Cruz-Santamaría Dulce M, Taxonera Carlos, Giner Manuel
Dulce M Cruz-Santamaría, Carlos Taxonera, Department of Gastroenterology, Hospital Clínico San Carlos, Complutense University of Madrid, 28040 Madrid, Spain.
World J Gastrointest Pathophysiol. 2012 Jun 15;3(3):60-70. doi: 10.4291/wjgp.v3.i3.60.
Acute pancreatitis (AP), defined as the acute nonbacterial inflammatory condition of the pancreas, is derived from the early activation of digestive enzymes found inside the acinar cells, with variable compromise of the gland itself, nearby tissues and other organs. So, it is an event that begins with pancreatic injury, elicits an acute inflammatory response, encompasses a variety of complications and generally resolves over time. Different conditions are known to induce this disorder, although the innermost mechanisms and how they act to develop the disease are still unknown. We summarize some well established aspects. A phase sequence has been proposed: etiology factors generate other conditions inside acinar cells that favor the AP development with some systemic events; genetic factors could be involved as susceptibility and modifying elements. AP is a disease with extremely different clinical expressions. Most patients suffer a mild and limited disease, but about one fifth of cases develop multi organ failure, accompanied by high mortality. This great variability in presentation, clinical course and complications has given rise to the confusion related to AP related terminology. However, consensus meetings have provided uniform definitions, including the severity of the illness. The clinical management is mainly based on the disease´s severity and must be directed to correct the underlying predisposing factors and control the inflammatory process itself. The first step is to determine if it is mild or severe. We review the principal aspects to be considered in this treatment, as reflected in several clinical practice guidelines. For the last 25 years, there has been a global increase in incidence of AP, along with many advances in diagnosis and treatment. However, progress in knowledge of its pathogenesis is scarce.
急性胰腺炎（AP）被定义为胰腺的急性非细菌性炎症状态，它源于腺泡细胞内消化酶的早期激活，可导致胰腺本身、附近组织及其他器官受到不同程度的损害。因此，它是一种始于胰腺损伤、引发急性炎症反应、包含多种并发症且通常会随时间逐渐缓解的病症。已知多种情况可诱发这种疾病，但其内在机制以及这些机制如何导致疾病发生仍不清楚。我们总结一些已明确的方面。有人提出了一个阶段序列：病因因素在腺泡细胞内引发其他有利于急性胰腺炎发展的情况，并伴有一些全身性事件；遗传因素可能作为易感性和调节因素参与其中。急性胰腺炎是一种临床表现差异极大的疾病。大多数患者病情较轻且局限，但约五分之一的病例会发展为多器官功能衰竭，死亡率很高。这种在表现、临床过程和并发症方面的巨大差异导致了与急性胰腺炎相关术语的混乱。然而，共识会议提供了统一的定义，包括疾病的严重程度。临床管理主要基于疾病的严重程度，必须针对纠正潜在的诱发因素并控制炎症过程本身。第一步是确定病情是轻度还是重度。我们回顾了在这种治疗中需要考虑的主要方面，这在一些临床实践指南中有所体现。在过去25年里，急性胰腺炎的全球发病率有所上升，同时在诊断和治疗方面也取得了许多进展。然而，在其发病机制方面的知识进展却很匮乏。
