The relationship between prolactin levels and the results of holter monitoring in patients with stable angina of tension and gastroesophageal reflux disease.

OBJECTIVE: The aim: Determine the possible relationship between prolactin levels and the results of Holter monitoring in patients with stable angina of tension and gastroesophageal reflux disease (GERD). PATIENTS AND METHODS: Materials and methods: The study included 118 patients with stable angina of tension of I-II functional class. Of these, 88 patients with stable angina of tension with comorbid GERD (A, B, C), who were included in the second group of the study and 30 patients with isolated stable angina of tension which formed the 1st group. All patients who were included in the study prior to treatment were evaluated for serum prolactin levels and Holter monitoring. RESULTS: Results: In patients with stable angina of tension and GERD, prolactin levels exceed the norm levels and are higher than the level of prolactin in the group with isolated stable angina (p<0,05), as well as the number of episodes of painful and painless myocardial ischemia and their duration (p<0,05). The presence of a comorbidity with GERD provokes an increase in the total duration of episodes of ischemia per day in patients with stable angina compared to those in patients with no GERD. A direct linear relationship was founded between prolactin serum levels and the number of episodes of pain in myocardial ischemia in patients with stable angina and GERD per day, and between the total duration of episodes of myocardial ischemia and prolactin levels. CONCLUSION: Conclusions: In patients with stable angina and GERD, in 70.4% of cases, the level of prolactin exceeds the norm in 2,6 times, and is higher than the level of prolactin in the isolated group of stable angina. For the comorbidity of stable angina and GERD, the number of episodes of painful, painless myocardial ischemia and their duration is more than once in the group of patients with stable angina without GERD (p<0.05).

The role of endothelial dysfunction in the progression mechanisms of non-alcoholic steatohepatitis in patients with obesity and chronic kidney disease.

OBJECTIVE: Introduction: The study increase in the incidence of non-alcoholic steatohepatitis (NASH) on the background of obesity and chronic kidney disease (CKD) in people of working age in Ukraine and in the world necessitates the research into mechanisms of mutual burden and the search for new factors in the pathogenesis of this comorbidity progression . The aim: To establish the role of endothelial dysfunction in the mechanisms of mutual burden and progression of non-alcoholic steatohepatitis and chronic kidney disease in patients with obesity. PATIENTS AND METHODS: Materials and methods: 135 patients were examined: of which 52 patients with non-alcoholic steatohepatitis with obesity I degree (1 group), 53 patients with nonalcoholic steatohepatitis with comorbid obesity of the I degree and chronic kidney disease of the І-ІІ stage (group 2). The control group consisted of 30 practically healthy persons of the corresponding age and sex. The average age of patients was (45.8 ± 3.81) years. RESULTS: Results: The results of the study showed that in patients with NASH, a significant increase in the content of NO in the blood was detected in comparison with the index in PHP (p <0,05) in group 1 - in 2,1 times, in the 2nd group - in 2,6 times (p <0,05). The role of nitrosative stress in the pathogenesis of NASH was proved, the confirmation of which is the increase in the concentration of nitrosothiols, peroxynitrite and other metabolites NO in the blood. Increased peroxynitrite formation due to the generation of NO by leukocytes is an important aspect of the damaging effect and inflammation process in NASH. Pathological hyperproduction of NO by endothelial cells and leukocytes from inflammatory infiltrates in the liver contributes to the development of nitrosative stress in NASH. The established hypernitrate in blood may also be considered compensatory in response to hyperproduction of ET-1 in all observational groups. CONCLUSION: Conclusions: Confirmation of the presence of endothelial dysfunction (ED) in patients with NASH with CKD resulted in a probable growth of the number of desquamated endothelial cells (DEC) in the 2nd group of patients in 1.9 times (p2 <0.05). Generation by neutrophils during the exacerbation of NASH of a significant number of active forms of oxygen and nitrogen and hyperproduction of endothelial cells and endometrial lymphocytes with progressive damage to the endothelium (growth of DEC) leads to significant ED, accompanied by mosaic angiospasm of the arteries due to hyperproduction of ET-1 and parectic vasodilatation of the veins of the portal vein system because of the hyperproduction of NO.