PECULIARITIES OF THE CLINICAL COURSE OF NON-ALCOHOLIC STEATOHEPATITIS AGAINST THE BACKGROUND OF THE CHRONIC KIDNEY DISEASE OF THE I-III STAGE WITH SECONDARY ARTERIAL HYPERTENSION.

The article addresses the theoretical generalization of the clinical study of non-alcoholic steatohepatitis peculiarities in comorbidity with obesity and chronic kidney disease of the І-ІІІ stage, characterized by higher frequency and intensity of clinical and biochemical syndromes, the manifestation of which is likely to increase the occurrence of secondary arterial hypertension (portal hypertension syndromes, cholestasis, mesenchymal inflammation). Comorbid course of non-alcoholic steatohepatitis with chronic kidney disease is characterized by higher degree of liver steatosis compared to the patients with only non-alcoholic steatohepatitis (p<0.05), and a higher diagnostic threshold of the hepatorenal index values, which correlates with the Steato-test index (p<0.001) with strong interdependence.

[Condition of neurohumoral regulation of bronchial tone and gallbladder in patients with chronic cholecystitis and chronic obstructive pulmonary disease].

UNLABELLED: SUMMARY The paper presents data from a study of the neuroendocrine regulation of nonstriated muscles, bronchial tree and the gallbladder tones by means of an assessment of the adrenergic and cholinergic systems state in patients, suffering from chronic obstructive pulmonary disease and chronic acalculous cholecystitis. Adrenergic and cholinergic activities as well as cortisol secretion have significantly changed. OBJECTIVE: To study the features of adrenergic and cholinergic regulations of bronchial tone and that of the gallbladder in patients with combined course of chronic acalculous cholecystitis and chronic obstructive pulmonary disease. MATERIALS AND METHODS: 92 patients were involved in the study: 30 patients with COPD (1st group), 30 patients with COPD of comorbid CAC in the acute phase (2nd group), 32 patients with CAC in the acute phase (3rd group) and a control group--30 practically healthy individuals (PHI) of the respective age. RESULTS AND DISCUSSION: All the patients with COPD and COPD combined with CAC had a marked predominance of the parasympathetic nervous system, as evidenced by the established significant decrease of CDE (Table) in patients with isolated COPD is 1.4 times (p < 0.05), in patients with COPD combined with CAC--there was more intense inhibition of enzyme activity--in 1.8 times (p < 0.05) and in patients with CAC of the 3rd group there were identical changes--a decreased activity of CDE in 1.6 times (p < 0.05) with significant intergroup differences between the groups (p < 0.05). An analysis of the studies showed significant changes in the CDE of the surveyed individuals. For instance, the CDA in the individuals of groups 1 and 2 was lower by 1.6 and 2.4 times respectively (p < 0.001) than in the group of PHI; in the patients of the 3rd group--the changes were minor--a decline of 14.6% (p < 0.05) compared with practically healthy individuals (Table). Participation of sympathoadrenal system in the pathogenesis of COPD occurrence has been proved, however, in patients with COPD and CAC, the ability to deposit CA, when combined with CAC has significantly dropped. The study of cortisol density in the blood serum of the patients under examination showed its significant drop in all groups observed. For instance, the first group patients' blood contained 2.7 times (p < 0.05) less cortisol than that of PHI; in the patients of the second group the inhibition of the functional state of the adrenal cortex was even more intense--cortisol was lower than its index in the control group by 3.7 times (p < 0.05); the 3d group patients had the maximum drop in cortisol secretion by 1.7 times (p < 0.05) with reliable intergroup difference. CONCLUSIONS: The base of regulatory neuroendocrine and paracrine mecganisms imbalance, contributing to a development of COPD, is the cholinergic imbalance (reduction in blood acetylcholinesterase activity, hypertensive sphincter of Oddi dysfunction), adrenergic imbalance, reduction in catecholamine-depositing erythrocytes function, hypokinetic gallbladder dysfunction, adrenal dysfunction (decreased cortisol levels) that contribute to the development and progression of chronic cholecystitis against a background of hypokinetic gallbladder dysfunction.