Late-onset depression has been associated with history of vascular disease and atherosclerosis. As immune dysregulation is critically involved in vascular disease. We hypothesized that responsiveness of late onset depression can be associated with level of inflammatory markers in these subjects.

Role of inflammatory mediator in antidepressant responses in late onset depression.

To study C-reactive protein as predictor of antidepressant response in late onset depression.

Depressed patient (as per ICD 10 DCR) age > 60 years recruited from department of psychiatry and complete clinical assessment done and base line depression severity measure on Hamilton Depression Rating Scale (HDRS). C reactive protein level was assessed at base line. Patient prescribed antidepressant medication and at 8 week follow up re assed for depression severity in HDRS. Data analyzed with spss.21 and spearman correlation was used.

Mean age of responder (n = 6) 63.5 ± 4.9 year and HDRS at base line 16 ± 1.9. Mean age of partial responder or non-responder (n = 19) 65.1 ± 6.1 year and HDRS at base line 18.5 ± 3.9. Continuous decrease in depression severity during study period and antidepressant response rate was 24%. Base line CRP level had negative correlation with antidepressant responsiveness (r = –0.6, P < 0.05).

Late onset depression was less responsive to antidepressant medication and poor antidepressant response rate was associated with higher level of CRP in late onset depression.

Document not received.

The authors have not supplied their declaration of competing interest.