PENTRAXIN-3 LEVEL IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE AND ARTERIAL HYPERTENSION COMORBIDE COURSE DEPENDING ON ENDOTHELIAL DYSFUNCTION PARAMETERS*
Keywords:nonalcoholic fatty liver disease, arterial hypertension, oxidative stress, endothelial dysfunction, pentraxin-3.
The object of this research was to find out the possible relation between pentraxin-3, AH progression stage and ED in patients with NAFLD and AH comorbide course. Materials and methods. 46 patients with NAFLD were examined. They were sorted into 3 groups: group A (15 patients with NAFLD), group B (11 patients with NAFLD combined with AH stage 1) and group C (20 patients with NAFLD combined with AH stage 2). Control group (group D) was formed of 15 apparently healthy people. Pentraxin-3, endothelial nitric oxide (eNOS), endothelium-dependent vasodilation (EDVD), C-reactive protein (CRP), fibrinogen and uric acid levels were determined in this study. Results and discussion. It has been established that the level of pentraxin-3 in blood plasma is significantly increased in the groups B and C compared with group A (p < 0,05) and group D (p < 0.01). Also, a significant increase of pentraxin-3 level in the group C compared with the group B was found (p < 0.05). The negative correlation was found between pentraxin-3 and eNOS (R = – 0.76; p < 0.05) and EDVD (R = – 0,73; р < 0,05). The positive correlation was found between pentraxin-3 and levels of CRP (R = + 0.78; p < 0.05), fibrinogen (R = + 0,39; р < 0,05) and uric acid (R = + 0,41; р < 0,05). Conclusions. The research performed has showed that the patients with NAFLD and AH comorbide course have statistically higher pentraxin-3 levels compared to the patients with isolated NAFLD course. Correlation between pentraxin-3, eNOS, CRP and EDVD in hypertensive patients with NAFLD may indicate the pathogenetic role of pentraxin-3 in the ED development and progression in this cohort of patient. It has been found that pentraxin-3 levels and endothelial reactivity parameters were statistically increased through AH progression in patients with NAFLD with underlying AH, that may indicate an independent effect of AH on the endothelial dysfunction development.
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