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At least 19 recordsLinked to original sources
PubMed2005

Molecular mechanisms of alcoholic pancreatitis.

Alcoholic pancreatitis is a major complication of alcohol abuse. Since only a minority of alcoholics develop pancreatitis, there has been a keen interest in identifying the factors that may confer individual susceptibility to the disease. Numerous possibilities have been evaluated including diet, drinking patterns and a range of inherited factors. However, at the present time, no susceptibility factor has been unequivocally identified. In contrast, considerable progress has been made with respect to the constant effects of alcohol on the pancreas. The molecular mechanisms of alcohol-induced pancreatic injury are being increasingly defined with an emphasis, in recent years, on the acinar cell itself as the principal site on ethanol-related damage. It has now been established that the acinar cell is capable of metabolizing alcohol and that the direct toxic effects of alcohol and/or its metabolites on acinar cells may predispose the gland to autodigestive injury in the presence of an appropriate triggering factor. A significant recent development relates to the characterization of pancreatic stellate cells, increasingly implicated in alcoholic pancreatic fibrosis. Here the current concepts regarding the mechanisms/pathways mediating alcohol-induced pancreatic injury are outlined.

Alcoholism↗
PubMed1978

A clinical investigation of chronic pancreatitis--comparative study between alcoholic pancreatitis and non-alcoholic pancreatitis--.

An analysis of 89 cases with chronic pancreatitis revealed 56% of chronic alcoholic pancreatitis (AP). The sex ratio was 47 males to 3 females and the mean age at onset was 42.4 years in AP and 49.3 years in chronic non-alcoholic pancreatitis (NAP). The 'total amount' of alcohol consumption was correlated to the onset. In AP, the abdominal pain was apt to relapse and severe in nature, furthermore painless pancreatitis was seen in 6%. The association with diabetes or calcification (38%) were more frequently seen in AP. The calcifications in AP appeared to be smaller in size and distributed diffusely or localized in cephalic portion. A striking frequency of liver dysfunctions (39 cases) were demonstrated, however, cirrhosis was rare in AP. The P-S test dysunctions in NAP were frequently reversible in the follow up study, while even some of chronic asymptomatic alcoholics developed clinical signs of pancreatitis during the observed period and proceeded to definite AP, of whom pancreatic dysfunctions showed fluctuation and eventual progression. In other words, even pain free intervals the pancreatic inflammation in susceptible persons may proceed to ultimated destruction of the pancreas. The fatality from chronic pancreatitis was rare (12.3%), which was related diabetes mellitus.

Adult↗
PubMed1989

[Clinical study on alcoholic pancreatitis in alcoholics (especially in ERP findings)].

The pancreatic functions (PFD test and 75g GTT), pancreatic enzymes (serum-amylase, urine-amylase, serum-elastase I and serum-lipase), alcohol consumption histories, clinical symptoms, histological findings in the liver and ERP findings have been examined in 66 alcoholic patients. Fourty two out of 66 cases (64%) showed abnormal ERP findings which were compatible with chronic pancreatitis. But among these 42 cases, only 9 cases (21%) showed clinical symptoms such as epigastralgia, back pain, diarrhea and emaciation which suggest the existence of chronic pancreatitis. The degree of liver damage, alcohol consumption have no significant correlation with ERP findings. Furthermore, the severe alcoholic pancreatitis occurred in patients having mild liver injury more than those having severe liver injury such as cirrhosis. And the data of pancreatic functions and enzymes could not confirm ERP findings especially in patients with mild and moderate pancreatic injury when compared to normal ERP findings. We concluded that asymptomatic alcoholic pancreatitis occurred more frequently in painless alcoholic. It may be not suitable for only using the normal pancreatic functions test to diagnose the alcohol induced chronic pancreatitis.

Adult↗
PubMed1980

[Acute alcoholic pancreatitis].

Alcoholism is the commonest cause of acute pancreatitis in South Africa. The pathogenesis and pathological abnormalities are reviewed, and stress is laid on the importance of chronic underlying changes on which an acute inflammatory process is superimposed. The clinical picture, the more important special investigations, and the present views on treatment are discussed.

Acute Disease↗
PubMed2007

Incidence of alcoholic pancreatitis in Japanese alcoholics: survey of male sobriety association members in Japan.

OBJECTIVE: To estimate the incidence of alcoholic pancreatitis, a dependence questionnaire survey was administered to male members of the sobriety association in Japan. METHODS: Questionnaires asking about age, age at start of alcohol drinking, amount of alcohol consumption, duration of drinking, the initiated age of abstinence, medical history of pancreatitis, the age at diagnosis of pancreatitis, and the etiology of pancreatitis were sent to 7876 male members of a sobriety association in Japan. RESULTS: Of 4120 members who replied to the questionnaire, 857 (20.8%) had a medical history of pancreatitis. Of these 857 members, 418 (10.1%) had been diagnosed with alcoholic pancreatitis, 32 (0.8%) as gallstone pancreatitis, and 407 (9.9%) with unknown etiology or etiology forgotten. A clear history of pancreatitis and information on habitual heavy drinking and the consumed amount of alcohol could be obtained from 373 of the 418 members diagnosed with alcoholic pancreatitis and from 345 of the 407 members with pancreatitis of unknown etiology. These 718 respondents were considered to be true alcoholic pancreatitis cases, with an extrapolated incidence of 9.1% (718/7876) to 17.4% (718/4120) cases of alcoholic pancreatitis in alcoholics in Japan. Alcoholics with a history of pancreatitis began drinking at relatively younger age and consumed a significantly greater amount of alcohol per day compared with 3113 alcoholics without a medical history of pancreatitis. CONCLUSION: This survey suggests that the incidence of alcoholic pancreatitis in alcoholics is much higher than previously reported.

Adult↗
PubMed1975

Standard and augmented secretin testing in chronic pancreatic alcoholic disease.

Sequential standard (1.0 U./kg.) and augmented (4.0-5.0 U./kg.) secretin response to the pancreas has been briefly compared in normal subjects and in patients with combinations of alcoholism, cirrhosis and alcoholic pancreatitis. The results of sequential testing led to the conclusion that, for clinical purposes, the standard test is adequate for the diagnosis of well established pancreatic pathologies causing gross destruction of the parenchyma. The augmented test is of particular value when the response to 1 U./kg. produced equivocal results, inasmuch as augmented stimulation enhances the masked secretory deficiency. The administration of the augmented stimulus to alcoholic patients yielded data which suggest a new hypothesis of pathogenesis for alcoholic pancreatitis, e.g., the postsecretin response pattern of minimal pancreatic inflammatory pathology is hypersecretion. Alcohol is thought to induce fatty degeneration of the pancreatic cell initially. Continued injury leads to necrosis and fibrosis.

Alcoholism↗
PubMed1991

Pancreatic enlargement in alcoholic pancreatitis: prevalence and natural history.

We determined the prevalence and natural history of pancreatic enlargement by abdominal ultrasonography or computed tomography in 72 patients with alcoholic pancreatitis. Pancreatic enlargement was observed in 54 patients (75%); it was diffuse in 28 (52%) and focal in 26 (48%). The focal enlargement was frequently cystic (50%), while the diffuse enlargement was only occasionally cystic (7%). Sequential imaging of the pancreas in 29 patients demonstrated partial to total resolution of pancreatic enlargement in greater than 50% during 6 months of follow-up. Determination of serum amylase and p-isoamylase activity was neither sensitive nor specific for pancreatic enlargement in alcoholic pancreatitis.

Acute Disease↗
PubMed1983

Prevalence of normal serum amylase levels in patients with acute alcoholic pancreatitis.

Acute alcoholic pancreatitis is uncommonly diagnosed when the serum amylase level is normal. We defined acute alcoholic pancreatitis as a clinical syndrome in which hyperamylasemia was not a necessary component and sought support for the diagnosis by ultrasonography and computed tomography of the pancreas. In 68 episodes of acute alcoholic pancreatitis identified in a one-year period, the serum amylase level was normal at the time of hospital admission in 32%. In 40 episodes, we performed ultrasonography and computed tomography within 48 hr of admission. The diagnosis was supported by ultrasonography in 43%, by computed tomography in 68%. Ultrasonography and computed tomography supported the diagnosis as frequently in patients with normal serum amylase levels as in patients with hyperamylasemia. We conclude that patients with acute alcoholic pancreatitis frequently have normal serum amylase levels. The widespread clinical practice of relying solely on hyperamylasemia to establish the diagnosis of acute alcoholic pancreatitis is unjustified and should be abandoned.

Acute Disease↗
PubMed1976

Comparison of pancreatic dysfunction in chronic alcoholic pancreatitis and chronic gallstone pancreatitis.

Comparative assessments of the endocrine and exocrine functions of the pancreas associated with gallstone pancreatitis or alcoholic pancreatitis were performed in a series of 86 patients, 20 with cholelithiasis, 12 with chronic alcoholism, 24 with chronic gallstone pancreatitis and 30 with chronic alcoholic pancreatitis and 32 healthy subjects were served as controls. The patients with cholelithiasis showed exocrine hypersecretion of the pancreas. In the patients with gallstone pancreatitis, all the assessed parameters of exocrine function were depressed. On the other hand, no pancreatic exocrine dysfunction was dispalyed in cases with chronic alcoholism. In the non-calcifying alcoholic pancreatitis, both the volume output and the the maximum concentration and output of bicarbonate were diminished but depression in amylase output was not seen. All these parameters were lowered in patients with calcifying pancreatitis. Elevation of hexosamine concentration in the pancreatic juice was evident in alcoholic pancreatitis as compared with gallstone pancreatitis, being particularly prominent in cases of non-calcifying pancreatitis. Patients with alcoholic pancreatitis were observed to secrete viscous pancreatic juice richer in amylase and hexosamine content, than those in the patients with gallstone pancreatitis. Endocrine dysfunction of the pancreas is more frequent and intense in alcoholic pancreatitis than in gallstone pancreatitis.

Alcoholism↗
PubMed1997

Clinical value of serum pancreatic enzymes in acute alcohol intoxication and acute alcoholic pancreatitis.

BACKGROUND AND AIMS: The aim of this study was to evaluate the incidence in the serum of elevated levels of amylase, pancreatic isoamylase, and lipase in acute alcohol intoxication among occasional drinkers and chronic alcoholics, and to assess the diagnostic ability of the three enzymes for acute alcoholic pancreatitis. PATIENTS AND METHODS: One-hundred and seventeen consecutive subjects with acute alcohol intoxication but no abdominal pain (47 occasional drinkers, 70 chronic alcoholics), and 17 with acute alcoholic pancreatitis were studied. For all subjects serum amylase, pancreatic isoamylase, and lipase were determined using commercially available kits. RESULTS: Among occasional drinkers, serum amylase levels were abnormally high in 6 subjects (13%), whereas serum pancreatic isoamylase and lipase were abnormally high in one, (2%). In chronic alcoholics without abdominal pain serum amylase and lipase were abnormally high in 10 subjects (14%) but serum pancreatic isoamylase in only 7 (10%). In patients with acute alcoholic pancreatitis, serum amylase and pancreatic isoamylase were abnormally high in 16 of the 17 patients (94%), whereas serum lipase was abnormally high in all. CONCLUSIONS: Chronic alcohol abuse, but not occasional alcohol intoxication, may cause pancreatic damage. Amylase, pancreatic isoamylase and lipase determinations in the serum are all equally useful in the diagnosis of acute alcoholic pancreatitis.

Acute Disease↗
PubMed1981

HLA antigens in chronic idiopathic pancreatitis compared with chronic alcoholic pancreatitis.

HLA A and B antigens in 46 patients with chronic pancreatitis were studied in Japan. Patients were divided into the two groups according to the etiology of the disease: one was chronic idiopathic pancreatitis (18 cases) and the other was chronic alcoholic pancreatitis (28 cases). One hundred twenty unrelated subjects were also examined as control. HLA B5 was detected in 14 of 18 cases of chronic idiopathic pancreatitis, which was significantly higher statistically than in control (P less than 0.001, corrected P less than 0.05). In contrast, no HLA antigens of locus A and B were found which had a relationship to chronic alcoholic pancreatitis. These results suggest that some genetic factors may be implicated in the development of chronic idiopathic pancreatitis and differing from that of alcoholic pancreatitis.

Adult↗
PubMed1986

Acute (nonprogressive) alcoholic pancreatitis: prospective longitudinal study of 144 patients with recurrent alcoholic pancreatitis.

Over the last 10 years, a series of 144 consecutive patients with alcoholic recurrent pancreatitis have been studied prospectively at regular intervals with particular regard to exocrine function, calcifications, pancreatographic ductal changes, and histopathology of the pancreas. Based upon the long-term course, the patients were classified into two groups; group A (n = 95), those with chronic pancreatitis (78 of them with calcifications); and group B (n = 49), those with acute (nonprogressive) pancreatitis. The duration of disease from onset was 2-19 years (median, 9.7 and 8.3 years, respectively, in group A and B). The two groups were comparable at onset of the disease in age, sex, number of episodes of pancreatitis, and number of pseudocysts. In group A, all 95 cases fulfilled the strict diagnostic criteria of chronic pancreatitis within the period of observation (e.g., progressive exocrine insufficiency and/or typical morphological changes, particularly calcifications). In group B, the exocrine function remained normal over the entire period of observation. No histologic evidence of chronic pancreatitis was detected in five of seven large pancreatic specimens. Marked to moderate ductal changes were found in 10 of 16 patients in group B (despite normal exocrine function). Our data suggest that about one third of patients of the present series with alcoholic (recurrent) pancreatitis did not progress toward chronic (progressive) pancreatitis, although some demonstrated morphological alterations (except calcifications) in association with normally preserved exocrine function (residual scars?). The pathogenetic factor(s) responsible for progression (or nonprogression) of alcoholic (recurrent) pancreatitis to chronic pancreatitis remain(s) to be elucidated.

Acute Disease↗
PubMed1994

Pancreatic fibrosis in patients with chronic alcohol abuse: correlation with alcoholic pancreatitis.

OBJECTIVES: To investigate the incidence and histological features of pancreatic fibrosis, including chronic alcoholic pancreatitis, in patients with a history of chronic alcohol abuse. METHODS: Forty-six autopsy cases of alcoholic dependence syndrome, 53 cases of chronic alcoholism, and 30 cases of chronic alcoholic pancreatitis were studied histopathologically. RESULTS: Fibrosis was seen in 33 of 46 cases of alcoholic dependence syndrome, 20 of 53 cases of chronic alcoholism, and all 30 cases of chronic alcoholic pancreatitis. Fibrosis was categorized into three types: intralobular, perilobular, and mixed intralobular and perilobular sclerosis. In chronic alcoholic pancreatitis, fibrosis was found mainly in perilobular, or interlobular, areas, and in some advanced cases extended into intralobular areas, so that the pancreatic tissue was completely replaced by fibrosis. Hence, interlobular fibrosis was found in all cases of chronic alcoholic pancreatitis. In contrast, in cases that had predominantly intralobular fibrosis, which were usually cases of alcoholic dependence syndrome, the pancreatic tissue had not completely disappeared, even at an advanced stage, and some parenchymal regeneration similar to that seen in hemochromatosis was observed. CONCLUSION: Interlobular and intralobular pancreatic fibrosis associated with alcohol abuse appears in distinct pathological patterns with differing mechanisms.

Alcoholism↗
PubMedDate not supplied

Management of pancreatic pseudocysts in chronic alcoholic pancreatitis with duct dilatation.

Twenty-one patients with pancreatic pseudocysts secondary to alcoholic pancreatitis were treated by cystojejunostomy (16), cystoduodenostomy (4) and external drainage (1). In all patients, the duct of Wirsung was drained into a defunctionalized loop of the jejunum at the same operation. There was no early or late mortality. Pseudocyst recurrence did not occur, and only one patient (4.7%) had light pain recurrence in the follow-up period. The importance of providing an outflow route for the obstructed pancreatic duct, and not just for the pseudocyst, is stressed due to this experience with patients affected by underlying chronic pancreatitis.

Alcoholism↗
PubMed1992

Cholinergic hypothesis of alcoholic pancreatitis.

Chronic alcohol intake interferes especially with the two main pathways regulating exocrine pancreatic secretion: the cholinergic and the pancreozymin pathway. Recently, a new theory of the pathogenesis of alcoholic pancreatitis was proposed emphasizing disordered agonist-receptor interaction at the level of pancreatic acinar cells. Accordingly, alcohol-induced alterations in the control of exocrine pancreatic secretion result in hyperstimulation of pancreatic acinar cells and their muscarinic receptors, mimicking the mechanism of acute pancreatitis caused by scorpion sting, intoxication with an anti-acetylcholinesterase-containing insecticide or supramaximal doses of secretagogues. The present review emphasizes the role of these alcohol-induced secretory alterations in the pathogenesis of alcoholic pancreatitis.

Acetylcholine↗