Alina Kępka1, Piotr Zwierz2, Sylwia Chojnowska3, Agnieszka Ochocińska4, Ewa Skorupa4, Marek Szczepański5, Sławomir Dariusz Szajda6, Napoleon Waszkiewicz7. 1. Department of Biochemistry, Radioimmunology and Experimental Medicine, The Children's Memorial Health Institute of Warsaw, Warsaw, Poland. Electronic address: a.kepka@ipczd.pl. 2. Provincial Sanitary - Epidemiological Station, Bialystok, Poland. 3. Faculty of Health Sciences, Lomza State University of Applied Sciences, Lomza, Poland. 4. Department of Biochemistry, Radioimmunology and Experimental Medicine, The Children's Memorial Health Institute of Warsaw, Warsaw, Poland. 5. Department of Neonatology and Newborn Intensive Care Unit, Medical University of Bialystok, Bialystok, Poland. 6. Faculty of Health Sciences, Lomza State University of Applied Sciences, Lomza, Poland; Department of Psychiatry, Medical University of Bialystok, Bialystok, Poland. 7. Department of Psychiatry, Medical University of Bialystok, Bialystok, Poland.
Abstract
BACKGROUND: Serum aspartate, alanine aminotransferases (AST, ALT), and plasma carnitine are all indirect biomarkers of alcohol abuse. Carnitine transfers long-chain fatty acids from cytoplasm to mitochondria for β-oxidation. The aim of the study was to determine the relationship between daily alcohol intake, time of alcohol dependence, plasma carnitine, and serum aminotransferases. PATIENTS: We studied 26 men who were addicted for 2-30 years, consuming ethanol from 75 to 700 g/day (alcoholic group), as well as 17 healthy men (control group). RESULTS: In alcoholics, compared to the controls, we found: a significant increase in serum: AST (p = 0.0014), ALT (p = 0.0071), AST/ALT ratio (p < 0.000); significantly lower plasma free carnitine (FC) (p = 0.0316) and total carnitine (TC) (p = 0.0349); and a significant negative correlation between FC (r = -0.6200; R2 = 0.3844; p = 0.0007), TC (r = -0.4365; R2 = 0.1905; p = 0.0258), and time of alcohol dependence, suggesting carnitine as an indirect marker of alcohol abuse. We did not find any significant correlation between FC, TC, and levels of alcohol or aminotransferase activity. CONCLUSION: In the alcoholic group, there was an increase in serum activity of AST, ALT, and AST/ALT ratio that confirms liver injury. In addition, we found low plasma FC and TC, which may indicate damage to mitochondrial β-oxidation caused by alcohol metabolites. The significantly higher plasma FC and TC in patients consuming the most, compared to patients consuming smaller doses of alcohol, may be caused by a lower carnitine demand of injured liver cells, decreased urinary carnitine excretion by impaired renal tubules, and leakage of carnitine into the blood from damaged muscles by the higher quantities of alcohol. The negative correlation between carnitine concentration and time of alcohol dependence may suggest the potential use of carnitine for treatment of alcohol abuse.
BACKGROUND: Serum aspartate, alanine aminotransferases (AST, ALT), and plasma carnitine are all indirect biomarkers of alcohol abuse. Carnitine transfers long-chain fatty acids from cytoplasm to mitochondria for β-oxidation. The aim of the study was to determine the relationship between daily alcohol intake, time of alcohol dependence, plasma carnitine, and serum aminotransferases. PATIENTS: We studied 26 men who were addicted for 2-30 years, consuming ethanol from 75 to 700 g/day (alcoholic group), as well as 17 healthy men (control group). RESULTS: In alcoholics, compared to the controls, we found: a significant increase in serum: AST (p = 0.0014), ALT (p = 0.0071), AST/ALT ratio (p < 0.000); significantly lower plasma free carnitine (FC) (p = 0.0316) and total carnitine (TC) (p = 0.0349); and a significant negative correlation between FC (r = -0.6200; R2 = 0.3844; p = 0.0007), TC (r = -0.4365; R2 = 0.1905; p = 0.0258), and time of alcohol dependence, suggesting carnitine as an indirect marker of alcohol abuse. We did not find any significant correlation between FC, TC, and levels of alcohol or aminotransferase activity. CONCLUSION: In the alcoholic group, there was an increase in serum activity of AST, ALT, and AST/ALT ratio that confirms liver injury. In addition, we found low plasma FC and TC, which may indicate damage to mitochondrial β-oxidation caused by alcohol metabolites. The significantly higher plasma FC and TC in patients consuming the most, compared to patients consuming smaller doses of alcohol, may be caused by a lower carnitine demand of injured liver cells, decreased urinary carnitine excretion by impaired renal tubules, and leakage of carnitine into the blood from damaged muscles by the higher quantities of alcohol. The negative correlation between carnitine concentration and time of alcohol dependence may suggest the potential use of carnitine for treatment of alcohol abuse.