Features of the connective tissue metabolism, the content of adipokines and cytokeratin-18 in patients with non-alcoholic steatohepatitis combined with osteoarthritis and obesity
DOI:
https://doi.org/10.14739/2310-1210.2019.4.173182Keywords:
nonalcoholic steatohepatitis, connective tissue, adipokines, cytokeratin-18Abstract
Aim. To determine the indices of connective tissue metabolism, adipokines and cytokeratin-18 in non-alcoholic steatohepatitis patients with osteoarthritis and obesity comorbidities.
Materials and methods. 90 patients were examined and divided into three groups: group 1 (n = 30) included patients suffering from OA grade II–III according to Kellgren and Lawrence classification with normal body mass (BMI = 21–25 kg/m2), group 2 (n = 30) – patients with NASH and OB without OA (BMI > 30 kg/m2), group 3 (n = 30) – patients with OA with NASH and OB (BMI more than 30 kg/m2). The control group consisted of 30 age-matched practically healthy persons (PHP). The average age of patients was 62.3 ± 5.7 years.
Results. In NASH patients with OB and OA, there is a significant increase in the synthesis of collagen and glycosaminoglycans which is accompanied by ineffective resorption of newly formed collagen due to inhibition of the collagenolytic activity of blood plasma in NASH arising from activation of proteinase inhibitors (α2-MG), a significant imbalance in the metabolic system of connective tissue, which, particularly in OA and OB comorbidities, leads to progressive fibrosis of the liver and its functions impairment. It has been established that blood adipokines level not only depends on body weight, but also reflects the risk for occurrence of nosologies associated withOB.
Conclusions. In patients with NASH and morbidOB, a significant increase in collagen and glycosaminoglycans synthesis was observed. Adipokine deficiency, found in the work, can play a significant pathogenetic role in the development and progression of NASH as well asOB and OA. Adipokines leptin and adiponectin and also cytokeratin-18 may serve as sensitive risk markers for comorbid diseases development and could be candidates for their measurements inclusion in the diagnostic algorithm for NASH, OA,OB and their combination.
References
Babak, O. Ya., & Andreeva, A. О. (2013) Hormonalni zminy v zhyrovii tkanyni khvorykh na hipertonichnu khvorobu i ozhyrinnia [The hormonal changes in adipose tissue in patients with hypertension against the background of obesity]. Ukrainskyi terapevtychnyi zhurnal, 1, 63–7. [in Ukrainian].
Babak, O. Ya., & Lapshyna, K. A. (2016) Lechebnaya taktika u pacientov s nealkogol'noj zhirovoj bolezn'yu pecheni s uchetom urovnya citokeratina-18 v plazme krovi [Therapeutic strategy in patients with non-alcoholic fatty liver disease, considering cytokeratin-18 level determination in blood plasma]. Suchasna hastroenterolohiia, 2, 15–20. [in Russian].
Golovach, I. Yu. (2014) Osteoartrit: sovremennye fundamental'nye i prikladnye aspekty patogeneza zabolevaniya [Osteoarthritis: modern fundamental and applied aspects of the pathogenesis of the disease]. Bol'. Sustavy. Pozvonochnik, 3, 54–8. [in Russian].
Dynnyk, N. V. (2016) Zastosuvannia neinvazyvnykh biomarkeriv ta mistse tsytokeratynu 18 u diahnostytsi patsiientiv z nealkoholnoiu zhyrovoiu khvoroboiu pechinky [The use of non-invasive biomarkers and cytokeratin 18 in the diagnosis of patients with non-alcoholic fatty liver disease]. Ukrainskyi naukovo-medychnyi molodizhnyi zhurnal, 2, 12–8. [in Ukrainian].
Alam, S., Alam, M., Alam, S. M., Chowdhury, Z., & Kabir, J. (2015). Prevalence and Predictor of Nonalcoholic Steatohepatitis (NASH) in Nonalcoholic Fatty Liver Disease (NAFLD). Journal of Bangladesh College of Physicians and Surgeons, 32(2), 71–77. doi: 10.3329/jbcps.v32i2.26034
Casteda, S., Roman-Blas, J. A., Largo, R., & Harrero-Beaumont, G. (2014) Osteoartritis: a progressive disease with chaning phenotypes. Rheumatology (Oxford), 53(1), 1–3. doi: 10.1093/rheumatology/ket247
Chakraborty, J. B., Oakley, F., & Walsh, M. J. (2012) Mechanisms and biomarkers of apoptosis in liver disease and fibrosis. Int J Hepatol, 2012, 648915. doi: 10.1155/2012/648915
Fujii, H., & Kawada, N. (2012) Inflammation and fibrogenesis in steatohepatitis. J Gastroenterol, 47(3), 215–25. doi: 10.1007/s00535-012-0527-x
Haima, P. (2014) Non-invasive Detection of Liver Injury and Fatty Liver Disease. Use of the Apoptosis Specific Biomarker Cytokeratin-18 (ccK18) to detect non-alcoholic steatohepatitis (NASH) and predict progressive liver disease. Switzerland: TECOmedical Group. 16 p.
K-Kutala, B., Bedossa, P., Guedj, J., Asselah, T., Martinot-Peignoux, M., Duval, X., & Marcellin, P. (2015) Patients with chronic hepatitis C without advanced fibrosis and hepatocellular carcinoma: a retrospective clinical-pathological study. Dig Liver Dis., 47(4), 296–302. doi: 10.1016/j.dld.2014.12.010
Liang, J., Liu, F., Wang, F., Han, T., Jing, L., Ma, Z., & Gao Y. (2017) A Noninvasive Score Model for Prediction of NASHin Patients with Chronic HepatitisBand Nonalcoholic Fatty Liver Disease. Biomed Res Int, 2017, 8793278. doi: 10.1155/2017/8793278
Rosso, C., Caviglia, G. P., Abate, M. L., Vanni, E., Mezzabotta, L., Touscoz, G. A., et al. (2016) Cytokeratin 18-Aspartate396 apoptotic fragment for fibrosis detection in patients with non-alcoholic fatty liver disease and chronic viral hepatitis. Dig Liver Dis., 48(1), 55–61. doi: 10.1016/j.dld.2015.09.008
Yang, Z. H., Yang, S. X., Qin, C. Z., & Chen, Y. X. (2015) Clinical values of elevated serum cytokeratin-18 levels in hepatitis: a meta-analysis. Hepat Mon, 15(5), e25328. doi: 10.5812/hepatmon.15(5)2015.25328
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