Oktoberfest Binge Drinking and Acute Pancreatitis: Is There Really No Relationship?
2011; Elsevier BV; Volume: 9; Issue: 11 Linguagem: Inglês
10.1016/j.cgh.2011.07.022
ISSN1542-7714
Autores Tópico(s)Alcohol Consumption and Health Effects
Resumo"The presence or absence, the severity or rate of progress of the pancreatic lesion does not appear to vary with the quantity of alcohol ingested. Apparently, it may attack an individual who has had little or no previous indulgence … while it may completely spare a chronic and severe alcoholic. Alcohol alone is not enough."1Weiner H.A. Tennant R.A. A statistical study of acute hemorrhagic pancreatitis (hemorrhagic necrosis of pancreas).Am J Med Sci. 1938; 196: 167Crossref Google Scholar"The … first attack usually occurred against a background of a heavy alcoholic intake of about 5–15 years' duration …. Relationship of the attack to an alcoholic binge or a night's over-indulgence was of paramount importance, but in many the amount of alcohol consumed was not necessarily greater than, or indeed as much as, that taken with impunity on previous occasions."2Marks I.N. Bank S. The aetiology, clinical features and diagnosis of pancreatitis in the South Western Cape; a review of 243 cases.S Afr Med J. 1963; 37: 1039-1053PubMed Google Scholar Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar in this issue of Clinical Gastroenterology and Hepatology directly or obliquely address 3 questions that have plagued pancreatologists for generations regarding "drunkard's pancreas."4Friedreich N. Diseases of the pancreas.in: Ziemssen H. Cyclopedia of the practice of medicine. William Wood, New York1878: 549-630Google Scholar (1) How much chronic alcohol ingestion can cause alcoholic chronic pancreatitis? (2) Can increased alcohol ingestion (bingeing) by persons with alcoholic chronic pancreatitis induce an attack of "acute pancreatitis?" (3) Does binge drinking induce an attack of acute pancreatitis in persons without an alcohol history, no history of previous attacks, no chronic pancreatitis, and no other etiology for pancreatitis? Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar report that the overall incidence of acute pancreatitis does not increase during Oktoberfest. Their analyses, however, do not allow firm answers to the 3 questions posed above and do not exclude the possibility that short-term bingeing leads to acute attacks of alcoholic pancreatitis. There is no controversy that alcohol causes chronic pancreatitis. In the 19th century Heinrich Claessen in 18425Claessen H. Die Krankheiten der Bauchspeicheldrüse. DuMont-Schauberg, Köln1842Google Scholar and Nikolaus Friedreich in 18784Friedreich N. Diseases of the pancreas.in: Ziemssen H. Cyclopedia of the practice of medicine. William Wood, New York1878: 549-630Google Scholar suggested an association between alcohol and pancreatitis and the latter coined the term "drunkard's pancreas." The connection between alcohol and chronic pancreatitis was not conclusively established, however, until the 20th century, beginning with case-reports/series,6Myers W.K. Keefer C.S. Acute pancreatic necrosis in acute and chronic alcoholism.N Engl J Med. 1934; 110: 1376-1380Crossref Google Scholar, 7Clark E. Pancreatitis in acute and chronic alcoholism.Am J Dig Dis. 1942; 9: 428Crossref Scopus (34) Google Scholar autopsy studies,1Weiner H.A. Tennant R.A. A statistical study of acute hemorrhagic pancreatitis (hemorrhagic necrosis of pancreas).Am J Med Sci. 1938; 196: 167Crossref Google Scholar, 6Myers W.K. Keefer C.S. Acute pancreatic necrosis in acute and chronic alcoholism.N Engl J Med. 1934; 110: 1376-1380Crossref Google Scholar, 7Clark E. Pancreatitis in acute and chronic alcoholism.Am J Dig Dis. 1942; 9: 428Crossref Scopus (34) Google Scholar, 8Egdahl A. A review of one hundred and five reported cases of acute pancreatitis, with special reference to etiology; with report of two cases.Johns Hopkins Hospital Bulletin. 1907; 18: 130-136Google Scholar and definitive clinical-anatomical studies by Comfort et al9Comfort M.W. Gambill E.E. Baggenstoss A.H. Chronic relapsing pancreatitis; a study of 29 cases without associated disease of the biliary or gastrointestinal tract.Gastroenterology. 1946; 6: 376-408PubMed Google Scholar in 1946. The amount and the length of exposure of alcohol required to cause chronic pancreatitis is uncertain and varies greatly among studies. Small studies indicate there is no clear alcohol toxicity threshold on the human pancreas but there is a dose-response relationship between drinking and the incidence of acute10Lindkvist B. Appelros S. Manjer J. et al.A prospective cohort study of smoking in acute pancreatitis.Pancreatology. 2008; 8: 63-70Abstract Full Text PDF PubMed Scopus (83) Google Scholar and chronic pancreatitis.11Durbec J.P. Sarles H. Multicenter survey of the etiology of pancreatic diseases Relationship between the relative risk of developing chronic pancreaitis and alcohol, protein and lipid consumption.Digestion. 1978; 18: 337-350Crossref PubMed Scopus (231) Google Scholar Durbec and Sarles11Durbec J.P. Sarles H. Multicenter survey of the etiology of pancreatic diseases Relationship between the relative risk of developing chronic pancreaitis and alcohol, protein and lipid consumption.Digestion. 1978; 18: 337-350Crossref PubMed Scopus (231) Google Scholar calculated an increased relative risk of 1.4 for chronic pancreatitis with 20 g per day compared with no alcohol intake. Three additional studies support the concept that the low cutoff (>20 g per day) used by Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar has a pathophysiological impact on the pancreas, but likely as a disease modifier rather than cause of pancreatitis. Mayo Clinic investigators, in a large natural history study of 347 patients with onset of chronic pancreatitis after age 35 years, evaluated an idiopathic group with no alcohol intake (n = 41), a low alcohol intake group ( 2 drinks per day was a strong independent risk factor for necrotizing pancreatitis, independent of etiology.13Papachristou G.I. Papachristou D.J. Morinville V.D. et al.Chronic alcohol consumption is a major risk factor for pancreatic necrosis in acute pancreatitis.Am J Gastroenterol. 2006; 101: 2605-2610Crossref PubMed Scopus (56) Google Scholar In a small meta-analysis of 2 case-control studies (n = 247 patients), Corrao et al14Corrao G. Bagnardi V. Zambon A. et al.A meta-analysis of alcohol consumption and the risk of 15 diseases.Prev Med. 2004; 38: 613-619Crossref PubMed Scopus (782) Google Scholar observed an increasing relative risk for developing chronic pancreatitis with ingesting 25, 50, and 100 g per day. A subsequent systematic review and meta-analysis of 6 studies and 1671 patients with attacks of pancreatitis due to alcohol (mixed population with acute or chronic pancreatitis) indicated there was a similar nearly exponential dose-response relationship between alcohol consumption and by the categorical analysis the risk of pancreatitis increased at a threshold of ≥4 drinks per day.15Irving H.M. Samokhvalov A.V. Rehm J. Alcohol as a risk factor for pancreatitis A systematic review and meta-analysis.JOP. 2009; 10: 387-392PubMed Google Scholar Similarly, Yadav et al16Yadav D. Hawes R.H. Brand R.E. et al.Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis.Arch Intern Med. 2009; 169: 1035-1045Crossref PubMed Scopus (312) Google Scholar reported in a recent, large multicenter study a threshold of ≥5 drinks per day increased the risk of chronic pancreatitis but surprisingly not recurrent acute pancreatitis, possibly due to insufficient power to discern a difference or the impact of reducing alcohol consumption after the first attack.17Nordback I. Pelli H. Lappalainen-Lehto R. et al.The recurrence of acute alcohol-associated pancreatitis can be reduced: a randomized controlled trial.Gastroenterology. 2009; 136: 848-855Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar, 18Pelli H. Lappalainen-Lehto R. Piironen A. et al.Risk factors for recurrent acute alcohol-associated pancreatitis: a prospective analysis.Scand J Gastroenterol. 2008; 43: 614-621Crossref PubMed Scopus (63) Google Scholar In Yadav's study, 88% of very heavy drinkers (≥5 drinks per day) in the chronic pancreatitis group binged (defined as >6 drinks per day for ≥3 consecutive days) compared with only 8% of heavy drinkers (>3 and 80 g per day),21Lankisch P.G. Assmus C. Maisonneuve P. et al.Epidemiology of pancreatic diseases in Lüneburg County A study in a defined german population.Pancreatology. 2002; 2: 469-477Abstract Full Text PDF PubMed Scopus (175) Google Scholar is a borderline amount considered to cause pancreatitis. Furthermore, there is no information regarding the duration alcohol was ingested. Twenty grams per day of alcohol is slightly less than the definition of heavy drinking by the National Center of Health Statistics, which defined drinking in terms of drinks per week as light (≤3), moderate (men 4–14; women 4–7), and heavy (men >14; women >7).22National Center of Health StatisticsHealth, United States, 2006 With Chartbook on Trends in the Health of Americans. National Center of Health Statistics, Hyattsville, MD2006Google Scholar This definition of heavy drinking (>25 g per day), however, is much lower than conventional criterion of "heavy drinking" to assign the etiology of pancreatitis to alcohol when a minimum of 50–80 g per day of alcohol is consumed over at least 6 years.23Layer P. Yamamoto H. Kalthoff L. et al.The different courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis.Gastroenterology. 1994; 107: 1481-1487Abstract Full Text PDF PubMed Google Scholar, 24Müllhaupt B. Truninger K. Ammann R. Impact of etiology on the painful early stage of chronic pancreatitis: a long-term prospective study.Z Gastroenterol. 2005; 43: 1293-1301Crossref PubMed Scopus (50) Google Scholar Phillip et al,3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar however, reported that those with presumed acute pancreatitis due to alcohol (they use the term "AAP") ingested 72.8 g per day during Oktoberfest, similar to that ingested chronically, and in line with criteria used by others.10Lindkvist B. Appelros S. Manjer J. et al.A prospective cohort study of smoking in acute pancreatitis.Pancreatology. 2008; 8: 63-70Abstract Full Text PDF PubMed Scopus (83) Google Scholar, 11Durbec J.P. Sarles H. Multicenter survey of the etiology of pancreatic diseases Relationship between the relative risk of developing chronic pancreaitis and alcohol, protein and lipid consumption.Digestion. 1978; 18: 337-350Crossref PubMed Scopus (231) Google Scholar Of note this amount of alcohol is greater than the 57 g per day ingested by the 6 million persons visiting Oktoberfest. These data raise questions about the accuracy of diagnoses of AAP and whether subgroups of patients ingested greater amounts of alcohol immediately prior to the attack of AAP. More than alcohol ingestion is involved in the development of alcoholic pancreatitis. Approximately 25–56 million American adults older than 18 years are dependent upon or abuse alcohol,25Hasin D.S. Stinson F.S. Ogburn E. et al.Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions.Arch Gen Psychiatry. 2007; 64: 830-842Crossref PubMed Scopus (1711) Google Scholar but no more than 3% of them develop AAP.26Lankisch P.G. Lowenfels A.B. Maisonneuve P. What is the risk of alcoholic pancreatitis in heavy drinkers?.pancreas. 2002; 25: 411-412Crossref PubMed Scopus (107) Google Scholar, 27Yadav D. Eigenbrodt M.L. Briggs M.J. et al.Pancreatitis: prevalence and risk factors among male veterans in a detoxification program.Pancreas. 2007; 34: 390-398Crossref PubMed Scopus (62) Google Scholar These data, along with observations that total alcohol consumption is not greater among heavy drinkers who develop pancreatitis versus those who do not,11Durbec J.P. Sarles H. Multicenter survey of the etiology of pancreatic diseases Relationship between the relative risk of developing chronic pancreaitis and alcohol, protein and lipid consumption.Digestion. 1978; 18: 337-350Crossref PubMed Scopus (231) Google Scholar, 28Stigendal L. Olsson R. Alcohol consumption pattern and serum lipids in alcoholic cirrhosis and pancreatitis A comparative study.Scand J Gastroenterol. 1984; 19: 582-587PubMed Google Scholar, 29Wilson J.S. Bernstein L. McDonald C. et al.Diet and drinking habits in relation to the development of alcoholic pancreatitis.Gut. 1985; 26: 882-887Crossref PubMed Scopus (59) Google Scholar, 30Bourliere M. Barthet M. Berthezene P. et al.Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?.Gut. 1991; 32: 1392-1395Crossref PubMed Scopus (112) Google Scholar indicate that additional cofactors participate in precipitating AAP, such as smoking, dietary factors, hereditary effects, alcohol type31Apte M.V. Pirola R.C. Wilson J.S. Mechanisms of alcoholic pancreatitis.J Gastroenterol Hepatol. 2010; 25: 1816-1826Crossref PubMed Scopus (82) Google Scholar or reducing the risk of AAP (eg, caffeinated coffee).32Morton C. Klatsky A.L. Udaltsova N. Smoking, coffee, and pancreatitis.Am J Gastroenterol. 2004; 99: 731-738Crossref PubMed Scopus (94) Google Scholar Smoking, in particular, is emerging as major risk for chronic pancreatitis (see meta-analysis33Andriulli A. Botteri E. Almasio P.L. et al.Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis.Pancreas. 2010; 39: 1205-1210Crossref PubMed Scopus (93) Google Scholar), a proposal dating to Claessen in 1842 or earlier.5Claessen H. Die Krankheiten der Bauchspeicheldrüse. DuMont-Schauberg, Köln1842Google Scholar For example, the multicenter study by Yadav et al16Yadav D. Hawes R.H. Brand R.E. et al.Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis.Arch Intern Med. 2009; 169: 1035-1045Crossref PubMed Scopus (312) Google Scholar reported that alcohol and cigarette smoking are independent risks for chronic pancreatitis but found no significant interaction between these risks because there were too few patients with the combination of nonsmoking and heavy drinking and also too few with heavy smoking and nondrinking. Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar found that patients with AAP had a significantly greater cigarette smoking exposure compared with nonalcoholic acute pancreatitis and were more commonly younger and men. The importance of these and other factors is unclear as data are insufficient/unavailable in their report3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar to discern an impact upon the development of AAP. A potential strength of the Phillip study3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar would have been to provide data to answer questions 2 and 3 (see Introduction of the Editorial). Unfortunately, they appear to have included patients with and without chronic alcoholic pancreatitis in the group of patients presumed to have "acute pancreatitis" due to alcohol (AAP), precluding answers to these questions. They state 15 of 69 total AAP patients in the 3 control periods had acute alcohol-induced chronic pancreatitis. It is unclear, however, whether these 15 patients had chronic pancreatitis and the remainder (n = 54) did not; how these 2 groups of patients were distributed among the 3 observation periods; and how much alcohol these 2 groups ingested chronically and immediately before the attack of AAP. Reporting alcohol intake only for entire groups may obscure differences in alcohol ingestion among subgroups. Multiple studies indicate that patients who develop AAP frequently report short-term heavy drinking or bingeing.2Marks I.N. Bank S. The aetiology, clinical features and diagnosis of pancreatitis in the South Western Cape; a review of 243 cases.S Afr Med J. 1963; 37: 1039-1053PubMed Google Scholar, 7Clark E. Pancreatitis in acute and chronic alcoholism.Am J Dig Dis. 1942; 9: 428Crossref Scopus (34) Google Scholar, 9Comfort M.W. Gambill E.E. Baggenstoss A.H. Chronic relapsing pancreatitis; a study of 29 cases without associated disease of the biliary or gastrointestinal tract.Gastroenterology. 1946; 6: 376-408PubMed Google Scholar, 17Nordback I. Pelli H. Lappalainen-Lehto R. et al.The recurrence of acute alcohol-associated pancreatitis can be reduced: a randomized controlled trial.Gastroenterology. 2009; 136: 848-855Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar, 34Imrie C.W. Observations on acute pancreatitis.Br J Surg. 1974; 61: 539-544Crossref PubMed Scopus (59) Google Scholar Typically, and particularly in binge drinkers, an attack begins 12–48 hours after cessation of drinking ("the afternoon after the night before"),2Marks I.N. Bank S. The aetiology, clinical features and diagnosis of pancreatitis in the South Western Cape; a review of 243 cases.S Afr Med J. 1963; 37: 1039-1053PubMed Google Scholar strongly suggesting that there is a relationship between a bout of alcohol ingestion and onset of an attack of acute pancreatitis. For multiple reasons, however, it remains unclear whether alcohol bingeing is responsible for precipitating AAP. Most investigators assume that patients who develop AAP have long-term heavy drinking.2Marks I.N. Bank S. The aetiology, clinical features and diagnosis of pancreatitis in the South Western Cape; a review of 243 cases.S Afr Med J. 1963; 37: 1039-1053PubMed Google Scholar, 7Clark E. Pancreatitis in acute and chronic alcoholism.Am J Dig Dis. 1942; 9: 428Crossref Scopus (34) Google Scholar, 9Comfort M.W. Gambill E.E. Baggenstoss A.H. Chronic relapsing pancreatitis; a study of 29 cases without associated disease of the biliary or gastrointestinal tract.Gastroenterology. 1946; 6: 376-408PubMed Google Scholar, 16Yadav D. Hawes R.H. Brand R.E. et al.Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis.Arch Intern Med. 2009; 169: 1035-1045Crossref PubMed Scopus (312) Google Scholar, 34Imrie C.W. Observations on acute pancreatitis.Br J Surg. 1974; 61: 539-544Crossref PubMed Scopus (59) Google Scholar Some studies indicated that binge drinking uncommonly associates with AAP,35Saint E.G. Acute pancreatitis.Med J Aust. 1954; 2: 536-543PubMed Google Scholar, 36Mayday G.B. Pheils M.T. Pancreatitis: a clinical review.Med J Aust. 1970; 1: 1142-1144PubMed Google Scholar, 37Kager L. Lindeberg S. Agren G. [Alcohol consumption and pancreatitis in men–an intensive study of a one year material].Nord Med. 1971; 85: 413PubMed Google Scholar and case-control studies with control populations of heavy drinkers without pancreatitis and heavy drinkers with liver disease have not resolved whether short-term heavy drinking or bingeing increases the incidence of AAP among heavy drinkers.28Stigendal L. Olsson R. Alcohol consumption pattern and serum lipids in alcoholic cirrhosis and pancreatitis A comparative study.Scand J Gastroenterol. 1984; 19: 582-587PubMed Google Scholar, 29Wilson J.S. Bernstein L. McDonald C. et al.Diet and drinking habits in relation to the development of alcoholic pancreatitis.Gut. 1985; 26: 882-887Crossref PubMed Scopus (59) Google Scholar, 37Kager L. Lindeberg S. Agren G. [Alcohol consumption and pancreatitis in men–an intensive study of a one year material].Nord Med. 1971; 85: 413PubMed Google Scholar Moreover, Strum and Spiro38Strum W.B. Spiro H.M. Chronic pancreatitis.Ann Intern Med. 1971; 74: 264-277Crossref PubMed Scopus (96) Google Scholar evaluated 894 admissions of Yale students for a first-attack of acute pancreatitis and failed to find a single instance of a patient 21 years or younger admitted with acute pancreatitis after a single drinking bout and no history of chronic alcohol ingestion; 2 patients 21 years old or younger had AAP but both had a 2-year history of heavy drinking. The authors concluded there is usually a "delay between the start of steady heavy drinking and the first clinical manifestation of alcoholic pancreatitis" and that "temperate persons who indulge in an acute alcoholic bout will not ordinarily develop acute pancreatitis." Although Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar report admission to hospital approximately 23 to 35 hours after the onset of pain, data are insufficient to determine if alcohol drinking precipitated AAP, how long after cessation of drinking patients had onset of pain and were admitted to hospital, and whether there were differences between patients with underlying alcoholic chronic pancreatitis and those with first-attack of AAP and no other known etiology for pancreatitis. Quantitative data about binge drinking prior to a first attack of AAP is available but limited. Nordback et al17Nordback I. Pelli H. Lappalainen-Lehto R. et al.The recurrence of acute alcohol-associated pancreatitis can be reduced: a randomized controlled trial.Gastroenterology. 2009; 136: 848-855Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar established a diagnosis of first attack AAP in 120 patients based on long-term heavy alcohol intake and exclusion of other etiologies. Daily alcohol consumption was significantly greater the week prior to AAP compared with the prior 2 months (P < .001) and was greater in each of the 2 groups randomized to different counseling: group 1 (65 vs 48 g per day) and group 2 (84 vs 56 g per day). In a separate study the investigators raised the hypothesis that the first-attack AAP may be precipitated by the alcohol withdrawal from an acute increase in alcohol consumption because they observed that 71% of the patients developed symptoms during the withdrawal period (43% at 1–24 hours and 28% at ≥25 hours) compared with 29% during the active drinking period.39Nordback I. Pelli H. Lappalainen-Lehto R. et al.Is it long-term continuous drinking or the post-drinking withdrawal period that triggers the first acute alcoholic pancreatitis?.Scand J Gastroenterol. 2005; 40: 1235-1239Crossref PubMed Scopus (16) Google Scholar This observation corresponds to the old aphorism referred to earlier that attacks of pancreatitis occur "the afternoon after the night before."2Marks I.N. Bank S. The aetiology, clinical features and diagnosis of pancreatitis in the South Western Cape; a review of 243 cases.S Afr Med J. 1963; 37: 1039-1053PubMed Google Scholar In summary, the answers to the 3 questions (raised in the Introduction of the Editorial) are emerging but are not entirely clear. Drinking 4 to 5 drinks per day or more for 16 to ≥35 years (but likely shorter durations) associates with the greatest risk for developing alcoholic chronic pancreatitis and ingesting <2 drinks per day may not increase risk. Cofactors other than alcohol, particularly cigarette smoking, are important and influence individual susceptibility of drinkers for developing pancreatitis. It is uncertain if and how much alcohol is necessary during a binge to induce an attack of "acute pancreatitis" in persons with established or without chronic alcoholic pancreatitis, but there is evidence that bingeing or acute withdrawal after bingeing precipitates an attack. Phillip et al3Phillip V. Huber W. Hagemes F. et al.Incidence of acute pancreatitis does not increase during Oktoberfest, but is higher than previously described in Germany.Clin Gastroenterol Hepatol. 2011; 9: 995-1000Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar showed that there was no increased incidence of hospital admission for pancreatitis associated with Oktoberfest. Use caution, however, in interpreting their results as suggesting that acute ingestion of alcohol does not precipitate attacks of "acute pancreatitis." Incidence of Acute Pancreatitis Does Not Increase During Oktoberfest, but Is Higher Than Previously Described in GermanyClinical Gastroenterology and HepatologyVol. 9Issue 11PreviewIncreased alcohol consumption can lead to acute pancreatitis (AP). We investigated whether the incidence of alcohol-induced AP increased during the Munich Oktoberfest in 2008, at which 6.6 million liters of beer were sold within 16 days. Full-Text PDF
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