World J Gastroenterol. 2009 Nov 14;15(42):5260-5. doi: 10.3748/wjg.15.5260.
The incidence of acute pancreatitis, an inflammation of the pancreas, is increasing worldwide. Pancreatic injury is mild in 80%-90% of patients who recover without complications. The remaining patients may develop a severe disease with local complications such as acinar cell necrosis, abscess and remote organ injury including lung injury. The early prediction of the severity of the disease is an important goal for physicians in management of patients with acute pancreatitis in order to optimize the therapy and to prevent organ dysfunction and local complications. For that purpose, multiple clinical scale scores have been applied to patients with acute pancreatitis. Recently, a new problem has emerged: the increased severity of the disease in obese patients. However, the mechanisms by which obesity increases the severity of acute pancreatitis are unclear. Several hypotheses have been suggested: (1) obese patients have an increased inflammation within the pancreas; (2) obese patients have an increased accumulation of fat within and around the pancreas where necrosis is often located; (3) increase in both peri- and intra-pancreatic fat and inflammatory cells explain the high incidence of pancreatic inflammation and necrosis in obese patients; (4) hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators; and (5) ventilation/perfusion mismatch leading to hypoxia associated with a low pancreatic flow might reduce the pancreatic oxygenation and further enhance pancreatic injury. Recent experimental investigations also show an increased mortality and morbidity in obese rodents with acute pancreatitis and the implication of the adipokines leptin and adiponectin. Such models are important to investigate whether the inflammatory response of the disease is enhanced by obesity. It is exciting to speculate that manipulation of the adipokine milieu has the potential to influence the severity of acute pancreatitis.
全球范围内，急性胰腺炎（胰腺炎症）的发病率正在上升。80%-90%的患者胰腺损伤较轻，无并发症即可康复。其余患者可能会发展为重症疾病，出现局部并发症，如腺泡细胞坏死、脓肿和远处器官损伤，包括肺损伤。早期预测疾病的严重程度是医生管理急性胰腺炎患者的一个重要目标，以便优化治疗并预防器官功能障碍和局部并发症。为此，已经有多种临床评分应用于急性胰腺炎患者。最近，出现了一个新问题：肥胖患者的疾病严重程度增加。然而，肥胖使急性胰腺炎加重的机制尚不清楚。已经提出了几种假说：（1）肥胖患者的胰腺内炎症增加；（2）肥胖患者的胰腺内和周围积聚了更多的脂肪，坏死通常发生在这些部位；（3）胰周和胰内脂肪以及炎症细胞的增加可以解释肥胖患者胰腺炎症和坏死的高发生率；（4）肥胖相关的肝功能障碍可能通过改变炎症介质的解毒作用增强全身炎症反应；（5）通气/灌注不匹配导致与低胰流相关的缺氧可能会降低胰腺的氧合作用，并进一步加重胰腺损伤。最近的实验研究还表明，肥胖的急性胰腺炎啮齿动物的死亡率和发病率增加，以及瘦素和脂联素等脂肪因子的作用。这些模型对于研究疾病的炎症反应是否因肥胖而增强非常重要。推测脂肪因子环境的调节有可能影响急性胰腺炎的严重程度，这令人兴奋。
