Alcoholic Pancreatitis

Schneider, Alexander; Singer, Manfred V.

doi:10.1159/000090169

Cited by 28 publications

(24 citation statements)

References 122 publications

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“…Two factors that cause AP are alcohol and gallstones, which play different roles and have different pathogenic mechanisms leading to pancreatic acinar cell damage. Alcohol abuse is the most common cause of AP in men, whereas gallstone migration into the bile duct is the main cause of AP in women (Dufour and Adamson, 2003;Schneider and Singer, 2005;Venneman et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Influence of interleukin-1β and interleukin-6 gene polymorphisms on the development of acute pancreatitis

Chi¹,

Chen²,

Huang³

2015

Genet. Mol. Res.

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ABSTRACT. We investigated the association between 3 main proinflammatory cytokines [interleukin (IL)-1b and IL-6] and the risk of acute pancreatitis. Polymerase chain reaction-restriction fragment length polymorphism was used to genotype IL-1β +3954 C/T (rs1143634) and IL-1β -511 C/T (rs16944) and IL-6 -174 G/C (rs1800795) and IL-6 -634 C/G (rs1800796). The genotype distributions of IL-1β +3954 C/T (rs1143634) and IL-1β -511 C/T (rs16944) and IL-6 -174 G/C (rs1800795) and IL-6 -634 C/G (rs1800796) were in HardyWeinberg equilibrium for the control group. Multivariate regression analyses showed that subjects carrying the rs1143634 TT genotype had a significantly increased risk of acute pancreatitis, with an adjusted odds ratio (95% confidence interval) of 2.11 (1.03-4.51). Subjects carrying the IL-1β rs1143634 TT genotype had a significantly increased risk of acute pancreatitis in our Chinese population.

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Section: Introductionmentioning

confidence: 99%

Influence of interleukin-1β and interleukin-6 gene polymorphisms on the development of acute pancreatitis

Chi¹,

Chen²,

Huang³

2015

Genet. Mol. Res.

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Section: Introductionmentioning

confidence: 99%

“…However, tissue damage is a major component of alcoholic pancreatitis [14,15] . Multiple theories have been suggested in explanation of the pathomechanisms of alcohol-induced pancreatitis [3,[14][15][16][17] . While typically excessive and prolonged alcohol use is associated with alcoholic pancreatitis, an acute alcohol consumption event or binge drinking can also trigger acute pancreatitis [18] .…”

Section: Introductionmentioning

confidence: 99%

Effect of Ethanol on Inflammatory Responses

et al. 2007

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Background/Aims: Alcohol use alters inflammatory cell responses. While alcohol has direct effects on pancreatic acinar cells, activation of inflammatory cells is a major component of the pathology of alcoholic pancreatitis. Methods: The effects of acute or chronic alcohol exposure were evaluated in human monocytes on the production of TNFα or IL-10 production, pro-inflammatory gene and nuclear factor-ĸB (NF-ĸB) activation. Results: Moderate, acute alcohol consumption or equivalent doses of alcohol in vitro had anti-inflammatory effects on monocyte activation via inhibition of pro-inflammatory genes and NF-ĸB activation, inhibition of TNFα production and augmentation of the anti-inflammatory cytokine, IL-10. In contrast, acute alcohol treatment augmented NF-ĸB activation and TNFα production and inhibited IL-10 levels in the presence of complex stimulation with combined TLR2 and TLR4 ligands. Prolonged alcohol exposure also resulted in an increase in NF-ĸB and TNFα production in response to TLR4 stimulation with LPS. Conclusion: These results suggest that alcohol can either attenuate or promote inflammatory responses that are critical in pancreatitis. Our results support the hypothesis that both acute alcohol intake in the presence of complex stimuli (such as necrotic cells) and chronic alcohol exposure result in hyper-responsiveness of monocytes to inflammatory signals and may contribute to increased inflammation in pancreatitis.

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“…The other cofactors are yet to be determined, but could be environmental, genetic, race or concomitant risk factors such as smoking and nutrition [for reviews, see [60,61,62,63]]. The prevalence of smoking increases with the amount of alcohol consumed.…”

Section: Alcohol Smoking and Pancreasmentioning

confidence: 99%

Alcohol and Smoking

Singer

Feick

Gerloff³

2011

Dig Dis

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The WHO ranks smoking and alcohol consumption as the first and third leading causes of the global burden of disease in industrialized countries, using disability-adjusted life years (DALYs) as a combined measure of premature death and disability. Smoking is responsible for 12.2% of all DALYs and alcohol consumption for 9.2%. For example in Germany, annually 110,000–140,000 humans die prematurely because of cigarette smoking and 40,000 because of alcohol drinking. In Europe and the USA, more than 20% of all hospitalized men and more than 9% of all hospitalized women suffer from alcohol-associated diseases. In Germany, about 2.0 million people in the age group 18–64 years (3.8% of all Germans) are alcohol abusers and 1.3 million people (2.4%) are alcohol-dependent. Alcohol can cause acute as well as chronic damage in nearly all body organs. Smoking damages also nearly every human body organ and is worldwide the most important single preventable health risk factor as well as the main cause for premature mortality in industrial countries. One third of the adult Germans as well as of the world population are active smokers; men smoke more frequently than women (34.0 vs. 25.1%). In this review a short overview will be given on the most important deleterious effects of alcohol and smoking. The most recent data about the pathophysiological relevance of non-alcoholic compounds of alcoholic beverages will also be discussed.

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Alcoholic Pancreatitis

Cited by 28 publications

References 122 publications

Influence of interleukin-1β and interleukin-6 gene polymorphisms on the development of acute pancreatitis

Influence of interleukin-1β and interleukin-6 gene polymorphisms on the development of acute pancreatitis

Effect of Ethanol on Inflammatory Responses

Alcohol and Smoking

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