Uomo Generoso, Manes Gianpiero
Department of Internal Medicine, Cardarelli Hospital, Naples, Italy.
Dig Dis. 2007;25(3):282-4. doi: 10.1159/000103903.
Chronic pancreatitis (CP) still remains a challenging clinical problem with many controversial issues regarding pathogenesis, outcome, and treatment. The disease comprises a spectrum of disorders that culminate as a final step in the destruction of the pancreas. Complex interaction does exist between genetic, environmental and immunologic factors leading to development of the disease. Multiple risk factors interact in a multiple-step model; the pancreatic injury may occur through different mechanisms with transition between an acute pancreatitis condition to recurrent pancreatitis and, finally, to CP. Most patients have multiple risk factors and the overall risk is a product of all risk factors in additive or multiplicative fashion. Susceptibility to develop CP in alcoholics depends on the expression of single gene mutation or is derived from complex genetic polymorphism; in addition, smoking habit can influence the risk of pancreatic calcifications and severity in alcoholic and idiopathic CP. Alteration of the immune response induced by gene mutations and/or environmental factors represents the main determinant of pancreatic fibrosis, the end-stage histologic feature from all CP etiologies.
慢性胰腺炎(CP)仍然是一个具有挑战性的临床问题,在发病机制、预后和治疗等方面存在许多争议性问题。该疾病包括一系列紊乱,最终导致胰腺的破坏。遗传、环境和免疫因素之间确实存在复杂的相互作用,从而导致该疾病的发生。多种风险因素在多步骤模型中相互作用;胰腺损伤可能通过不同机制发生,从急性胰腺炎状态转变为复发性胰腺炎,最终发展为慢性胰腺炎。大多数患者有多种风险因素,总体风险是所有风险因素以相加或相乘方式作用的结果。酗酒者患慢性胰腺炎的易感性取决于单基因突变的表达或源于复杂的基因多态性;此外,吸烟习惯会影响酒精性和特发性慢性胰腺炎患者胰腺钙化的风险和严重程度。基因突变和/或环境因素引起的免疫反应改变是胰腺纤维化的主要决定因素,胰腺纤维化是所有慢性胰腺炎病因的终末期组织学特征。