Features of changes in anticoagulant hemostasis system in patients with hypertensive disease with concomitant hyperuricemia
DOI:
https://doi.org/10.15587/2519-4798.2018.148791Keywords:
hyperuricemia, hypertension, antithrombin III, protein C, Hageman-dependent fibrinolysis, atherosclerosisAbstract
Aim of the research was to study the state of anticoagulant and fibrinolytic units of the hemostasis system in patients with hypertension associated with hyperuricemia.
Materials and methods. We surveyed 133 people (80 male and 53 female), whose average age was 56.19±7.29 years, all patients were divided into 3 groups. The first main group was 54 patients with arterial hypertension with concomitant hyperuricemia, the second group was made up of 50 patients with hypertension and normal uric acid levels, and the third – 15 patients with hyperuricemia without increase in blood pressure, and the control group consisted of 14 practically healthy subjects comparable in age and sex. Hyperuricemia was determined at uric acid levels >7 mg/dL (>413 μmol/L). The activity of anticoagulant and fibrinolytic units of hemostasis was studied as a result of conducting of special laboratory tests: antithrombin III, protein C, plasminogen and XIIa-dependent fibrinolysis. Non-parametric statistical methods were used to analyze the data: U-Mann-Whitney, probable differences were considered at p<0.05.
Results. In the examination of patients, we found suppression of the activity of antithrombin III, in the first group of patients, 23 % was large in terms of the control group, while the difference between the groups (in groups I and II) was 18.3 %. The protein C activity in the first group was reduced by 25.7 % compared with the control group and by 14.8 % less than that of group II. When comparing the parameters of the anticoagulating potential of blood groups among patients, it was determined that the level of antithrombin III was the lowest in patients with group I, namely 18.3 % when compared with group III (p <0.001) and 23.1 % when compared with II group (p <0.001). The protein C was the lowest in patients in group I by 14.8 % compared with group III (p <0.001) and by 25.7 % when compared with group II (p <0.001).
Plasminogen (PG) was suppressed in all groups of patients: at hypertension by 16.7 % (p <0.01), with hyperuricemia by 32.1 % (p<0.001), with hypertension with concomitant hyperuricemia by 26.7 % (p<0.001). A significant increase in the activity of indicators of Hageman-dependent fibrinolysis was also found, in group I of patients with combined course of Hageman-dependent fibrinolysis, it was 3.5 times more (p<0.001), compared to the control group, in group II patients this indicator was 2.2 times more than in patients of the control group (p<0.001), and in group III patients 2.8 times (p<0.001).
Conclusion. In hypertensive disease without concomitant hyperuricemia, AT III and protein C decreased, reflecting the anticoagulant potential of blood plasma, and in hypertensive patients associated with concomitant hyperuricemia, an even greater decrease in plasma hemostasis and prolonged fibrinolysis time was observed
References
- Versteeg, H. H., Heemskerk, J. W. M., Levi, M., Reitsma, P. H. (2013). New Fundamentals in Hemostasis. Physiological Reviews, 93 (1), 327–358. doi: http://doi.org/10.1152/physrev.00016.2011
- Platonova, T. N., Gornitskaya, O. V., Chernyshenko, T. M. et. al. (2013). Determination of protein C activity and its role in clinical laboratory diagnosis. Laboratory diagnostics, 3, 3–8.
- Lucking, A. J., Gibson, K. R., Paterson, E. E., Faratian, D., Ludlam, C. A., Boon, N. A. et. al. (2013). Endogenous Tissue Plasminogen Activator Enhances Fibrinolysis and Limits Thrombus Formation in a Clinical Model of Thrombosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 33 (5), 1105–1111. doi: http://doi.org/10.1161/atvbaha.112.300395
- Barkagan, Z. S., Momot, A. P. (2001). Diagnosis and controlled therapy of haemostasis disorders. Moscow: Nyediamed, 296.
- Droste, D. W., Ringelstein, E. B. (2002). Evaluation of Progression and Spread of Atherothrombosis. Cerebrovascular Diseases, 13, 7–11. doi: http://doi.org/10.1159/000047783
- Leys, D. (2001). Atherothrombosis: A Major Health Burden. Cerebrovascular Diseases, 11, 1–4. doi: http://doi.org/10.1159/000049137
- Bokarev, I. N., Bokarev, M. I. (2002). Thrombophilia, venous thrombosis and their treatment. Clinical medicine, 5, 4–8.
- Volterrani, M., Iellamo, F., Sposato, B., Romeo, F. (2016). Uric acid lowering therapy in cardiovascular diseases. International Journal of Cardiology, 213, 20–22. doi: http://doi.org/10.1016/j.ijcard.2015.08.088
- Tuttle, K. R., Short, R. A., Johnson, R. J. (2001). Sex differences in uric acid and risk factors for coronary artery disease. The American Journal of Cardiology, 87 (12), 1411–1414. doi: http://doi.org/10.1016/s0002-9149(01)01566-1
- Platonova, T. M., Savchuk, O. M., Chernyshenko, T. M. (2000). Determination of the activity of the tissue activator plasminogen and the content of soluble fibrin in the plasma of patients with various pathological conditions. Laboratory diagnostics, 2, 15–17.
- Borghi, C., Rosei, E. A., Bardin, T., Dawson, J., Dominiczak, A., Kielstein, J. T. et. al. (2015). Serum uric acid and the risk of cardiovascular and renal disease. Journal of Hypertension, 33 (9), 1729–1741. doi: http://doi.org/10.1097/hjh.0000000000000701
- Crouse, J. R., Toole, J. F., McKinney, W. M., Dignan, M. B., Howard, G., Kahl, F. R. et. al. (1987). Risk factors for extracranial carotid artery atherosclerosis. Stroke, 18 (6), 990–996. doi: http://doi.org/10.1161/01.str.18.6.990
- Nieto, F. J., Iribarren, C., Gross, M. D., Comstock, G. W., Cutler, R. G. (2000). Uric acid and serum antioxidant capacity: a reaction to atherosclerosis? Atherosclerosis, 148 (1), 131–139. doi: http://doi.org/10.1016/s0021-9150(99)00214-2
- Kanellis, J., Watanabe, S., Li, J. H., Kang, D. H., Li, P., Nakagawa, T. et. al. (2003). Uric Acid Stimulates Monocyte Chemoattractant Protein-1 Production in Vascular Smooth Muscle Cells Via Mitogen-Activated Protein Kinase and Cyclooxygenase-2. Hypertension, 41 (6), 1287–1293. doi: http://doi.org/10.1161/01.hyp.0000072820.07472.3b
- Kang, D.-H., Park, S.-K., Lee, I.-K., Johnson, R. J. (2005). Uric Acid-Induced C-Reactive Protein Expression: Implication on Cell Proliferation and Nitric Oxide Production of Human Vascular Cells. Journal of the American Society of Nephrology, 16 (12), 3553–3562. doi: http://doi.org/10.1681/asn.2005050572
- Fang, J., Alderman, M. H. (2000). Serum uric acid and cardiovascular mortality the NHANES I epidemiologic follow-up study, 1971–1992. National Health and Nutrition Examination Survey. Jama, 283 (18), 2404–2410. doi: http://doi.org/10.1001/jama.283.18.2404
- Corry, D. B., Eslami, P., Yamamoto, K., Nyby, M. D., Makino, H., Tuck, M. L. (2008). Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin–angiotensin system. Journal of Hypertension, 26 (2), 269–275. doi: http://doi.org/10.1097/hjh.0b013e3282f240bf
- Romney, G., Glick, M. (2009). An Updated Concept of Coagulation With Clinical Implications. The Journal of the American Dental Association, 140 (5), 567–574. doi: http://doi.org/10.14219/jada.archive.2009.0227
- Lucking, A. J., Gibson, K. R., Paterson, E. E., Faratian, D., Ludlam, C. A., Boon, N. A. et. al. (2013). Endogenous Tissue Plasminogen Activator Enhances Fibrinolysis and Limits Thrombus Formation in a Clinical Model of Thrombosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 33 (5), 1105–1111. doi: http://doi.org/10.1161/atvbaha.112.300395
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2018 Maria Valigura
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.