The researchers concluded that “This proof-of-concept study suggests that TNF antagonism does not exhibit generalized efficacy in TRD.” However, they noted three interesting findings, pointing to a highly complex interrelationship between inflammation and TRD.

  • Participants with a high level of inflammation at baseline responded preferentially to infliximab.
  • Infliximab-treated participants with a low level of inflammation appeared to fare worse than those treated with placebo.
  • Increased inflammation predicted a poor response to placebo.

The researchers commented, “Taken together, the data suggest that there is a subgroup of patients with TRD who have increased inflammation and respond to cytokine antagonism but not to placebo.” The authors regarded these findings as important because they represent a “first step in the personalization of antidepressant therapy” and they “provide promise for future development and elaboration to inflammatory biomarkers that identify patients who may be uniquely responsive to immune-targeted therapy.”

REFERENCES
1. Miller AH, Maletic V, Raison CL. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009;6;(9):732–741.

2. Messay B, Lim A, Marsland AL. Current understanding of the bi-directional relationship of major depression and inflammation. Biol Mood Anxiety Disord. 2012 Feb 28;2(1):4.


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3. Rush AJ, Trivedi MH, Wisniewski SR, et al. Acute and longer-term outcomes in depressed outpatients requiring one or more treatment steps: A STAR*D report. Am J Psychiatry. 2006;163(11):1905–1917.

4. Raison CL, Rutherford RE, Woolwine BJ, et al. A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression. Arch Gen Psychiatry. Published online: September 3, 2012. Available at: http://archpsyc.jamanetwork.com/article.aspx?doi=10.1001/2013.jamapsychiatry.4. Accessed: November 7, 2012.