College of Medicine, China Medical University, Taichung, Taiwan.
Department of Psychiatry, Cathay General Hospital, Taipei, Taiwan; School of Medicine, Fu Jen Catholic University, Taipei, Taiwan.
Brain Behav Immun. 2020 Aug;88:125-131. doi: 10.1016/j.bbi.2020.05.044. Epub 2020 May 17.
IFN-α-induced depression in patients undergoing hepatitis C virus (HCV) treatment provides powerful support for the inflammation hypothesis of depression. Most studies have focused on the occurrence of depressive symptoms, but there has been no study yet in depression-free HCV patients receiving IFN-α. We hypothesized that HCV patients who did not develop depression after IFN-α exposure might have a lower incidence of depressive disorders after the IFN-α treatment.
We conducted a twelve-year population-based cohort study of chronic HCV patients who received IFN-α therapy. The data were obtained from the Taiwan National Health Insurance Research Database. The study cohort was patients without any depressive disorder nor antidepressant use before and during IFN-α therapy. They were matched randomly by age, sex income and urbanization at a ratio of 1:4 with the control cohort of HCV patients without IFN-α therapy. The follow-up started after the last administration of IFN-α, and the primary outcome was the incidence of depressive disorders after IFN-α therapy.
A total of 20,468 depression-free subjects were identified from records of HCV patients receiving IFN-α therapy. Patients without IFN-α-induced depression were associated with a significantly lower incidence (per 10,000 person-years) of new-onset depressive disorders (126.8, 95% Confidential Interval [CI] of 118.5-135.6) as compared to the control cohort (145.2, 95% CI of 140.0-150.6) (p < 0.001). After adjusting for age, sex, income, urbanization and comorbid diseases, the crude hazard ratio for the incident depressive disorder was 0.87 (95% CI, 0.80-0.87) and the adjusted hazard ratios was 0.79 (95% CI, 0.72-0.87) for IFN-α-induced depression-free subjects as compared to the controls.
Our study indicates that IFN-α treated depression-free patients have a lower risk for depressive disorders. This hypothesized mechanism might derive from an IFN-α-induced resilience factor as yet to be defined.
Our study might suggest a new possibility for a new pharmacological strategy against depression.
干扰素-α(IFN-α)诱导的丙型肝炎病毒(HCV)治疗患者的抑郁为抑郁的炎症假说提供了有力的支持。大多数研究都集中在抑郁症状的发生上,但目前还没有研究关注无抑郁症状的 HCV 患者在接受 IFN-α 治疗后的情况。我们假设,IFN-α 暴露后未发生抑郁的 HCV 患者在 IFN-α 治疗后发生抑郁障碍的风险可能较低。
我们进行了一项为期 12 年的基于人群的 HCV 患者队列研究,这些患者接受了 IFN-α 治疗。数据来自台湾全民健康保险研究数据库。研究队列由 IFN-α 治疗前后无任何抑郁障碍或使用抗抑郁药的慢性 HCV 患者组成。按照年龄、性别、收入和城市化程度,以 1:4 的比例随机与未接受 IFN-α 治疗的 HCV 患者对照队列相匹配。随访从最后一次 IFN-α 给药开始,主要结局是 IFN-α 治疗后抑郁障碍的发生率。
共从接受 IFN-α 治疗的 HCV 患者的记录中确定了 20468 例无抑郁的患者。与对照队列相比(145.2,95%置信区间[CI]:140.0-150.6),无 IFN-α 诱导性抑郁的患者新发抑郁障碍的发生率(每 10000 人年)显著较低(126.8,95%CI:118.5-135.6)(p<0.001)。在校正年龄、性别、收入、城市化程度和合并症后,新发抑郁障碍的粗风险比为 0.87(95%CI:0.80-0.87),IFN-α 诱导无抑郁的患者的调整风险比为 0.79(95%CI:0.72-0.87)。
本研究表明,IFN-α 治疗无抑郁的患者发生抑郁障碍的风险较低。这种假设的机制可能源于尚未确定的 IFN-α 诱导的恢复力因素。
我们的研究可能为针对抑郁的新药理学策略提供了新的可能性。