Inflammatory processes are connected to major depressive disorder, but there is uncertainty as to whether individual differences in inflammatory biomarkers could be used to prescribe medication to patients that is likely to be the most effective for them.
Researchers from Dalhousie University in Halifax, Nova Scotia, Canada, came up with an hypothesis that C-reactive protein (CRP), a commonly available marker of systemic inflammation, predicts differential response to the serotonin reuptake inhibitor escitalopram (Lexapro) and the norepinephrine reuptake inhibitor nortriptyline (Pamelor).
CRP levels at baseline predicted differences in treatment outcomes on the Montgomery-Åsberg Depression Rating Scale (MADRS) with the two medications, study researcher Rudolf Uher, MD, PhD, and colleagues reported in the American Journal of Psychiatry. Higher MADRS score indicate more severe depression.
Patients with CRP levels less than 1 mg/L at baseline had higher average improvements on MADRS scores with escitalopram than with nortriptyline, whereas those with higher baseline CRP levels showed more improvement on MADRS scores with nortriptyline than with escitalopram.
The interactions between CRP and medications explain more than 10% of individual-level variance in treatment outcomes, according to the researchers.
“An easily accessible peripheral blood biomarker may contribute to improvement in outcomes of major depressive disorder by personalizing treatment choice,” they concluded.
Major depressive disorder has been linked with inflammatory processes, but it is unclear whether individual differences in levels of inflammatory biomarkers could help match patients to treatments that are most likely to be beneficial.
The authors tested the hypothesis that C-reactive protein (CRP), a commonly available marker of systemic inflammation, predicts differential response to escitalopram (a serotonin reuptake inhibitor) and nortriptyline (a norepinephrine reuptake inhibitor).