Abstract
Interferon alpha (IFN-α)-treated patients commonly develop depression during the therapy period. Although most IFN-α-induced depressive disorders achieve remission after IFN-α therapy, no studies have examined the long-term mood effects of IFN-α treatment. We conducted a 12-year population-based cohort study of hepatitis C virus (HCV)-infected patients who were older than 20 years and had received IFN-α therapy. The sample was obtained from the Taiwan National Health Insurance Research Database. The cohort included patients with and without IFN-α-induced depression, matched randomly by age, sex and depression history, at a ratio of 1:10. The follow-up started after the last administration of IFN-α and was designed to determine the incidence of recurrent depressive disorder after IFN-α therapy. A total of 156 subjects were identified as having IFN-α-induced depression and achieving full remission after IFN-α therapy. The overall incidence of recurrent depressive disorders among patients with and without IFN-α-induced depression was 56.8 (95% confidence interval (CI), 42.4–76.1) and 4.1 (95% CI, 2.9–5.8) cases, respectively, per 100 000 person-years, P<0.001. The adjusted hazard ratios for recurrent depressive disorder were 13.5 (95% CI, 9.9–18.3) in the IFN-α-treated cohort and 22.2 (95% CI, 11.2–44.2) in the matched cohort for IFN-α-induced depression patients after adjusting for age, sex, income, urbanization and comorbid diseases. IFN-α-induced depression was associated with a high risk of recurrent depression. It was not a transient disease and might be considered an episode of depressive disorder. Continuation therapy might be considered, and further research is needed.
Highlights
Remitted major depressive disorder patients have been studied for a number of years,6 the understanding of the mechanisms underlying its recurrence remains limited because most studies investigate major depressive disorder during the acute phase
The crude hazard ratio (HR) for recurrent depressive disorder were 14.4 and 19.0 for interferon. aAdjusted for age (IFN)-α-induced depression patients in the IFN-α-treated and matched cohorts, respectively
To the best of our knowledge, this was the first nationwide study to examine the association between recurrent depressive disorder and IFN-α-induced depression in an hepatitis C virus (HCV)-infected population
Summary
Major depressive disorder is a highly recurrent illness, and its recurrence is an important reason for its burden. Population studies have found a ⩾ 40–75% lifetime recurrence of major depressive disorder among patients who have recovered from their first depressive episode. remitted major depressive disorder patients have been studied for a number of years, the understanding of the mechanisms underlying its recurrence remains limited because most studies investigate major depressive disorder during the acute phase.7Interferon alpha (IFN-α)-induced depression is a common and severe psychiatric disorder in IFN-α therapy for hepatitis C virus (HCV)-infected patients. Population studies have found a ⩾ 40–75% lifetime recurrence of major depressive disorder among patients who have recovered from their first depressive episode.. Remitted major depressive disorder patients have been studied for a number of years, the understanding of the mechanisms underlying its recurrence remains limited because most studies investigate major depressive disorder during the acute phase.. Interferon alpha (IFN-α)-induced depression is a common and severe psychiatric disorder in IFN-α therapy for hepatitis C virus (HCV)-infected patients. Therapeutic administration of IFN-α leads to depression in up to 50% of patients, and up to 30% of patients develop IFN-α-induced depression (a major depressive episode according to Diagnostic and Statistical Manual of Mental Disorders, 4th edn diagnostic criteria) within the first 3 months.. Almost all patients experience acute sickness, including symptoms of fatigue, malaise, myalgia, arthralgia, anorexia, apathy and cognitive impairment. IFN-α administration to humans replicates multiple pathologies central to depression, thereby providing support for the notion that endogenous cytokines that mediate innate immune responses can contribute to the state of depression.
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