Читать книгу Clinical Pancreatology for Practising Gastroenterologists and Surgeons - Группа авторов - Страница 70

Starting with acinar cell injury by a variety of pancreatic toxins, systemic inflammation occurs as early as the first few hours of the inciting parenchymal injury [15]. SIRS is a clinically evident syndrome that is a manifestation of the host’s exaggerated immune response to a local organ injury. SIRS secondary to sterile pancreatic inflammation is the predominant event in the first two weeks and its severity and progression to organ failure determines the fate of patients [2]. SIRS has long been recognized as a harbinger of disease severity. Several studies have shown that SIRS, especially when persistent for 48 hours or longer, is associated with increased risk of mortality [23].

At a biomarker level, white blood cell count, CRP, procalcitonin, and a variety of proinflammatory cytokines have been incorporated into different prediction models [47–51]. None of the cytokines, chemokines, damaged associated molecular pattern levels, or adipokines are routinely available for use. As such, a widely available acute‐phase reactant, CRP at levels above 20 mg/dl, is a commonly used inclusion criterion for studies examining predicted severe pancreatitis [20,21]. Leukocytosis is a criterion included in the SIRS criteria, Imrie score, and Acute Physiology, Age, and Chronic Health Evaluation (APACHE)‐II score. Procalcitonin has repeatedly been shown to be associated with infected necrosis and organ failure [52–54]. IL‐6 is a potent proinflammatory cytokine and is the most extensively studied cytokine with a strong association with severe pancreatitis with good accuracy (Table 4.2). TNF‐α is another potent proinflammatory cytokine but due to the inaccuracies inherent in its measurement, studies examining TNF‐α as a predictor of severity are scarce [65].