Glycoconjugates in the detection of alcohol abuse

Abstract

Up to 30% of all hospital admissions and health-care costs may be attributable to alcohol abuse. Ethanol, its oxidative metabolites, acetaldehyde and ROS (reactive oxygen species), non-oxidative metabolites of alcohol [e.g. FAEEs (fatty acid ethyl esters)] and the ethanol-water competition mechanism are all involved in the deregulation of glycoconjugate (glycoprotein, glycolipid and proteoglycan) metabolic processes including biosynthesis, modification, transport, secretion, elimination and catabolism. An increasing number of new alcohol biomarkers that are the result of alcohol-induced glycoconjugate metabolic errors have appeared in the literature. Glycoconjugate-related alcohol markers are involved in, or are a product of, altered glycoconjugate metabolism, e.g. CDT (carbohydrate-deficient transferrin), SA (sialic acid), plasma SIJ (SA index of apolipoprotein J), CETP (cholesteryl ester transfer protein), β-HEX (β-hexosaminidase), dolichol, EtG (ethyl glucuronide) etc. Laboratory tests based on changes in glycoconjugate metabolism are useful in settings where the co-operativeness of the patient is impaired (e.g. driving while intoxicated) or when a history of alcohol use is not available (e.g. after trauma). In clinical practice, glycoconjugate markers of alcohol use/abuse let us distinguish alcoholic from non-alcoholic tissue damage, having important implications for the treatment and management of diseases.

Alcohol withdrawal syndrome: mechanisms, manifestations, and management

“…Carbohydrate‐deficient transferrin (CDT) is the most available and studied biomarker and has a high specificity for severe AUD 37. CDT values are not markedly influenced by medications except by immunosuppressants.…”

Decrease in salivary lactoferrin output in chronically intoxicated alcohol-dependent patients

“…After alcohol intake, the level of acetaldehyde in saliva strikingly exceeds the level in systemic blood. From saliva, acetaldehyde, ethanol, and other metabolites of alcohol and toxins such as reactive oxygen species (ROS) or fatty acid ethyl esters (FAEEs), easily reach all local tissues [5][6][7][8][9]. The lack of lactoferrin concentration decrease in our earlier acute alcohol intoxication study [7] might be the result of the lack of salivary flow data.…”

“…In alcohol abusers, ethanol replaces water from hydrogen bonds of hydrophilic domains of proteins, which increases the fluidity of parenchymal cell membranes of salivary glands. Replacement of water by ethanol impairs the activation of cAMP in the membrane, Ca 2+ mobilization, and finally impairs the secretory process [5][6][7][8][9]. The decrease in SF may also be the result of alcohol withdrawal syndrome stress.…”

“…The decrease in SF may also be the result of alcohol withdrawal syndrome stress. Alcohol www.fhc.viamedica.pl withdrawal syndrome stress is characterized by a significant central and peripheral sympathetic hyperactivity, hypercortisolemia, reduced food intake and fluid diet (which reduces mastication that stimulates SF), and reduced number of muscarinic receptors as well as reduced secretion/action of paracrine gastrointestinal hormones and transmitters such as somatostatin, PP peptide, and cholecystokinin [5,9,[40][41][42].…”

“…Acute local mucosa damage is reversible and proportional to the concentration of alcohol. Ethanol immediately diffuses into saliva and oral tissues, reaching in saliva and oral tissues higher concentrations than in plasma [4][5][6][7][8][9]. Acetaldehyde, the main metabolite of ethanol, also damages oral tissues [10].…”