SUMMARY -Alcohol addiction is a heterogeneous psychiatric disorder according to both phenotype and etiology. Difference in phenotype characteristics manifests in the manner the addiction arises, history of the alcoholic and history of drinking, comorbid disorders, and the phenomenon of abstinence difficulties. Concerning the etiology of alcoholism, the disease itself is considered to be a consequence of an interactive influence of the environment and genetic factors. Numerous researches conducted in the last decades discovered many aspects of the biochemical, cell and molecular bases of alcohol addiction, leading to a conclusion that alcoholism is, like many other addictions, a brain disease. By recognizing alcoholism as a disease which basically implies changes of the neurobiological mechanisms, as well as a clear genetic basis, it was supposed that the disease, having its basis solely in the symptomatology, is essentially heterogeneous. By trying to solve the problem of a clinically heterogeneous nature of the disease during the last fifty years, various sub-classifications of such patients have been suggested. According to Cloninger, subtypes of alcoholism differ also according to changes in the brain neurotransmission systems, i.e. it is supposed that patients suffering from alcoholism type 1 have a more pronounced dopaminergic transmission deficit, while dopaminergic transmission is not disturbed significantly in patients diagnosed with alcoholism type 2, who, however, have a significant lack of serotonergic transmission. In such a way, Cloninger actually presented the basis of the so-called neurobiological alcoholism model. Since he has connected differences in neurotransmission with differences in personality characteristics, this model is also known as the psychobiological model of alcoholism. The characteristic of alcoholism type 1 is avoiding damage (Harm Avoidance, HA) decreased dopamine transmission and increased serotonin transmission, while the significant characteristic of alcoholism type 2 is seeking for excitement (Novelty Seeking, NS), unchanged dopamine transmission and decreased serotonin transmission. These neurochemical differences among alcoholism subtypes represent the basis for a different therapy approach. Intake of alcohol changes different gene expression in the human brain. The inheritance model of alcoholism is not fully explained, however, it is considered that the disease is connected to a larger gene number included in neurotransmission, cell mechanisms and general metabolic function, with a simultaneous influence of the environment. The contribution of genetic factors is stronger in certain types of alcoholism and thus we have been confronted in the last years of alcoholism research with studies researching the connections of some alcoholism subtypes with the polymorphism phenomenon in the genes coding the synaptic proteins included in the alcoholism etiology. The primary role of monoamine oxidase (MAO) in the brain is catalysis of deamination of the oxidative neurotransmitter a...

Drinking alcoholic beverages is one of the oldest socially acceptable forms of behavior which can lead to the development of alcohol addiction. Long-term alcohol drinking has, together with numerous psychological and somatic complications, harmful consequences for the oral health. Patients suffering from alcoholism generally have poorer oral hygiene, dental care, periodontal status, fewer teeth, more carious lesions, gingival diseases, inter-dental papillae bleeding and deep gingival pockets associated with bone loss, as well as higher rate of oropharyngeal cancer. The changes in the oral microbiome affect the immune system, metabolism of carcinogens and digestion, which also leads to the development of local oral diseases as well as systemic gastrointestinal and cardiovascular illnesses. Harmful impact of alcohol on oral health can be direct, caused by local toxic effects of alcohol and as a consequence of systemic diseases associated with alcohol drinking, causing changes in the entire oral mucosa. Poor dietary habits additionally contribute to a poorer dental status while frequent simultaneous usage of tobacco products additionally increases the risk of developing periodontitis, tooth loss and oral carcinoma. Excessive alcohol drinking can seriously affect the oral cavity where, despite easy access via clinical examination, we still lack clinical data and a clear mechanism of development of the described changes.

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In trying to dissociate the effect of alcohol and tobacco use on platelet monoamine oxidase-B (MAO-B) activity, we compared the enzyme kinetics in controls (n = 66) and alcohol-dependent patients (n = 81), subdivided according to the severity of both, alcohol and tobacco use. Platelet MAO-B kinetics was measured spectrophotofluorimetrically in chronic alcohol intoxication and after 3 weeks abstinence. In alcoholic patients, an increased Michaelis-Menten constant (16%, p < 0.01) was shown, notwithstanding smoking status. Maximal velocity did not differ between patients and controls when adjusted for smoking. In cigarette smokers, a highly significant dose-dependent reduction of platelet MAO velocity (40%, p < 0.001) was demonstrated, with a similar degree of reduction in patients and controls. Tobacco use itself had no influence on MAO affinity. No differences were shown between subtype 1 and 2 alcoholics, or between the day of admission and the 21st day of abstinence. In conclusion, it seems that both, alcohol and tobacco consumption, may contribute to the lowering of overall platelet MAO-B activity. The effect of alcohol is small, due to interference with substrate binding, and not alteration of catalytic activity. In contrast, the effect of cigarette smoking is pronounced and relates to the dose-dependent reduction of platelet MAO velocity, with no influence on its affinity.

In March 2020, three months after the first cases surfaced in the Chinese city of Wuhan, WHO declared a global pandemic of the novel coronavirus, which by than had already spread through a great number of countries all over the world. In order to protect the health of healthcare workers and patients, activities and measures of disease prevention have been taken; in such circumstances, psychiatry found itself faced with various challenges, one of them being the preservation of the continuity of electroconvulsive therapy (ECT) in patients with severe or refractory psychiatric disorders. Such patients are a priority and demand immediate treatment in hospital settings adapted to epidemiological circumstances. Having studied the instructions and recommendations of the competent authorities, as well as reviewing available literature, this paper presents the most important measures for the smooth performance of ECT in conditions associated with the COVID-19 disease.

Alcohol dependence (AD) is a complex disorder with a poorly understood etiology. In this study, we investigated the relationship between genetic variation in the TPH2 gene, which encodes the enzyme responsible for serotonin synthesis in the brain, and both AD and personality traits, with attention to Cloninger’s types of AD. The study included 373 healthy control subjects, 206 inpatients with type I AD, and 110 inpatients with type II AD. All subjects were genotyped for the functional polymorphism rs4290270 in the TPH2 gene, and AD patients completed the Tridimensional Personality Questionnaire (TPQ). The AA genotype and the A allele of the rs4290270 polymorphism were more frequent in both patient groups compared with the control group. In addition, a negative association was found between the number of A alleles and TPQ scores for harm avoidance in patients with type II, but not type I, AD. These results support the involvement of genetic variations of the serotonergic system in the pathogenesis of AD, especially type II AD. They also suggest that in a subset of patients, genetic variation of TPH2 could potentially influence the development of AD by affecting the personality trait of harm avoidance.

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