Metabolic disorders in patients with arterial hypertension with concomitant obesity
Journal Title: Український терапевтичний журнал - Year 2019, Vol 0, Issue 3
Abstract
Objective — further investigation of the pathogenetic triggers of arterial hypertension with concomitant obesity. Materials and methods. Examinations involved 111 patients with arterial hypertension (AH) with concomitant obesity (main group) and 18 patients with AH without obesity (comparison group). The age of the patients in the main group ranged from 41 to 67 years, on average (53.6 ± 7.35) years. The control group consisted of 24 practically healthy persons of representative age, which on average was (53.5 ± 7.7) years. The comparison group consisted of 18 patients with 1—2 degree arterial hypertension of the Ist and IInd stages, with an average age of (52.25 ± 6.41) years without obesity. Dopamine (DA) level was determined from the data from the daily excretion of dopamine with urine using a fluorometric method. The direct determination of angiotensin II (ATII) and aldosterone (ALD) was performed using an immune-enzymatic analysis. The concentration of lipids was determined using an enzymatic colorimetric method. Results and discussion. In patients with AH, a violation of the dopamine metabolism was detected in 88.8 % of patients with concomitant obesity and 69.2 % of patients without obesity, manifested by a decrease in the DA excretion with urine in 2.3 times (p < 0.001) and 2.0 times (p < 0.001), respectively, in comparison with the control group. The presence of concomitant obesity resulted in more profound disorder in the dopaminergic system, that manifested is the decreased DA levels in the daily urine by 14.6 % compared to patients with isolated AH (p < 0,001). Hyperactivation of renin-angiotensin-aldosterone system (RAAS) was more pronounced in patients with AH with concomitant obesity, accompanied by high levels of ATII and ALD: (47.45 ± 18.8) and (220.17 ± 108.8) versus (42.1 ± 5.2) pg/ml and (172.1 ± 18.9) pg/ml (p < 00.05; p < 0.001), (15.28 ± 2.9) and (119.78 ± 31.6) pg/ml (p < 0.001) in the group of patients with isolated AH and control respectively. The threshold DA range was 875—1060 mmol/l, with an excess of which the frequency of pathological levels of ALD and ATII significantly decreased (p < 0.05). Patients with AH, concomitant obesity and disturbances of dopamine metabolism has more pronounced atherogenic lipid profile, than patients with hypertension without obesity. Conclusions. As a result of the study, several violations of dopamine metabolism in patients with AH and associated obesity have been established. They manifested in the inhibition of the dopaminergic system, that confirmed the pathogenetic role of DA in the development of obesity against the background of hyperactivation of the renin-angiotensin-aldosterone system.
Authors and Affiliations
V. O. Sobol, V. G. Lizogub, O. G. Puzanova, Yu. O. Moshkovska
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