Pitchumoni C S, Agarwal N, Jain N K
Department of Gastrenterology, Our Lady of Mercy Medical Center, Bronx, New York.
Am J Gastroenterol. 1988 Jun;83(6):597-606.
The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
急性胰腺炎（AP）的多系统受累反映了胰腺产生多种强效血管活性肽、激素和酶的能力。各种预后标准是对这些代谢紊乱的早期评估。低钙血症的发病机制是多因素的，长期以来一直被认为是AP严重程度的指标。甲状旁腺激素（PTH）-降钙素失衡、胰高血糖素、胃泌素和其他胰腺激素与PTH-降钙素的相互作用、游离脂肪酸在血清钙与白蛋白结合中的作用以及钙离子在肌肉和肝脏中的转运，最近已有描述，但仍存在相互矛盾的理论。然而，钙皂形成这一历史悠久的理论却广为接受。急性胰腺炎中的高血糖、低血糖和偶尔的酮症酸中毒已得到深入研究。高脂血症与急性胰腺炎之间复杂的因果关系需要进一步研究。凝血异常似乎由活化的胰蛋白酶引发，它们在微血管凝血中的作用似乎为主要器官功能障碍形成了一个统一的假说，但这需要进一步研究。成人呼吸窘迫综合征可能是活性酶消化肺表面活性物质和/或微血管血栓形成的结果。心功能抑制和休克被怀疑是由血管活性肽如缓激肽或心肌抑制因子引起的，其结构尚未阐明。急性胰腺炎中的肾素-血管紧张素改变和肾脏并发症在文献中很少受到关注。急性胰腺炎患者因视网膜血管血栓形成而出现中度视觉障碍甚至失明的情况幸运地并不常见。皮下脂肪坏死、关节痛和胰腺脑病等表现虽罕见但很有趣。尽管关于急性胰腺炎并发症发病机制的复杂性已有大量文献，但在特定并发症的预防和管理方面进展甚微。希望在急性胰腺炎中诱导的酶紊乱的修正方面开展进一步工作，将实现其有效治疗并预防严重并发症。
