Epidemiology of alcoholic liver disease

Saunders, John B.; Latt, Noeline

doi:10.1016/0950-3528(93)90002-a

Cited by 38 publications

(19 citation statements)

References 111 publications

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“…Indeed, native livers from hepatitis C-infected patients here and in other studies often showed morphology of chronic hepatitis rather than alcohol injury ( Table 1), suggesting that alcohol had exacerbated viral damage rather than the other way around (19,20). In alcoholics, the presence and severity of clinical liver disease correlate with hepatitis C seropositivity (17,21); alcohol may increase hepatitis C replication and liver injury (22) and accelerate fibrosis (23). Hence, such cases might be better regarded as a subgroup of the coexistent diagnosis (hepatitis C) rather than alcohol liver disease, especially when considering the impact of pretransplant diagnosis on graft outcome.…”

Section: Discussionmentioning

confidence: 99%

Liver Transplantation for Alcoholic Cirrhosis: Long Term Follow-Up and Impact of Disease Recurrence1

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Liver Transplantation for Alcoholic Cirrhosis: Long Term Follow-Up and Impact of Disease Recurrence1

et al. 2001

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“…It has been estimated that around two billion people drink ethanol on a regular basis . Ethanol consumption has long been recognized as a major cause of liver disease, but it can also affect the gastrointestinal (GI) tract and is associated with the development of oral, esophageal, and colorectal cancers . Ethanol as well as its metabolites can cause damage that includes decreased intestinal motility and cytotoxic and mutagenic effects .…”

Section: Introductionmentioning

confidence: 99%

Ethanol metabolism and its effects on the intestinal epithelial barrier

Elamin¹,

Masclee²,

Dekker³

et al. 2013

Nutr Rev

162

130

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Ethanol is widely consumed and is associated with an increasing global health burden. Several reviews have addressed the effects of ethanol and its oxidative metabolite, acetaldehyde, on the gastrointestinal (GI) tract, focusing on carcinogenic effects or alcoholic liver disease. However, both the oxidative and the nonoxidative metabolites of ethanol can affect the epithelial barrier of the small and large intestines, thereby contributing to GI and liver diseases. This review outlines the possible mechanisms of ethanol metabolism as well as the effects of ethanol and its metabolites on the intestinal barrier. Limited studies in humans and supporting in vitro data have indicated that ethanol as well as mainly acetaldehyde can increase small intestinal permeability. Limited evidence also points to increased colon permeability following exposure to ethanol or acetaldehyde. In vitro studies have provided several mechanisms for disruption of the epithelial barrier, including activation of different cell-signaling pathways, oxidative stress, and remodeling of the cytoskeleton. Modulation via intestinal microbiota, however, should also be considered. In conclusion, ethanol and its metabolites may act additively or even synergistically in vivo. Therefore, in vivo studies investigating the effects of ethanol and its byproducts on permeability of the small and large intestines are warranted.

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“…However, several observations suggest that other factors should interact with alcohol consumption in causing liver damage. [18][19][20] In alcoholics, liver histology is normal in 5% to 25% of biopsies and 18% of autopsy findings, 21 and cirrhosis develops at a low yearly incidence rate of around 2%. 16 Thus, only 10% to 25% of alcoholics will suffer from cirrhosis during their life.…”

mentioning

confidence: 99%

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

Corrao

Aricò²

1998

Hepatology

301

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Although alcohol intake and hepatitis C virus (HCV) infection are the major determinants of liver cirrhosis (LC) in Western countries, the joint effect of these two factors on LC risk has not yet been adequately studied. We used data from two hospital-based case-control studies performed in Italy. Cases were 285 cirrhotic patients admitted for the first time to district hospitals for liver decompensation. Controls were 417 patients admitted during the same period, and in the same hospitals as the cases, for acute diseases unrelated to alcohol. Alcohol consumption was expressed as lifetime daily alcohol intake (LDAI). Serum HCV antibodies (anti-HCV) were detected using a secondgeneration test and recombinant immunoblotting assay. We found a dose-effect relationship between LDAI and the risk of LC in both anti-HCV-negative and -positive subjects. Considering the extreme LDAI categories (LDAI ‫؍‬ 0 g, lifetime teetotalers, and LDAI ‫؍‬ 175 g), the LC odds ratios increased from 1.0 (reference category) to 15.0 (95% CI, 7.1-31.7) and from 9.2 (95% CI, 2.0-43.2) to 147.2 (95% CI, 42.1-514.3) in anti-HCV-negative and -positive patients respectively. The interaction between LDAI and HCV showed an additive structure for LDAI F50 g/day and a multiplicative structure for consumption G125 g/day. Alcohol intake and HCV infection are independent risk factors for symptomatic liver cirrhosis, each being sufficient to induce the disease. In subjects with high alcohol intake, the coexistence of HCV infection multiplies the alcohol-associated risk of cirrhosis. In subjects with low alcohol intake, other factors could be involved. (HEPATOLOGY 1998;27:914-919.)Alcohol intake represents the main determinant of liver cirrhosis in Italy 1,2 and other Western countries. 3 Evidence in this respect has been given by ecological, 3-5 prevalence, 6-9 case-control, 10-15 and cohort 16,17 studies. However, several observations suggest that other factors should interact with alcohol consumption in causing liver damage. [18][19][20] In alcoholics, liver histology is normal in 5% to 25% of biopsies and 18% of autopsy findings, 21 and cirrhosis develops at a low yearly incidence rate of around 2%. 16 Thus, only 10% to 25% of alcoholics will suffer from cirrhosis during their life. 22 Among these interacting factors, the role of chronic infection with hepatitis B virus is still debated. [23][24][25][26] Similarly, despite the initial suggestion that chronic infection with hepatitis C virus (HCV) may multiplicatively interact with alcohol intake in determining cirrhosis, 27 recent evidence suggests that these two factors act independently. 28 The aim of the present study was to assess, using a case-control design, the risk of developing liver cirrhosis associated with alcohol intake, HCV infection, and the combined action of these factors. PATIENTS AND METHODS Selection of Cases and Controls.We used the data from two hospitalbased case-control studies performed with the same design in two different periods and in two different Italian areas.The desi...

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Epidemiology of alcoholic liver disease

Cited by 38 publications

References 111 publications

Liver Transplantation for Alcoholic Cirrhosis: Long Term Follow-Up and Impact of Disease Recurrence1

Liver Transplantation for Alcoholic Cirrhosis: Long Term Follow-Up and Impact of Disease Recurrence1

Ethanol metabolism and its effects on the intestinal epithelial barrier

Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis

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