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Original Research

Inflammatory Biomarkers in 70 Depressed Inpatients With and Without the Metabolic Syndrome

Sara Zeugmann, MA, MSc; Arnim Quante, MD; Isabella Heuser, MD, PhD; Ralf Schwarzer, PhD; and Ion Anghelescu, MD, PhD

Published: February 9, 2010

Article Abstract

Objective: Chronic subclinical inflammation may be associated with the metabolic syndrome as well as with depression. We examined the impact of the metabolic syndrome on concentrations of inflammatory biomarkers in major depression.

Method: Data for 70 inpatients with major depressive disorder (diagnosed according to ICD-10 and DSM-IV), and with or without the metabolic syndrome, were assessed 4 to 5 weeks after admission to the clinic of the Department of Psychiatry, Charité-University Medicine, Berlin, between 2005 and 2007. The metabolic syndrome was defined according to the criteria of the International Diabetes Federation (2005). Immunologic biomarkers assessed included adiponectin, resistin, serum amyloid A (SAA), C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), soluble E-selectin, and CD40 ligand (CD40L). Severity of depression was measured with the 17-item Hamilton Depression Rating Scale.

Results: After regressional correction for confounding variables and covariates, a 2-factorial analysis of variance (metabolic syndrome’ ‰×’ ‰time) revealed that the metabolic syndrome’s presence affected adiponectin (F43,1′ ‰=’ ‰5.56; P’ ‰<‘ ‰.05) and IL-6 levels (F25,1′ ‰=’ ‰6.80; P’ ‰<‘ ‰.05) significantly. There was also a trend for effects on fibrinogen levels (F47,1′ ‰=’ ‰3.66; P’ ‰=’ ‰.06).

Conclusions: This is the first study to evaluate the putative additive effect of the metabolic syndrome on a panel of 9 inflammatory biomarkers
in depression. Our findings support an additive effect on some (adiponectin, IL-6, and trendwise for fibrinogen) markers. Patients with the metabolic syndrome and major depression are at higher risk for more frequent and more severe cardiovascular side effects than their counterparts without the metabolic syndrome.

J Clin Psychiatry 2010;71(8):1007-1016

Submitted: October 2, 2008; accepted February 23, 2009.

Online ahead of print: February 9, 2010 (doi:10.4088/JCP.08m04767blu).

Corresponding author: Sara Zeugmann, MA, MSc, Department of Psychiatry, Charité-University Medicine, Eschenallee 3, Berlin 14050, Germany (

Volume: 71

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