Legalization of medical cannabis has occurred in 33 states and the District of Columbia, and recreational use has increased exponentially since 2013. As a result, it is important to understand how cannabis interacts with other drugs and has potential risks for patients on concomitant medications. Components of medical cannabis can inhibit or compete for several cytochrome P450 (CYP) hepatic isoenzymes, UDP‐glucuronosyltransferases, and P‐glycoprotein. These enzymes and transporters are involved in the metabolism and absorption of numerous medications, including anticoagulants (ACs) and antiplatelet agents (APs), potentially causing harmful drug‐drug interactions. ACs and/or APs are often prescribed to high‐risk patients with cardiac conditions, a history of myocardial infarction, or stroke. Cannabis may cause these medications to be less efficacious and put patients at risk for recurrent cardiovascular and cerebrovascular events. Several case reports show cannabis may inhibit the metabolism of warfarin because of CYP2C9 interactions, resulting in increased plasma concentrations, increased international normalized ratio, and risk of bleeding. Cannabidiol inhibits CYP2C19, an isoenzyme responsible for the transformation of clopidogrel to its active thiol metabolite. This interaction could lead to subtherapeutic levels of active metabolite and possibly increased stroke risk. Within this review, a total of 665 articles were screened from PubMed and EMBASE. Four case reports, 1 in vitro study, and 1 pharmacokinetic article were found to be of relevance. This review serves to examine reported and potential cannabis interactions with APs/ACs to help inform patients and health care providers of possible risks and knowledge gaps.

IntroductionAspirin and clopidogrel are mainstays in secondary stroke prevention; however, some patients do not demonstrate optimal antiplatelet effects from these therapies.ObjectivesThe primary objective of this study was to determine if pharmacist medication intervention paired with anti‐platelet medication monitoring with whole blood aggregometry improved responsiveness to antiplatelet treatment when compared with standard‐of‐care, alone in patients at risk of recurrent stroke or transient ischemic attack (TIA).MethodsThis retrospective chart review at an outpatient neurology practice examined patients treated post‐stroke or post‐TIA between 2005 and 2017. Patients were categorized as either having undergone platelet function testing (PFT) with pharmacist intervention and standard‐of‐care or standard‐of‐care alone. Patient populations for each group were matched based on age, sex, and ABCD2 risk scores. Pharmacotherapeutic management and interventions were assessed in each group.ResultsA total of 342 patients were included as two matched groups (n = 171 for each group) with parallel baseline characteristics. Drug‐drug interactions were identified (P < .0001), and counseling on adherence (P = .0008) occurred statistically significantly more often with a pharmacist involved in patient care. After pharmacist intervention and PFT, 83% of patients were considered responsive to their antiplatelet therapy compared with 27% at baseline in the pharmacist intervention group (P < .0001).ConclusionPharmacist interventions optimized secondary stroke/TIA prophylaxis therapy, decreased drug‐drug interactions, and increased adherence counseling. Patients who underwent PFT and pharmacist intervention transitioned from nonresponsive to responsive to their antiplatelet therapy regimen.

Purpose/Background Extensive research has been conducted comparing the metabolic characteristics of older second-generation antipsychotics (SGAs); minimal data exist comparing the long-term metabolic effects of SGAs approved in the last 10 years. Methods/Procedures A retrospective chart review of patients treated with brexpiprazole, lurasidone, asenapine, cariprazine, and iloperidone (newer SGAs) for at least 6 weeks at an outpatient psychiatric practice was conducted. Patients treated with olanzapine, an older SGA, were included as a comparator. Metabolic characteristics were collected at baseline, approximately 6 weeks, 12 weeks, and for up to 12 months. Findings/Results Of the newer SGAs, there were statistically significant increases in patients' average weight at 12 weeks and 1 year or less with brexpiprazole (2.48 lb, P = 0.02; 5.97 lb, P = 0.01) and iloperidone (4.54 lb, P < 0.01; 5.13 lb, P = 0.02). Brexpiprazole and iloperidone resulted in significant increases in body mass index, up to a 0.90-kg/m2 average increase in patients taking brexpiprazole at 1 year or less. Minimal weight gain was seen with cariprazine (4.25 lb, P = 0.42) and asenapine (1.80 lb, P = 0.62) at 1 year or less after treatment initiation. Although not statistically significant, lurasidone showed an average weight loss of up to 0.60 lb at 1 year or less (P = 0.56). Implications/Conclusions Although some weight gain was seen with the newer SGAs, all demonstrated significantly favorable metabolic characteristics compared with olanzapine. Monitoring of weight and metabolic parameters remain important in patients treated with SGAs.