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)

Recognising the inhibitory activity of acetazolamide upon acid gastric secretion and its favorable effects in the treatment of gastric ulcer which we have described (see reference) - we applied the therapeutical testing by acetazolamide in the differentiation of benign from malignant niches of the stomach. Acetazolamide was administered orally at doses of 25-30 mg per kilogram body weight in a long term trial, together with 3 gr sodium bicarbonate, 1 gr potassium bicarbonate, 1.5 gr magnesium oxide per day and an increased quantity of liquids, to 741 patients with radiologically demonstrated ulcer craters. The fundamental criterion was the size of the niche as established by radiologic examination. In all gastric ulcers the size of the niche was considerably reduced after 7-9 days of treatment with acetazolamide; the niche disappeared in 2-3 weeks. This favorable result was obtained without diet and rest. In 38 cases in which there was no significant radiologic change of the niche after 7-9 days of treatment with acetazolamide - the malignancy of the niche was confirmed. The simplicity and the effectiveness of this rapid therapeutic test, makes it useful in the differentiation of benign from a malignant ulcer craters.
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PMID:Therapeutic testing by acetazolamide in the differentiation of a benign from a malignant niche. 88 70

The present experiment demonstrated that relatively high doses of acetazolamide (100 and 200 mg/kg s.c.) induced severe gastric hemorrhagic ulceration in rats. This ulceration was aggravated by oral administration of HC1, but was inhibited by NaHCO3. Further, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were affirmed by an increase in serotonin and histamine released from the stomach after acetazolamide treatment. Acetazolamide injection also increased the protein level, but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increases in serotonin and histamine released may also have been contributing factors for gastric ulcer formation.
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PMID:Pathogenesis of gastric ulceration produced by acetazolamide in rats. 632 41

The present study demonstrated that acetazolamide (100 and 200 mg/kg, s.c.) induced severe gastric hemorrhagic ulceration in rats. The ulceration was aggravated by oral administration of HCl, but was inhibited by NaHCO3. Furthermore, the severity of ulceration was also decreased by pretreatment with methysergide, chlorpheniramine, or cimetidine. These protective effects were accompanied by an increase in serotonin and histamine released from the stomach. Acetazolamide injection also increased the protein level but reduced the sialic acid content in the gastric secretion, indicating that the gastric mucosal barrier may have been damaged. Prostaglandin E2 content of the gastric mucosa was not affected by the drug; however, carbonic anhydrase activity was markedly reduced in a dose-dependent manner. Thus, it is suggested that the ulceration induced by acetazolamide is mainly due to the inhibition of carbonic anhydrase activity and mucus secretion. The increase in serotonin and histamine release also may have been the contributing factors for gastric ulcer formation.
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PMID:Study of the damaging effects of acetazolamide on gastric mucosa in rats. 644 31