Sk Das

Biomarkers of alcoholism: an updated review

Alcoholic beverages, and the problems they engender, have been familiar in human societies since the beginning of recorded history. Among a variety of blood tests used to aid the diagnosis of alcohol consumption and related disorders, laboratory tests are particularly useful in settings where cooperativeness is suspected or when a history is not available. Biochemical and haematological tests, such as gamma-glutamyltransferase activity, aspartate aminotransferase activity and erythrocyte mean corpuscular volume, are established markers of alcohol intake. Carbohydrate-deficient transferrin is the only test approved by the FDA for the identification of heavy alcohol use. Total serum sialic acid and sialic acid index of Apolipoprotein J have the potential to be included in a combination of measurements providing an accurate, more exact, assessment of alcohol consumption in a variety of clinical and research settings. Several other markers with considerable potential for measuring recent alcohol intake include beta-hexosaminidase, acetaldehyde adducts and the urinary ratio of serotonin metabolites, 5-hydroxytryptophol and 5-hydroxyindoleacetic acid. These markers provide hope for more sensitive and specific aids to diagnosis and improved monitoring of alcohol intake.Review Article Biomarkers of alcoholism: an updated review S. K. Das , L. Dhanya & D. M. Vasudevan Department of Biochemistry, Amrita Institute of Medical Sciences, Kerala, India The Publisher of the above referenced article, published in Journal of Scandinavian Journal of Clinical and Laboratory Investigation, 2008; 68(2): 81 – 92 (DOI: 10.1080/00365510701532662), retracts this manuscript. A substantial portions of the text and data in this paper were not original and had been previously published in a paper by Martin A. Javors & Bankole A. Johnson, Current status of carbohydrate defi cient transferrin,total serum sialic acid, sialic acid index of apolipoprotein J and serum b-hexosaminidase as markers for alcohol consumption. Addiction, 2003:98;(Suppl. 2), 45 – 50 Scandinavian Journal of Clinical and Laboratory Investigation published this article in good faith, and on the basis of warranties made by the corresponding author regarding the originality of the work. The article is retracted from all editions. The author accepts this action. We thank the author for his cooperation in this matter. Jens Petter Berg Editor-in-Chief Scandinavian Journal of Clinical & Laboratory Investigation, 2012; 72: 343

Consequences of Alcohol Consumption on Neurotransmitters -An Overview

Alcohol one of the important products of the global addiction alters brain function by interacting with multiple neurotransmitter systems, thereby disrupting the delicate balance between inhibitory and excitatory neurotransmitters. Alcohol positively reinforces drinking by producing a mild euphoria. The reinforcing effects of alcohol are mediated by several neurochemical systems and are associated with some of the behavioral manifestations of intoxication. Alcohol consumption is initially accompanied by decreased attention, alterations in memory, mood changes and drowsiness. Generally all vital functions of brain depend on a delicate balance between excitatory and inhibitory neurotransmission,which in turn dependent on short and long term alcohol consumption. Detailed understanding of alcohols mechanism of action on the neurotransmitters of brain is a prerequisite in discovering effective treatments for both alcohol abuse and alcoholism. This review covers the elaborate literature on the subject and highlights the functions and interactions of neurotransmitters and alcoholism.

Evaluation of blood oxidative stress‐related parameters in alcoholic liver disease and non‐alcoholic fatty liver disease

Oxidative stress is implicated in the pathogenesis of liver disease. We investigated oxidative stress‐related parameters and correlated with clinical findings in 35 non‐alcoholic fatty liver disease (NAFLD) patients, 38 alcoholic liver disease (ALD) patients and 38 normal subjects. NAFLD patients showed significantly higher body mass index, cholesterol, LDL‐cholesterol, VLDL‐cholesterol levels and transaminase activities compared to the other two groups. Haematological parameters were significantly altered in ALD patients and were reported only in male subjects. Glutathione content, catalase activity, glutathione reductase activity and glutathione peroxidase activity in NAFLD patients were reduced by 10.7u2005%, 18.5u2005%, 8.1u2005% and 16.8u2005%, respectively, and in ALD patients by 21.8u2005%, 29.6u2005%, 24.3u2005% and 45.3u2005%, respectively, compared to the normal group. However, thiobarbituric acid reactive substance content, superoxide dismutase activity and glutathione s‐transferase activity were increased by 35.2u2005%, 31.6u2005% and 5.4u2005%, respectively, in NAFLD patients, and in ALD patients by 75.2u2005%, 72.7u2005% and 32.4u2005%, respectively, compared to the normal group. Oxidative stress is associated with collagen production and leads to fibrosis. Type IV collagen level in NAFLD patients (190.6±83u2005ng/mL) was significantly higher than in the normal group (124.5±14.5u2005ng/mL) and lower than in ALD patients (373.4±170u2005ng/mL). While type IV collagen level of >124u2005ng/mL was a predictor of NAFLD patients from normal subjects, elevated ALT (>40u2005IU/L) activity could discriminate either of the liver disease patients from normal subjects.

RETRACTED: Biomarkers of alcoholism: an updated review

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Genesis of hepatic fibrosis and its biochemical markers

Liver fibrosis is characterized by an abnormal hepatic accumulation of extracellular matrix (ECM) that results from both increased deposition and reduced degradation of collagen fibres. Fibrotic liver injury results in activation of the hepatic stellate cell (HSC). Surrogate markers are gradually being substituted for biomarkers that reflect the complex balance between synthesis and degradation of the extracellular matrix. Once the hepatic stellate cell is activated, the preceding matrix changes and recurrent injurious stimuli will perpetuate the activated state. The ECM directs cellular differentiation, migration, proliferation and fibrogenic activation or deactivation. The metabolism of the extracellular matrix is closely regulated by matrix metalloproteinases (MMP) and their specific tissue inhibitors (TIMP). Although liver biopsy combined with connective tissue stains has been a mainstay of diagnosis, there is a need for less invasive methods. These diagnostic markers should be considered in combination with liver function tests, ultrasonography and clinical manifestations.

Drugs and non-alcoholic steatohepatitis

Health complications associated with obesity include diabetes, hypertension, hyperlipidemia, cardiovascular disease, and associated co-morbidities including non-alcoholic steatohepatitis (NASH). Additionally, NASH has been associated with several drugs. Though steatohepatitis is a rare form of drug induced liver disease, it has generated great interest in the recent past. Oral hypoglycemic agents, lipid lowering agents, antihypertensives, and antiobesity medication underlie a significant proportion of well-recognized hepatotoxicity. While some medications have predictable toxicity, many more are associated with idiosyncratic reactions. The toxic mechanism appears to involve mitochondrial injury, impaired β -oxidation, generation of reactive oxygen species and ATP depletion. If a drug is suspected, it is probably prudent to stop this medication.