State of anticoagulant and fibrinolytic systems of blood in patients with hypertension in combination with non-alcoholic fatty liver disease
DOI:
https://doi.org/10.15587/2519-4798.2018.147805Keywords:
hypertension, non-alcoholic fatty liver disease, anticoagulant, blood fibrinolytic activityAbstract
Aim of the research. To determine the state of the anticoagulant and fibrinolytic activity of blood in patients with hypertension and concomitant non-alcoholic fatty liver disease.
Methods. 132 patients were examined. 45 patients with hypertension stage II (HT) with concomitant non-alcoholic fatty liver disease (NAFLD), 31 patients with NAFLD without HT, 41 patients with HT without concomitant NAFLD. The control group - 15 healthy individuals of comparable age and sex. To achieve the aim the study of the anticoagulant and fibrinolytic link was carried out by special laboratory studies.
Results. When compared with the control group, the level of Antithrombin III decreased by 16.4 % in the HT group (p<0.01) and in the NAFLD group (p<0.01), HT+NAFLD – by 20.3 % (p<0.001). The level of Protein C in patients with hypertension decreased by 26 % (p<0.001), with NAFLD – by 9.5 % (p<0.05), with NAFLD+HT – by 14.1 % (p<0.01). Plasminogen decreased in HT – by 15 % (p<0.001), NAFLD – by 20.9 % (p<0.001), NAFLD+HT – by 16.5 % (p<0.001). The duration of Hageman-dependent fibrinolysis is increased in all groups compared to control: in the HT group – by 47 % (p<0.001), in the NAFLD group – by 78 % (p<0.001), in the NAFLD+HT group – 2.4 times (p<0.001).
Conclusions. Suppression of anticoagulant hemostasis is observed in patients with hypertension and with NAFLD. The decrease in the fibrinolytic activity of the blood system is reflected in the extension of the dissolution time of the fibrin clot in the group of patients with hypertension, NAFLD, NAFLD combined with HT. The level of plasminogen decreased to the same extent in patients with hypertension and with the combination of hypertension and NAFLD but isolated NAFLD had a stronger effect on this indicator. NAFLD is a risk factor for thrombophilic changes in the blood
References
- Williams, B., Mancia, G., Spiering, W., Agabiti Rosei, E., Azizi, M., Burnier, M. et. al. (2018). 2018 ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal, 39 (33), 3021–3104. doi: http://doi.org/10.1093/eurheartj/ehy339
- Gajalakshmi, V., Lacey, B., Kanimozhi, V., Sherliker, P., Peto, R., Lewington, S. (2018). Body-mass index, blood pressure, and cause-specific mortality in India: a prospective cohort study of 500 810 adults. The Lancet Global Health, 6 (7), e787–e794. doi: http://doi.org/10.1016/s2214-109x(18)30267-5
- Lewington, S., Clarke, R., Qizilbash, N., Peto, R., Collins, R. (2002). Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet, 360 (9349), 1903–1913. doi: http://doi.org/10.1016/s0140-6736(02)11911-8
- Momot, A. P. (2015). The problem of thrombophilia in clinical practice. Russian Journal of Children Hematology and Oncology, 2 (1), 36–48. doi: http://doi.org/10.17650/2311-1267-2015-1-36-48
- Lee, K. W., Lip, G. Y. H. (2003). Effects of Lifestyle on Hemostasis, Fibrinolysis, and Platelet Reactivity. Archives of Internal Medicine, 163 (19), 2368. doi: http://doi.org/10.1001/archinte.163.19.2368
- Junker, R., Heinrich, J., Schulte, H., Erren, M., Assmann, G. (1998). Hemostasis in normotensive and hypertensive men: results of the PROCAM study. The prospective cardiovascular Münster study. Journal of Hypertension, 16 (7), 917–923. doi: http://doi.org/10.1097/00004872-199816070-00004
- Woodward, M., Lowe, G. D., Rumley, A., Tunstall-Pedoe, H., Philippou, H., Lane, D. A., Morrison, C. E. (1997). Epidemiology of coagulation factors, inhibitors and activation markers: The Third Glasgow MONICA Survey. II. Relationships to cardiovascular risk factors and prevalent cardiovascular disease. British Journal of Haematology, 97 (4), 785–797. doi: http://doi.org/10.1046/j.1365-2141.1997.1232935.x
- Makris, T. K., Tsoukala, C., Krespi, P., Hatzizacharias, A., Gialeraki, A., Papargyriou, J. et. al. (1997). Haemostasis balance disorders in patients with essential hypertension. Thrombosis Research, 88 (2), 99–107. doi: http://doi.org/10.1016/s0049-3848(97)00222-3
- Corseaux, D., Ollivier, V., Fontaine, V., Huisse, M.-G., Philippe, M., Louedec, L. et. al. (2002). Hemostasis imbalance in experimental hypertension. Molecular Medicine, 8 (4), 169–178. doi: http://doi.org/10.1007/bf03402009
- Rinella, M. E. (2015). Nonalcoholic Fatty Liver Disease. JAMA, 313 (22), 2263–2273. doi: http://doi.org/10.1001/jama.2015.5370
- Bril, F., Cusi, K. (2017). Management of Nonalcoholic Fatty Liver Disease in Patients With Type 2 Diabetes: A Call to Action. Diabetes Care, 40 (3), 419–430. doi: http://doi.org/10.2337/dc16-1787
- Byrne, C. D., Targher, G. (2015). NAFLD: A multisystem disease. Journal of Hepatology, 62 (1), S47–S64. doi: http://doi.org/10.1016/j.jhep.2014.12.012
- Fotbolcu, H., Zorlu, E. (2016). Nonalcoholic fatty liver disease as a multi-systemic disease. World Journal of Gastroenterology, 22 (16), 4079–4090. doi: http://doi.org/10.3748/wjg.v22.i16.4079
- Potze, W., Siddiqui, M. S., Boyett, S. L., Adelmeijer, J., Daita, K., Sanyal, A. J., Lisman, T. (2016). Preserved hemostatic status in patients with non-alcoholic fatty liver disease. Journal of Hepatology, 65 (5), 980–987. doi: http://doi.org/10.1016/j.jhep.2016.06.001
- Kopec, A. K., Joshi, N., Luyendyk, J. P. (2016). Role of hemostatic factors in hepatic injury and disease: animal models de-liver. Journal of Thrombosis and Haemostasis, 14 (7), 1337–1349. doi: http://doi.org/10.1111/jth.13327
- Essalmani, R., Susan-Resiga, D., Guillemot, J., Kim, W., Sachan, V., Awan, Z. et. al. (2017). Thrombin activation of protein C requires prior processing by a liver proprotein convertase. Journal of Biological Chemistry, 292 (25), 10564–10573. doi: http://doi.org/10.1074/jbc.m116.770040
- Chapin, J. C., Hajjar, K. A. (2015). Fibrinolysis and the control of blood coagulation. Blood Reviews, 29 (1), 17–24. doi: http://doi.org/10.1016/j.blre.2014.09.003
- Jin, R., Krasinskas, A., Le, N.-A., Konomi, J. V., Holzberg, J., Romero, R., Vos, M. B. (2016). Association between plasminogen activator inhibitor-1 and severity of liver injury and cardiovascular risk in children with non-alcoholic fatty liver disease. Pediatric Obesity, 13 (1), 23–29. doi: http://doi.org/10.1111/ijpo.12183
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2018 Bazhenova Nataliia
This work is licensed under a Creative Commons Attribution 4.0 International License.
Our journal abides by the Creative Commons CC BY copyright rights and permissions for open access journals.
Authors, who are published in this journal, agree to the following conditions:
1. The authors reserve the right to authorship of the work and pass the first publication right of this work to the journal under the terms of a Creative Commons CC BY, which allows others to freely distribute the published research with the obligatory reference to the authors of the original work and the first publication of the work in this journal.
2. The authors have the right to conclude separate supplement agreements that relate to non-exclusive work distribution in the form in which it has been published by the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.