Effect of alcohol on duodenal-pancreatic reflux

Rosato, Ernest F.; Butler, Charles J.; Grossman, Robert; Mullen, James L.; Skerrett, Philip V.; Rosato, Francis E.

doi:10.1016/0002-9610(73)90032-9

Cited by 7 publications

(3 citation statements)

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“…[33][34][35][36][37][38] • The rapid activation of pancreatic zymogens by the physiological action of enterokinase and bile salts, and the neutralization of protease inhibitors.…”

Section: Discussionmentioning

confidence: 99%

“…• The recurrent episodes of acute AP, precipitated by D-PR, and associated with a pressure gradient from the duodenum to the PD that exceeds that proven to cause D-PR and pancreatitis in man, monkeys, dogs, and rats. [33][34][35][36][37][38] • The rapid activation of pancreatic zymogens by the physiological action of enterokinase and bile salts, and the neutralization of protease inhibitors. • The site of zymogen activation-intraductal-shown by the presence of active enzymes within the ducts.…”

Section: Discussionmentioning

confidence: 99%

“…When alcohol was used to distend the duodenal loop instead of saline, D-PR occurred at a lower pressure and was further lowered by chronic alcohol ingestion. 38 Trypsinogen, kallikreinogen, and proelastase are all rapidly activated in the duodenal loop model; all 3 pancreatic proteases induce reflux pancreatitis 39 and the destructive effect of elastase in the canine and human pancreas is welldocumented. 21,39 ImportantarticlesbyMü ller-Wieland 34 and Anderson 35 have been neglected (one was in a German journal, 34 the other was not readily accessible 35 ), and their relevance to the pathogenesis of pancreatitis was not understood.…”

Section: Motility Disturbancesmentioning

confidence: 99%

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Neurological Damage and Duodenopancreatic Reflux in the Pathogenesis of Alcoholic Pancreatitis

McCutcheon

2000

Arch Surg

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To present a new theory on the pathogenesis of acute alcoholic pancreatitis based on experimental data, the significance of which has not been recognized, and on evidence from the current literature.Hypothesis: That chronic alcoholism damages muscarinic receptors in the pancreas, duodenum, and Oddi sphincter, producing heightened sensitivity to acetylcholine, stimulation of protein-rich pancreatic juice, hypertonicity of the duodenum and esophagus, relaxation of the Oddi sphincter, and intraduodenal pressures exceeding those shown to cause duodenopancreatic reflux and acute pancreatitis in humans and experimental animals.Outcome: The duodenopancreatic reflux mechanism can explain all of the clinical features of acute alcohol pan-creatitis, including the intraductal site and rapid activation of zymogens by enterokinase, the recurrent episodes of pancreatitis, the precipitation of protein plugs by partial proteolytic hydrolysis, the severe vascular changes, the relation to infection by the most direct route, and the progression to chronic pancreatitis via the necrosis-fibrosis sequence.Conclusions: Damage to the nervous system, with a time lag of 5 to 15 years between the onset of heavy drinking and the development of neurological disorders (peripheral neuropathy and cerebellar degeneration), is a characteristic complication of chronic alcoholism. The similarity to events in alcoholic pancreatitis is striking.

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“…[33][34][35][36][37][38] • The rapid activation of pancreatic zymogens by the physiological action of enterokinase and bile salts, and the neutralization of protease inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%