Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A significant association has previously been found between a betazole-induced decrease in serum group I pepsinogen (PG I) levels and a low peak acid output (PAO) in symptomatic patients with vagotomy and gastric resection or a drainage procedure. This study compares the effect of betazole on serum PG I levels and gastric acid output in 245 unoperated patients (115 duodenal ulcer, 25 prepyloric ulcer, 32 gastric ulcer, 73 nonulcer) and in 73 symptomatic postoperative patients (15 subtotal gastric resection, 28 vagotomy and gastric resection, 30 vagotomy and drainage). A negative serum PGI response (2-hr serum PG I level less than 92% of basal) occurred in 10 (4.1% of the unoperated patients and in 31 (42.5%) of the postoperative patients. Seven (70%) of the former and 29 (93.5%) of the latter patients had a PAO of less than 10 mEq per hr, indicating that a negative serum PG I response is associated with a low PAO in both unoperated and postoperative patients. The PAO was greater than 10 mEq per hr in 93.1% of the 277 patients with a 2-hr serum PG I level of more than 92% of basal. Additional studies revealed that neither aspiration of gastric juice nor perfusion of the stomach with acid altered the serum PG I response. This suggests that topical acid does not modulate the effect of betazole on serum PG I levels. Finally, a negative serum PG I response has been shown to be paradoxical, in that gastric pepsin levels have been found to increase over basal concurrently with the decrease in serum PG I levels.
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PMID:Effect of betazole on serum group I pepsinogen levels: relationship to gastric acid output in unoperated and postoperative patients. 84 14

The CURE peptic ulcer clinic started in April 1974. Patients (mostly veterans) with documented ulcer disease were interviewed regularly and inpatient hospitalizations were reviewed for follow-up periods of up to 6 years. Data from 245 male ulcer patients, 190 with duodenal ulcer alone and 55 with both documented duodenal ulcer (DU) and gastric ulcer (GU), were analyzed to assess the natural history of ulcer disease and factors predicting the severity of its course. Eleven percent of clinic patients had a complication (bleeding requiring a transfusion, perforation, or obstruction) during follow-up. Complication rates were about 2.7% per year for those with no prior complication, and about 5% per year for those with a prior complication. No patient variables or ulcer markers were related to the likelihood of a complication. Patients with both DU and GU were similar to patients with DU alone on many background variables, but the combined ulcer group had a significantly higher frequency of blood group nonsecretors, increased incidence of cigarette smoking, and greater frequency of complications or ulcer hospitalization prior to entry into the study and during follow-up. These factors, together with our failure to find differences in aggressive factors (acid output and PGI), suggests that DU + GU represents a different disease entity marked by additional defects in mucosal defense.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of duodenal ulcer patients. 666 43

It has been assumed that cyclooxygenase-2 (COX-2) is solely responsible for inflammatory processes. Recently, this view has been challenged because COX-2-selective agents caused a delay of gastric ulcer healing and exacerbation of inflammation in rats. To further characterize organ-specific toxic effects of selective and nonselective COX inhibitors, we assessed the eicosanoid release from different rat organs ex vivo after oral administration of the COX-2-selective inhibitor NS-398 and the unselective COX inhibitors diclofenac, meloxicam, and ketorolac. Prostanoid and leukotriene release from tissue fragments of the stomach, kidney, lung, and brain were determined after ex vivo incubation of tissue fragments in Tyrode's solution for 10 min at 37 degrees C. Ketorolac (0.1, 0.3, and 0.9 mg/kg) inhibited prostanoid release from all organs most potently and led to a significant increase of leukotriene release from the lung. Effects of diclofenac and meloxicam (1, 3, and 9 mg/kg each) were similar for all organs tested. At 9 mg/kg, 6keto-prostaglandin F (PGF)(1alpha) release from gastric mucosa was reduced by 79.1 +/- 11.4 and 87.6 +/- 7.7% and PGE(2) release from rat kidney was inhibited by 60.4 +/- 6.8 and 78.6 +/- 16.6% by diclofenac and meloxicam, respectively. NS-398 did not reduce prostanoid release from the lung. Consistent with the reported constitutive expression of COX-2, prostanoid release from kidney and brain was reduced by 20 to 30%. The release of 6keto-PGF(1alpha) from gastric mucosa was reduced by 34.7 +/- 22.2% at 3 mg/kg and by 86.9 +/- 12.7% at 9 mg/kg. At these doses, NS-398 has been previously shown to be COX-2 selective. Because PGF(1alpha) is the stable breakdown product of PGI(2), these results suggest that COX-2 contributes to PGI(2) synthesis in the rat stomach.
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PMID:Effects of selective and unselective cyclooxygenase inhibitors on prostanoid release from various rat organs. 1068 36