TY - JOUR
T1 - Inflammation and clinical response to treatment in depression
T2 - A meta-analysis
AU - Strawbridge, R.
AU - Arnone, D.
AU - Danese, Andrea
AU - Papadopoulos, Andrew
AU - Herane Vives, A.
AU - Cleare, Anthony
PY - 2015/10/1
Y1 - 2015/10/1
N2 - The depressive state has been characterised as one of elevated inflammation, which holds promise for better understanding treatment-resistance in affective disorders as well as for future developments in treatment stratification. Aiming to investigate alterations in the inflammatory profiles of individuals with depression as putative biomarkers for clinical response, we conducted a meta-analyses examining data from 35 studies that investigated inflammation before and after treatment in depressed patients together with a measure of clinical response. There were sufficient data to analyse IL-6, TNFα and CRP. Levels of IL-6 decreased with antidepressant treatment regardless of outcome, whereas persistently elevated TNFα was associated with prospectively determined treatment resistance. Treatment non-responders tended to have higher baseline inflammation, using a composite measure of inflammatory markers. Our findings suggest that elevated levels of inflammation are contributory to treatment resistance. Combining inflammatory biomarkers might prove a useful tool to improve diagnosis and detection of treatment refractoriness, and targeting persistent inflammation in treatment-resistant depression may offer a potential target for the development of novel intervention strategies.
AB - The depressive state has been characterised as one of elevated inflammation, which holds promise for better understanding treatment-resistance in affective disorders as well as for future developments in treatment stratification. Aiming to investigate alterations in the inflammatory profiles of individuals with depression as putative biomarkers for clinical response, we conducted a meta-analyses examining data from 35 studies that investigated inflammation before and after treatment in depressed patients together with a measure of clinical response. There were sufficient data to analyse IL-6, TNFα and CRP. Levels of IL-6 decreased with antidepressant treatment regardless of outcome, whereas persistently elevated TNFα was associated with prospectively determined treatment resistance. Treatment non-responders tended to have higher baseline inflammation, using a composite measure of inflammatory markers. Our findings suggest that elevated levels of inflammation are contributory to treatment resistance. Combining inflammatory biomarkers might prove a useful tool to improve diagnosis and detection of treatment refractoriness, and targeting persistent inflammation in treatment-resistant depression may offer a potential target for the development of novel intervention strategies.
KW - Biological markers
KW - Depression
KW - Depressive disorder
KW - Inflammation
KW - Treatment-resistant
UR - http://www.scopus.com/inward/record.url?scp=84936805954&partnerID=8YFLogxK
U2 - 10.1016/j.euroneuro.2015.06.007
DO - 10.1016/j.euroneuro.2015.06.007
M3 - Article
SN - 0924-977X
VL - 25
SP - 1532
EP - 1543
JO - European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
JF - European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
IS - 10
ER -