PS-BPC12-7: ANTI-INFLAMMATORY AND PRO-INFLAMMATORY BIOMARKERS IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE AND HYPERTENSION

Abstract

Introduction: Non-alcoholic fatty liver disease (NAFLD) affects up to 50% of patients with hypertension (HT). Research data indicate a decrease in the activity of anti-inflammatory biomarkers with a simultaneous increase in the levels of pro-inflammatory agents. Objective: To assess the changes in anti-inflammatory systems (using kallistatin, IL-10) and pro-inflammatory activity (using IL-1β; and high-sensitivity CRP (hsCRP)) in patients with NAFLD under the influence of concomitant HT. Design and method: 63 patients with NASH and HT and 52 patients with isolated NASH were examined. Plasma kallistatin, IL-10, IL-1β; and hsCRP levels were evaluate using ELISA. The results were statistically processed using standard methods. Results: Kallistatin levels in patients with NAFLD and HT were on average 65.03 ng/ml (95% CI 61.38; 68.68), which was significantly lower than in the group with isolated NAFLD (83.42 ng/ml (95% CI 81.89; 84.94), p < 0.001) and control results (111.70 ng/ml (95% CI 106.14; 113.22), p < 0.001). The level of anti-inflammatory IL-10 in the group of NAFLD and HT also reached minimal values (12.69 pg/ml (95% CI 11.93; 12.95) against 14.34 pg/ml (95% CI 13.27; 14,34) in the group with isolated NAFLD (p < 0.001) and 16.19 pg/ml (95% CI 15.15; 17.74) in the control group (p < 0.001)). The opposite results were observed in the study of IL-1β; content, which was increased in the group with NAFLD and HT (17.55 pg/ml (95% CI 17.06; 19.73) versus 15.72 pg/ml (95% CI 15,25; 17.44) in the group with isolated NAFLD (p < 0.001) and 8.26 (95% CI 7.79; 8.46) in the control group (p < 0.001)). In addition, patients with NAFLD and HT had an increase in CRP (7.90 mg/l (95% CI 7.96; 8.75) versus 6.55 mg/l (95% CI 6.47; 7.57) in the group with isolated NAFLD (p < 0.001) and 2.07 mg/l (95% CI 1.83; 2.85 mg/l) in the control group (p < 0.001)). It has been shown that with the progression of HT in patients with NAFLD, the level of kallistatin significantly decreases (p < 0.001, p = 0.011 for the HT stage and BP grade) and IL-10 (p < 0.001) with a simultaneous increase in IL-1β; (p < 0.001) and CRP levels (p < 0.001). Conclusions: Thus, patients with NAFLD and HT are likely to experience changes in biomarker status toward a pro-inflammatory profile and deepening of these deviations with the progression of concomitant hypertension.