Hepatic outcomes among adults taking duloxetine: a retrospective cohort study in a US health care claims database.
Hepatic outcomes among adults taking duloxetine: a retrospective cohort study in a US health care claims database.
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DOI：
10.1186/s12876-015-0373-4
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发表时间：
2015-10-14
影响因子：
2.4
通讯作者：
Dore DD
中科院分区：
文献类型：
--
作者：
Lin ND;Norman H;Regev A;Perahia DG;Li H;Chang CL;Dore DD
已报告使用度洛昔单抗后发生肝损伤。本研究在美国大型健康保险数据库中进一步检查了度洛西汀的肝脏安全性。在美国商业保险人群（2004年8月1日至2010年12月31日）的倾向评分匹配队列分析中，我们比较了开始度洛西汀治疗的抑郁症和无肝病患者与对照药物（文拉法辛或选择性5-羟色胺再摄取抑制剂[SSRI]，以及未经治疗的抑郁症患者）。我们估计了经病历证实的肝相关死亡、肝衰竭和其他临床显著肝损伤的发生率（IR）和95%置信区间（CI）。在30，844例度洛沙坦启动者中，21，000例与文拉法辛启动者相匹配，28，479例与SSRI启动者相匹配，22，714例与未经治疗的患者相匹配。无肝脏相关死亡或肝功能衰竭病例。与文拉法辛开始治疗者相比，度洛沙坦开始治疗者中其他无其他病因记录的临床显著肝损伤的IR更高，但无统计学显著性（0.7/1000人-年[PY] [95% CI：0.2 − 1.5] vs. 0.0/1000 PY [95% CI：0.0 − 0.3]）和SSRI（0.4/1000 PY [95% CI：0.1 − 1.0] vs. 0.0/1000 PY [95% CI：0.0 − 0.3]）。度洛西汀和未治疗患者的IR相似（0.5/1000 PY [95% CI：0.1 - 1.3] vs. 0.5/1000 PY [95% CI：0.1 - 1.5]）。当考虑肝脏结局时，不考虑其他病因，观察到相似的结果。我们的研究结果，虽然没有统计学意义，但可能表明与文拉法辛和可能的SSRI相比，度洛沙坦启动者中除肝脏相关死亡或肝功能衰竭外的肝损伤发生率更高，但未接受治疗的患者除外。这些差异仍然与机会一致，并且不能排除风险升高。
Hepatic injury has been reported following duloxetine use. This study further examines the hepatic safety of duloxetine in a large US health insurance database. In this propensity score-matched cohort analysis in a US commercially insured population (01 August 2004 to 31 December 2010), we compared individuals with depression and without liver disease who initiated duloxetine to comparators (venlafaxine or selective serotonin reuptake inhibitors [SSRIs], and individuals with pharmacologically untreated depression). We estimated incidence rates (IR) and 95 % confidence intervals (CI) for medical record-confirmed hepatic-related death, liver failure, and other clinically significant hepatic injury. Among 30,844 duloxetine initiators, 21,000 were matched to venlafaxine initiators, 28,479 to SSRI initiators, and 22,714 to untreated patients. There were no cases of hepatic-related death or liver failure. IRs of other clinically significant hepatic injury without documented alternate etiologies were higher but not statistically significant among duloxetine initiators compared to initiators of venlafaxine (0.7/1000 person-years [PY] [95 % CI: 0.2 − 1.5] vs. 0.0/1000 PY [95 % CI: 0.0 − 0.3]) and SSRIs (0.4/1000 PY [95 % CI: 0.1 − 1.0] vs. 0.0/1000 PY [95 % CI: 0.0 − 0.3]). IRs were similar among duloxetine and untreated patients (0.5/1000 PY [95 % CI: 0.1 − 1.3] vs. 0.5/1000 PY [95 % CI: 0.1 − 1.5]). When hepatic outcomes were considered irrespective of alternate etiologies, similar results were observed. Our findings, while not statistically significant, may suggest a higher incidence of hepatic injury other than hepatic-related death or liver failure among duloxetine initiators compared to venlafaxine and possibly SSRIs, but not untreated patients. These differences remain consistent with chance, and an elevated risk cannot be ruled in or out.