21 February 2020 In General Health

The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies.

In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case-control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies.

The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7- 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy.

The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor.

There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine

05 December 2018 In General Health

The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case-control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7- 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor. There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.

27 July 2018 In Cardiovascular System

BACKGROUND: Although epidemiological evidence for the beneficial effect of low alcohol consumption on myocardial infarction is strong, the impact of heavy drinking episodes is less clear.

OBJECTIVES: The aim of this study was to investigate a possible association between the risk for acute myocardial infarction occurrence and alcohol consumption.

METHODS: Our hospital-based case-control study comprised 374 participants (187 newly diagnosed patients with myocardial infarction and 187 controls, individually matched by gender, age, and place of residence). This study was performed in Kragujevac (a city in Serbia) during 2010. Logistic regression analysis was used to determine odds ratio (OR) with 95% confidence intervals (95% CI).

RESULTS: The history of alcohol consumption in patients with acute myocardial infarction and their controls did not differ significantly: the percentage of those that were consuming alcohol was slightly higher in cases (54.5%) than in controls (50.3%). The habit of binge drinking during the previous 12 months was significantly more common in cases (25.1%) than in controls (12.8%): adjusted OR = 2.2 (95%CI = 1.2-4.2, p = 0.017), p for trend = 0.015. Analysis of binge drinking by age, gender and place of residence revealed that the increase in risk for acute myocardial infarction was associated with older age (adjusted OR = 5.1, 95%CI = 1.7-15.1, p for trend = 0.010), male gender (adjusted OR = 2.3, 95%CI = 1.1-5.2, p for trend = 0.028) and rural place of residence (adjusted OR = 4.8, 95%CI = 1.3-18.5, p for trend = 0.033).

CONCLUSION: Our results suggest that binge drinking is associated with twice the risk for myocardial infarction compared to not drinking. Since consumption of alcohol is very common in the Serbian population, the effect of binge drinking on myocardial infarction should be considered an important public health issue.

04 August 2017 In General Health

Meta-analyses of alcohol use, alcohol dosage and alcohol-related problems as risk factors for tuberculosis incidence were undertaken. The global alcohol-attributable tuberculosis burden of disease was also re-estimated.Systematic searches were conducted, reference lists were reviewed and expert consultations were held to identify studies. Cohort and case-control studies were included if there were no temporal violations of exposure and outcome. Risk relations (RRs) were pooled by using categorical and dose-response meta-analyses. The alcohol-attributable tuberculosis burden of disease was estimated by using alcohol-attributable fractions.36 of 1108 studies were included. RRs for alcohol use and alcohol-related problems were 1.35 (95% CI 1.09-1.68; I2: 83%) and 3.33 (95% CI 2.14-5.19; 87%), respectively. Concerning alcohol dosage, tuberculosis risk rose as ethanol intake increased, with evidence of a threshold effect. Alcohol consumption caused 22.02 incident cases (95% CI 19.70-40.77) and 2.35 deaths (95% CI 2.05-4.79) per 100 000 people from tuberculosis in 2014. Alcohol-attributable tuberculosis incidence increased between 2000 and 2014 in most high tuberculosis burden countries, whereas mortality decreased.Alcohol consumption was associated with an increased risk of tuberculosis in all meta-analyses. It was consequently a major contributor to the tuberculosis burden of disease.

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