By Thomas S. May
RHODES, GREECE -- June 19, 2007 -- Patients with multiple sclerosis (MS) often become depressed, and it is commonly believed that the depression is related to disease modifying treatment (DMT) with Interferon-beta. However, the results of a new study presented here at the 17th Meeting of the European Neurological Society (ENS) contradict this notion.
The study was performed by Stephen Kirzinger, MD, assistant professor, University of Louisville School of Medicine, Louisville, Kentucky, United States, and colleagues, and it involved a retrospective chart review of 112 patients with MS who had been treated either with Interferon-beta or with Glatiramer Acetate (GA) for up to 48 months.
To determine the relationship between DMT and depressive symptoms, patients were evaluated for depression using the Beck Depression Inventory (BDI) at baseline (within 6 weeks of initiating a DMT) and at each subsequent visit. In addition, patients' response to DMT was also evaluated using various measures such as the Expanded Disability Status Scale (EDSS), Modified Fatigue Impact Scale (MFIS), and the CogniStat (to assess cognitive impairment).
To be included in the study, patients must have completed a BDI within 6 weeks of starting their DMT. Sixty-seven subjects fulfilled this criterion and were included in the analysis. Forty-two had been exclusively on Interferon-beta and 25 received GA therapy.
An analysis of the results revealed no statistically significant difference between the two treatment groups with respect to the presence of depression, the investigators reported. They also noted that treatment with antidepressant medication did not significantly alter the results. Patients on Interferon-beta had a mean BDI score of 12.3 (SD=8), whereas patients treated with GA had a mean score of 12.1 (SD=7.7).
These findings do not support the common perception that disease modifying therapy with Interferon-beta is associated with depressive symptoms, the researchers concluded.
[Presentation title: Depression: Relationship to Disease-modifying Therapy. Abstract P284]
