Anthracyclines are effective antineoplastic drugs; however, their use is constrained by dose-dependent cardiotoxicity. Vascular endothelial dysfunction is an early independent event in cardiovascular diseases and may precede anthracycline-induced cardiotoxicity. Brachial flow-mediated dilation (FMD) is a non-invasive technique for evaluating vascular endothelial function. We evaluated the evidence on anthracycline-induced vascular endothelial dysfunction in cancer patients and survivors using FMD. Studies measuring FMD in anthracycline-treated active cancer patients or survivors were retrieved from inception to August 2024 using PubMed, Embase, and Scopus. The primary outcome was the difference in FMD between anthracycline-treated patients and healthy controls or baseline. We performed the meta-analysis using a random-effects model and evaluated the certainty in effect estimates. Overall, 18 studies (n = 841 patients) met the inclusion criteria. Compared to the baseline, a non-significant change toward a decline in FMD was observed. However, a significant reduction in FMD was observed in anthracycline-treated patients compared to healthy controls (standardized mean difference (SMD): − 0.6082; 95% CI: − 0.8963 to − 0.3201; p < 0.0001). Subgroup analyses revealed consistent significant reductions in FMD for childhood cancers (SMD: − 0.7189; 95% CI: − 0.9903 to − 0.4476; p < 0.0001), while adult cancers showed no significant difference. No significant publication bias was detected overall for healthy control comparisons. High heterogeneity was observed in the included studies (I² = 81.7808% versus healthy controls and I² = 75.6876% for childhood cancers subgroup analysis). Anthracyclines induce vascular endothelial dysfunction, indicated by lower FMD in cancer patients and survivors, particularly among those with childhood cancers, who might be at risk of long-term cardiovascular complications.

Pharmacogenomics (PGx) is a crucial part of precision medicine; however, its integration into clinical practice has been slow, primarily due to knowledge gaps regarding pharmacogenomics among healthcare professionals (HCPs). Pharmacogenomics education is considered the most influential barrier to the successful implementation of PGx. In the Middle East and North Africa (MENA) region, several studies have highlighted the lack of PGx education among students and HCPs. This scoping review aims to provide an overview of the existing literature on how PGx is delivered in the curricula and its impact on knowledge acquisition among students and HCPs in the MENA region. A database search of PubMed, Embase, and CINAHL was conducted up to June 2023. Outcomes included PGx education availability, curriculum placement, mode of delivery, and knowledge level. Seven cross‐sectional studies were identified (2014–2023), with 57% from the Gulf region. PGx education is mostly taught to undergraduates (71%) through didactic lectures (100%), with only a few studies reporting a standalone course (29%). Participants demonstrated low (43%) to moderate (43%) knowledge levels, assessed using objective scales or subjective self‐assessment after completion of the course. Reported barriers to implementing PGx education included knowledge gaps, economic constraints, and system sustainability. PGx education in the MENA region is delivered mainly as an integrated course in professional programs including pharmacy and medicine, and the overall knowledge level was low to moderate. Future research could focus on providing more detailed reporting of the PGx educational landscape, developing standardized assessment tools, and evaluating actual knowledge acquisition among different professions.

Background/Objective: Sepsis remains a major cause of morbidity and mortality worldwide, making early risk stratification and prognosis critical. Vascular endothelial dysfunction is a hallmark of sepsis pathogenesis, with evidence suggesting that endothelial injury may occur early, preceding organ failure. Brachial flow-mediated dilation (FMD), a validated noninvasive ultrasound technique measuring endothelium-dependent vasodilation, serves as a surrogate marker of endothelial function, where lower FMD values reflect impaired function. This systematic review and meta-analysis aimed to evaluate the validity and quality of evidence on using FMD to measure vascular endothelial dysfunction in septic patients by comparing FMD (i) between septic patients and non-septic controls and (ii) between sepsis non-survivors and survivors. Methods: PubMed, Embase, Scopus, and Web of Science were searched until November 2024 for clinical studies assessing FMD in septic patients. A random-effects model was used for the meta-analysis, and quality of studies was assessed using the Newcastle–Ottawa Scale. Results: Eight studies were included, and seven underwent quantitative synthesis (385 septic patients, 106 non-survivors and 217 survivors). Compared with non-septic controls, septic patients demonstrated significantly lower FMD (pooled standardized mean difference (SMD) = −2.1617; 95% CI −3.8349 to −0.4885; p = 0.0113; I² = 98.2939%). Within the sepsis cohort, non-survivors showed significantly attenuated FMD compared to survivors (pooled SMD = −0.7003; 95% CI −1.1133 to −0.2873; p = 0.001; I² = 60.5593%). Conclusions: FMD shows potential as a surrogate marker of endothelial dysfunction for sepsis risk assessment, as evident by lower FMD in septic patients, particularly non-survivors.

Background/Objectives: Understanding the patterns of inappropriate antibiotic prescribing is crucial to design antimicrobial stewardship interventions. This systematic review evaluated the prevalence and types of inappropriate antibiotic prescribing among dialysis patients. Methods: Four electronic bibliographic databases including PubMed, Embase, Scopus, and CINAHL, were searched. Supplementary search was conducted using Google Scholar and by manually checking the reference list of selected studies. Selected studies include those published in the English language since inception of the databases until October 2024. Two independent reviewers screened, selected, and extracted the data for qualitative synthesis. Results: Of the 784 records identified from the databases, 13 studies fulfilled the eligibility criteria. Eight of the studies (42.6%) were from the USA. Antibiotic prescribing rate ranging from 16 to 75.5% was reported among dialysis patients, with vancomycin (6.5–100%), piperacillin-tazobactam (2.4–44.5%), meropenem (2.1–25.8%), metronidazole (2.1–16.4%), cefazolin (4.3–13.6%), and ceftriaxone (1.3–10.8%) being the most commonly prescribed antibiotics. The studies showed that 20–65.7% of prescriptions are inappropriate, mostly due to inappropriate dosing (25.5–100%), lack of an indication (5.5–73.9%), and inappropriate choice/spectrum (23.6–69.7%). Conclusions: Antibiotic prescribing among dialysis population is higher than the rate reported among hospitalized patients. High rate of broad-spectrum antibiotic prescribing coupled with the high rate of inappropriate antibiotic prescribing indicate the need for the implementation of antimicrobial stewardship programs in dialysis settings.

Background: Triple-negative breast cancer (TNBC) has a poor prognosis and limited targeted therapies, with anthracyclines being key treatments. However, many patients show reduced responsiveness to these treatments, affecting their outcomes. Arachidonic acid metabolites, specifically epoxyeicosatrienoic acids (EETs) produced by cytochrome P450 (CYP) epoxygenase enzymes, have been implicated in TNBC progression. However, limited data exist on the role of CYP epoxygenase gene expression in the responsiveness of anthracycline-based therapy in TNBC. Thus, we aimed to test the contribution of these CYPs in anthracycline responsiveness among patients with TNBC and to explore whether inhibition of CYP epoxygenase can potentiate the anti-cancer activity of anthracyclines. Methods: Our study used the KM-plotter database to retrieve and extract patients’ data with TNBC. The patients were assigned to two cohorts: responders or less-responders to anthracycline based on relapse-free survival. Additionally, the effects of the CYP epoxygenase inhibitor MSPPOH in combination with doxorubicin were evaluated in the TNBC cell line. Results: The present study shows that TNBC patients with lower responsiveness to anthracycline-based therapy exhibited higher levels of CYP2C8, CYP2C9, and CYP2C19. We also found that these CYP2Cs could be potential biomarkers for predicting anthracycline responsiveness. Using human TNBC cells, we show that a selective CYP2C epoxygenase inhibitor, MSPPOH, significantly potentiates the anti-cancer effect of anthracycline. Conclusions: Collectively, this study provides preliminary evidence that CYP2C epoxygenase is involved in the therapeutic response to anthracyclines in TNBC, suggesting that these enzymes may serve as predictive biomarkers. However, given the limitations of using a public database and a single TNBC cell line, continued validation within larger, independent patient cohorts is needed.