PubMed · 3282314
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S Taurand. 1988. [Insulin (2)].. https://pubmed.ncbi.nlm.nih.gov/3282314/
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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.
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.
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