Serum TNF-α levels in relation to alcohol consumption and common TNF gene polymorphisms

Gonzalez-Quintela, Arturo; Campos, Joaquín; Loidi, Lourdes; Quinteiro, Celsa; Pérez, Luis‐Fernando; Gudé, Francisco

doi:10.1016/j.alcohol.2008.04.008

Cited by 55 publications

(37 citation statements)

References 33 publications

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“…Patients with alcoholic hepatitis have higher circulating TNF-α levels compared to heavy drinkers with inactive cirrhosis, heavy drinkers without liver disease, and persons with neither alcoholism nor liver disease, and high levels correlate with mortality [22]. A large number of animal and human studies have found the serum concentrations of TNF-α, IL-1, IL-6, IL-8, IL-10, IL-12, IFNs, MCP-1, PDGF, and TGF-β to be elevated in both chronic and acute alcohol-induced liver disease [11,20,21,22,23,24,25,26,27,28,29,30,31,32] (fig. 1).…”

Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Farkas

Kemény

2013

Skin Pharmacol Physiol

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Emerging evidence suggests that excessive alcohol consumption is associated with psoriasis. In alcoholics, antipsoriatic treatments are less efficient, but more toxic and an additional challenge is poor therapeutic compliance. There is a correlation between excess alcohol intake and increased risk of infections, but on the other hand alcohol and its metabolites can trigger a persistent systemic inflammation, mediated by pro-inflammatory cytokines released from activated Kupffer cells in the liver and from monocytes in the circulation. Ethanol and its metabolites can also enhance lymphocyte and keratinocyte activation and proliferation and can increase the mRNA levels of genes characteristic for proliferating keratinocytes. In this review, we discuss the mechanisms by which alcohol contributes to psoriasis development focusing on liver, systemic inflammation and skin.

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Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Farkas

Kemény

2013

Skin Pharmacol Physiol

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“…However, no significant association was found with different alcohol-related hepatic diseases [17,[23][24][25][26] or with AD [10] .…”

Section: Tnf-␣ -308 (Rs1800629 G/a)mentioning

confidence: 68%

“…Three studies that enrolled heavy drinkers as controls were excluded [14][15][16] . We also excluded a control subsample of heavy drinkers from a fourth study [17] . Four other studies were not considered because the minimal duration of chronic alcohol intake was not indicated [18] or was less than 5 years [19][20][21] (see PRISMA flow diagram, fig.…”

Section: Resultsmentioning

confidence: 99%

“…The 'A' allele has been related to increased TNF-␣ expression [22] . A positive association was reported between 'A' allele excess and alcohol-related steatohepatitis [23] , alcoholic liver cirrhosis [24] , and advanced liver disease [17] , but not confirmed in three other studies of AALD [25][26][27] .…”

Section: Tnf-␣ -238 (Rs361525 G/a)mentioning

confidence: 99%

“…Three of them included subgroups of patients without liver disease [17,24,25] . A first metaanalysis including all patients (4,040 alleles) found a significant association (z = 2.31, p = 0.02; OR = 1.36, CI: 1.05-1.76) and an absence of heterogeneity (Q = 2.01, p = 0.85 with I 2 = 0%) ( fig.…”

Section: Tnf-␣ -238 (Rs361525 G/a)mentioning

confidence: 99%

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Association of Inflammation Genes with Alcohol Dependence/Abuse: A Systematic Review and a Meta-Analysis

Kébir

Gorsane²,

Blecha³

et al. 2011

Eur Addict Res

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The aim of the present work was to systematically review all association studies of inflammation genes with alcohol dependence/alcohol abuse (AD/AA) and to perform a meta-analysis. Odds ratios (ORs) were estimated by contrasting the ratio of counts of the ‘high-risk’ versus ‘low-risk’ alleles in AD/AA cases versus controls. Data reported in at least three published studies were available for four genetic polymorphisms [TNF-α -238 (rs361525, G/A); TNF-α -308 (rs1800629, G/A); IL-1RA (VNTR [86 bp]_n); IL-10 -592 (rs1800896, C/A)]. In total, nine meta-analyses were performed. Of these, only the TNF-α -238 polymorphism showed a significant association with AD/AA (OR = 1.36, 95% CI: 1.05–1.76). This risk remained significant and increased slightly when we considered only patients with advanced alcohol-related liver disease (AALD) (OR = 1.5, 95% CI: 1.13–1.98) but not when we considered only patients without AALD (OR = 1.08, 95% CI: 0.5–2.35). Sensitivity analysis showed that this genetic association is derived from the AALD phenotype rather than from AD. Our approach is limited by our phenotype definition; some studies included chronic heavy drinkers (minimal daily consumption of 80 g for a minimal duration of 10 years) but without a standardized psychiatric assessment.

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Alcohol use and the development of periodontal pockets: An 11‐year follow‐up study

Sankaranarayanan

Saxlin

Knuuttila

et al. 2020

Journal of Periodontology

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Background: This study investigates whether alcohol use predicts the periodontal pocket development over an 11-year follow-up period. Methods: The study participants' periodontal condition was examined both in the Health 2000 and 2011 Surveys (BRIF8901). Participants were aged 30 to 65 years, dentate, periodontally healthy, and did not have diabetes or rheumatoid arthritis in 2000. Periodontal outcome measures in 2011 were the number of teeth with deepened (≥4 mm) periodontal pockets and the presence of deepened periodontal pockets. The exposure in 2000 was alcohol use (amount [g/week], frequency [any alcohol or different beverages]). Incidence rate ratios (IRRs) with 95% confidence intervals (CI) were estimated using negative binomial regression model and Poisson regression model with a robust variance estimator. Results: Overall, the amount of alcohol use or use over the risk limit in 2000 was inconsistently associated with the development of periodontal pockets (IRRs varied from 0.6 to 1.0). The frequency of alcohol use (any alcohol or different beverages) had an inconsistent association with the presence of periodontal pockets (IRRs varied from 0.5 to 1.2) while there was an inverse association with the number of teeth with periodontal pockets. Among smokers, there were no clear associations between any of the exposures and either of the outcomes. The same was found among non-smokers except an inverse association was found between frequency of alcohol use and the number of teeth with periodontal pockets. Conclusion: Alcohol use was not consistently associated with the periodontal pocket development over a period of 11 years.

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Serum TNF-α levels in relation to alcohol consumption and common TNF gene polymorphisms

Cited by 55 publications

References 33 publications

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Association of Inflammation Genes with Alcohol Dependence/Abuse: A Systematic Review and a Meta-Analysis

Alcohol use and the development of periodontal pockets: An 11‐year follow‐up study

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