Effect of centrally administered prolactin on gastric and duodenal ulcers in rats

The effect of centrally administered prolactin on gastric acid secretion and experimentally-induced gastric and duodenal ulcers was studied. The acute gastric ulcer models used were pylorus ligation, indomethacin-induced and ethanol-induced gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by cysteamine hydrochloride. In pylorus ligated rats, prolactin (1 microg/kg icv) produced 45% increase in gastric content volume, significant increase in free acidity (P < 0.001), total acidity (P < 0.001) and ulcer index (P < 0.001). It did not show any significant effect on ethanol-induced and indomethacin-induced gastric ulcers. Prolactin increased the ulcer index (P < 0.001) and ulcer score (P < 0.05) in acetic acid-induced chronic gastric ulcers. It also increased ulcer area (P < 0.05) in cysteamine-induced duodenal ulcers. Therefore, the proulcerogenic activity of prolactin was due to its gastric hypersecretory effect.     

Effect of peroxisome proliferator-activated receptor-alpha agonist (bezafibrate) on gastric secretion and gastric cytoprotection in rats

The effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) on gastric secretion and gastric cytoprotection was evaluated using five different models of gastric ulcers: acetic acid-induced chronic gastric ulcers, pylorus ligation, ethanol-induced, indomethacin-induced and ischemia-reperfusion-induced gastric ulcers. Bezafibrate, a PPAR-alpha agonist was administered at two different doses of 10 and 100 mg/kg body weight intraperitoneanally. Both doses of bezafibrate showed significant antiulcer effect in ethanol-induced, indomethacin-induced and pylorus ligation-induced gastric ulcers. Bezafibrate increased healing of ulcer in acetic acid-induced chronic gastric ulcer model. Both doses were also effective in preventing gastric lesions induced by ischemia-reperfusion. It was concluded that PPAR-alpha activation increases healing of gastric ulcers and also prevents development of gastric ulcers in rats.     

2,3-Dimercaptopropanol, a thiol chelator, alleviates gastroduodenal ulcers in rats

Earlier studies have implicated reactive oxygen species and transitional metals in the pathogenesis of gastric lesions. In this study, we have evaluated the effect of 2,3-dimercaptopropanol (DMP), a thiol compound and metal chelator, on chemically induced gastroduodenal ulcers in rats. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with DMP (3-100 mg/kg, i.p.). The effect of orally administered DMP on cysteamine-induced duodenal ulcers and ethanol-induced gastric ulcers was also tested. The level of nonprotein sulfhydryls (NP-SH) and gastric wall mucus was measured in the glandular stomach of rats treated with ethanol. None of the dose of DMP affected the volume or acidity of gastric secretion. Low doses of DMP (3 and 10 mg/kg) significantly reduced cysteamine-induced duodenal ulcers, whereas the high doses (30 and 100 mg/kg) were ineffective in this model. All the doses of DMP significantly and dose dependently attenuated ethanol-induced gastric lesions. The adverse effects of ethanol on gastric wall mucus and NP-SH were significantly and dose dependently reversed by DMP. In conclusion, the protective effects of DMP appear to be independent of gastric acid secretion and may be associated with counteracting the oxidative stress by replenishing glutathione and reducing the pool of transition metals.     

Effect of tyrosine administration on duodenal ulcer induced by cysteamine in the rat

Duodenal ulcers were produced by administering cysteamine to rats. Pretreatment with the catecholamine precursor, L-tyrosine (40 mg/100 g i.p. for 5 days), decreased the intensity of duodenal ulcers induced by cysteamine. Equimolar doses of tyrosine methyl ester (51.2 mg/100 g i.p. or s.c.) were equally effective in reducing ulcer intensity. Other amino acids (i.e., alanine, aspartic acid, glutamic acid, glycine, leucine, lysine, tryptophan and valine) did not prevent experimental duodenal ulcers. Coadministration of other large neutral amino acids (e.g., leucine and valine) that compete with tyrosine for uptake into the brain did not inhibit the effect of tyrosine on duodenal ulcers induced by cysteamine. Gastric, duodenal and brain dopamine concentrations were increased 1 hr after the injection of tyrosine methyl ester (25.6 mg/100 g s.c.). These results suggest that the effect of tyrosine on duodenal ulcer induced by cysteamine may be mediated by changes in gastrointestinal dopamine metabolism.     

Gastroprotection of (-)-α-bisabolol on acute gastric mucosal lesions in mice: the possible involved pharmacological mechanisms

(-)-α-Bisabolol is an unsaturated, optically active sesquiterpene alcohol obtained by the direct distillation essential oil from plants such as Vanillosmopsis erythropappa and Matricaria chamomilla . (-)-α-Bisabolol has generated considerable economic interest, since it possesses a delicate floral odor and has been shown to have anti-septic and anti-inflammatory activity . The aim of this work was to evaluate the gastroprotective action of (-)-α-bisabolol on ethanol and indomethacin-induced ulcer models in mice, and further investigate the pharmacological mechanisms involved in this action. The oral administration of (-)-α-bisabolol 100 and 200 mg/kg was able to protect the gastric mucosa from ethanol (0.2 mL/animal p.o.) and indomethacin-induced ulcer (20 mg/kg p.o.). Administration of l -NAME (10 mg/kg i.p.), glibenclamide (10 mg/kg i.p.) or indomethacin (10 mg/kg p.o.) was not able to revert the gastroprotection promoted by (-)-α-bisabolol 200 mg/kg on the ethanol-induced ulcer. Dosage of gastric reduced glutathione (GSH) levels showed that ethanol and indomethacin reduced the content of non-protein sulfhydryl (NP-SH) groups, while (-)-α-bisabolol significantly decreased the reduction of these levels on ulcer-induced mice, but not in mice without ulcer. In conclusion, gastroprotective effect on ethanol and indomethacin-induced ulcer promoted by (-)-α-bisabolol may be associated with an increase of gastric sulfydryl groups bioavailability leading to a reduction of gastric oxidative injury induced by ethanol and indomethacin.     

Effects of pretreatment with clonidine, lithium and quinine on the activities of antidepressant drugs in the mouse tail suspension test

Summary— The aim of the present study was the investigation of pretreatment effects with clonidine (0.06 mg/kg, intraperitoneal [ip]), lithium (1 mEq, ip) or quinine (0.5 mg/kg, ip) on the activities of various drugs acting on noradrenergic and/or serotonergic systems in the mouse tail suspension test. Drugs used in the present study included: the tricyclic antidepressants imipramine and dothiepin, the heterocyclic antidepressant trazodone, the 5-HT reuptake inhibitor (SSRI) fluoxetine, the atypical antidepressants mianserin and iprindole, the 5-HT_1A receptor agonist ipsapirone, the 5-HT_2A/2C receptor antagonist ritanserin, and the 5-HT₃ receptor antagonist ondansetron. Clonidine, lithium and quinine differentially enhanced the effects of several psychotropic drugs administered at sub-active doses. The activity of iprindole (32 mg/kg, ip) was not potentiated by pretreatment with clonidine, lithium or quinine. Our results suggest that lithium exerted additive effects via postsynaptic 5-HT_1A receptor activation, quinine via potassium ion channel blockade of 5-HT₃ receptors, while clonidine did so primarily via action at 5-HT₂ receptors.     

5-HTP induced diarrhea as a carcinoid syndrome model in mice?

Summary— Serotonin (5-HT) is present in the gastrointestinal tract and is probably one of the compounds responsible for diarrhea in patients presenting with carcinoid syndrome. Intraperitoneal administration of L-5-hydroxytryptophan (L-5-HTP) at doses of 25 to 100 mg/kg dramatically increase defecation in mice. In this new paradigm, counting fecal boli deposited is simple and the appraised or inhibition of diarrhea induced by ip 25 mg/kg of L-5-HTP is very clear, with a good reproducibility of scores. L-5-HTP needs to be metabolized into 5-HT to be active; benserazide, an inhibitor of decarboxylase, antagonized the diarrhea induced by 5-HT. Among the 5-HT antagonists used in interaction with 5-HT, only those of the 5-HT₃ type (ondansetron, granisetron, tropisetron) and, to a lesser extent 5-HT₂ type (ritanserin), decreased the diarrhea induced by 5-HTP. The 5-HT₄ receptor agonists from the benzamide family (metoclopramide and zacopride) increased defecation in mice but the effect failed to reach statistical significance.     

YM022, a highly potent and selective CCKB antagonist inhibiting gastric acid secretion in the rat, the cat and isolated rabbit glands

Summary— We investigated the effects of the novel CCK_B/gastrin antagonist YM022 on gastric acid secretion in vivo and in vitro, compared to CI-988 and L365.260 as reference antagonists. In the anaesthetized rat, pentagastrin-induced stimulation of gastric acid secretion was dose-dependently and up to 100% inhibited by iv administration of YM022 with an ID₅₀ of 0.009 ± 0.0006 μmol/kg h in comparison to 0.6 ± 0.03 and 3.40 ± 0.05 μmol/kg h for CI-988 and L-365,260, respectively. In the gastric fistula cat, iv administration of YM022 produced a similar inhibitory effect with an ID₅₀ of 0.02 μmol/kg in comparison to 1.6 and 2.5 μmol/kg for CI-988 and L-365,260, respectively. Furthermore, bolus injection of 0.6 μmol/kg YM022 produced 100% inhibition within 30 min and 85% inhibition was still observed after 3 h. In the isolated rabbit gastric glands, CCK₈-stimulated ¹⁴C-aminopyrine uptake was inhibited according to the following rank order of potency: YM022 (IC₅₀ = 0.0012 μM) ≫ CI-988 (IC₅₀ = 0.2 μM) ≫ L365.260 (IC₅₀ = 2.8 μM). Unlike with L365.260, no influence of CI-988 and YM022 on histamine-stimulated acid output was shown in this study. Thus, YM022 is a highly potent and selective gastric CCK₈/gastrin receptor antagonist and has a long-lasting inhibitory effect on gastric acid secretion.     

Absence of tolerance in duodenal ulcer patients treated for 28 days with a bedtime dose of roxatidine or ranitidine

Summary— There is much experimental work on the occurrence of tolerance to the antisecretory effect of H₂-receptor antagonists in healthy subjects, while data on its development in patients with duodenal ulcer are poor and conflicting. Moreover, this phenomenon has not been studied previously with 24 h gastric pH-metry in patients with active duodenal ulcer. For these reasons, we carried out a prospective pharmacodynamic investigation in 48 patients with endoscopically proven duodenal ulcer using the well-established once daily dosing schedule of H₂ blockers. They were studied by means of 24 h continuous endoluminal pH-metry which was performed before, on d1 and d28 after receiving an oral bedtime dose (2200 hours) of either roxatidine 150 mg or ranitidine 300 mg, given in randomized and single-blind fashion. Eight patients did not complete the study for various reasons and 82% of ulcers healed after 4 weeks of therapy. Gastric pH was higher ( P < 0.001) on d1 and d28 than basal values during all time periods, but the evening, with both H₂ blockers. There was no significant difference between pH values of d1 and d28 in any time interval with both roxatidine and ranitidine. There was also no difference in pharmacodynamic data between the two active treatments. We conclude that tolerance does not develop after 1 month's treatment with a bedtime dose of H₂ antagonist in patients with active duodenal ulcer and therefore data gathered on this phenomenon in healthy subjects are not applicable to ulcer patients.     

Gastrointestinal motor and secretory responses to cholinergic stimulation in humans. Differential modulation by muscarinic and cholecystokinin receptor blockade

Abstract. The present study investigated how a cholinergic agonist modifies interdigestive motility and secretion of the upper gastrointestinal tract and how muscarinic and cholecystokinin receptor blockade interfere with this direct cholinergic stimulation. In eight healthy volunteers, gastrointestinal motor and secretory responses to bethanechol (12.5, 25, and 50 μg kg^-1 h^-1) with and without a background of atropine (5 μg kg^-1 h^-1) or loxiglumide (10 mg kg^-1 h^-1) were studied. Stepdoses of bethanechol caused a parallel stimulation of antroduodenal motility and gastropancreatic secretion ( P < 0.01) without inducing a fed pattern. However, duration of phase I was shortened ( P < 0.05). Only high doses of bethanechol enhanced gastrin ( P < 0.05), cholecystokinin ( P < 0.05), and pancreatic polypeptide ( P < 0.01) release. Atropine completely antagonized motor and secretory responses to cholinergic stimulation. Loxiglumide left cholinergically stimulated motility and pancreatic enzyme secretion unaltered. With co-infusion of bethanechol and loxiglumide, PP release dropped by 63% ( P < 0.01); gastric acid output, gastrin and CCK release increased by 56%, 16%, and 25%, respectively ( P < 0.05). We conclude that stimulation by a cholinergic agonist preserves the interdigestive pattern. Low dose muscarinic receptor blockade abolishes cholinergic stimulation over the full dose range. Inhibition of somatostatin release would explain stimulation of gastrin release and gastric acid secretion with co-infusion of bethanechol and loxiglumide. Endogenous CCK appears to interact with direct cholinergic stimulation at the pancreatic PP cell and the gastric D-cell but not at pancreatic acinar and antroduodenal smooth muscle cells.     

Effect of histamine on regional cerebral blood flow in man

Regional cerebral blood flow (rCBF) was measured using the intra-arterial ¹³³Xe technique in 35 or 256 areas of a hemisphere. In seven patients rCBF was measured in the resting state and following intracarotid (i.c.) infusion of histamine 10–50 μg/min. In four patients histamine was infused intravenously in a dose of 25–40 μg/min. Histamine caused no significant change in mean arterial blood pressure or arterial PCO₂. There was no significant change in mean hemispheric blood flow during i.v. or i.c. histamine infusion. No change in the regional distribution of hemispheric blood flow was observed. Experimental histamine headache is most likely of extracranial origin.     

Stimulation of gastric mucus output by somatostatin in man

Abstract. Effects of i.v. somatostatin on the gastric mucus output during a 60 min infusion of pentagastrin were examined in five healthy subjects. Experiments were also made with prior indomethacin administration to suppress the synthesis of endogenous prostaglandins. N-acetyl neuraminic acid, a sialic acid, was measured in the gastric aspirates as an index of gastric mucus.
Somatostatin increased significantly the gastric mucus output in a dose-related way. The output increased to 158 ± 14% and 216 ± 24% of the control level by 1 and 2 μg kg^-1 h^-1 somatostatin, respectively. The increase induced by somatostatin was prevented by prior indomethacin. With indomethacin alone the mucus output was not different from in controls.
Thus somatostatin has augmentory effects on the gastric mucus, which can be blocked by indomethacin, indicating that endogenous prostaglandins are involved in the augmentation.
Somatostatin prevents stress ulcerations in the rat, assumedly by inhibiting the gastric acid secretion. This study suggests that additional mechanisms may contribute to the protective action of somatostatin on the gastric mucosa.     

Human corticotropin-releasing hormone and thyrotropin-releasing hormone modulate the hypercapnic ventilatory response in humans

Human corticotropin-releasing hormone (hCRH) and thyrotropin-releasing hormone (TRH) are known to stimulate ventilation after i.v. administration in humans. In a placebo-controlled, single-blind study we aimed to clarify if both peptides act by altering central chemosensitivity. Two subsequent CO₂-rebreathing tests were performed in healthy young volunteers. During the first test 0.9% NaCl was given i.v.; during the second test 200 μg of hCRH ( n  = 12) or 400 μg of TRH ( n  = 6) was administered i.v.. Nine subjects received 0.9% NaCl i.v. during both rebreathing manoeuvres. The CO₂–response curves for the two tests were compared within the same subject. In the hCRH group a marked parallel shift of the CO₂–response curve to the left was observed after hCRH ( P  < 0.01). The same effect occurred following TRH but was less striking ( P  = 0.05). hCRH and TRH caused a reduction in the CO₂ threshold. The CO₂–response curves in the control group were nearly identical. The results indicate an additive effect of both releasing hormones on the hypercapnic ventilatory response in humans, presumably independent of central chemosensitivity.     

Essential oil of Croton zehntneri and its major constituent anethole display gastroprotective effect by increasing the surface mucous layer

Croton zehntneri, a plant native to northeastern Brazil, is widely used in folk medicine to treat gastrointestinal problems and has rich essential oil content. The effects of the essential oil of Croton zehntneri (EOCZ) and its main constituent anethole on several models of gastric lesions were studied in mice and rats. Oral treatment with EOCZ and anethole, both at doses of 30–300 mg/kg, caused similar and dose‐dependent gastroprotection against ethanol‐ and indomethacin‐induced gastric damage, but did not change cold‐restraint stress‐induced ulcers in rats. Furthermore, EOCZ and anethole (both at 30 and 300 mg/kg) similarly and significantly increased the mucus production by the gastric mucosa, measured by Alcian blue binding, in ethanol‐induced ulcer model. However, at the same doses, neither EOCZ nor anethole promoted significant alteration in gastric production of non‐protein sulfhydryl groups. In pylorus‐ligated model, neither EOCZ nor anethole (both at 30 and 300 mg/kg) had a significant effect on the volume of gastric juice, pH, or total acidity. The results of this study show for the first time that EOCZ possesses a gastroprotective potential, an effect mostly attributed to the action of anethole. This activity is related predominantly to the ability of EOCZ and anethole to enhance the production of gastric wall mucus, an important gastroprotective factor. Furthermore, they suggest that EOCZ has potential therapeutic application for the treatment of gastric ulcers.     

Vasoactive substances in early dumping syndrome: effects of dumping provocation with and without octreotide

In patients after gastric surgery, early dumping symptoms can be provoked by oral glucose challenge. Octreotide effectively prevents the occurrence of dumping symptoms. We have studied plasma renin activity (PRA), aldosterone and atrial natriuretic peptide (ANP) concentrations in nine patients with early dumping, 10 surgical control subjects and nine healthy control subjects after an oral glucose challenge preceded by either placebo or 25 μg of octreotide subcutaneously (s.c.). In the dumping group, basal PRA was signifi-cantly ( P  < 0.01) higher (3.9 ± 0.6 μg L⁻¹ h⁻¹) than in either surgical or healthy control subjects (1.1 ± 0.3 μg L⁻¹ h⁻¹ and 1.1 ± 0.2 μg L⁻¹ h⁻¹ respectively) and showed a significant rise after glucose ingestion to 5.4 ± 0.9 μg L⁻¹ h⁻¹ that did not occur in control subjects. Aldosterone concentration showed a concomitant rise. In dumping patients, plasma ANP decreased after glucose ingestion from 31 ± 6 ng L⁻¹ to 21 ± 5 ng L⁻¹ ( P  < 0.05). This decrease did not occur in control subjects. Early dumping is associated with an activation of the renin–aldosterone axis and a decrease in plasma ANP, reflecting a hypovolaemic state. Octreotide prevents the occurrence of these changes.     

Effect of carbenoxolone on gastric prostaglandin E2 levels in patients with peptic ulcer disease following vagal and pentagastrin stimulation

The influence of oral carbenoxolone sodium (50 mg X 3 daily) on prostaglandin E2 release into gastric juice has been examined in nine peptic ulcer patients (duodenal ulcer, n = 6; prepyloric ulcer, n = 1; gastric ulcer, n = 2) during modified sham feeding and following bolus stimulation of acid secretion by pentagastrin (6 micrograms/kg). Carbenoxolone increased the overall mean of prostaglandin E2 concentrations in gastric juice following modified sham feeding by 32 +/- 9% (mean +/- SEM; P less than 0.02) and decreased the acidity slightly but significantly (P less than 0.05). A marked rise in prostaglandin E2 levels (46 +/- 11%; n = 5; P less than 0.02) was observed in for duodenal ulcer patients and the patient with a prepyloric ulcer responding to therapy (i.e., pain relief and ulcer healing within 4 weeks of treatment). A significant peak (P less than 0.05) related to modified sham feeding was observed only during medication, while a late gradual increase in prostaglandin E2 levels--not associated with vagal stimulation--occurred both in control and carbenoxolone experiments. No significant differences were observed following pentagastrin stimulation. The initial peak in prostaglandin E2 levels observed during medication favours the notion that the mechanism of drug action relies on inhibition of enzymatic degradation while the late increase in prostaglandin E2 levels may be explained by artificial prostaglandin formation during the aspiration procedure.     

Central and peripheral opioid modulation of gastric relaxation induced by feeding in dogs

The influence of i.v. vs. i.c.v. administration of [( D-Ala2, MetPhe4, Gly-ol5]enkephalin (DAMGO) and morphine), kappa U 50488 and ethylketocyclazocine and delta ([D-Pen2, D-Pen5]enkephalin (DPDPE)] opioid agonists on gastric relaxation induced by a standard meal was evaluated in conscious dogs with strain-gauge transducers implanted on the gastric fundus and antrum. Under control conditions, the amplitude of the gastric relaxation in response to feeding was 2.46 +/- 0.23 g. Given i.v. 10 min before feeding, both U 50488 (10 micrograms/kg) and ethylketocyclazocine (10 micrograms/kg) significantly (P less than .01) reduced the amplitude of the gastric relaxation by 57 and 68%, respectively, whereas DAMGO and morphine (10 micrograms/kg i.v.) increased markedly the response to feeding by 67 and 51%, respectively. In contrast, DPDPE had no effect on the gastric relaxation induced by feeding. Previous administration of naloxone (0.3 mg/kg i.v.) or MR 2266 (0.3 mg/kg i.v.) blocked the effect of U 50488 on gastric relaxation with no effect per se on the amplitude of response; naloxone also blocked the increase in gastric relaxation induced by DAMGO. When administered i.c.v. (0.1 microgram/kg) DAMGO induced a significant (P less than .05) increase in the amplitude of gastric relaxation whereas U 50488 and DPDPE (0.1 and 1 microgram/kg i.c.v.) had no effect. The effect of i.c.v. DAMGO on gastric relaxation was unaffected by a previous i.v. administration of SR 58002C (1 mg/kg). Truncal vagotomy blocked the increase in gastric relaxation induced by DAMGO (10 micrograms/kg i.v.), but did not change the effect of U 50488 (10 micrograms/kg i.v.) on gastric relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative evaluation of ulcer prevention efficacy of orally, rectally and sublingually administered omeprazole in three acute gastric ulcer models in rats

Summary— Ulcer prevention efficacy of orally, rectally and sublingually administered omeprazole was evaluated and compared using ulcer index and percentage inhibition of ulcerogenecity in three different acute gastric ulcer models viz, indomethacin, 0.6N HCl and aspirin (after pylorus ligation) induced ulcers in rats. The ulcer prevention efficacy after oral, rectal and sublingual administration were statistically significant ( P < 0.01) in all the models. The differences in ulcer index and percentage inhibition of ulcerogenecity for rectal and sublingual administration were insignificant ( P < 0.05) in indomethacin and HCl induced ulcers and were significant ( P < 0.05) in aspirin induced ulcers. The ulcer prevention activity was significantly higher ( P < 0.05) after rectal and sublingual routes when compared to oral administration in all three models evaluated. Results revealed a faster onset and higher extent of pharmacodynamic activity of omeprazole after rectal and sublingual administration.     

Potentiating effects of nicorandil on the adenosine A2 receptor-mediated vasodepression in rats: potential role for KATP channels

Summary— The effects of nicorandil on systemic blood pressure (SBP) and heart rate (HR) responses to adenosine were compared with those to N⁶-cyclopentyladenosine (CPA), a selective adenosine A, receptor agonist, and 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA), a selective adenosine A₂ receptor agonist, in anesthetized rats. When injected intravenously (iv), single bolus doses of CPCA (0.01–1.0 μg/kg), like adenosine (30 μg/kg), elicited dose-dependent decreases in SBP scarcely affecting HR, while CPA (0.03–1.0 μg/kg) produced only reduction of HR without influencing SBP. The enhancement of the vasodepressor response to CPCA, like adenosine, was induced by the iv infusion of either nicorandil (10 μg/kg per min) or cromakalim (0.1 μg/kg per min), but the response to CPA in HR remained unmodified during the infusion of nicorandil as well as cromakalim. After iv treatment with glibenclamide (20 mg/kg), an adenosine triphosphate (ATP)-sensitive K⁺ channel blocker, or 3,7-dimethyl-1-propargylxanthine (DMPX) (1 mg/kg), a selective antagonist of adenosine A₂ receptor, not only CPCA action but also the enhancement of CPCA action by nicorandil and cromakalim were significantly attenuated. Similar results were obtained in the case of single bolus iv adenosine. The present result indicates that the augmentation of the adenosine action by nicorandil appears to be mediated by activation of ATP-sensitive K⁺ channels, closely linked with stimulation on A₂ receptors by adenosine.     

Time trends in the prevalence of Helicobacter pylori infection in patients with peptic ulcer disease: a single-center retrospective study in Shanghai

ObjectiveThe present study aimed to investigate the recent trends in Helicobacter pylori infection associated with peptic ulcer disease in a large population in Shanghai.MethodsWe analyzed the medical records of all patients who had undergone upper gastrointestinal endoscopy (EGD) for uninvestigated dyspepsia at Ren Ji Hospital between 2013 and 2019 to determine the prevalence of H. pylori infection in patients with peptic ulcers.ResultsPeptic ulcers were found in 40,385 of the 383,413 patients who underwent EGD during the study period. Over the 7-year study period, the annual prevalence of H. pylori among patients receiving EGD declined from 32.2% to 26.5%. H. pylori was present in 60% of ulcers and the incidence was higher (66.9%) in duodenal compared with gastric ulcers (48.5%). The proportion of H. pylori-associated gastric ulcers declined from 52.2% to 49.3% and that of H. pylori-positive duodenal ulcers declined from 70.0% to 63.9%.ConclusionThe prevalence of H. pylori-positive peptic ulcers, mainly duodenal ulcers, fell from 2013 to 2019. However, the proportion of non-H. pylori-associated peptic ulcer disease increased, especially in elderly people, possibly due to the use of nonsteroidal anti-inflammatory drugs. Further research is needed to confirm this hypothesis.