Zhang XiPing, Wu Dijiong, Jiang Xinge
Department of General Surgery, Hangzhou First People's Hospital; Zhejiang University of Traditional Chinese Medicine. Hangzhou, Zhejiang Province, China.
JOP. 2009 Jan 8;10(1):8-14.
One of the most common complications of acute pancreatitis is acute lung injury, during which intercellular adhesion molecule-1 (ICAM-1) plays an important role by participating in leukocyte adhesion and activation as well as by inducing the "cascade effect" of inflammatory mediators, pulmonary microcirculation dysfunction and even acute respiratory distress syndrome, multiple organ failure or death. Although it is generally believed that the modulatory mechanism of ICAM-1 during this process is associated with the activation of nuclear transcription factor kappa B which is mediated by IL-1, IL-6, IL-18 and oxygen free radical, etc., further studies are still required to clarify it. Since the upregulation of ICAM-1 expression in the lung during acute lung injury is one of main pathogeneses, the early detection of the ICAM-1 expression level may contribute to the prevention and treatment of acute lung injury. Moreover, reducing pulmonary ICAM-1 expression levels through treatment with anti-ICAM-1 monoclonal antibody (aICAM-1) and antagonists of the neurokinin 1 receptor, etc., should have a positive effect on protecting the lungs during acute pancreatitis. This review aims to further clarify the relationship between ICAM-1 and acute pancreatitis complicated by acute lung injury, and therefore provides a theoretical basis for the formulation of corresponding therapeutic measures in clinical practice for acute pancreatitis.
急性胰腺炎最常见的并发症之一是急性肺损伤，在此过程中，细胞间黏附分子-1（ICAM-1）通过参与白细胞黏附和活化以及诱导炎症介质的“级联效应”、肺微循环功能障碍甚至急性呼吸窘迫综合征、多器官功能衰竭或死亡发挥重要作用。尽管一般认为ICAM-1在此过程中的调节机制与由白细胞介素-1、白细胞介素-6、白细胞介素-18和氧自由基等介导的核转录因子κB的激活有关，但仍需要进一步研究来阐明。由于急性肺损伤期间肺中ICAM-1表达上调是主要发病机制之一，早期检测ICAM-1表达水平可能有助于急性肺损伤的防治。此外，通过抗ICAM-1单克隆抗体（aICAM-1）和神经激肽1受体拮抗剂等治疗降低肺中ICAM-1表达水平，对急性胰腺炎期间的肺保护应具有积极作用。本综述旨在进一步阐明ICAM-1与急性胰腺炎并发急性肺损伤之间的关系，从而为临床实践中制定急性胰腺炎相应治疗措施提供理论依据。
