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The statins are widely used worldwide to reduce risk for cardiovascular events in both the primary and secondary prevention settings. Although generally quite safe, the statins can be associated with a variety of serious side adverse effects, including myalgia, myopathy, and changes in plasma enzymes of hepatic origin. Although rare, the most serious of these is rhabdomyolysis. Several drugs can interfere with the metabolism and disposal of the statins, thereby increasing risk for adverse events. It is important that clinicians treating patients with statins be aware of the potential for drug-drug interactions between each statin and specific other drugs and take measures to prevent them. The prediction of potential drug-drug interactions derives from basic pharmacokinetic principles. Certain drug interactions are predicted by measuring the effect of interacting drugs on blood plasma concentrations of the statin. Individual patient variations resulting in part from polymorphisms in the metabolizing enzymes confound some of these predictions. Based on these known effects, a new classification for predicting statin drug interactions is proposed. This report discusses likely prescription and nonprescription interactions as well as potential alternatives for special populations.

The extracted cases from the AERS indicate continuing reports of thrombotic events associated with the use of one C1 esterase inhibitor product among patients with hereditary angioedema. The AERS is incapable of establishing a causal link and detecting the true frequency of an adverse event associated with a drug; however, potential signals of C1 esterase inhibitor product-associated thrombotic events among patients with hereditary angioedema were identified in the extracted combination cases.

Introduction: Currently available omega-3 (OM-3) fatty acid products in the US are either nonprescription dietary supplements (e.g., fish oils) or prescription (Rx) medications. As such, we aimed to describe critical therapeutic differences among the OM-3 fatty acids, focusing on differences between fish oil supplements and Rx OM-3s. Methods: A narrative review of known papers salient to this topic was conducted. Results: Despite the multiple purported clinical benefits, the published evidence for OM-3 dietary supplements is generally insufficient, inconsistent, or negative. Rx OM-3 products are indicated as an adjunct to diet to reduce triglycerides (TG) in adults with severe hypertriglyceridemia (TG C 500 mg/dl). Recently, the Rx eicosapentaenoic acid (EPA)-only OM-3, icosapent ethyl, demonstrated cardiovascular (CV) risk reduction among statin-treated patients at high risk of CV disease in a large CV outcomes trial (CVOT), and is now also indicated as an adjunct to maximally tolerated statin therapy to reduce the risk of myocardial infarction, stroke, coronary revascularization, and unstable angina requiring hospitalization in adult patients with elevated TG (C 150 mg/ dL) and established CVD or diabetes mellitus and C 2 additional risk factors for CVD. In contrast to the rigorous regulatory standards for safety, efficacy, and manufacturing of medications (whether Rx or over the counter), the Food and Drug Administration manages dietary supplements as food. Issues specific to OM-3 dietary supplements include variable content, labeling inconsistencies, and poor product quality/impurity. Given these issues, OM-3 dietary supplements should not be substituted for Rx OM-3 products. The efficacy of the EPA-only Rx OM-3 product in a large CVOT cannot be extrapolated to other OM-3 products. Conclusion: Consumers and health care providers need to recognize critical differences between Rx and OM-3 dietary supplements to ensure appropriate use of each OM-3 product.

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After oral administration of eprosartan to healthy volunteers, bioavailability is approximately 13%, with peak plasma concentrations occurring 1-2 hours after an oral dose in the fasted state. Food slows the rate of absorption and changes the overall extent by less than 25%, which is unlikely to be of clinical consequence. Plasma concentrations increase in a slightly less than dose-proportional manner from 100-800 mg. There is no evidence of significant accumulation of eprosartan with long-term therapy. The drug's terminal elimination half-life is typically 5-9 hours after oral administration. The agent is highly protein bound (approximately 98%), with low plasma clearance (approximately 130 ml/minute) and small volume of distribution (approximately 13 L). It is primarily unmetabolized by the liver, with less than 2% of an oral dose recovered in the urine as a glucuronide. Biliary (primary) and renal excretion contribute to its elimination. No dosage adjustment is required in patients with mild to moderate renal impairment. Although an increase in systemic exposure to eprosartan was observed in the elderly, in patients with hepatic impairment, and in those with severe renal disease, this finding is unlikely to be of clinical consequence, based on the drug's excellent safety and tolerability profile (doses up to 1200 mg) in phase III clinical trials in hypertensive patients. Eprosartan can be safely administered to these special populations without an initial dosage adjustment, with subsequent dosing individualized based on tolerability and response.