Effect of different retention doses of ultrasound-guided polidocanol chemical ablation for benign cystic-solid thyroid nodules.

OBJECTIVE: To assess the influence of varying retention doses of ultrasound-guided polidocanol chemical ablation for benign cystic-solid thyroid nodules. METHODS: A retrospective study was conducted from December 2019 to January 2022, including 78 patients with benign cystic-solid thyroid nodules, of which 31 received polidocanol chemical ablation alone, 23 received polidocanol chemical plus thermal ablation, and 24 received open surgery. Patients who received polidocanol chemical ablation were assigned into groups based on the retention dose of polidocanol: 0 %, 10 %, 20 %, 30 %, and 50 %. Follow-ups were done at 1, 3, 6, and 12 months postoperatively. The volume of the nodules, postoperative complications, and recurrence of the nodules were examined before treatment and during follow-up visits. RESULTS: Total operation time and intraoperative bleeding volume for patients who received ablation were substantially lower than those for patients who received open surgery (P < 0.001). Among patients in the polidocanol chemical ablation group, volume shrinkage rate of thyroid nodules in the 10 % retention dose group was significantly lower than that in the 0 % retention dose group at 1, 3, and 6 months postoperatively (P < 0.05). The 30 % retention dose group had the highest nodule shrinkage rate (98.46 ± 1.55 %) at 12 months postoperatively, which was significantly higher than that in the 50 % retention dose group (P < 0.05). Among patients in the polidocanol chemical and thermal ablation group, the volume shrinkage rate of thyroid nodules in the 10 % and 30 % retention dose groups at 1 month postoperatively was significantly lower than that in the 0 % retention dose group (P < 0.05). Although volume shrinkage rate in the 20 % retention dose group after thermal ablation was higher than that in the 0 % retention dose group, the difference was not statistically significant (P > 0.05). In terms of adverse reactions, the incidence of hoarseness and coughing was higher in the open surgery group than in the polidocanol chemical ablation and polidocanol chemical and thermal ablation groups, but there was no significant difference (P > 0.05). CONCLUSION: Chemical ablation with polidocanol was safe and effective for therapy of benign cystic-solid thyroid nodules, and the optimal retention dose may be between 20 % and 30 %. Patients with poor efficacy from chemical ablation alone can receive safe and effective treatment through thermal ablation.

Dopamine Burden Triggers Cholesterol Overload Following Disruption of Synaptogenesis in Minimal Hepatic Encephalopathy.

The contribution of Dopamine (DA) to minimal hepatic encephalopathy (MHE) has been demonstrated. However, recent studies have revealed that cholesterol (CHO) treatment substantially increased the risk of dementia. The objectives of this study were to investigate whether CHO was induced by DA overload and its involvement in DA-induced cognitive impairment in MHE. Our study showed that DA treatment triggered CHO biosynthesis via the activation of JNK3/SREBP2 signaling pathway in primary cultured astrocytes. Conditioned media from DA-treated astrocytes increased CHO uptake by primary cultured neurons and disrupted synaptic formations; at the same time, inhibition of CHO synthesis and transportation from astrocytes diminished the disruption of synaptogenesis, which indicates the involvement of CHO in the perturbation of neural synaptogenesis in vitro. Secondary secretion of DA from primary cultured neurons was stimulated by CHO secreted from astrocytes. DA induced synergistic decreases of PPARγ/pERK/pCREB expressions in the presence of CHO in neurons, leading to synergistic synaptic impairment. Memory impairments were observed in MHE/DA-treated rats, which were partially rescued by atorvastatin (ATVS) treatment, confirming the involvement of CHO burden in vivo. Overall, our study suggests that DA overload triggers obvious CHO production from astrocytes. Excessive CHO in turn triggered neurons to secrete abundant DA and DA burden in combination with CHO overload elicit the cognitive decline and memory loss via PPARγ/ERK/CREB pathway in MHE.