THE THE MAIN CLINICAL AND PATHOGENETIC FEATURES OF THE COMORBID COURSE OF NON-ALCOHOLIC STEATOHEPATITIS, OBESITY AND HYPERTENSION
DOI:
https://doi.org/10.11603/1811-2471.2023.v.i2.13825Keywords:
non-alcoholic steatohepatitis, obesity, hypertension, metabolic syndromeAbstract
SUMMARY. The incidence of nonalcoholic steatohepatitis (NASH) in the population is 20–40 %, in obese patients – 50–90 %. The presence of NASH significantly reduces the quality of life of patients. The presence of concomitant arterial hypertension in patients can cause a cascade of reactions of mutual burdens, which will lead to the progression of all comorbid diseases.
The aim – to investigate the differences between clinical and laboratory parameters in the comorbid course of NASH on the background of obesity. In addition, we studied the state of hepatic circulation and the functional state of the endothelium depending on the presence of comorbid hypertension.
Material and Methods. Systematic review with further analysis, comparison, systematization and generalization of scientific literature in MEDLINE, Cochrane and PubMed databases of relevant articles on the study of psychological characteristics of women of childbearing age diagnosed with psychogenic infertility.
Results. In recent years, NASH has increasingly been seen as an additional independent risk factor for cardiovascular disease and a predictor of its complications. The course of NASH under conditions of comorbidity with obesity in comparison with the isolated course is characterized by a predominance of hypertension of II degree (60.0 %), increased variability of systolic blood pressure (SBP) during the day with increasing duration of “pressure load” during the day. The comorbid course of NASH with obesity and hypertension (HT) there is a significant activation of the processes of liver tissue fibrosis, the content of protein-bound oxyproline in the blood, fibronectin, hexosamines, sialic acids, fucose, not bound to protein due to the activation of fibroblast growth factor, in response to which there is usually inadequate compensatory activation of collagenolysis (increase in the content of free oxyproline in the blood, which was inhibited by excessively activated proteinase-inhibitory system).
Conclusions. The comorbidity of NASH with HT and obesity is a powerful pathogenetic factor that worsens the quality of life of patients to a much greater extent than the severity of a single disease. It's crucial to have multidisciplinary approach in the treatment of people with comorbidity of HT with NASH on the background of obesity.
References
Molina-Molina, E., Krawczyk, M., Stachowska, E., Lammert, F., & Portincasa, P. (2019). Non-Alcoholic Fatty Liver Disease in Non-Obese Individuals: Prevalence, Pathogenesis and Treatment. Clin. Res. Hepatol. Gastroenterol., 43(6), 638-645. DOI: 10.1016/j.clinre.2019.04.005. DOI: https://doi.org/10.1016/j.clinre.2019.04.005
Fabbrini, E., Sullivan, S., & Klein, S. (2010). Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology, 51(2), 679-89. DOI: 10.1002/hep.23280. DOI: https://doi.org/10.1002/hep.23280
Friedman, S.L., Neuschwander-Tetri, B.A., Rinella, M., & Sanyal, A.J. (2018). Mechanisms of NAFLD development and therapeutic strategies. Nat. Med., 24(7), 908-922. DOI: 10.1038/s41591-018-0104-9. DOI: https://doi.org/10.1038/s41591-018-0104-9
Younossi, Z.M. (2016). Global epidemiology of nonalcoholic fatty liver disease—meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology, 64(1), 73-84. DOI: 10.1002/hep.28431. DOI: https://doi.org/10.1002/hep.28431
Loomba, R., & Sanyal, A.J. (2013). The global NAFLD epidemic. Nat. Rev. Gastroenterol. Hepatol., 10(11), 686-690. DOI: 10.1038/nrgastro.2013.171. DOI: https://doi.org/10.1038/nrgastro.2013.171
Kuzminova, N.V., Gribenyuk, O.V., Osovska, N.Y., & Knyazkova, I.I. (2016). Arterial hypertension, obesity and non-alcoholic fatty liver disease: is there any connection? Arterial Hypertens., 20(4), 216-227. DOI: 10.5603/AH.2016.0025. DOI: https://doi.org/10.5603/AH.2016.0025
Ekstedt, M. (2006). Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology, 44(4), 865-873. DOI: 10.1002/hep.21327. DOI: https://doi.org/10.1002/hep.21327
Mandryk, O.Y. (2014). Peculiarities of of nonalcoholic steatohepatitis course in patients with arterial hypertension. Ways of drug correction. Extended abstract of candidates thesis. Chernivtsi: Bukovinian State Medical University [in Ukrainian].
Lade, A., Noon, L.A., & Friedman, S.L. (2014). Contributions of metabolic dysregulation and inflammation to nonalcoholic steatohepatitis, hepatic fibrosis, and cancer. Curr. Opin. Oncol., 26, 100-107. DOI: 10.1097/CCO.0000000000000042. DOI: https://doi.org/10.1097/CCO.0000000000000042
Käräjämäki, A.J. (2017). Non-alcoholic fatty liver disease with and without metabolic syndrome: different long-term outcomes. Metabolism, 66, 55-63. DOI: 10.1016/j.metabol.2016.06.009. DOI: https://doi.org/10.1016/j.metabol.2016.06.009
