Introduction
The non-invasive identification of liver fibrosis related to metabolic-associated steatotic liver disease is crucial for risk stratification in children [1]. Non-invasive tests, including serum collagen-derived and inflammatory markers, may represent a good surrogate for risk stratification [2].
Aims & Methods
The aim of our study was to investigate the differences in fibrosis and inflammation markers in children with metabolic-associated steatotic liver disease (MASLD) depending on the liver fibrosis presence.
94 patients aged 9 to 17 years (average age 12.15 ± 2.51 years) were included in the study. According to body mass index, transient elastography (Fibroscan®502 touch, Echosens, France) data patients were divided into 4 groups: 1 group consisted of 27 obese patients with MASLD and liver fibrosis ≥F1 (METAVIR), 2 group - 35 obese patients with MASLD without fibrosis, 3 group - 18 obese patients without MASLD, 4 group (control) - 14 patients with normal weight without MASLD. Serum content of hydroxyproline free (HPf) and hydroxyproline protein-bound (HPp/b) according to Osadchuk and glycosaminoglycans (GAG) according to Rimington were evaluated. Serum IL-10 and IL-6 levels were evaluated by an ELISA kit (Wuhan Fine Biotech Co., Ltd, China).
Results
The levels of serum HPp/b were elevated in 100% of 1 group children compared to the control group as well as in 86.9% and 53.8% of 2 and 3 group children respectively (p˂0,05). HPp/b /HPf ratio was increased in children of 1 group by 1.4 times (p<0.05), 2 group - by 1.4 times (p<0.05), 3 group - by 1.3 times (p<0.05) in comparison with the control group. Correlation of HPp/b /HPf ratio with CAP (r=0,307; р<0,05), liver stiffness (r=0,323; р<0,05) was found. Serum GAG content in 1 group of children was 1.3 times (p<0.05) higher as well as IL-6 /IL-10 ratio was 5,4 times higher in comparison with the control group (p<0.05).
Conclusion
Thus, an imbalance between the collagen synthesis and degradation in obese MASLD children was revealed combined with a shift towards pro-inflammatory cytokine production, which might promote fatty liver fibrosis development.
References
- Armandi A, Michel M, Gjini K, Emrich T, Bugianesi E, Schattenberg JM. Emerging concepts in the detection of liver fibrosis in non-alcoholic fatty liver disease. Expert Rev Mol Diagn. 2023;23(9):771-782. doi:10.1080/14737159.2023.2242779
- Hammerich L, Tacke F. Hepatic inflammatory responses in liver fibrosis. Nat Rev Gastroenterol Hepatol. 2023;20(10):633-646. doi:10.1038/s41575-023-00807-x