ppi
7 interactions related to ppi
omeprazole + magnesium
Long-term omeprazole use (typically >1 year) is associated with hypomagnesemia, likely via impaired active intestinal magnesium transport through TRPM6/TRPM7 channels. The FDA issued a formal Drug Safety Communication in 2011 warning of serious adverse events including arrhythmia, tetany, and seizures.
omeprazole + calcium
Omeprazole impairs absorption of calcium carbonate (the most common supplemental form) because dissolution and ionization require an acidic gastric environment. Long-term PPI use is associated with increased risk of hip, wrist, and spine fractures, prompting an FDA labeling change in 2010-2011.
pantoprazole + magnesium
Pantoprazole, like all PPIs, is associated with hypomagnesemia after long-term use, likely via impaired active intestinal magnesium transport (TRPM6/TRPM7). The FDA included pantoprazole in its 2011 Drug Safety Communication on PPI-induced hypomagnesemia, which can cause arrhythmia, tetany, and seizures.
esomeprazole + vitamin b12
Esomeprazole, the S-isomer of omeprazole, profoundly suppresses gastric acid required to liberate vitamin B12 from food proteins, impairing its absorption with long-term use. Studies confirm a dose- and duration-dependent reduction in serum B12 with chronic PPI therapy.
omeprazole + vitamin b12
Omeprazole suppresses gastric acid, which is required to cleave vitamin B12 from dietary proteins before it can bind intrinsic factor and be absorbed in the ileum. Long-term use (typically >2 years) is associated with measurably lower serum B12 levels and increased risk of clinical deficiency.
omeprazole + st. john's wort
St. John's wort potently induces CYP3A4 and CYP2C19, the enzymes responsible for omeprazole metabolism. Co-administration significantly lowers omeprazole plasma concentrations, reducing its acid-suppressing efficacy and potentially compromising treatment of GERD, ulcers, or H. pylori eradication.
omeprazole + iron
Omeprazole reduces absorption of nonheme (plant and supplemental) iron by raising gastric pH, which prevents the reduction of ferric (Fe3+) to absorbable ferrous (Fe2+) iron. Recent research also shows PPIs upregulate hepcidin and downregulate duodenal ferroportin, directly blocking iron export from enterocytes.