RESUMO
Objective The serum S100B level reflects brain injury after stroke .This study was to explore the features of ser-um S100 B in post-stroke depression patients and its change after anti-depression treatment . Methods Totally 52 of the 95 post-stroke depression inpatients were included in this study .All the patients were treated with escitalopram for 8 weeks followed evaluation of their depression status and the therapeutic effects with Hamilton Depression Scale -17.The serum S100B concentration was detected before and after the treatment .Thirty-six post-stroke patients without depression and another 36 normal controls were recruited for com-parison of the serum S100B concentration.Response is defined as the reduction rate of HAMD-17≥50% after the treatment . Results The serum S100 B levels of the post-stroke depression patients , non-depression post-stroke patients, and normal controls were ([0.44 ± 0.14] vs [0.36 ±0.09] vs [0.21 ±0.10] μg /L, F=41.88, P=0.000), those of the male and female post-stroke depression patients at the baseline were ([0.46 ±0.16] vs [0.43 ±0.14] μg /L, t=0.7062, P=0.4833), and those of the ischemic stroke and hem-orrhagic stroke patients at the baseline were ([0.42 ±0.12] vs [0.47 ±0.15] μg /L, t=1.3097, P=0.1963).The reductions of the S100B level in the response and non-response groups were ([0.13 ±0.03] vs [0.04 ±0.01] μg /L, t=11.6595, P=0.0000). Conclusion The serum S100 B level in post-stroke depression patients is higher than in non-depression post-stroke patients and normal controls, which is not associated with gender or stroke types .The decrease of serum S100B predicts the efficacy of anti-depression treatment.
RESUMO
<p><b>OBJECTIVE</b>To assess the association of BDNF gene Val66Met polymorphism with efficacy of antidepressant treatment and plasma BDNF level.</p><p><b>METHODS</b>Two hundred and forty-nine ethnic Han Chinese patients with depression(study group), who have met the diagnostic criteria of DSM-IV, were prescribed with venlafaxine or paroxetine. Two hundred and two healthy individuals were recruited as the control group. General demographic information such as gender, age, educational status, occupation, and marriage status were collected. HAMD-17 was adopted as the primary rating tool to evaluate the severity of depression on the baseline and at the end of 1st, 2nd, 4th, 6th week of treatment. PCR-restriction fragment length polymorphism was applied to determine the Val66Met polymorphism of the BDNF gene in the two groups. Plasma BDNF concentration was measured with ELISA before and after 6 weeks of treatment.</p><p><b>RESULTS</b>No significant differences have been found in HAMD scores and reduction of HAMD scores on the baseline and at the end of 1 st, 2nd, 4th, 6th weeks of treatment for each genotype. Nor were significant differences found in the Val66Met genotypes and allelic frequency between patients who achieved remission or not after 6 weeks' treatment as well as the healthy volunteers. The plasma BDNF level in depression patients was lower than that in healthy controls. The BDNF level has increased significantly after 6 weeks' treatment with both venlafaxine and paroxetine, but was still lower than the healthy controls. The BDNF level in the patients achieved remission who were treated with venlafaxine was similar to the normal controls, while those treated with paroxetine was still lower than normal controls. The BDNF level in patients who have not achieved remission was lower than normal controls. The BDNF level was not associated with the Val66Met polymorphism on the baseline and the end of 6th week.</p><p><b>CONCLUSION</b>No association has been found between the efficacy of venlafaxine or paroxetine and the BDNF Val66Met polymorphism. The BDNF level of patients with depression is significantly lower than healthy controls on the baseline, and can be enhanced with the treatment. Particularly, the BDNF level in patients who achieved remission after the treatment of venlafaxine can rise to normal. The level of BDNF has certain value in the forecasting of efficacy in the anti-depression therapy. BDNF level is not associated with the Val66Met polymorphism of the BDNF gene.</p>