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Biomedical subjects

I Kisfalvi

Publications and source records attributed to I Kisfalvi.

At least 19 recordsLinked to original sources
PubMed1999

Efficacy of two different dosage regimens of omeprazole, amoxycillin and metronidazole for the cure of Helicobacter pylori infection.

BACKGROUND: While addition of metronidazole to the omeprazole-amoxycillin combination has been shown to be advantageous, the optimal dosage and drug distribution of the antimicrobials has not been sufficiently evaluated. AIM: To investigate the efficacy of two different regimens of omeprazole, amoxycillin and metronidazole for the cure of Helicobacter pylori infection. METHODS: Two hundred and fifty-five patients with H. pylori associated duodenal ulcers were randomly treated with either a 1-week regimen of omeprazole 20 mg b.d., amoxycillin 1000 mg b.d. and metronidazole 800 mg b.d. (OAM b.d.) or a combination of omeprazole 40 mg o.d., amoxycillin 500 mg t.d.s. and metronidazole 400 mg t.d.s. (OAM t.d.s.). All patients subsequently received omeprazole 20 mg o.d. for an additional 3 weeks. H. pylori status was assessed by histology and 13C-UBT prior to treatment and 8 weeks after randomization. Additional biopsies were obtained for H. pylori culture to determine primary and secondary resistance to metronidazole by agar dilution. RESULTS: Two hundred and thirty-seven patients were included in the intention-to-treat analysis and 198 patients in the per protocol analysis. With intention-to-treat analysis, the cure rate was 77% after treatment with OAM b.d. (95% CI, 69%-85%) and 76% after OAM t. d.s. therapy (95% CI, 67%-83%). Ulcer healing (intention-to-treat analysis) was documented in 95% of patients in the OAM b.d. group (n=122) and in 97% of patients in the OAM t.d.s. group (n=115). Adverse events were reported in 26 (20%) and in 18 (14%) patients in the OAM b.d. and OAM t.d.s. groups, respectively. None resulted in discontinuation of treatment. Overall primary resistance of H. pylori against metronidazole was found in 22 of 116 strains (19%). CONCLUSIONS: The combination of omeprazole, amoxycillin and metronidazole achieves about an 80% cure rate of H. pylori infection even in active ulcers. The total daily dose, and the choice of twice or three times daily dosing does not seem critical with this regimen.

Aged↗
PubMed1996

Effect of dexloxiglumide and spiroglumide, two new CCK-receptor antagonists, on gastric emptying and secretion in the rat: evaluation of their receptor selectivity in vivo.

BACKGROUND: Clear definition of the role of CCK in the physiology of gastric motor activity has been long hampered by the lack of specific and potent nonpeptide antagonists of CCK-receptors. The availability of such compounds has stimulated a broad array of investigations into the physiological actions of this hormone and to examine its putative role in certain diseases. AIMS: The effect of two recently developed CCK-receptor antagonists, namely dexloxiglumide and spiroglumide, on gastric emptying and secretion as well as their selectivity towards CCKA- and CCKB-receptors in vivo was studied in the rat. METHODS: Gastric emptying was quantified by using a liquid noncaloric meal labelled with phenol red. Acid secretion was measured by titration in conscious rats. RESULTS: The putative CCKA-antagonist, dexloxiglumide, administered by intravenous route, was able to inhibit CCK-8-induced delay of gastric emptying in a dose-dependent fashion, with an ID50 (95% CL) of 1.14 (0.84-1.53) mg/kg. Similarly, the putative CCKB-gastrin-antagonist, spiroglumide, proved to be capable of inhibiting dose-dependently pentagastrin-induced acid hypersecretion, its ID50 being 20.1 (8.67-46.4) mg/kg. On the other hand, dexloxiglumide, at doses able to almost completely block CCKA mediated effects (i.e. delay of gastric emptying), was ineffective against pentagastrin-induced acid hypersecretion. Similarly, spiroglumide, at doses which inhibit by 55% CCKB-gastrin mediated effects (i.e. acid secretion) was inactive when tested against CCK-8 induced delay of gastric emptying. CONCLUSIONS: These results demonstrate in vivo that dexloxiglumide is a selective antagonist for CCKA-receptors whereas spiroglumide is selective for CCKB-gastrin-receptors. These compounds are therefore useful tools for discriminating between different subclasses of CCK-receptors in vivo and might have a therapeutic potential in motility or acid-related disorders.

Animals↗
PubMed1983

Gastric acid and serum gastrin response to sham feeding, and the effect of cimetidine on the response to sham feeding in duodenal ulcer patients.

Sham feeding resulted in a significant increase of gastric acid secretion in 12 male patients with duodenal ulcer. No significant change in serum gastrin concentration was produced by sham feeding. Reproducibility of gastric acid response to sham feeding was very good (r = 0.74). The mean peak 30 min acid output amounted to 9.5 +/- 1.0 mmol/30 min following sham feeding. That was 46.5% of the 30 min peak acid output elicited by pentagastrin infusion administered in a dose of 1.5 micrograms/kg/h. Cimetidine in a dose of 2 mg/kg/h almost completely reduced (by 85%) the gastric acid secretion induced by sham feeding. Cimetidine did not cause any change in serum gastrin concentration during and after sham feeding.

Adult↗
PubMed1982

Effect of calcitonin on bombesin-stimulated gastric acid secretion in patients with duodenal ulcer.

Intravenous infusion of bombesin (0.9 micrograms/kg/hour) caused a significant increase in gastric acid secretion and serum gastrin concentration in 8 duodenal ulcer patients. Intravenous infusion of calcitonin (2 MRCU/kg/hour) produced a significant decrease in gastric acid output and in integrated gastrin output produced by bombesin infusion (0.9 micrograms/kg/hour) in the same 8 patients with duodenal ulcer. Percentage of inhibition was 49.7 and 40.8, respectively. Simultaneous infusion of calcitonin and bombesin caused no significant difference in serum calcium concentration. It is suggested that the inhibitory effect of calcitonin on acid secretion elicited by bombesin is produced, at least in part, by a fall in serum gastrin caused by bombesin. In addition, calcitonin might directly inhibit the parietal cells by releasing endogenous gastric somatostatin.

Adult↗
PubMed1980

Effect of calcitonin on basal and pentagastrin- and calcium-stimulated gastric acid secretion in patients with duodenal ulcer.

Synthetic salmon calcitonin infused intravenously in a pharmacological dose of 2 MRCU/kg/hour resulted in an abrupt and profound inhibition of basal and pentagastrin and calcium induced gastric acid secretion in patients with duodenal ulcer. The inhibition in the sixth 15-minute period of the intravenous infusion of calcitonin amounted to 98.7% (basal acid secretion), 51.8% (pentagastrin-stimulated acid secretion) and 80.9% (calcium-induced acid secretion). There were no significant alterations in the serum calcium and gastrin levels during the intravenous infusion of calcitonin. The slight decrease in serum gastrin concentration in the first 30 minutes of calcitonin infusion cannot explain the strong inhibition of gastric acid secretion produced by calcitonin. It is assumed that calcitonin inhibits directly the parietal cells.

Adult↗
PubMed1979

Inhibition of bombesin-stimulated gastric acid secretion by secretin, glucagon and caerulein in patients with duodenal ulcer.

The inhibitory effects of intravenous infusions of secretin, glucagon and caerulein on the gastric acid response to bombesin were studied in 8 duodenal ulcer patients. Bombesin was found to be a very potent stimulator of gastric acid secretion in patients with duodenal ulcer. There were no significant differences in acid outputs per 15-min period between bombesin infused in a dose of 0.9 microgram/kg/h and pentagastrin infusion administered in a maximal dose, at a rate of 6.0 microgram/kg/h. Secretin (1 U/kg/h), glucagon (30 microgram/kg/h) and caerulein (0.1 microgram/kg/h) produced significant decreases in gastric acid secretion evoked by bombesin given in a dose of 0.9 microgram/kg/h. Percentages of inhibition were 48.6, 45.2 and 35.5, respectively. It is supposed that secretin and glucagon given in pharmacological doses are capable of interfering with the action of gastrin released from antrum by means of bombesin on the parietal cell by noncompetitive kinetics. Caerulein administered in a pharmacological dosis, however, can inhibit the effect of gastrin released by bombesin on the parietal cells by a competitive kinetic.

Adult↗
PubMed1978

Inhibitory effect of glucagon, secretin and caerulein on gastric acid secretion stimulated by pentagastrin in patients with duodenal ulcer.

In 10 duodenal ulcer patients gastric acid secretion was stimulated by intravenous infusion of 1.5 microgram pentagastrin per kilogram hour. When acid secretion had reached a plateau, glucagon in a dose of 30 microgram per kilogram hour, secretin in a dose of 1 IU per kilogram hour or caerulein in a dose of 0.1 microgram per kilogram hour were infused into a separate vein for one hour during the intravenous infusion of pentagastrin. Using these doses, each drug produced about 30 per cent inhibition given separately. The highest degree of inhibition was obtained by the combination of glucagon and secretin. The inhibition reached the sum of the inhibitions after glucagon and secretin administered separately. Caerulein added to glucagon or secretin could slightly increase the inhibitory effect of these drugs given separately. Caerulein, however, failed to increase inhibition when glucagon and secretin were infused simultaneously.

Adult↗
PubMed1978

Intragastric titration of peptone-stimulated gastric acid secretion.

Fourteen male patients with duodenal ulcer were stimulated by a 10% peptone meal, and acid secretion was measured by continuous intragastric titration. The results were compared to the effects of intravenous infusion of pentagastrin given in a dose of 6.0 microgram/kg-hour on gastric acid secretion in the same 14 patients. Acid secretion reached the peak in the third 15-min period after peptone instillation and it was similar to that peak acid output/15 min produced by infusion of pentagastrin. Acid secretion in response to peptone in the second hour gradually diminished towards the basal level, on the contrary, during i.v. infusions of pentagastrin the acid secretion was well sustained. The acid response to peptone solution or pentagastrin infusion did not differ significantly in the first hour, but in the second hour the difference was significant. It is concluded that the gastric acid secretion induced by peptone is comparable to the effect of the highest dose of pentagastrin infusion only in the first hour. Reproducibility of gastric response to peptone and to pentagastrin infusion was very good (r = 0.79 and 0.87, respectively).

Adult↗
PubMed1975

Failure of pentagastrin to potentiate the effect of histamine.

The gastric secretory response to pentagastrin and histamine administered jointly in maxiumum does by the subcutaneous route and in intravenous infusion, and in lower doses in infusion has been compared to the response to each of the two drugs administered by itself. No potentiating action was observed, some additive action was found on infusion of the drugs and even this action was confined to the lowest dose-levels.

Drug Synergism↗