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PURPOSE: Thirst is a symptom of dehydration and one of the main complications affecting postoperative outcomes and comfort. Persistent water scarcity can have a detrimental effect on the cognitive function and psychology of patients. However, the current evidence about the prevalence and risk factors for postoperative thirst is not fully understood. Therefore, this study aims to investigate the prevalence and risk factors of postoperative thirst and provide guidance for clinical practice. DESIGN: Systematic review and meta-analysis. METHODS: We searched PubMed, Cochrane Library, Web of Science, Embase, Clinicaltrials.gov, China National Knowledge Infrastructure, and Wanfang Database. Eligible studies were evaluated using the Agency for Healthcare Research and Quality. The collected data were pooled and analyzed using Stata15.0. FINDINGS: A total of 11 cross-sectional studies were included involving 20,612 patients. Eight studies reported prevalence and the pooled prevalence of postoperative thirst was 76.8% (95% confidence interval [CI]: 0.664 to 0.858). Five studies contributed to meta-syntheses of risk factors for postoperative thirst. The results indicated that sex (odds ratio [OR] = 1.44, 95% CI = 1.13 to 1.84, I2 = 80.2%, P = .006), anesthesia drug (OR = 1.48, 95% CI = 1.06 to 2.06, I2 = 94.8%, P < .001), surgical type (OR = 0.66, 95% CI = 0.49 to 0.9, I2 = 77.9%, P = .004) were statistically associated with postoperative thirst. CONCLUSIONS: Our study shows a high prevalence of postoperative thirst. Sex, anesthesia drug, and surgical type are risk factors that influence postoperative thirst. Nurses and other health care professionals should routinely assess the postoperative thirst of patients and perform targeted interventions to alleviate their distressing symptoms and improve the quality of care.
RESUMO
BACKGROUND: Liver injury is common in severe acute pancreatitis (SAP). Excessive autophagy often leads to an imbalance of homeostasis in hepatocytes, which induces lipid peroxidation and mitochondrial iron deposition and ultimately leads to ferroptosis. Our previous study found that milk fat globule epidermal growth factor 8 (MFG-E8) alleviates acinar cell damage during SAP via binding to αvß3/5 integrins. MFG-E8 also seems to mitigate pancreatic fibrosis via inhibiting chaperone-mediated autophagy. AIM: To speculate whether MFG-E8 could also alleviate SAP induced liver injury by restoring the abnormal autophagy flux. METHODS: SAP was induced in mice by 2 hly intraperitoneal injections of 4.0 g/kg L-arginine or 7 hly injections of 50 µg/kg cerulein plus lipopolysaccharide. mfge8-knockout mice were used to study the effect of MFG-E8 deficiency on SAP-induced liver injury. Cilengitide, a specific αvß3/5 integrin inhibitor, was used to investigate the possible mechanism of MFG-E8. RESULTS: The results showed that MFG-E8 deficiency aggravated SAP-induced liver injury in mice, enhanced autophagy flux in hepatocyte, and worsened the degree of ferroptosis. Exogenous MFG-E8 reduced SAP-induced liver injury in a dose-dependent manner. Mechanistically, MFG-E8 mitigated excessive autophagy and inhibited ferroptosis in liver cells. Cilengitide abolished MFG-E8's beneficial effects in SAP-induced liver injury. CONCLUSION: MFG-E8 acts as an endogenous protective mediator in SAP-induced liver injury. MFG-E8 alleviates the excessive autophagy and inhibits ferroptosis in hepatocytes by binding to integrin αVß3/5.
