[HORMONAL-GENETIC SCREENING IN PATIENTS, SUFFERING GASTRODUODENAL ULCER HEMORRHAGE].

Genetic-hormonal regulation plays a key pathophysiologic role in a blood loss on background of complicated gastroduodenal ulcer disease, but a clinical significance of some genes of compensatory steroidogenesis remains unrevealed. Examination of 63 patients, using a chain reaction with polymerase (CRP); analysis of length of restriction fragments (CRP-RFLP) and immunohistochemical investigation of gastroduodenal mucosa were performed on the base of a Sumsky Rural Clinical Hospital. Trustworthy difference of distribution of polymorphic genes ESR1 and VKORC1 in patients of both gender in presence of the ulcer hemorrhage was not revealed, excluding genotype A/A VKORC1, what trustworthy more frequently was revealed in women (p < 0.05). There was established, that intact zone of gastric fundus owes immunoreactivity towards alpha-receptors of estrogen in nuclei of epitheliocytes and stromocytes. Diagnosis of polymorphic gene VKORC1 and expression of the estrogen receptors may serve the base for pathogenetic therapy in patients with hemorrhage occurrence.

[BIOLOGICAL RESERVOIRS AS A THE RESPONSE OF THE ORGANISM TO INJURY AND PROOF FOR METABOLIC CORRECTION IN GASTRODUODENAL HEMORRHAGE IN PATIENTS WITH HIGH OPERATING-ANESTHETIC RISK].

In the authors opinion in the process of self-regulation the human body creates some biological reservoirs in response to damage (disturbance of homeostasis) for constant internal environment In cases of decompensation and depletion of these pools metabolic correction is necessary. This opinion was based on the results of the endoscopic metabolic hemostasis in ulcer gastroduodenal bleeding in patients with high operational and anesthetic risk.

[Gastroduodenal mucosa sensitivity to estrogen in ulcers complicated by hemorrhage].

Expression of alpha-receptors of estrogen (RE) in accordance to immunohistochemical (IHC) labeling in gastroduodenal mucosa cells was studied up in patients, suffering the ulcer disease and without it. In 4 patients (group I) a gastroduodenal mucosa affection was revealed, they were operated on for hemorrhage from gastroduodenal ulcers; in 3 patients (group II) gastroduodenal mucosa affection was not observed; in 4 patients (group III, control), a mammary gland cancer was diagnosed, a positive reaction on alpha-RE was noted. In groups I and II the biopsies were studied, obtained from pylorus and gastric fundus, as well as from duodenal ampula, and in a group III--obtained from the tumor. In a control group a positive labeling of nuclei was revealed in biopsies. In patients of groups I and II the alpha-RE expression by cellular nuclei was not revealed, but, the lots of positive IHC labeling of cytoplasm in glandular and stromal mucosal cells of the investigated gut were noted. Positive IHC labeling of cytoplasm for alpha-RE witnesses about sensitivity to them in norma and pathological processes. But, a trustworthy difference of alpha-RE expression by cellular nuclei was not noted. For confirmation or denial of this hypothesis further clinical and IHC investigations are needed.

Weak up-regulation of serum response factor in gastric ulcers in patients with co-morbidities is associated with increased risk of recurrent bleeding.

BACKGROUND: Serum response factor (SRF) is crucial for gastric ulcer healing process. The study determined if gastric ulcer tissues up-regulate SRF and if such up-regulation correlated with co-morbidities and the risk of recurrent bleeding. METHODS: Ulcer and non-ulcer tissues were obtained from 142 patients with active gastric ulcers for SRF expression assessed by immunohistochemistry. Based on the degree of SRF expression between these two tissue types, SRF up-regulation was classified as strong, intermediate, and weak patterns. The patients were followed-up to determine if SRF up-regulation correlated to recurrent bleeding. RESULTS: Gastric ulcer tissues had higher SRF expression than non-ulcer tissues (p < 0.05). Patients with strong SRF up-regulation had lower rates of stigmata of recent hemorrhage (SRH) on the ulcer base than the others (p < 0.05). Multivariate logistic regression confirmed that co-morbidities and weak SRF up-regulation were two independent factors of recurrent gastric ulcer bleeding (p < 0.05). Combining both factors, there was an 8.29-fold (95% CI, 1.31~52.62; p = 0.03) higher risk of recurrent gastric ulcer bleeding. CONCLUSIONS: SRF expression is higher in gastric ulcer tissues than in non-ulcer tissues. Weak SRF up-regulation, combined with the presence of co-morbidities, increase the risk of the recurrent gastric ulcer bleeding.

[Free radical processes in patients with the gastro-intestinal bleedings].

The role of the free radical processes (FRP) is shown and objectified in the development of the ulcer gastro-intestinal bleedings (UGIB). It is revealed on the first day of hospitalization already. The greatest imbalance of the FRP is registered in heavy patients with acute UGIB. It appeared like decrease of the oxygen and activation of the lipid FRP disregulation. Unheavy patients have FRP changes refer to the oxygen part of the oxidation process only. Intensification FRP in process of increase of weight disease consists in decrease activity oxygen and increase a lipid disbalance. FRP disbalance has long time proceeds, last till the patient's discharge. Results of the research prove as much as possible early inclusion in a complex of medical actions antoixidant therapy. The high efficiency of the energetic corrector reamberin in a dose of 400-800 ml was shown in patients with UGIB.

Intragastric pH with oral vs intravenous bolus plus infusion proton-pump inhibitor therapy in patients with bleeding ulcers.

BACKGROUND & AIMS: Intravenous bolus plus infusion proton pump inhibitor (PPI) therapy is recommended for patients with bleeding ulcers and higher risk stigmata. If frequent oral dosing of PPIs provided similar antisecretory effect, this might be preferred based on ease and cost. METHODS: Patients presenting with overt bleeding due to ulcers had intragastric pH probes placed after endoscopy and baseline pH recorded. They were randomly assigned to intravenous lansoprazole (90-mg bolus followed by 9-mg/h infusion) or oral lansoprazole (120-mg bolus followed by 30 mg every 3 hours). pH was recorded for 24 hours. RESULTS: Intragastric pH was > 6 for 67.8% of the study period with intravenous PPI (n = 32) and 64.8% with oral PPI (n = 34): difference, 3.0%; 95% confidence interval (CI): -9.2% to 15.2%. Intragastric pH was > 6 for > 60% of the study period in 22 (68.8%) patients receiving intravenous and 22 (64.7%) patients receiving oral PPI: difference, 4.0%; 95% CI: -18.7% to 26.8%. At 1 hour, mean pHs for intravenous vs oral were 5.3 +/- 0.4 vs 3.3 +/- 0.4, respectively (difference, 2.0; 95% CI: 0.8-3.1; P = .001). At > or = 1.5 hours, 95% CIs of the differences for all hourly mean pHs included zero. Mean pH rose above 6 after 2-3 hours of intravenous PPI and 3-4 hours of oral PPI. CONCLUSIONS: Frequent oral PPI may be able to replace the currently recommended intravenous bolus plus infusion PPI therapy in patients with bleeding ulcers, although the possibility that intravenous PPIs are superior cannot be definitively excluded given our relatively wide confidence intervals. Intravenous PPI provides more rapid increase in pH, reaching mean pH of 6 approximately 1 hour sooner than oral PPI.

Role of the NO/cGMP/K(ATP) pathway in the protective effects of sildenafil against ethanol-induced gastric damage in rats.

BACKGROUND AND PURPOSE: Sildenafil is a selective inhibitor of cGMP-specific phosphodiesterase. Sildenafil, acting via NO-dependent mechanisms, prevents indomethacin-induced gastropathy. Activation of ATP-sensitive potassium channels (K(ATP)) is involved in gastric defence. Our objective was to evaluate the role of the NO/cGMP/K(ATP) pathway in the protective effects of sildenafil against ethanol-induced gastric damage. EXPERIMENTAL APPROACH: Rats were treated with L-NAME (1 or 3 mg kg(-1), i.p.) or with L-arginine (200 mg kg(-1), i.p.) + L-NAME (3 mg kg(-1), i.p.), the guanylate cyclase inhibitor, ODQ (10 mg kg(-1), i.p.), glibenclamide (0.1, 0.3, 1 or 3 mg kg(-1), i.p.) or with glibenclamide (1 mg kg(-1), i.p.) + diazoxide (3 mg kg(-1), i.p.). After thirty minutes, the rats received sildenafil (1 mg kg(-1), by gavage), followed by intragastric instillation of absolute ethanol (4 ml kg(-1)) to induce gastric damage. One hour later, gastric damage (haemorrhagic or ulcerative lesions) was measured with a planimetry programme. Samples of stomach were also taken for histopathological assessment and for assays of tissue glutathione and haemoglobin. KEY RESULTS: Sildenafil significantly reduced ethanol-induced gastric damage in rats. L-NAME alone, without L-arginine, significantly reversed the protection afforded by sildenafil. Inhibition of guanylate cyclase by ODQ completely abolished the gastric protective effect of sildenafil against ethanol-induced gastric damage. Glibenclamide alone reversed sildenafil's gastric protective effect. However, glibenclamide plus diazoxide did not alter the effects of sildenafil. CONCLUSIONS: Sildenafil had a protective effect against ethanol-induced gastric damage through the activation of the NO/cGMP/K(ATP) pathway.

Sildenafil reduces alcohol-induced gastric damage: just say 'NO'.

Although sildenafil (Viagra) and other phosphodiesterase V (PDE V) inhibitors are increasingly recognized for their use in the treatment of male erectile dysfunction and perhaps more recently pulmonary artery hypertension, less is known of their potential beneficial effects in other situations. Medeiros et al., in the current issue of the British Journal of Pharmacology, report that sildenafil dramatically reduces alcohol-induced gastric damage in rats. The authors provide convincing evidence that such protection not only occurs via the nitric oxide (NO)/cGMP pathway, but also involves regulation of ATP-sensitive potassium channels. Therefore, in addition to exerting anti-impotence efficacy, PDE V inhibitors may provide significant beneficial effects from mucosal injury induced by alcohol.

Gastric protection by alpha-melanocyte-stimulating hormone against ethanol in rats: involvement of somatostatin.

The proopiomelanocortin-derived tridecapeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is a neuropeptide that exerts broad anti-inflammatory actions in mammals. This study aimed to investigate the effect of alpha-MSH on ethanol-induced gastric ulcer in rats and to evaluate the involvement of endogenous somatostatin in the actions of the peptide. The rats received 1 mL 75% ethanol or saline orally. alpha-MSH was given (25 micro g/rat; i.p.) alone or following the somatostatin antagonist cyclo-(7-aminoheptanoyl-PH-E-d-Trp-Lys-THR) (10 microM/kg; i.p.) administration. Gastric lesions were scored macroscopically and microscopically following decapitation at 30 min after ethanol challenge. Gastric malondialdehyde (MDA) level, myeloperoxidase (MPO) activity and mast cell counts were assessed. Ethanol-induced gastric hemorrhagic lesions were characterized by increased gastric MDA level, MPO activity and mast cell counts. alpha-MSH treatment decreased the extent of tissue injury and reversed tissue MDA level, MPO activity and mast cell counts. The effect of the peptide on the severity of gastric lesions, MDA level and MPO activity was reversed by the somatostatin antagonist. In conclusion, alpha-MSH is beneficial in a rat model of gastric ulcer via mechanisms which partly involve the endogenous somatostatin.

Role of circadian rhythm and endogenous melatonin in pathogenesis of acute gastric bleeding erosions induced by stress.

Stress that appears as a consequence of burns, surgical trauma and life threatening conditions is a serious clinical entity, can result in acute gastric mucosal lesions. Such stress lesions can develop in response to the imbalance between the aggressive factors promoting mucosal damage and the gastric mucosal defense mechanisms including predominantly gastric blood flow (GBF), biosynthesis of gastroprotective prostaglandins (PG) and enhanced mucus/bicarbonate secretion. Melatonin, a major hormone of pineal gland, whose activity is also abundant in the gastrointestinal tract, was shown to inhibit gastric acid secretion, augment GBF and scavenge free radicals, resulting in the attenuation of stress-induced gastric lesions. Melatonin is released during the night but little is known about the effect of circadian rhythm and day/night alterations in melatonin secretion on the formation of stress-induced gastric lesions. Using rats with intact pineal glands and those with removed pineal glands (pinealectomy) exposed to water immersion and restraint stress (WRS) at both, day and night hours, we studied the effect of light and nocturnal melatonin on the formation of these lesions, and accompanying changes in GBF and plasma melatonin levels. It was found that the gastric mucosa exposed to WRS of various time duration's lasting 1.5, 3 and 6 h, time-dependently increased the number of gastric lesions and this effect was accompanied by the time-dependent fall in the GBF and an increase in the plasma and luminal melatonin levels. Pinealectomy augmented WRS-induced lesions at each time intervals of WRS and produced a marked fall in the GBF and plasma and luminal melatonin levels at each time interval of WRS tested. WRS lesions were significantly reduced at night hours and showed circadian variations in plasma levels melatonin with significantly higher plasma melatonin levels at night than in the day and with a greater magnitude of damage induced in the daily hours than at night hours. WRS-induced gastric mucosal lesions were markedly enhanced in pinealectomized rats, both at day and night, and this was accompanied by a significant fall in plasma melatonin levels Stress that appears as a consequence of burns, surgical trauma and life threatening conditions is a serious clinical entity, can result in acute gastric mucosal lesions. Such stress lesions can develop in response to the imbalance between the aggressive factors promoting mucosal damage and the gastric mucosal defense mechanisms including predominantly gastric blood flow (GBF), biosynthesis of gastroprotective prostaglandins (PG) and enhanced mucus/bicarbonate secretion. Melatonin, a major hormone of pineal gland, whose activity is also abundant in the gastrointestinal tract, was shown to inhibit gastric acid secretion, augment GBF and scavenge free radicals, resulting in the attenuation of stress-induced gastric lesions. Melatonin is released during the night but little is known about the effect of circadian rhythm and day/night alterations in melatonin secretion on the formation of stress-induced gastric lesions. Using rats with intact pineal glands and those with removed pineal glands (pinealectomy) exposed to water immersion and restraint stress (WRS) at both, day and night hours, we studied the effect of light and nocturnal melatonin on the formation of these lesions, and accompanying changes in GBF and plasma melatonin levels. It was found that the gastric mucosa exposed to WRS of various time duration's lasting 1.5, 3 and 6 h, time-dependently increased the number of gastric lesions and this effect was accompanied by the time-dependent fall in the GBF and an increase in the plasma and luminal melatonin levels. Pinealectomy augmented WRS-induced lesions at each time intervals of WRS and produced a marked fall in the GBF and plasma and luminal melatonin levels at each time interval of WRS tested. WRS lesions were significantly reduced at night hours and showed circadian variations in plasma levels melatonin with significantly higher plasma melatonin levels at night than in the day and with a greater magnitude of damage induced in the daily hours than at night hours. WRS-induced gastric mucosal lesions were markedly enhanced in pinealectomized rats, both at day and night, and this was accompanied by a significant fall in plasma melatonin levels with a pronounced reduction in mucosal generation of PGE(2) and GBF and by a small increase in plasma melatonin levels during the dark phase. We conclude that 1) stress-induced gastric bleeding erosions exhibit circadian rhythm with an increase in the day and attenuation at night and that these fluctuations in the formation of stress-induced gastric damage may depend upon the melatonin synthesis 2) the progressive increase in plasma melatonin in pinealectomized animals exposed to various time intervals of WRS suggests that extra-pineal melatonin possibly that derived from gastrointestinal tract, play an important role in the gastric mucosal defense against stress-induced gastric damage.

[Changes of duodenal biochemical content in the early duodenal recurrent hemorrhage].

The dynamics of the indices changes concerning the general protein, urea and glucose content was investigated in 32 mongrel dogs while modelling the hemorrhage from duodenum and its early recurrence. There was established that the urea content and somewhat the general protein content reflect most accurately the hazard of the early recurrent hemorrhage occurrence.

The effect of regular and high doses of omeprazole on the intragastric acidity in patients with bleeding peptic ulcer treated endoscopically: a clinical trial with continuous intragastric pH monitoring.

OBJECTIVE: In peptic ulcer bleeding (PUB), pH level >4 is considered necessary to prevent dissolving of a formed fibrin clot. The effect of regular or high doses of omeprazole on the intragastric pH in patients with acute PUB was studied. METHODS: In our earlier study, after endoscopic therapy, PUB patients were randomized to receive a regular dose of intravenous omeprazole (20 mg; i.e. 60 mg/3 days) or a high dose of omeprazole (80 mg bolus + 8 mg/h; i.e. 652 mg/3 days). Of these 142 analysed and reported patients, 13 PUB patients also had intragastric pH monitoring for these 3 days; seven of these patients had a regular dose and six received a high dose of omeprazole. RESULTS: The mean 24-h intragastric pH (regular versus high dose) on day 1 was 4.9 +/- 1.6 versus 6.3 +/- 0.5 (P = 0.035), on day 2 was 4.9 +/- 1.8 versus 6.7 +/- 0.3 (P = 0.001), and on day 3 was 5.7 +/- 1.1 versus 6.7 +/- 0.5 (P = NS). The medians of the intragastric pH were 6 versus 6.5 (P = 0.082) on day 1, 5.8 versus 6.8 (P = 0.001) on day 2, and 6.2 versus 6.8 (P = 0.17) on day 3. The proportion of time when pH <4 on day 1 was 29.2 +/- 34.1 versus 5.4 +/- 5.7% (P = NS). CONCLUSIONS: A regular dose of omeprazole raises the mean and median 24-h intragastric pH >4 in patients with PUB. This reduction in the acidity together with endoscopic therapy is probably sufficient to maintain haemostasis. A high dose of omeprazole keeps the pH almost constantly >6.

Effect of lysozyme chloride on betel quid chewing aggravated gastric oxidative stress and hemorrhagic ulcer in diabetic rats.

AIM: To evaluate the protective effect of lysozyme chloride on betel quid chewing (BQC) aggravated gastric oxidative stress and hemorrhagic ulcer in rats with diabetes mellitus (DM). METHODS: Male Wistar rats were challenged intravenously with streptozotocin (65 mg/kg) to induce DM. Rats were fed with regular pellet food or BQC-containing diets. After 90 d, rats were deprived of food for 24 h. Rat stomachs were irrigated for 3 h with normal saline or simulated gastric juice. Rats were killed and gastric specimens were harvested. RESULTS: An enhancement of various gastric ulcerogenic parameters, including acid back-diffusion, mucosal lipid peroxide generation, as well as decreased glutathione levels and mucus content, were observed in DM rats. After feeding DM rats with BQC, an exacerbation of these ulcero-genic parameters was achieved. Gastric juice caused a further aggravation of these ulcerogenic parameters. Daily intragastric lysozyme chloride dose-dependently inhibited exacerbation of various ulcerogenic parameters in those BQC-fed DM rats. CONCLUSION: (1) Gastric juice could aggravate both DM and BQC-fed DM rat hemorrhagic ulcer; (2) BQC exacerbated gastric hemorrhagic ulcer in DM rats via enhancing oxidative stress and reducing defensive factors; (3) lysozyme chloride effectively protected BQC aggravated gastric damage in DM rats.

[Application of the proton pump inhibitors in treatment of an acute gastro-intestinal bleeding of the ulcer etiology].

The results of treatment of 53 patients, suffering an acute gastro-intestinal bleeding of the ulcer etiology are adduced. The proton pump inhibitor Omez infusion have promoted the improvement of the patients treatment results.

Gastric mucosal resistance to acute injury in experimental portal hypertension.

1. The gastric mucosa of portal hypertensive rats exhibits important microvascular changes and a nitric oxide (NO)-dependent hyperemia. This study analyses whether portal hypertensive mucosa exhibits changes in its ability to withstand aggression. 2. Portal hypertension was induced by partial portal vein ligation (PPVL) or common bile duct ligation (CBDL) and gastric damage was induced by oral administration of ethanol or aspirin. Experiments were performed in conscious or anaesthetized rats and some animals were pre-treated with the NO-synthesis inhibitor L-NAME. 3. Conscious PPVL or CBDL rats showed an increased resistance to the damaging effects of ethanol. Oral administration of aspirin produced less gastric damage in PPVL conscious rats than in the control group. 4. The protective effects of portal hypertension were maintained in animals anaesthetized with ketamine and absent when pentobarbital was employed. 5. Pre-treatment with L-NAME restored the damaging effects of ethanol and aspirin in PPVL rats without modifying the level of damage in control animals. 6. Gastric bleeding induced by oral aspirin, as measured by the luminal release of (51)Cr-labelled erythrocytes, was significantly greater in PPVL rats than in control animals. 7. Semi-quantitative analysis by RT--PCR of the mRNA for endothelial NO-synthase (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS) levels showed that the expression of iNOS was slightly increased in both the gastric mucosa and smooth muscle of PPVL rats. No changes were observed in eNOS and nNOS expression. 8. Conscious portal hypertensive rats exhibit an enhanced resistance to acute gastric damage which is absent under the influence of some types of anaesthesia and seems related to an increased synthesis of nitric oxide. However, mucosal lesions in these animals show an augmented bleeding per area of injury.

Inhibition of Helicobacter pylori-induced cyclo-oxygenase-2 aggravates NSAID-caused gastric damage in Mongolian gerbils.

BACKGROUND: The effect of Helicobacter pylori infection on non-steroidal anti-inflammatory drug-induced gastric mucosal injury is controversial. AIM: To examine the effect of the interaction between H. pylori and non-steroidal anti-inflammatory drugs on gastric mucosal injury. METHODS: Mongolian gerbils infected with H. pylori were treated with indometacin at 8 mg/kg for 2 days or 7 days. Mucosal damage was assessed by macroscopic and histological examination, and myeloperoxidase activity was measured as an index of neutrophil infiltration. The expression levels of cyclo-oxygenase proteins were determined by Western blot analysis and cyclo-oxygenase activity. RESULTS: A 2-day course of indometacin did not cause an increase in gastric damage in H. pylori-infected Mongolian gerbils compared to uninfected gerbils, while a 7-day course of indometacin caused additive gastric damage in H. pylori-infected animals. H. pylori infection induced cyclo-oxygenase-2 expression in the stomach. Treatment with indometacin for 2 days did not significantly affect cyclo-oxygenase activity in H. pylori-infected animals, while treatment for 7 days inhibited both cyclo-oxygenase-1 and cyclo-oxygenase-2 activities. Pre-treatment with a selective cyclo-oxygenase-2 inhibitor aggravated mucosal injury in H. pylori-infected animals treated or not treated with indometacin for 2 days. CONCLUSIONS: Our results suggest that cyclo-oxygenase-2 protein induced by H. pylori infection may be involved in the defence of the gastric mucosa against damage caused by non-steroidal anti-inflammatory drugs. Therefore, inhibition of cyclo-oxygenase-2 activity may enhance non-steroidal anti-inflammatory drug-caused gastric damage in H. pylori-infected animals.

Role of histamine and acid back-diffusion in modulation of gastric microvascular permeability and hemorrhagic ulcers in Salmonella typhimurium-infected rats.

Documentation concerning the pathogenesis of gastric hemorrhagic ulcer in Salmonella typhimurium (Salmonella typhi)-infective disease is lacking. This research first proposed that alterations of mast cell histamine release, gastric acid back-diffusion and mucosal microvascular permeability are important in modulating gastric ulcer and hemorrhage in Salmonella typhi-infected rats. Additionally, effects of several histamine-related drugs on this ulcer model were evaluated. Male Wistar rats were deprived food for 36 h. Live cultures of Salmonella typhi (OU 5045, 1 x 10(10) CFU in 1.0 mL of sterilized phosphate buffer saline) were challenged, intrajejunally to rats just before withdrawal of food. Control rats received the same volume of sterilized vehicle only. Rat stomachs were irrigated for 3 h with either normal saline or simulated gastric juice. Gastric acid back-diffusion, mucosal histamine concentration, microvascular permeability as well as luminal hemoglobin content and ulcer areas were determined. Severe gastric hemorrhage and mucosal ulcerations, particularly in acidic stomachs, were observed in Salmonella typhi-infected rats. A positive correlation of histamine to gastric hemorrhage and ulcer was found in those rats with Salmonella typhi-infection. This hemorrhagic ulcer in Salmonella typhi-infected rats was effectively ameliorated by intraperitoneal ketotifen, diphenhydramine and ranitidine but was worsen by exogenous histamine or diamine oxidase. In conclusion, enhancement of acid back-diffusion, mast cell histamine release and microvascular permeability is important in modulating gastric hemorrhage and ulcer in Salmonella typhi-infected rats.

Prostaglandin E2 in duodenal ulcer complications.

Prostaglandins are presumed to have cytoprotective properties and may play a role in the pathogenesis of duodenal ulcer and its complications. To evaluate this hypothesis, 35 patients with either duodenal ulcer bleeding (18 patients) or gastric outlet obstruction (17 patients) were investigated. Biopsies were taken from gastroduodenal tissues and secretions for prostaglandin E2 (PGE2) levels. These levels were compared to those taken from the same areas during a later endoscopy. A correlation was found between the severity of the clinical endoscopic findings and PGE2 levels. Increased levels of PGE2 were found in the quiescent phase and decreased levels found during the deteriorated phase. These differences of PGE2 levels were found to be of significant value (P less than 0.002). Furthermore, the patients in which the PGE2 levels were decreased at second endoscopy needed surgery. PGE2 may, thus, be a factor in duodenal ulcer pathogenesis and its complications, and be used as a prognostic marker and guide.

The influence of intravenous omeprazole on intragastric pH and outcomes in patients with peptic ulcer bleeding after successful endoscopic therapy--a prospective randomized comparative trial.

BACKGROUND/AIMS: The role of omeprazole in preventing rebleeding in patients with peptic ulcer bleeding after successful endoscopic therapy has been controversial. In this study, we used 3 different formulas of intravenous omeprazole in the above patients. We wished to compare the intragastric pH and outcomes among them. METHODOLOGY: Between July 1996 and May 1997, after having obtained initial hemostasis with endoscopic therapy, a total of 20 patients with peptic ulcer bleeding (spurting/oozing/non-bleeding visible vessel: 6/4/10) received intravenous bolus of omeprazole 20 mg every 3 hours; 20 patients (3/5/12) received intravenous bolus of omeprazole 40 mg every 6 hours; and, 20 patients (5/4/11) received intravenous bolus of omeprazole 80 mg every 12 hours for 3 days. One intragastric pH meter (Gastrograph Mark III, Medical Instruments Corp. Switzerland) was used to record 24-hour intragastic pH. RESULTS: The intragastric pH in the patients receiving omeprazole 20 mg every 3 hours was 6.1, 6.0-6.2 (mean: 95% CI); in patients receiving omeprazole 40 mg every 6 hours it was 6.4, 6.2-6.5; and, in patients receiving omeprazole 80 mg every 12 hours it was 5.8, 5.7-5.9. The duration of intragastric pH > 6.0 in omeprazole 20 mg every 3 hours was 70.9%, 57.3%-84.4% (mean: 95% CI); in omeprazole 40 mg every 6 hours it was 83.1%, 73.1%-93.1%; and, in omeprazole 80 mg every 12 hours it was 66%, 51.5%-80.4%. Patients with peptic ulcers receiving omeprazole 40 mg intravenous bolus every 6 hours had the highest intragastric pH as compared with the other 2 groups (p < 0.0001). There were no significant differences concerning rebleeding rates, volume of blood transfusion, hospital stay, numbers of operation and mortality among the 3 groups. CONCLUSIONS: After initial hemostasis had been obtained, patients with peptic ulcer bleeding receiving 40 mg intravenous bolus every 6 hours had the highest intragastric pH. However, they had similar outcomes with the other 2 groups.