11/2020, p. 3-9
Biological aspects of narcology

Disruption of Relationship Between Cortisol and Neurotrophic Brain Factor in Patients with Chronic Alcoholism.

Didkovskij N.A., Malashenkova I.K., Ogurcov D.P., Krynskij S.A., Hajlov N.A., Chekulaeva E.I., Zaharova N.V., Parhomenko A.A., Sobolev E.S., Bryun E.A.

Аннотация:
Background. Chronic alcoholism (CA) is a severe illness with a wide range of organ pathologies and little therapy options. An increased level of cortisol and systemic inflammation play an important role in the pathogenesis of CA. Suppression of the production of neurotrophins, primarily of the brain-derived neurotrophic factor (BDNF), is considered to be one of the mechanisms of the development of addiction, cognitive impairment, and neurodegeneration in patients with CA. Aim: to study the levels of cortisol and BDNF and their possible relationship with systemic inflammation in patients with stage 2 alcoholism. Method. Thirty patients (25 men and 5 women) with the 2-nd stage of alcoholism in the stage of recovery from alcoholic psychosis were studied. Control group was composed of 30 healthy volunteers of comparable sex and age. Serum levels of BDNF, cortisol, cytokines IL-1β, TNFα, IL-8, IL-6, and C-reactive protein (CRP) were determined by ELISA. Results. It was found that in CA there were signs of systemic inflammation – an increase in the levels of pro-inflammatory mediators, CRP and cortisol. In patients with higher levels of cortisol, the levels of IL-6, IL-8 and CRP were significantly higher. In addition, with CA, broken correlation between the levels of cortisol and BDNF was revealed – with an increase in cortisol> 400 nmol/L, the content of BDNF was significantly lower than with a level of cortisol <400 nmol / L. Normally, there is a positive correlation between the level of cortisol and BDNF, the maximum production of which occurs in the morning, while in patients with CA we found a moderate negative correlation between the level of BDNF and cortisol. The revealed disorders may be related to an increase in the neurotoxicity (excitotoxicity) of alcohol at the XA2 stage, because excessive concentrations of proinflammatory mediators and cortisol through neuroimmune communications enhance neuroinflammation and neuronal damage, and the level of production of the most important protective BDNF appears to be insufficient to counteract neuronal damage. Conclusion. The results reflect the prospects of further research for the formation of the prognosis of the disease and the selection of rehabilitation and therapy programs.

Ключевые слова:
chronic alcoholism, cortisol, BDNF, IL-1β, TNFα, IL-8, IL-6 and C-reactive protein.