ABSTRACT
Aims: Obstructive sleep apnea (OSA) is characterized by episodic sleep state-dependent upper airway collapse. OSA can markedly decrease quality of life (QoL) and productivity. Continuous Positive Airway Pressure (CPAP) has been used as an effective treatment for OSA. Recently, uvulopalatopharyngoplasty (UPPP) treatment has emerged as effective management among patients with OSA, especially non-adherent ones to conventional therapies such as CPAP. Our aim was to determine whether CPAP and UPPP treatment could improve the quality of life in patients with moderate OSA. Design: Prospective. Setting: Patients with moderate OSA, confirmed by polysomnography from March 2019 to March 2020, participated. CPAP and UPPP treatments were considered for patients according to their preferences. The Sleep Apnea Quality of Life Index (SAQLI) questionnaire before and after treatment was completed. Methods: Change in their QoL was compared between the CPAP group and UPPP treatment. In addition, QoL was compared between these groups and patients who did not receive any of these treatment methods. Results: Seventy-eight patients were included in treatment groups, 40 using CPAP and 38 undergoing UPPP treatment. Furthermore, 10 patients who did not receive treatment were considered the control. Both methods of treatment significantly (p < 0.001) improved QoL, but UPPP treatment was superior (p = 0.042) to CPAP. There was a poor correlation between post-treatment BMI (0.037), Respiratory Disturbance Index (RDI) (0.096), age (0.022), and post-treatment SAQLI score. Conclusion: Based on these results, CPAP and UPPP treatment can improve QoL. UPPP treatment could be considered an effective arm of OSA management among the study population.
ABSTRACT
BACKGROUND: Previously, observational studies showed that amlodipine can mitigate calcineurin inhibitor- and contrast-induced acute kidney injury (AKI). Herein, we aimed to measure the effect of amlodipine on renal ischemia/reperfusion (I/R) injury and find the underlying mechanisms. MATERIALS AND METHODS: Bilateral renal I/R was induced by clamping the hilum of both kidneys for 30 min. The first dose of amlodipine 10 mg/kg was gavaged before anesthesia. The second dose of amlodipine was administered 24 h after the first dose. Forty-eight hours after I/R, rats were anesthetized, and their blood and tissue specimens were collected. RESULTS: Amlodipine significantly decreased the elevated serum levels of creatinine and blood urea nitrogen (BUN) and mitigated tissue damage in hematoxylin & eosin (H&E) staining. Amlodipine strongly reduced the tissue levels of malondialdehyde (MDA), interleukin 1ß (IL1ß), and tumor necrosis factor α (TNF-α). Amlodipine enhanced antioxidant defense by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2) and Sestrin2. Furthermore, amlodipine significantly improved mitochondrial biogenesis by promoting Sestrin2/peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α)/mitochondrial transcription factor A (TFAM) pathway. It also enhanced autophagy and attenuated apoptosis, evidenced by increased LC3-II/LC3-I and bcl2/bax ratios after renal I/R. CONCLUSION: These findings suggest that amlodipine protects against renal I/R through Nrf2/Sestrin2/PGC-1α/TFAM Pathway.