 59%. A low dose of omeprazole (20 mumol/kg x 2) also raised the gastric gastrin content (41%), whereas no change was noted on treatment with a low dose of ranitidine (125 mumol x 4). Following recovery for 28 days no significant increases in gastrin were observed. 1, 3, 7, 14 or 28 days of treatment with omeprazole (80 mumol/kg x 2) gradually increased the gastric gastrin content being significantly raised already after 3 days. We conclude that a) measuring the tissue gastrin content may be the preferable method when changes in gastrin following long-term treatment with acid inhibiting drugs are to be determined, b) the amount of gastrin in the stomach increases rapidly following treatment with omeprazole and is approximately doubled following 28 days of treatment and c) after treatment for 28 days omeprazole was found to cause greater elevations in the tissue gastrin content than ranitidine despite similar degrees of basal acid inhibition.
Analysis of Variance↗
Studies of a proposed mechanism regulating parietal cell emptying.
We have proposed and provided experimental evidence for the existence of a mechanism controlling the output of hydrochloric acid from the parietal cells. On stimulation of the cells, histamine not only activates the H+/K-pump but also prevents acid from leaving the cell. The delay may be caused by cAMP activation. When the appropriate conditions have been obtained, the acid leaves the cell and enters the gastric lumen. A delay in onset of acid secretion is convenient from several points of view. For example, salivary amylase, which is responsible for approximately 50% of the carbohydrate digestion, will have time to exert its digesting effect in the stomach before the pH decreases and the enzyme becomes inactivated. Also, bicarbonate secretion will be started before high concentrations of acid have been obtained in the stomach and thereby contributes to protection of gastric mucosa.
Aminopyrine↗
The effect of omeprazole and ranitidine on ulcer healing, relief of symptoms, and incidence of adverse events in the treatment of duodenal ulcer patients.
In a Swedish double-blind multicenter study involving 143 patients, the new proton pump inhibitor omeprazole (30 mg taken as a single morning dose) was compared with ranitidine (400 mg b.i.d.). Clinical assessment and laboratory investigations were carried out at 2 and 4 weeks, and again at 6 weeks if patients had not healed earlier. Endoscopy was repeated at two-weekly intervals until the ulcer was healed. The patients in the two treatment groups were well matched prior to treatment. There was a higher ulcer healing rate in the omeprazole group (70%) than in the ranitidine group (55%) after two weeks of treatment. This difference reached statistical significance in 128 patients adhering to the protocol as shown by a logit model analysis with drug, ulcer size and smoking as the prognostic factors (p = 0.04). There were no major differences between the two treatment groups in terms of symptomatic relief. Both drugs were generally well tolerated, and the number of adverse events in the two treatment groups were similar. After healing, 127 patients entered a follow-up study, with endoscopy either after 6 months or on recurrence of symptoms. There was no significant difference between the two treatment groups, with the relapse frequency within 6 months being 39% in the omeprazole group and 47% in the ranitidine group. These results, with a 15 percentage points higher ulcer healing rate for omeprazole as compared with H2-receptor antagonists after two weeks, are in accordance with results reported in other studies.
Duodenal Ulcer↗
Time course of inhibition of gastric acid secretion by omeprazole and ranitidine in gastric fistula rats.
Basal, pentagastrin- and histamine-stimulated acid secretion were measured in gastric fistula rats treated with the H+/K(+)-ATPase inhibitor, omeprazole, and the H2-receptor antagonist, ranitidine. All doses of omeprazole (20, 30, 40, 80, 400 mumol/kg) and ranitidine (125, 187.5, 250, 375 mumol/kg) essentially abolished the basal acid output for various periods of time. Omeprazole, 80 mumol/kg, administered twice daily, reduced the 24-h basal acid secretion more effectively than did 400 mumol/kg given once daily. Four daily administrations of ranitidine reduced the 24-h basal acid output to a similar extent as omeprazole administered twice. Omeprazole (20, 80 mumol/kg) was more effective than ranitidine (125, 375 mumol/kg) in inhibiting acid secretion evoked by maximal doses of pentagastrin (650 nmol/kg per h) and histamine dihydrochloride (136 mumol/kg), whereas this difference was less pronounced for the inhibition of acid responses induced by a threshold dose (1.1 mumol/kg) of histamine. The inhibition evoked by omeprazole (80 mumol/kg x 2) and ranitidine (375 mumol/kg x 4) of basal and histamine (1.1 and 136 mumol/kg)-induced acid secretion was similar after 1 and 4 weeks of treatment. After the end of drug administration, the acid secretion induced by threshold doses of histamine was significantly elevated in the omeprazole-treated rats, whereas no significant hypersecretion of acid was seen during the recovery period in rats treated with ranitidine. Plasma gastrin concentrations were significantly elevated after 4 weeks of treatment with omeprazole but returned to pretreatment levels after 4 weeks of recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Digital ambulatory monitoring of small-bowel motility.
This paper describes a new technique for ambulatory long-term monitoring of small-bowel motility. Intraluminal pressure was measured with a silicon catheter with two strain-gauge transducers spaced 15 cm apart. Pressure data were stored in a portable memory unit. Initial studies showed that a recording frequency of 2 Hz was sufficient for obtaining reliable motility measurements. Twelve-hour recordings of motility in the upper jejunum were done in 12 healthy volunteers. After a 1964-kJ meal the median duration of fed-state motility was 4.6 h (3.4-5.3 h, interquartile range). The activity front of the migrating motor complex propagated with a velocity of 2.7-5.3 cm/min, and the median cycle length was 77 (40-103) min. The frequency of contractions in the activity front was 11.4 (10.9-11.6)/min at the proximal transducer. This new technique enables small-bowel motility to be monitored over longer periods of time and with much less inconvenience to the patient than previously used methods.
Adult↗
Effects of long-term hypergastrinaemia on the ultrastructure of enterochromaffin-like cells in the stomach of the rat, hamster and guinea pig.
The present report describes the ultrastructure of the enterochromaffin-like (ECL) cells in the stomach of the rat, hamster and guinea pig, and the ultrastructural consequences of long-term hypergastrinaemia evoked either by continuous infusion of synthetic human (Leu15)-gastrin-17 for 4 weeks (rats) or by daily treatment with large doses of the antisecretory agent omeprazole for 2-10 weeks (rats, hamsters and guinea pigs). As a result, the ECL cells increased greatly in size (maximal effect after 2 weeks of omeprazole treatment, no further gain in size after 4 or 10 weeks). Also the endoplasmic reticulum and Golgi area were enlarged. The most conspicuous feature of the ECL cells is the cytoplasmic vesicles, which are of varying size and either devoid of a dense core or with a small, often eccentrically located dense core. The vesicles probably represent the main storage site of the secretory products of the ECL cell. In addition, the cytoplasm contains granules, which differ from the vesicles in that they possess a more or less electron-dense core, surrounded by a narrow halo. The size of the vesicles ranged from small to very large, while the granules were uniformly small. Many vesicles were seen to lie very close together, some displaying an irregular outline (vacuole-like vesicles), at times giving the impression that they were undergoing fusion. The profile size (median value) of the vesicles was unaffected by gastrin infusion for 4 weeks. However, there was a tendency to a relative increase in the number of very small vesicles. In contrast, the vesicles became larger during the omeprazole treatment. Also, the number of vesicles that seemed to be engaged in fusion increased after omeprazole treatment but not after gastrin infusion. The observations support the view that ECL cells are influenced by gastrin. The effects of gastrin infusion and of omeprazole treatment on ECL cell ultrastructure were not completely identical. It cannot be excluded that the omeprazole-evoked achlorhydria evokes effects unrelated to those of hypergastrinaemia on the ECL cells, or that endogenous gastrins may evoke effects that are in some ways distinct from those of synthetic human (Leu15)-gastrin-17. Alternatively, the additional effects seen after long-term omeprazole treatment may reflect simply the duration of the hypergastrinaemic stimulus.
Animals↗
Time-course of development and reversal of gastric endocrine cell hyperplasia after inhibition of acid secretion. Studies with omeprazole and ranitidine in intact and antrectomized rats.
In intact rats plasma gastrin levels were increased during a 20-wk treatment course with either omeprazole or ranitidine. Although plasma gastrin levels were the same during treatment, the enterochromaffinlike (ECL) cell density increased approximately linearly with time at a rate correlated to the plasma gastrin level. Antrectomy prevented the ECL cell hyperplasia seen in omeprazole-treated rats, suggesting that it was not caused by omeprazole per se. Changes in ECL cell density roughly paralleled changes in oxyntic mucosal histidine carboxylase activity and histamine concentration. Treatment with omeprazole also raised stomach weight and antral gastrin and gastrin cell density, reduced antral somatostatin cell density, but did not affect enterochromaffin cell density. Within 19 days of cessation of a 10-wk treatment course, plasma gastrin levels, oxyntic mucosal histidine decarboxylase activity, and antral gastrin and somatostatin cell densities had returned to control levels. The stomach weight was normal within 5-10 wk, antral gastrin concentration within 10 wk, and oxyntic mucosal ECL cell density and histamine concentration within 20 wk. After renewed treatment with omeprazole for 10 wk starting 10 wk after completion of the first omeprazole treatment period, changes in all parameters were of similar magnitude in animals previously treated with omeprazole and those previously treated with vehicle. The results suggest that the effects described are reversible and that gastrin cells turn over more rapidly than ECL cells.
Animals↗
Transferability of a computer system for medical history taking and decision support in dyspepsia. A comparison of indicants for peptic ulcer disease.
The transferability of a British data base for differential diagnosis of dyspepsia using data obtained by computer interrogation was tested in 467 Swedish patients. The diagnostic value for peptic ulcer disease of symptoms such as frequent night pain relieved by food or antacids, smoking, family history of ulcer, food relief pain, male sex, and episodic pain was shown to be reproducible. However, for a number of symptoms their value for the diagnosis of peptic ulcer disease could not be reproduced in Swedish patients. The combined value of indicants was tested using a computer based algorithm for calculating diagnostic probabilities. The performance of this algorithm was poor when British data were applied to Swedish patients but reclassification of the Swedish patients on their own data base showed promising results. Crean and colleagues in Glasgow have developed a computer system for automated interrogation of patients with dyspepsia. The system utilises a large number of questions to obtain information regarding a maximum of 160 diagnostic indicants. The symptoms elicited from a patient can be compared with those of a large number of previously examined patients and the probabilities of ten different diagnoses can be calculated. The calculation of diagnostic probabilities is based on scores reflecting the diagnostic value of different symptoms in different diseases. After careful translation of questions the system has been transferred for use in Sweden. The present report is based on data from patients seen during the first two years with the system at a Swedish hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗