Previous studies have shown that infection-related cytokine increase of interleukin 6 (IL6) and tumor necrosis factor α (TNF-α) can cause suppression of cytochrome P450 3A4 (CYP3A4) enzymes.⁽¹⁾ Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been associated with increased cytokine levels, which may suggest suppression of CYP3A4 enzymes and downstream interaction with CYP-mediated drug metabolism including calcineurin inhibitors.

Tacrolimus (Tac), the most used immunosuppressive agent for orthotropic liver transplantation (LT), is a calcineurin inhibitor metabolized via CYP3A4 primarily in the liver and intestinal mucosa.⁽²⁾ This potential effect of CYP3A4 inhibition on immunosuppression (IS) management with Tac in LT recipients with SARS-CoV-2 infection has yet to be evaluated. We sought to characterize and evaluate our experience with Tac-based immunosuppressive management among LT recipients hospitalized for SARS-CoV-2 infection.

先前的研究表明，白细胞介素 6 (IL6) 和肿瘤坏死因子 α (TNF-α) 的感染相关细胞因子增加可引起细胞色素 P450 3A4 (CYP3A4) 酶的抑制。^{( 1 )}严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染与细胞因子水平升高有关，这可能表明 CYP3A4 酶受到抑制，下游与 CYP 介导的药物代谢（包括神经钙蛋白抑制剂）相互作用。

他克莫司 (Tac) 是正交异性肝移植 (LT) 中最常用的免疫抑制剂，是一种主要在肝脏和肠粘膜中通过 CYP3A4 代谢的钙调神经磷酸酶抑制剂。^{( 2 )} CYP3A4 抑制对感染 SARS-CoV-2 的 LT 接受者使用 Tac 进行免疫抑制 (IS) 管理的潜在影响尚未得到评估。我们试图描述和评估我们在因 SARS-CoV-2 感染住院的 LT 接受者中基于 Tac 的免疫抑制管理的经验。