Decreased Plasma Hydrogen Sulfide Level Is Associated With the Severity of Depression in Patients With Depressive Disorder.

Accumulating evidence has suggested a dysfunction of synaptic plasticity in the pathophysiology of depression. Hydrogen sulfide (H2S), an endogenous gasotransmitter that regulates synaptic plasticity, has been demonstrated to contribute to depressive-like behaviors in rodents. The current study investigated the relationship between plasma H2S levels and the depressive symptoms in patients with depression. Forty-seven depressed patients and 51 healthy individuals were recruited in this study. The 17-item Hamilton Depression Rating Scale (HAMD-17) was used to evaluate depressive symptoms for all subjects and the reversed-phase high-performance liquid chromatography (RP-HPLC) was used to measure plasmaH2S levels. We found that plasma H2S levels were significantly lower in patients with depression relative to healthy individuals (P < 0.001). Compared with healthy controls (1.02 ± 0.34 µmol/L), the plasma H2S level significantly decreased in patients with mild depression (0.84 ± 0.28 µmol/L), with moderate depression (0.62 ± 0.21µmol/L), and with severe depression (0.38 ± 0.18 µmol/L). Correlation analysis revealed that plasma H2S levels were significantly negatively correlated with the HAMD-17 scores in patients (r = -0.484, P = 0.001). Multivariate linear regression analysis showed that plasma H2S was an independent contributor to the HAMD-17 score in patients (B = -0.360, t = -2.550, P = 0.015). Collectively, these results suggest that decreased H2S is involved in the pathophysiology of depression, and plasma H2S might be a potential indicator for depression severity.

Aripiprazole for the treatment of duloxetine-induced hyperprolactinemia: A case report.

BACKGROUND: It is well known that aripiprazole co-treatment effectively reduces antipsychotic-induced hyperprolactinemia. However, the effectiveness of aripiprazole to treat high prolactin levels induced by antidepressant drugs with serotoninergic activity, such as duloxetine, remains unknown. CASE PRESENTATION: An 18-year-old female diagnosed with major depressive disorder (MDD) was treated with 100 mg sertraline once daily. After two weeks, galactorrhoea was observed. Blood biochemical tests revealed an elevated serum prolactin level of 241 ng/mL. Physiological causes and additional potential pathological causes were ruled out. Therefore, sertraline was cross tapered with mirtazapine. Galactorrhoea ceased, but the side-effect of sedation prompted a switch to 40 mg duloxetine twice daily. After two weeks, the patient developed menstrual irregularities and milky discharge concomitant with a serum prolactin level of 205 ng/mL. As a result, duloxetine was decreased to 60 mg once daily, and aripiprazole was initiated at 2.5 mg daily and titrated to 5 mg daily. Two weeks after the initiation of dual therapy, galactorrhoea stopped, and prolactin levels decreased to 118 ng/mL. After eight weeks, prolactin levels decreased to 39 ng/mL, and menstruation returned to normal. After antidepressant therapy finished, prolactin levels normalized to 19 ng/mL. CONCLUSION: The case suggests that adjunctive aripiprazole may be useful as a treatment option for duloxetine-induced hyperprolactinemia in MDD.