Alcohol and Pancreatitis

Sarles, H; Laugier, R.

doi:10.1159/000171083

Cited by 3 publications

(4 citation statements)

References 12 publications

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“…These basic pathological conditions are malnutrition and obesity, fatty liver, alcoholic hepatitis, and liver cirrhosis (9-11), esophagitis (12), gastritis (13), enterocolitis (14), pancreatitis (15), liver cancer, cardiomyopathy (16), pulmonary infections (17,18), polyneuritis, myelitis, encephalitis and delirium tremens (19), some blood diseases (20), etc. Mortality in alcoholics is increased, although, according to other statistics, those who drink up to 35 g alcohol per day present lower mortality than those who do not drink at all.…”

Section: Addiction To Alcohol (Alcoholism)mentioning

confidence: 99%

The alcoholic lung disease: Historical background and clinical features

et al. 2007

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Summary. The purpose of this review article is to prove the damage that alcohol causes to the respiratory system. We will make a brief review of alcohols history in the course of the centuries till nowadays. The problem of addiction to alcohol (alcoholism) will be examined for several countries.Alcohol's metabolism is another topic to be discussed parallel to its pharmacological action. In addition, alcohol's impact on the respiratory system varies from damaging the mucociliary system to the regulation of breathing and from the sleep apnea syndrome to diffusion disorders. "Alcoholic lung disease" constitutes a syndrome despite the fact that the damage of the lung due to concurrent smoking and drug use is often indistinguishable.

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Section: Addiction To Alcohol (Alcoholism)mentioning

confidence: 99%

The alcoholic lung disease: Historical background and clinical features

et al. 2007

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“…Once the pathogenetic process has started, episodes of acute AP, gallstone-associated pancreatitis, and idiopathic pancreatitis are clinically indistinguishable, 2,114,115 particularly at the time of the first attack. 115 The age and sex difference between the patients in the study by Sarles, 116 who had alcoholic or gallstoneassociated pancreatitis, was due to the fact that the alcoholics were mostly young men, and patients with gallstones are more often female and middle-aged.…”

Section: Relationship Between Acute and Chronic Pancreatitismentioning

confidence: 99%

“…Grö nroos and others [2][3][4] proposed a new theory of the pathogenesis of AP based on the fact that the hypersecretion of pancreatic juice protein in patients with AP is due to increased cholinergic tone; supramaximal stimulation by the cholecystokinin (CCK) analogue, cerulein, causes acute edematous "pancreatitis" in animals; poisoning by anticholinesterase insecticides in humans precipitates acute pancreatitis; and a 60% decrease in rat pancreatic muscarinic receptors was demonstrated after 8 months of alcohol intake. 4 However, acute AP and gallstoneassociated pancreatitis are characterized by the inappropriate, intrapancreatic activation of pancreatic zymogens; the release of active enzymes into the interstitial space, pancreatic circulation, and peritoneal and pleural effusions [5][6][7][8] ; and evidence of marked vascular damage and pancreatic necrosis.…”

mentioning

confidence: 99%

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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“…Protein plugs may be generated by increased secretion of proteins [7], by a different intraductal environment, includ-ing pH changes, by epithelial lesions or by prematurely activated pancreatic juice. Trypsin, one of the important factors in the activation of pancreatic juice under physiological conditions, may also be involved during premature intraductal activation [8].…”

Section: Introductionmentioning

confidence: 99%