[Treatment of Olanzapine-induced Hyperprolactinemia by Shaoyao Gancao Decoction].

Objective To observe the efficacy and safety of Shaoyao Gancao Decoction (SGD) in treating olanzapine induced hyperprolactinemia. Methods Totally 120 schizophrenia patients who took Olanzapine Tablet (OT) were assigned to the treatment group and the control group by random number table, 60 in each group. All patients took OT. Those in the treatment group additionally took SGD. The ther- apeutic course for all was 8 weeks. Serum levels of prolactin were measured before treatment and at the end of week 2, 4, and 8 after treatment. The spiritual symptoms of patients were assessed by Positive and Negative Syndrome Scale (PANSS) before treatment and at the end of week 8 after treatment. Adverse reactions were assessed using Treatment Emergent Symptom Scale (TESS) before treatment and at the end of week 8 after treatment. Results Compared with before treatment in the same group, ser- um levels of prolactin were significantly reduced in the treatment group at the end of week 4 and 8 after treatment (P <0. 05). There was no statistical difference in serum levels of prolactin in the control group among each time points (P > 0. 05). Compared with the control group, serum levels of prolactin de- creased significantly in the treatment group at the end of week 4 and 8 after treatment (P <0. 01). There was no statistical difference in PANSS between the two groups at the end of week 8 after treatment (P> 0. 05). Adverse reactions occurred in 5 cases (943%) of the treatment group and 4 cases (7. 14%) in the control group. They were manifested as insomnia, headache, constipation, and incapability of sitting quietly. There was no statistical difference in adverse reaction between the two groups (P'>0. 05). Con- clusions SGD could effectively improve olanzapine-induced hyperprolactinemia, and had no obvious effect on psychotic symptoms. It showed no obvious adverse reactions.

No association of the rs9722 C >T in the S100B gene and susceptibility to major depression in a Chinese population.

OBJECTIVE: Astroglial-derived protein S100B is known to play important roles in axonal growth, neural plasticity, and energy regulation. Disturbance of these neurodevelopmental processes is proposed as one of the etiologies for mood disorder, and genetic polymorphisms of S100B have a possibility to be in susceptibility to major depressive disorder (MDD). METHOD: We first investigated the association of the rs9722 C > T polymorphism of the S100B gene and susceptibility to MDD by comparing 152 major depressive patients with 150 healthy individuals in a Chinese population. RESULTS: The genotype frequencies of the S100B rs9722 C > T polymorphism were 30% (C/C), 56% (C/T), and 14% (T/T) in depressed patients, 32% (C/C), 53% (C/T), and 15% (T/T) in healthy volunteers, respectively. The allele frequencies of the S100B rs9722 C > T polymorphism were 58% (C allele) and 42% (T allele) in depressed patients, and 59% (C allele) and 41% (T allele) in healthy volunteers, respectively. CONCLUSION: There were no significant differences in the genotype distribution and allele frequencies between major depressive patients and healthy individuals. S100B rs9722 C > T polymorphism appears not to be an important factor in susceptibility to MDD in a Chinese population.

Association study of astrocyte-derived protein S100B gene polymorphisms with major depressive disorder in Chinese people.

OBJECTIVE: Astroglial-derived protein S100B is known to play important roles in axonal growth, neural plasticity, and energy regulation. Disturbance of these neurodevelopmental processes is proposed as one possible etiology for mood disorder. Therefore, we performed a genetic analysis of S100B in patients with major depressive disorder (MDD). METHOD: The polymorphisms of S100B were determined by polymerase chain reaction-restriction fragment length polymorphism in patients (n = 152) with MDD and healthy control subjects (n = 150). The genotypic and allelic distributions of 2 variants were analyzed in Chinese patients. RESULTS: Two single nucleotide polymorphisms did not display significant associations with MDD. However, there were significant differences in age of onset in 3 genotypes of S100B rs9722. Significant differences in the subgroup depression (first-episode and recurrent depression) were also shown in 3 genotypes of S100B rs9722 and rs11911834 in patients and control subjects (P < 0.05). CONCLUSIONS: Our findings did not suggest association of S100B gene polymorphisms in patients with MDD in China. We found there were differences in depressive episodes among different genotypes of S100B gene.

The effects of gender and numbers of depressive episodes on serum S100B levels in patients with major depression.

S100B protein is a calcium-binding protein mostly derived from glial cells, which exerts trophic or toxic effects on neural cell depending on its concentration. It has been reported that S100B played an important role as a potential marker in psychiatric disorders. Thus, we will explore the clinical implication of S100B in major depression, especially the effect of gender and numbers of depressive episodes on S100B. The levels of serum S100B were measured with enzyme-linked immunosorbent assay (ELISA) in 54 patients with major depression and 35 age-matched healthy controls. The S100B levels in major depressed patients were significantly higher than those in controls. The serum S100B levels in female patients were significantly higher than those in male patients. Patients with recurrent depressive episodes had significantly higher S100B levels than those in first-episode depression. Serum S100B levels were significantly positive related with the numbers of depressive episode, family history and cognitive disturbance scores. These findings confirmed an increase in serum S100B levels in major depressive patients and presence of a sexual dimorphism. Moreover, numbers of depressive episodes in depression seemed to have an additional increasing effect on S100B levels.