Decreased UA levels showed weak negative correlation with the presence of sadness and disturbed daily activities, higher CRP levels positively correlated with severe depression and the correlation between depression and fatigue was also observed (p < 0.05).
Participants with a high CRP levels had a significantly higher rate of depression than did those with a low hs-CRP levels (25.1% vs. 19.8%, p = 0.007).
Fatigued bereaved individuals (33%; SF-36 energy/vitality score 0-45) had significantly higher CRP levels (p < .05) as compared to non-fatigued bereaved individuals and reported higher levels of pain (p < .001), greater stress (p < .001), depression (p < .001), and sleeping problems (p < .001), as well as poorer social functioning (p < .001) and general health (p < .001) than those in the non-fatigued group.
Numerous studies have shown associations between an on-going depression and elevated serum levels of the acute-phase reactant C-reactive protein (CRP).
After adjustment for demographics, health indicators, and medication use, increased plasma CRP levels were more strongly associated with late-onset depression than early-onset depression (OR [95% CI]: 1.43 [1.05-1.94]).
These results confirm and extend previous findings suggesting that increased levels of CRP are associated with a later onset of depression and demonstrate that also NLR as a subclinical inflammatory marker is related to a later onset of depression.
Logistic regression analyses revealed that menstrual status, chronic diseases, serum inflammatory factors (CRP, IL-6 and TNF-α) and BDNF levels had independent predictive values for depression in patients with perimenopausal syndrome (P<0.05).
We aimed to investigate whether depression was associated with serum CRP levels in a cross-sectional analysis of a large cohort from a middle-income country.
Study participants are then assigned into one of two study strata: either into the 'Depression with inflammation' stratum (CRP levels > 3 mg/L); or into the 'Depression without inflammation' stratum (CRP levels ≤ 3 mg/L).
Our results show that CHD patients with depression had higher levels of CRP, IL-6 gene expression, and VEGF compared with CHD non-depressed, as well as lower plasma and saliva cortisol levels.
In total, physical function (J-HAQ, grip power, DASH, TUG, JSSF), quality of life (J-HAQ, General Health, EQ-5D) and depression (BDI-II) improved and disease activity (CRP, DAS28-CRP(4)) decreased significantly 6 and 12 months after surgery (p<.01), despite some differences in their outcomes by the preoperative disease activity and the surgical site.
IL-6 and CRP levels were elevated among those with lifetime depression and, among those with depression only, IL-6 methylation showed an inverse correlation with circulating IL-6 and CRP.
Compared with the levels in the schizophrenia group, the levels of CRP in the bipolar disorder and depression groups, the level of IFN-γ in the bipolar disorder group, and the levels of NGAL in the anxiety disorder and depression groups were significantly decreased (P < 0.05).
Inflammation is associated with depression, especially in women, and levels of C-reactive protein (CRP) and interleukin (IL)-6 predict response to antidepressant medications.
One hundred and twenty outpatients with IBD were recruited and: (a) completed questionnaires to record: age, sex, social support, socioeconomic status, anxiety and depression (n = 104), (b) underwent assessments of biases in emotional recognition (n = 112), emotional memory and reinforcement learning (c) had recorded from clinical records: type of IBD, duration of IBD, IBD activity and (d) provided blood for high-sensitivity C-reactive protein levels (n = 99).
IgM responses to NO-adducts and OSEs, especially malondialdehyde and myristic acid, and C-reactive protein (CRP) were inversely associated with TRYCAT pathway activity, whilst a lifetime depression and Pseudomonas putida were positively associated.
In four longitudinal studies, high levels of CRP were found to be associated with depression even after adjustment for BMI and weight loss, further corroborating the idea that other sources of peripheral inflammation might contribute to depressive symptoms.
Higher baseline CRP levels were associated lower depression severity (correlation coefficient=-0.63) with bupropion-SSRI combination but not with SSRI monotherapy (correlation coefficient=0.40).The overall remission rate was 41.5%.
Removing the interaction term, CES-D trajectory was associated with inflammation: higher levels of high-sensitivity C-reactive protein were observed in the subthreshold (β = 0.57, p = .004) and increasing depressive symptoms (β = 1.36, p < .001) trajectories compared with the no depression trajectory.
A complete clinical assessment, assessment of vascular risk factors, blood sample for the evaluation of serum CRP was obtained, and baseline depression severity was measured on Hamilton Depression Rating Scale (HDRS).