急性胰腺炎并发急性呼吸窘迫综合征的发病机制研究进展

Research progress on the pathogenesis of acute pancreatitis complicated by acute respiratory distress syndrome

急性胰腺炎(acute pancreatitis,AP)是消化系统中常见的急性腹痛疾病之一。导致AP疾病进展及致命的主要因素包括全身炎症反应综合征(SIRS)和多器官功能衰竭(MOF)。急性呼吸窘迫综合征(ARDS)作为AP最常见、最严重的早期并发症之一,与高病死率密切相关。然而,重症急性胰腺炎(SAP)并发ARDS的发病机制尚未完全阐明,可能与初始腺泡细胞损伤后核转录因子-κB(NF-κB)的激活、大量炎症介质释放以及免疫细胞介入等复杂因素相关,形成全身炎症瀑布反应。因此,本研究详细阐述NF-κB在AP发展早期的关键作用,揭示了NF-κB如何将初始腺泡损伤与全身炎症相关联,并导致肺泡弥漫性损伤。这不仅深化了临床医师对AP并发ARDS的理解,还为临床治疗提供潜在治疗靶点和理论依据。

Acute pancreatitis(AP)is a common acute abdominal pain disorder in the digestive system.Major factors contributing to disease progression and mortality include systemic inflammatory response syndrome(SIRS)and multiple organ failure(MOF).Acute respiratory distress syndrome(ARDS)is one of the most common and severe early complications of AP,closely associated with high mortality rates.However,the pathogenesis of severe acute pancreatitis(SAP)-associated ARDS remains incompletely understood.This may involve the factors such as the activation of nuclear factor-kappa B(NF-κB)following initial acinar cell injury,the release of large amounts of inflammatory mediators and the intervention of immune cells,contributing to a cascade of systemic inflammation.Therefore,based on the latest research findings,this paper elaborates on the pivotal role of NF-κB activation in early stages of AP inflammation progression and elucidates how it links initial acinar injury to systemic inflammation and leads to diffuse alveolar damage.This not only deepens clinicians’understanding of AP complicated by ARDS but also provides potential therapeutic targets and theoretical basis for clinical treatment.