Raison, C.L., Rutherford, R.E., Woolwine, B.J., Shuo, C., Schettler, P., Drake, D.F., . . . Miller, A.H. (2012). A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: The role of baseline inflammatory biomarkers. Archives of General Psychiatry, 1–11.doi:10.1001/2013.jamapsychiatry.4
To determine the effect of repeated intravenous injection of a monoclonal antibody, directed at the inflammatory cytokine tumor necrosis factor (TNF), on the mood of patients diagnosed with treatment-resistant depression (TRD); to note the effects of the intervention on the levels of inflammatory cytokines and high-sensitivity C-reactive protein (hs-CRP) and concentrations of TNF
Patients were randomized to receive either placebo or infliximab infusions of 5 mg/kg at baseline and at weeks 2 and 6. Assessments of clinical and inflammatory status (hs-CRP, TNF, and its soluble receptors I and II) were conducted at baseline and at weeks 1–4, 6, 8, 10, and 12.
Transition phase after active treatment
Randomized double-blind placebo-controlled trial
There were no differences in HAM-D score changes over time between groups. These scores declined significantly over time in both groups (p = 0.01). Subgroup analysis showed that, for patients with baseline hs-CRP concentration greater than 5 mg/L, those on infliximab had greater improvement in HAM-D scores (effect size = 0.41). Treatment response rates were not different between groups
Treatment with infliximab is not an effective intervention for treatment-resistant depression. However, as levels of hs-CRP increase, infliximab has greater effect. Antagonism of TNF is ineffective against treatment-resistant depression. More research is needed to determine inflammatory biomarkers in patients who may uniquely respond to immune-targeted therapies.
This study yields no results that can immediately be applied to practice. Nurse-researchers should consider constructing and implementing clinical trials aimed at exploring, developing, and understanding inflammatory biomarkers to identify immune-targeted therapeutic interventions.