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Alcoholism is a complicated disorder that is often characterised with refractoriness to treatment, chronic course, high comorbidity and frequently with aggressive and suicidal behaviour. The neurobiological basis of alcoholism is assumed to be associated with the altered functions of different neurotransmitter (opioid, GABA, dopamine or serotonin (5-hydroxytryptamine, 5-HT)) systems. The association between central serotonergic function and the development and maintenance of alcohol abuse and dependence is based on the preclinical and clinical data, which show decreased 5-HT function associated with alcohol abuse. Peripheral biochemical markers might be used to improve the understanding of the underlying neurobiology of alcoholism, but also for the screening, establishing the diagnosis, disease staging, prediction of the suicidal risk and prediction and monitoring of treatment. Since 5-HT synaptosomes in the central nervous system and platelets similarly store, release and metabolise 5-HT, blood platelets have been widely used as a limited peripheral model for the central serotonergic synaptosomes. Various 5-HT abnormalities are frequently found in alcoholism, and decreased plasma tryptophan levels, decreased but also unaltered concentration of platelet 5-HT, increased platelet 5-HT uptake, and decreased and unchanged platelet monoamine oxidase (MAO) activity in alcoholic subjects have been reported. Deficits in central 5-HT function in alcoholic subjects were also detected after a challenge tests with fenfluramine, m-clorophenylpiperasine, and 6-chloro-2-1-piperazinylpyrazine, which resulted in blunted prolactin and cortisol responses. Alcoholism is frequently associated with different comorbid psychiatric disorders (personality disorder, PTSD, anxious-depressive disorder, major depression, schizophrenia), and with nicotine addiction. Clinical diagnosis of alcoholism was made according to the DSM-IV criteria, using Structured clinical interview and CAGE. Different