BackgroundRestless Legs Syndrome (RLS) is a common neurological disorder. Growing evidence shows that dopaminergic dysfunction and iron deficiency are associated with the pathogenesis of RLS. Additionally, the dopaminergic system is linked with the hypothalamic-pituitary-thyroid (HPT) axis. Thus, the current study aimed to compare thyroid function between RLS patients and healthy subjects and investigate the associations with clinical characteristics of RLS.MethodsSerum levels of thyroid hormones were investigated in 102 first-episode drug-naïve RLS patients and 80 matched healthy controls (HCs). Baseline data and clinical characteristics were performed by professional personnel. In addition, multivariate regression was used to analyze the relationship between thyroid function and RLS.ResultsCompared with control group, RLS patients had significantly higher serum thyroid-stimulating hormone (TSH) levels (p < 0.001), and higher prevalence of subclinical hypothyroidism [Odds ratio (OR) 8.00; 95% confidence interval (CI) = 3.50–18.30; p < 0.001]. The Subclinical hypothyroidism rate (47.1 vs. 10%, p < 0.001) in RLS patients was higher than the HCs group. Regression analysis revealed that serum TSH (OR = 1.77; 95% CI = 1.41–2.23; p < 0.001) was independently associated with RLS. There was a statistically significant positive correlation between TSH and the Pittsburgh sleep quality index (PSQI) scores (r = 0.728, p < 0.001), and the International Restless Legs Scales (IRLS) points (r = 0.627, p < 0.001). Spearman correlation analysis showed that FT3 was positive correlated with HAMA14 score (r = 0.239, p = 0.015). In addition, compared with the good-sleeper group, poor-sleeper patients had significantly higher serum TSH levels (p < 0.001).ConclusionSerum levels of TSH and the prevalence of subclinical hypothyroidism were higher in RLS patients, indicating the imbalance between thyroid hormones (TH) and the dopaminergic system may contribute to the development of primary RLS. Additionally, the TH axis may influence the quality of sleep in RLS patients.

BackgroundRestless Legs Syndrome (RLS) is closely related to poorer sleep quality. Vitamin D can regulate sleep regulation, cell proliferation, and differentiation. To measure whether vitamin D has predictive value for poor sleep quality in RLS was our aim in this study.MethodsTo analyze the serum levels of 25-hydroxyvitamin D [25(OH)D] in 95 RLS patients. We used the Pittsburgh Sleep Quality Index (PSQI) to measure sleep quality. Subjects had been divided into a normal and poor-sleeper groups according to the PSQI score. Using correlation and regression analysis to explore underlying etiologies that affect sleep disorder in RLS patients.ResultsPatients in the poor-sleeper group had significantly lower vitamin D levels in comparison to the normal group. The serum vitamin D levels were negative correlate with PSQI scores after adjusting for confounding factors. In addition, regression analysis showed that vitamin D could act as a predictor for sleep disorders in RLS patients (odds ratio [OR] = 0.008, p = 0.004). The area under the curve (AUC), cut-off value, sensitivity, and specificity of serum vitamin D was 0.967 (95% CI 0.935–0.998), 16.84 ng/ml, 87.5%, and 93.7% by receiver operating characteristic (ROC) analysis.ConclusionOur study confirmed the relationship between poorer sleep quality and vitamin D in RLS. However, the causal relationship between vitamin D deficiency and RLS is currently inconclusive. The effect of vitamin D supplementation is needed to confirm as the therapeutic strategies for sleep disorders in RLS patients in future work.

Hypoxia occurs in physiological situations and several pathological situations, inducing oxidative stress. G straminea Maxim ( G.s Maxim) is a traditional Tibetan medicine that exerts several biological effects. This study focused on the protective effects of G.s Maxim in hypoxia-induced oxidative stress and apoptosis. We found that G. s Maxim significantly increased survival and reduced oxidative stress in hypoxic mice. Various extraction parts of G. s Maxim showed antioxidant activity and significantly improved survival in hypoxia-injured PC12 cells. G.s Maxim reduced hypoxia-induced cell apoptosis and leakage of lactate dehydrogenase. Hypoxic cells had increased malondialdehyde levels but reduced superoxide dismutase activity and G. s Maxim reversed these effects. Moreover, G. s Maxim suppressed hypoxia-induced apoptosis by inducing protein expression of B cell leukemia/lymphoma-2 and reducing the expression of hypoxia-inducible factor-1α, Bcl-2-associated X, and nuclear factor-k-gene binding. These findings suggest that G. s Maxim attenuates hypoxia-induced injury associated with oxidative stress and apoptosis.