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What is known and objective Acquired long QT syndrome secondary to drug‐induced QT prolongation and torsades de pointes has been reported for antiviral drugs. However, no studies have reported an association between corrected QT (QTc) prolongation and antiviral therapy in patients with novel coronavirus disease (COVID‐19). Case description We present two cases from our institution in which patients with COVID‐19 experienced QTc prolongation during treatment with antiviral therapy. Lopinavir/ritonavir, together with gender and drug‐drug interactions, may have contributed to the induction of QTc prolongation in those patients. What is new and conclusion Co‐administration of QT‐prolonging medications and drugs interfering with the metabolism of those medications must be considered in patients with COVID‐19. Careful analysis of electrocardiograms for QTc duration should be performed at baseline and during antiviral therapy to identify individuals at high risk of arrhythmias.

BackgroundVoriconazole (VRCZ) is commonly used as oral and intravenous (IV) formulations. Few studies have comprehensively analysed the variation factors for the weight-corrected VRCZ serum concentration/dose (C/D) ratio based on the administration route. We retrospectively investigated the risk factors that influence the VRCZ C/D ratio in patients treated with oral or IV formulations.MethodsA total of 325 patients were divided into two groups (IV and oral groups). Propensity score matching was performed and linear regression analyses were used to identify the risk factors that affect the VRCZ C/D ratio according to the administration route. Receiver operating characteristic (ROC) curves were also used to assess the predictive potential for VRCZ trough concentration >5 µg/mL.ResultsThe VRCZ C/D ratio in the oral group was significantly lower than that in the IV group (p<0.001). Propensity score matching resulted in 65 in the IV group matched with 65 in the oral group. Multivariate analysis showed that age (p=0.039), aspartate aminotransferase (AST) (p=0.016) and total bilirubin (TBIL) (p=0.041) levels were independent influencing factors of the VRCZ C/D ratio in the oral group. ROC curves showed that the predicted probability of combined age, AST and TBIL had maximal area under the curve (AUC) of 0.901 for VRCZ trough level >5 µg/mL. Meanwhile, the ratio of TBIL (p=0.005) and single dose (p=0.015) were independent factors in the IV group with ROCAUC of 0.781.ConclusionsTo obtain optimal VRCZ efficacy and safety, dose adjustment is required based on multiple factors that may cause the observed difference in the VRCZ C/D ratio and trough levels between oral and IV administration.

Flutamide-induced haemolytic anaemia is rare but can be fatal. We describe the case of an 88-year-old man with prostatic carcinoma who, in addition to clinically obvious jaundice, developed haemolytic anaemia after undergoing treatment with flutamide for 5 days. When flutamide was replaced with temporary adrenocortical hormone treatment and blood transfusion, the blood indices and liver function of the patient improved gradually. We emphasise the need for routine monitoring of blood counts for patients undergoing flutamide treatment, and highlight the importance of discontinuing flutamide immediately when haemolytic anaemia occurs.

Background Metformin, a rst-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. Therefore, this study was aimed to investigate the effect of metformin on ethanol-induced cardiomyocyte injury and its underlying mechanism.Methods and Results H9c2 cardiomyocytes were exposed to ethanol for 24 h to establish an ethanolinduced cardiomyocyte injury model, and followed by treatment with metformin in the presence or absence of Lapatinib (an ErbB2 inhibition). CCK8 and LDH assays demonstrated that metformin suppressed cardiomyocyte apoptosis induced by ethanol exposure. Furthermore, the up-regulated expressions of apoptosis-related proteins (Bax and C-CAS-3) were also reduced by metformin. In addition, our results showed that metformin activated the AKT/Nrf2 pathway, and then promoted Nrf2 nuclear translocation and the transcription of its downstream antioxidant genes (HO-1, CAT and SOD2), thereby inhibiting oxidative stress. Interestingly, we found that ErbB2 expression was signi cantly inhibited in ethanol-treated cardiomyocyte, which was markedly reversed by metformin. In contrast, Lapatinib largely abrogated the activation of AKT/Nrf2 signaling by metformin, accompanied by the increases in oxidative stress and cardiomyocyte apoptosis,indicating that metformin prevented ethanol-induced cardiomyocyte injury in an ErbB2-dependent manner.Conclusions In summary, our study provides the rst evidence that metformin protects cardiomyocyte against ethanol-induced oxidative stress and apoptosis by activating ErbB2-mediated AKT/Nrf2 signaling. Thus, metformin may be a potential novel treatment approach for alcoholic cardiomyopathy.