Analysis of pathophysiology in acute pancreatitis from the stand point of SIRS and CARS

急性胰腺炎是一种潜在的致命疾病。大多数患者出现系统性炎症反应综合征（SIRS），这是由炎症细胞因子引起的。在这种情况下，如果发生第二次攻击样感染，由先前炎症性损伤引起的中性粒细胞被进一步激活，导致远端器官功能障碍。另外，严重炎症损伤的患者也会经历一个抗炎期，即代偿性抗炎反应综合征（CARS）。这种情况的特点是产生抗炎细胞因子，从而抑制细胞因子反应，这可能导致免疫抑制。诱导重症胰腺炎后，细胞因子的产生在一段时间内明显受到抑制。在这种car条件下，脾细胞产生IL-2减少，引起细菌性腹膜炎后死亡率增加。这些结果表明SIRS中过度的细胞因子反应和CARS中防御系统的改变都可能导致远端器官功能障碍的发生。

Acute pancreatitis is a potentially fatal disease. Most patients develop systemic inflammatory response syndrome (SIRS), which is induced by inflammatory cytokines. In this condition, neutrophils primed by preceding inflammatory insult are further activated to cause distant organ dysfunction if the second attack-like infection occurs. Alternatively, patients with severe inflammatory insults also undergo an anti-inflammatory phase, the compensatory anti-inflammatory response syndrome (CARS). This condition is characterized by the production of anti-inflammatory cytokines and, as a result, suppression of cytokine response, which may result in immune suppression. After induction of severe pancreatitis, cytokine production was markedly suppressed for a while. In this CARS condition, production of IL-2 by splenocyte decreased and mortality rate after induction of bacterial peritonitis increased. These results suggest that both excessive cytokine response in SIRS and altered defense system in CARS may result in the development of distant organ dysfunction.