PMID- 18504118
OWN - NLM
STAT- MEDLINE
DCOM- 20090112
LR  - 20220309
IS  - 0924-9338 (Print)
IS  - 0924-9338 (Linking)
VI  - 23
IP  - 6
DP  - 2008 Sep
TI  - Depression, comorbidities and the TNF-alpha system.
PG  - 421-9
LID - 10.1016/j.eurpsy.2008.03.013 [doi]
AB  - Depression has frequently been reported to be associated with other physical 
      diseases and changes in the cytokine system. We aimed to investigate associations 
      between a medical history of depression, its comorbidities and cytokine plasma 
      levels in the Bavarian Nutrition Survey II (BVS II) study sample and in patients 
      suffering from an acute depressive episode. The BVS II is a representative study 
      of the Bavarian population aged 13-80years. The disease history of its 1050 
      participants was assessed through face-to-face interviews. A sub-sample of 568 
      subjects and 62 additional acutely depressed inpatients of the Max Planck 
      Institute of Psychiatry participated in anthropometric measurements and blood 
      sampling. Tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptor 
      (sTNF-R) p55 and sTNF-R p75 plasma levels were measured using enzyme-linked 
      immunosorbent assays. A history of depression was associated with a higher 
      incidence of high blood pressure, peptic ulcer, dyslipoproteinemia, osteoporosis, 
      allergic skin rash, atopic eczema and thyroid disease. Within the BVS II sample, 
      participants with a history of depression differed from subjects who had never 
      had depression with regard to sTNF-R p55 and sTNF-R p75 levels even when 
      controlling for age, BMI and smoking status. Acutely depressed inpatients showed 
      even higher levels of sTNF-R p55 and sTNF-R p75 than subjects in the normal 
      population. TNF-alpha levels were also significantly elevated in acutely 
      depressed patients. These results confirm earlier studies regarding the 
      comorbidities of depression and support the hypothesis that activation of the 
      TNF-alpha system may contribute to the development of a depressive disorder.
FAU - Himmerich, H
AU  - Himmerich H
AD  - Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804, Munich, 
      Germany. hhimmerich@ukaachen.de
FAU - Fulda, S
AU  - Fulda S
FAU - Linseisen, J
AU  - Linseisen J
FAU - Seiler, H
AU  - Seiler H
FAU - Wolfram, G
AU  - Wolfram G
FAU - Himmerich, S
AU  - Himmerich S
FAU - Gedrich, K
AU  - Gedrich K
FAU - Kloiber, S
AU  - Kloiber S
FAU - Lucae, S
AU  - Lucae S
FAU - Ising, M
AU  - Ising M
FAU - Uhr, M
AU  - Uhr M
FAU - Holsboer, F
AU  - Holsboer F
FAU - Pollmacher, T
AU  - Pollmacher T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080527
PL  - England
TA  - Eur Psychiatry
JT  - European psychiatry : the journal of the Association of European Psychiatrists
JID - 9111820
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (TNFRSF1A protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Acute Disease
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Chronic Disease/epidemiology
MH  - Comorbidity
MH  - Depressive Disorder/diagnosis/epidemiology/*immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II/*blood
MH  - Reference Values
MH  - Tumor Necrosis Factor-alpha/*blood
MH  - Young Adult
EDAT- 2008/05/28 09:00
MHDA- 2009/01/13 09:00
CRDT- 2008/05/28 09:00
PHST- 2007/10/08 00:00 [received]
PHST- 2008/03/18 00:00 [revised]
PHST- 2008/03/22 00:00 [accepted]
PHST- 2008/05/28 09:00 [pubmed]
PHST- 2009/01/13 09:00 [medline]
PHST- 2008/05/28 09:00 [entrez]
AID - S0924-9338(08)01527-7 [pii]
AID - 10.1016/j.eurpsy.2008.03.013 [doi]
PST - ppublish
SO  - Eur Psychiatry. 2008 Sep;23(6):421-9. doi: 10.1016/j.eurpsy.2008.03.013. Epub 
      2008 May 27.