PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1679670

Drug interactions with antisecretory agents.

P D Hansten
View original source ↗Export metadata ↓

Abstract

Antisecretory agents may affect the absorption, metabolism, and renal excretion of other drugs. Inhibition of gastric acid secretion may decrease the gastrointestinal absorption of drugs such as ketoconazole that dissolve poorly in the absence of adequate acid. With anti-secretory agents, the drug interaction mechanism most likely to result in adverse effects is the inhibition of hepatic oxidative drug metabolism, primarily a problem with cimetidine. Omeprazole also appears to inhibit the hepatic metabolism of some drugs, but available evidence indicates that it interacts with fewer drugs than cimetidine and the magnitude of the inhibition is lower. Cimetidine decreases the renal clearance of procainamide and its active metabolite, N-acetylprocainamide, probably through interference with active renal tubular secretion. In therapeutic doses, other H2-receptor antagonists probably have minimal effects on renal procainamide elimination.

Explore related subjects

Drug InteractionsHistamine H2 AntagonistsHumansKidneyLiverOmeprazoleJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P D Hansten. 1991. Drug interactions with antisecretory agents.. https://doi.org/10.1111/j.1365-2036.1991.tb00755.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Hospitalisations and emergency department visits due to drug-drug interactions: a literature review.

PURPOSE: Our objective was to evaluate the incidence of adverse patient outcomes due to drug-drug interactions (D-DIs), the type of drugs involved and the underlying reason. As a proxy for adverse patient outcomes, emergency department (ED) visits, hospital admissions and re-hospitalisations were assessed. METHODS: A literature search in the Medline and Embase database (1990-2006) was performed and references were tracked. An overall cumulative incidence was estimated by dividing the sum of the cases by the sum of the study populations. RESULTS: Twenty-three studies were found assessing the relationship between D-DIs and ED-visits, hospitalisations or re-hospitalisations. The studies with a large study size showed low incidences and vice versa. D-DIs were held responsible for 0.054% of the ED-visits, 0.57% of the hospital admissions and 0.12% of the re-hospitalisations. In the elderly population, D-DIs were held responsible for 4.8% of the admissions. Drugs most often involved were NSAIDs and cardiovascular drugs. The reasons for admissions or ED-visits, which were most often found were GI-tract bleeding, hyper- or hypotension and cardiac rhythm disturbances. CONCLUSION: This review provides information on the overall incidence of D-DIs as a cause of adverse patient outcomes, although there is still uncertainty about the impact of D-DIs on adverse patient outcomes. Our results suggest that a limited number of drugs are involved in the majority of cases and that the number of reasons for admission as a consequence of D-DIs seems to be modest.

Drug Interactions↗
PubMed2007

Drug-induced long QT and torsade de pointes: recent advances.

PURPOSE OF REVIEW: A wide array of drugs can cause marked QT prolongation with the associated risk of torsade de pointes. The large number of drugs with this potential, the correspondingly large number of patients exposed to such drugs, and the potentially fatal outcome make drug-induced long QT syndrome an important public health problem. This review focuses on mechanisms underlying QT prolongation and proarrhythmia, risk factors, including the role of genetic variants, and the unifying framework of reduced repolarization reserve. RECENT FINDINGS: While most drugs that prolong the QT block a specific potassium channel, novel mechanisms altering protein trafficking have been discovered. The progression to torsade de pointes may be less related to degree of QT prolongation than to drug effects on transmural dispersion or variability of repolarization. Our understanding of certain predisposing risk factors has been further refined. SUMMARY: Ongoing research continues to elucidate the mechanisms underlying drug-induced long QT syndrome. Importantly, studies are establishing improved predictors of risk for progression to torsade de pointes, in addition to the degree of QT prolongation, which is an imperfect predictor. Nonetheless, drug-induced long QT syndrome and torsade de pointes pose unique challenges for clinicians, researchers, drug-development programs, and regulatory agencies.

Drug Interactions↗