Torres Harrys A, Hosry Jeff, Mahale Parag, Economides Minas P, Jiang Ying, Lok Anna S
Department of Infectious Diseases, Infection Control and Employee Health, The University of Texas MD Anderson Cancer Center, Houston, TX.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI.
Hepatology. 2018 Jan;67(1):36-47. doi: 10.1002/hep.29344. Epub 2017 Nov 13.
Hepatitis C virus (HCV) reactivation in patients receiving cancer treatment has been reported in retrospective studies. We sought to determine prospectively the incidence, predictors, and clinical significance of HCV reactivation during cancer treatment. HCV-infected patients receiving cancer treatment at our institution between November 2012 and July 2016 were studied. Reactivation was defined as an increase in HCV-RNA ≥1 log IU/mL over baseline and hepatitis flare as an increase in alanine aminotransferase to ≥3 times the upper limit of normal. One hundred patients were studied, 50 with hematologic malignancies and 50 with solid tumors. Reactivation occurred in 23 (23%) patients, including 18 (36%) patients with hematologic malignancies and 5 (10%) patients with solid tumors. In univariate analysis, patients with reactivation were more likely than those without reactivation to have prolonged lymphopenia (median, 95 versus 22 days; P = 0.01) and to have received rituximab (44% versus 9%; P < 0.0001), bendamustine (22% versus 0%; P < 0.001), high-dose steroids (57% versus 21%; P = 0.001), or purine analogs (22% versus 5%; P = 0.02). Rituximab (odds ratio = 9.52; P = 0.001), and high-dose steroids (odds ratio = 5.05; P = 0.01) retained significance in multivariable analysis. Of the 23 patients with reactivation, 10 (43%) had hepatitis flare. No patient with reactivation experienced liver failure or liver-related death within 36 weeks after initiation of cancer treatment. Fourteen patients with hepatitis flare, six of whom had reactivation, required discontinuation or dose reduction of cancer treatment.
HCV reactivation occurred in 23% of HCV-infected patients receiving cancer treatment, and most had an unremarkable clinical course. However, reactivation can affect the cancer treatment plan. Our findings suggest that HCV infection should not contraindicate cancer therapy and infected patients should have access to multiple cancer treatments with close monitoring while receiving regimens associated with HCV reactivation. (Hepatology 2018;67:36-47).
回顾性研究报告了接受癌症治疗的患者中丙型肝炎病毒（HCV）再激活的情况。我们旨在前瞻性地确定癌症治疗期间HCV再激活的发生率、预测因素及临床意义。对2012年11月至2016年7月在我们机构接受癌症治疗的HCV感染患者进行了研究。再激活定义为HCV-RNA较基线水平增加≥1 log IU/mL，肝炎发作定义为丙氨酸氨基转移酶升高至正常上限的≥3倍。共研究了100例患者，其中50例为血液系统恶性肿瘤患者，50例为实体瘤患者。23例（23%）患者发生再激活，其中18例（36%）血液系统恶性肿瘤患者和5例（10%）实体瘤患者。单因素分析显示，发生再激活的患者比未发生再激活的患者更易出现长期淋巴细胞减少（中位数，95天对22天；P = 0.01），且更有可能接受利妥昔单抗（44%对9%；P < 0.0001）、苯达莫司汀（22%对0%；P < 0.001）、大剂量类固醇（57%对21%；P = 0.001）或嘌呤类似物（22%对5%；P = 0.02）治疗。利妥昔单抗（比值比 = 9.52；P = 0.001）和大剂量类固醇（比值比 = 5.05；P = 0.01）在多变量分析中仍具有显著意义。在23例发生再激活的患者中，10例（43%）出现肝炎发作。在开始癌症治疗后的36周内，没有发生再激活的患者出现肝衰竭或与肝脏相关的死亡。14例出现肝炎发作的患者，其中6例发生再激活，需要中断或减少癌症治疗剂量。
接受癌症治疗的HCV感染患者中23%发生HCV再激活，且大多数患者的临床病程无明显异常。然而，再激活可能会影响癌症治疗计划。我们的研究结果表明，HCV感染不应成为癌症治疗的禁忌证，感染患者在接受与HCV再激活相关的治疗方案时，应在密切监测下接受多种癌症治疗。（《肝脏病学》2018年；67卷：36 - 47页）
