Alcoholic pancreatitis: new pathogenetic insights.
Though amply described, alcoholic pancreatitis continues to stir controversy. One of the most debated points is whether it is a chronic disease since onset or progresses to a chronic form after repeated episodes of acute pancreatitis. Histologic studies on patients with pancreatitis have clearly shown that it is chronic since onset and that if necrotic acute pancreatitis develops in an alcoholic, it occurs in a pancreas damaged by chronic lesions. While the possibility cannot be wholly excluded that alcohol-related acute pancreatitis may develop in the absence of chronic lesions, such an occurrence would be rare. In addition to alcoholism, genetic factors play a determinant role in the pathogenesis of the disease. Genetic studies have suggested that in hereditary pancreatitis mutation of the cationic trypsinogen gene and serine peptidase inhibitor, Kazal type 1 (SPINK1) genes mutations of the may have pathogenetic importance; however, studies on alcoholic pancreatitis have produced disappointing results so far.
Lucrezio
L
L
Internal Medicine Institute, University of Bologna, Sant'Orsola Hospital, via Massarenti 9, Bologna, Italy.
Bassi
M
M
Migliori
M
M
Bastagli
L
L
Gullo
L
L
D000428:Alcohol Drinking / Q000009:adverse effects; D002352:Carrier Proteins / Q000235:genetics; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics; D006801:Humans; D009154:Mutation; D019283:Pancreatitis, Acute Necrotizing / Q000150:complications; D019512:Pancreatitis, Alcoholic / Q000209:etiology* / Q000235:genetics; D014357:Trypsin; D014359:Trypsin Inhibitor, Kazal Pancreatic; D014362:Trypsinogen / Q000235:genetics
C505032:CFTR protein, human; D002352:Carrier Proteins; C486642:SPINK1 protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D014359:Trypsin Inhibitor, Kazal Pancreatic; D014362:Trypsinogen; C489303:PRSS1 protein, human; D014357:Trypsin