Key result
Colloidal bismuth subcitrate significantly reduced aspirin-induced gastric microbleeding and mucosal damage compared to placebo, despite a similar ~85% reduction in PGE2 generation.
Why the study?
Does colloidal bismuth subcitrate reduce aspirin-induced gastric microbleeding and mucosal damage in healthy young male subjects?
RCT (n=10)
Double-blind
Does colloidal bismuth subcitrate reduce aspirin-induced gastric microbleeding and mucosal damage in healthy young male subjects?
Colloidal bismuth subcitrate protects against aspirin-induced gastric microbleeding and mucosal damage without preventing the suppression of prostaglandin E2 production.
Answers are grounded in this paper and cite their sources.
May support bismuth co-therapy in aspirin users at GI risk; extends mucosal protection beyond prostaglandin pathways.
Ten healthy young male subjects took part in a double-blind, placebo-controlled, crossover trial to assess the effect of colloidal bismuth subcitrate (De-No) on prostaglandin (PG) E2 generation and mucosal integrity in an aspirin (ASA)-treated stomach. After administration of ASA (2.5 g) plus placebo, a marked reduction in mucosal generation of PGE2 (by about 85%) was observed, and this was accompanied by a significant increase in gastric microbleeding and DNA loss and endoscopic and histologic damage of the mucosa. After the combination of De-Nol (300 mg four times daily) with ASA, mucosal generation of PGE2 showed a reduction similar to that in tests with ASA plus placebo, but gastric microbleeding and mucosal damage were significantly reduced. It is concluded that De-Nol has a protective action on ASA-induced gastric microbleeding and that this protection occurs despite a marked suppression of mucosal production of prostaglandins.
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Konturek et al. (1988) conducted an RCT in Healthy (n=10). Colloidal bismuth subcitrate (De-Nol) plus aspirin vs. Placebo plus aspirin (2.5 g) was evaluated on Gastric microbleeding and mucosal damage. Colloidal bismuth subcitrate significantly reduced aspirin-induced gastric microbleeding and mucosal damage compared to placebo, despite a similar ~85% reduction in PGE2 generation.
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