We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure [email protected]
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
It has been suggested that the activation of systemic inflammatory response in depression is associated with inflammatory changes in the brain (neuroinflammation) and may reflect the severity of the clinical symptoms in patients.
Objectives
To study the relationship between clinical and immune parameters in patients with endogenous depressive disorders for the possible use of these indicators for diagnostics of these conditions.
Methods
Patients with bipolar affective disorder (group 1) and recurrent depressive disorder (group 2) (F31, F32, F33) were examined before the therapy. Mentally healthy age- and gender-matched persons were investigated as controls. The severity of depressive symptoms was assessed by HDRS. The activity of inflammatory indicators (leukocyte elastase (LE) and 1-proteinase inhibitor (ɑ1-PI)), as well as the level of autoantibodies (AB) to S-100B and MBP, were measured in plasma.
Results
Group 1 was characterized by an increase of LE and ɑ1-PI activity in comparison with the control group (р<0.001; р=0.002) and group 2 (р<0.05). No significant difference in AB to neuroantigens was found. Group 2 was distinguished by the increase in activity of the inflammatory indicators (р<0.01; р<0.05) as well as the autoimmune reactions to neuroantigens compared with control one (р=0.03). The correlations between complex assessment of the immune system and the severity of depressive symptoms in both groups were revealed (χ2=6.1; p=0.013; χ2=4.8; p=0.05).
Conclusions
Revealed correlations suggest that inflammatory markers are involved in the pathogenesis of endogenous depressive disorders and can be used as an additional differential diagnostics criterion for the assessment of the clinical state of patients.
Disclosure
No significant relationships.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.