Agarwal N, Pitchumoni C S
Department of Surgery, Our Lady of Mercy Medical Center, Bronx, NY 10466.
Gastroenterologist. 1993 Jun;1(2):115-28.
Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
从炎症胰腺释放的蛋白水解酶、脂肪酶、激肽和其他活性肽，将胰腺炎症（一种腹膜后单器官疾病）转变为多系统疾病。成人呼吸窘迫综合征，除继发于微血管血栓形成外，可能是活性磷脂酶A（卵磷脂酶）的结果，该酶可消化表面活性剂的主要成分卵磷脂。心肌抑制和休克被怀疑继发于血管活性肽和心肌抑制因子。凝血异常范围可从散在的血管内血栓形成到严重的弥散性血管内凝血。急性肾衰竭已根据血容量不足和低血压来解释。急性胰腺炎（AP）中作为肾衰竭介质的肾素 - 血管紧张素改变有待研究。代谢并发症包括低钙血症、高脂血症、高血糖、低血糖和糖尿病酮症酸中毒，其中低钙血症长期以来被认为是预后不良的指标。低钙血症的发病机制是多因素的，包括钙皂形成、激素失衡（如甲状旁腺激素、降钙素、胰高血糖素）、游离脂肪酸 - 白蛋白复合物对钙的结合以及钙的细胞内转运。皮下脂肪坏死、关节炎和普尔夏视网膜病变较为罕见。AP的各种预后标准及其他相关实验室异常是全身效应的表现。对这些并发症的早期识别和适当处理已改善了重症AP的预后。
