Aldehyde dehydrogenase 2 polymorphism for development to hepatocellular carcinoma in <scp>E</scp>ast <scp>A</scp>sian alcoholic liver cirrhosis

Abe, Hiroshi; Aida, Yuta; Seki, Nobuyoshi; Sugita, Tomonori; Tomita, Yoichi; Nagano, Tomohisa; Itagaki, Munenori; Sutoh, Satoshi; Nagatsuma, Keisuke; Itoh, Kyoko; Matsuura, Tomokazu; Aizawa, Yoshifusa

doi:10.1111/jgh.12948

Cited by 23 publications

(29 citation statements)

References 37 publications

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“…It was suggested that metaregression was not always effective in explaining between-study heterogeneity [29]. In addition to metaregression, we conducted the Galbraith plot to explore heterogeneity, finding that the studies of Tomoda et al [19] and Abe et al [20] were the sources of heterogeneity for ALDH2 rs671. When these studies were omitted from the overall meta-analysis, the heterogeneity dropped down to 22.9% (P het = 0.247), without significantly affecting the pooled ORs.…”

Section: Discussionmentioning

confidence: 99%

“…Our meta-analysis suggested a lack of association between ALDH2 rs671 and HCC susceptibility, but we could not exclude the possibility that an interaction between ALDH2 rs671 and alcohol drinking may have a role in the development of HCC. Abe et al found that the profile of alcohol consumption and ALDH2 rs671 had a close relation, and ALDH2 rs671 and the consumptive period affected HCC development in patients with alcoholic liver cirrhosis [20]. In addition, the study by Liu et al suggested that the association between ALDH2 rs671 and HCC might be significantly mediated by habitual alcohol consumption [7].…”

Section: Discussionmentioning

confidence: 99%

“…The meta-regression results for rs2031920 were similar. Next, we conducted the Galbraith plot and accordingly singled out the studies of Tomoda et al [19] and Abe et al [20] as the main sources of heterogeneity for rs671 (graph not shown). Removing these studies decreased heterogeneity (P het = 0.247, I 2 = 22.9%), without significantly influencing the pooled ORs.…”

Section: Heterogeneity and Meta-regressionmentioning

confidence: 99%

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Relationship of ALDH2 rs671 and CYP2E1 rs2031920 with hepatocellular carcinoma susceptibility in East Asians: a meta-analysis

et al. 2020

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Background: Aldehyde dehydrogenase 2 (ALDH2) and cytochrome p450 2E1 (CYP2E1) are important alcoholmetabolizing enzymes. The aim of this meta-analysis was to evaluate the association of ALDH2 rs671 and CYP2E1 rs2031920 polymorphisms with hepatocellular carcinoma (HCC) susceptibility in East Asians. Methods: A systematic search strategy was implemented in MEDLINE, PubMed, Scopus, Embase, and China Academic Journals databases. Nineteen case-control studies were selected for inclusion. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated through random-effects or fixed-effects models. Subgroup analysis, meta-regression, sensitivity analysis, cumulative meta-analysis, and evaluation of publication bias were performed. Results: The overall meta-analysis did not find a significant association of ALDH2 rs671 and CYP2E1 rs2031920 genotypes with HCC susceptibility in East Asians. In addition, stratified analysis by country, Hardy-Weinberg equilibrium status, and source of controls also did not identify any association. Conclusion: The ALDH2 rs671 and CYP2E1 rs2031920 polymorphisms are not associated with HCC susceptibility in East Asians.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Heterogeneity and Meta-regressionmentioning

confidence: 99%

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Relationship of ALDH2 rs671 and CYP2E1 rs2031920 with hepatocellular carcinoma susceptibility in East Asians: a meta-analysis

et al. 2020

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“…In the present study, we found that most patients with a diagnosis of alcoholic LC were 40-49 years old, and four-fifths of the patients were diagnosed before they were 60 years old. This finding is probably due to the lower aldehyde dehydrogenase 2 activity, which is more susceptible to alcohol-induced liver injury in Asian and Chinese populations [20][21][22].…”

Section: Comparison With Other Studiesmentioning

confidence: 99%

Comorbidities and Outcome of Alcoholic and Non-Alcoholic Liver Cirrhosis in Taiwan: A Population-Based Study

Yang

Wang

Tsai

et al. 2020

IJERPH

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The prognosis of different etiologies of liver cirrhosis (LC) is not well understood. Previous studies performed on alcoholic LC-dominated cohorts have demonstrated a few conflicting results. We aimed to compare the outcome and the effect of comorbidities on survival between alcoholic and non-alcoholic LC in a viral hepatitis-dominated LC cohort. We identified newly diagnosed alcoholic and non-alcoholic LC patients, aged ≥40 years old, between 2006 and 2011, by using the Longitudinal Health Insurance Database. The hazard ratios (HRs) were calculated using the Cox proportional hazards model and the Kaplan–Meier method. A total of 472 alcoholic LC and 4313 non-alcoholic LC patients were identified in our study cohort. We found that alcoholic LC patients were predominantly male (94.7% of alcoholic LC and 62.6% of non-alcoholic LC patients were male) and younger (78.8% of alcoholic LC and 37.4% of non-alcoholic LC patients were less than 60 years old) compared with non-alcoholic LC patients. Non-alcoholic LC patients had a higher rate of concomitant comorbidities than alcoholic LC patients (79.6% vs. 68.6%, p < 0.001). LC patients with chronic kidney disease demonstrated the highest adjusted HRs of 2.762 in alcoholic LC and 1.751 in non-alcoholic LC (all p < 0.001). In contrast, LC patients with hypertension and hyperlipidemia had a decreased risk of mortality. The six-year survival rates showed no difference between both study groups (p = 0.312). In conclusion, alcoholic LC patients were younger and had lower rates of concomitant comorbidities compared with non-alcoholic LC patients. However, all-cause mortality was not different between alcoholic and non-alcoholic LC patients.

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“…Accumulating evidence suggests that a drinking habit for an individual with the ALDH2*2 allele increases the risk of cancerous diseases, including upper aerodigestive, gastric, colorectal, hepatic, and lung cancer [32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47]. For example, it was reported that individuals with the ALDH2*1/*2 genotype who were heavy drinkers (C46 g ethanol/day and C5 days/week) had a 38-fold greater risk of developing oesophageal cancer compared to non-drinking individuals with the ALDH2*1/*1 genotype, while drinkers with the ALDH2*1/*1 allele had only a 2-fold greater risk [47].…”

Section: Effect Of Aldh2*2 On Cancerous Diseasesmentioning

confidence: 99%

Roles of defective ALDH2 polymorphism on liver protection and cancer development

Matsumoto

Thompson

Chen³

et al. 2016

Environ Health Prev Med

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Aldehyde dehydrogenase 2 polymorphism for development to hepatocellular carcinoma in East Asian alcoholic liver cirrhosis

Abstract: In alcoholic liver cirrhosis, investigations of ALDH2 polymorphism and ethanol consumption profile are useful for prediction of HCC development.

Cited by 23 publications

References 37 publications

Relationship of ALDH2 rs671 and CYP2E1 rs2031920 with hepatocellular carcinoma susceptibility in East Asians: a meta-analysis

Relationship of ALDH2 rs671 and CYP2E1 rs2031920 with hepatocellular carcinoma susceptibility in East Asians: a meta-analysis

Comorbidities and Outcome of Alcoholic and Non-Alcoholic Liver Cirrhosis in Taiwan: A Population-Based Study

Roles of defective ALDH2 polymorphism on liver protection and cancer development

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