indication

Used to treat nausea, heartburn, indigestion, upset stomach, diarrhea, and other temporary discomforts of the stomach and gastrointestinal tract.

pharmacology

Bismuth subsalicylate displays anti-inflammatory action (due to salicylic acid) and also acts as an antacid and mild antibiotic. It can also cause a black tongue and black stools in some users of the drug, when it combines with trace amounts of sulfur in their saliva and gastrointestinal tract. This discoloration is temporary and harmless.

mechanism of action

As an antidiarrheal, the exact mechanism has not been determined. Bismuth subsalicylate may exert its antidiarrheal action not only by stimulating absorption of fluid and electrolytes across the intestinal wall (antisecretory action) but also, when hydrolyzed to salicylic acid, by inhibiting synthesis of a prostaglandin responsible for intestinal inflammation and hypermotility. In addition, bismuth subsalicylate binds toxins produced by Escherichia coli. Both bismuth subsalicylate and the intestinal reaction products, bismuth oxychloride and bismuth hydroxide, are believed to have bactericidal action. As an antacid, bismuth has weak antacid properties.

biotransformation

Based on in vitro dissociation data and in vivo animal data, bismuth subsalicylate is believed to be largely hydrolyzed in the stomach to bismuth oxychloride and salicylic acid. In the small intestine, nondissociated bismuth subsalicylate reacts with other anions (bicarbonate and phosphate) to form insoluble bismuth salts. In the colon, nondissociated bismuth subsalicylate and other bismuth salts react with hydrogen sulfide to produce bismuth sulfide, a highly insoluble black salt responsible for the darkening of the stools.

absorption

Following oral administration, absorption of the salicylate component from the small intestine is generally rapid and complete (>90%).

drug interactions

Acetazolamide: The salicylate, bismuth subsalicylate, at high dose increases the effect of the carbonic anhydrase inhibitor, acetazolamide.

Amprenavir: The antiacid decreases the absorption of amprenavir

Atazanavir: This gastric pH modifier decreases the levels/effects of atazanavir

Betamethasone: The corticosteroid, betamethasone, may decrease the effect of the salicylate, bismuth subsalicylate.

Fludrocortisone: The corticosteroid, fludrocortisone, may decrease the effect of the salicylate, bismuth subsalicylate.

Gliclazide: The salicylate, bismuth subsalicylate, increases the effect of the sulfonylurea, gliclazide.

Glyburide: The salicylate, bismuth subsalicylate, increases the effect of the sulfonylurea, glibenclamide.

Hydrocortisone: The corticosteroid, hydrocortisone, may decrease the effect of the salicylate, bismuth subsalicylate.

Methazolamide: The salicylate, bismuth subsalicylate, at high dose increases the effect of the carbonic anhydrase inhibitor, methazolamide.

Methotrexate: The salicylate, bismuth subsalicylate, increases the effect and toxicity of methotrexate.

Minocycline: Formation of non-absorbable complexes

Prednisolone: The corticosteroid, prednisolone, may decrease the effect of the salicylate, bismuth subsalicylate.

Prednisone: The corticosteroid, prednisone, may decrease the effect of the salicylate, bismuth subsalicylate.

Probenecid: The salicylate, bismuth subsalicylate, decreases the uricosuric effect of probenecid.

Tetracycline: Formation of non-absorbable complexes

Triamcinolone: The corticosteroid, triamcinolone, may decrease the effect of the salicylate, bismuth subsalicylate.