Clinical evidence of pathogenesis in chronic pancreatitis

Abstract

Chronic pancreatitis is a continuing inflammatory disease characterized by irreversible morphological change and, typically, by pain and permanent impairment of function. The pathogenesis of pancreatitis, either acute or chronic, is still controversial. There have been no widely accepted concepts to provide a reasonable explanation linking the known etiological factors and the pathophysiological aspects of the disease. Alcohol is undoubtedly the major etiological factor in most countries, and the relative importance of alcohol as a cause of chronic pancreatitis ranges from 40% to 90% in various countries. As fewer than 10% of alcoholics develop chronic pancreatitis, other nutritional or genetic influences are likely to be involved in the pathogenesis of alcoholic pancreatitis. Accessory pancreas incidentally found in patients with chronic alcoholic pancreatitis does not always have the pathological findings seen in the main pancreas. Integrity of the pancreatic duct seems to be another important factor for chronic alcoholic pancreatitis. Gene mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), cationic trypsinogen, and pancreatic secretory trypsin inhibitor have been investigated in idiopathic chronic pancreatitis. Molecular and cell biology research during the past few years has elucidated pathophysiological factors that are involved in the pathogenesis of chronic pancreatitis, but cannot demonstrate a common pathway between etiological factors and the pathogenesis or development of the disease.

Exocrine pancreatic insufficiency in pigeons

“…Pancreatic insufficiency in mammals is caused less commonly by chronic pancreatitis and rarely by pancreatic neoplasia (Williams, 1989;Birchard et al ., 1994a). In man, a chronic pancreatitis resulting in progressive destruction of pancreatic tissue (pancreatic fibrosis) is a common cause of exocrine pancreatic insufficiency (EPI) (Suda, 2000;Hayakawa et al ., 2002).…”

Long-term outcomes of autoimmune pancreatitis

“…In the typical long-term course of ordinary CP, pancreatic exocrine and endocrine dysfunctions occur owing to the destruction of acinar and Langerhans islet cells, inducing maldigestion and diabetes mellitus as clinical presentations[19]. At the time of AIP diagnosis, exocrine and endocrine insufficiencies were observed in 66%-81% and 46%-67% of cases, respectively[20-22].…”

Genetic Risk for Alcoholic Chronic Pancreatitis

“…The determination of the factors, genes, proteins, and cells involved; the pathways that govern its interactions; and where the defects are will provide a better understanding of the pathogenesis of the disease [10]. More than one theory attempts to explain the mechanisms responsible for the development of pancreatitis of alcoholic etiology [11]. The first, based on the study of pancreatic histology, shows the formation of ductal closures, secondary to increased protein content in pancreatic juice, is the change that leads to obstruction, fibrosis, and calcification.…”