【摘要】 目的 總結甲狀腺功能亢癥（甲亢）患者131I治療中的護理特點及經驗。 方法 2008年1-8月對收治的184例行131I治療的甲亢患者，依據131I治療特點采取針對性的護理措施：心理上幫助其消除緊張焦慮的情緒，飲食方面指導禁食碘物，并密切觀察病情及預防甲亢危象，對服藥中出現的一些不適癥狀及時對癥處理。 結果 184例經131I治療的甲亢患者3～6個月病情痊愈和緩解153例（83.15%），甲亢復發22例（11.96%），甲狀腺功能減退癥發生9例（4.89%）。 結論 有效對癥的護理措施是甲亢患者積極配合治療，早日獲得康復的重要因素。【Abstract】 Objective To summarize the nursing characteristics and experience for the patients with hyperthyroidism treated by 131I. Methods A total of 184 patients with hyperthyroidism underwent 131I treatment between January and August 2008 were included. We took care of the patients according to the therapeutic features of 131I treatment: helped them calm down, advised not eating iodine-containing food, observed the disease condition and dealt with the discomfort after medicated. Results In 184 patients with hyperthyroidism treated by 131I treatment for three to six months, 153 (83.15 %) were cured, 22 (11.96 %) recurred, and 9 (4.89 %) had hypothyroidism. Conclusion Comprehensive nursing is a key point to make the patients with hyperthyroidism cooperate and recover.
ObjectiveTo systematically review the pathophysiological mechanisms and clinical characteristics of hypertriglyceridemia-associated acute pancreatitis, with a particular focus on the role of the gut microbiota and the gut–pancreas axis, and to summarize emerging microbiota-targeted therapeutic strategies and future research directions. MethodsRelevant literature published in recent years was reviewed and analyzed. Evidence regarding epidemiological features, pathogenic mechanisms, alterations in gut microbial composition, and microbiota-based therapeutic approaches was synthesized to establish an integrated framework linking dyslipidemia, gut microbial dysbiosis, and acute pancreatitis. ResultsCurrent evidence suggests that hypertriglyceridemia contributes to the initiation and progression of acute pancreatitis through multiple mechanisms, including lipotoxic injury, inflammatory cascade activation, and microcirculatory dysfunction. Gut microbiota dysbiosis and impairment of intestinal barrier integrity are closely associated with disease severity. Microbial metabolites and immune-regulatory pathways may play important roles in disease progression. Microbiota-targeted interventions have demonstrated potential in modulating inflammation, maintaining intestinal barrier function, and restoring metabolic homeostasis; however, their clinical efficacy and safety require further validation. ConclusionsThe gut microbiota and the gut–pancreas axis may represent key regulatory links between hypertriglyceridemia and acute pancreatitis. Further elucidation of the underlying mechanisms and advancement of precision microbiome-based interventions may provide novel approaches for risk stratification, early intervention, and comprehensive management of hypertriglyceridemia-associated acute pancreatitis.
