Morphological substrate of platelet hemostasis damage in patients with type 2 diabetes mellitus and hypertension.

Authors

  • N. O. Pertseva ГУ «Днепропетровская медицинская академия МЗ Украины», Ukraine

DOI:

https://doi.org/10.26641/1997-9665.2015.4.57-65

Keywords:

diabetes mellitus type 2, arterial hypertension, platelet hemostasis, ultrastructure

Abstract

Background. Disorders of hemostasis in patients with arterial hypertension and diabetes mellitus type 2 are complex: growing aggregative activity of platelets and red blood cells, activation and degranulation of platelet antiaggregatory potential endothelium; reduced anticoagulant and fibrinolytic activity of blood. Objective. The purpose of this study was to determine the morphological changes of blood cells in patients with type 2 diabetes mellitus with hypertension. Methods. Ultrastructural analysis of platelets was performed in 60 patients with type 2 diabetes mellitus and hypertension and 5 volunteers – healthy individuals (control group). Results. The degree of alteration of platelet hemostasis depends on the quality level of glycemic control and albuminuria. Patients with optimal glycemic control, there is significantly increased relative content of activated platelets with preservation of normal and degranulated content aggregated forms and the appearance of individual platelets with alpha and delta granules imbalance. In patients with albuminuria and poor glycemic control has been a sharp violation of platelet hemostasis due to significant increase of the content of activated, degranulated and aggregated platelets release the contents of the majority of the granules, the development of intravascular hyperactivation of platelets, increasing the number of reversibly and irreversibly transformed erythrocytes, including the appearance of platelet-leukocyte aggregates. Conclusion. Morphological substrate of platelet hemostasis damage in patients with type 2 diabetes mellitus with hypertension is complex of ultrastructural changes of blood cells: intravascular platelet hyperactivation, an imbalance content of all types of granules, transformation of the red blood surface architecture, and the formation of different composition and size of platelet aggregates. This complex is found in all patients of this contingent and acts as an early predictor of the disease. The most sensitive quantitative characteristics of this complex is the relative content of activated and aggregated platelets, packing density of alpha- and delta-granules, level of inversely transformed red blood cells, the number of platelet aggregates.

References

  1. Shilov AM. Gipertenziya i reologiya krovi [Hypertension and blood rheology]. Moscow: BARS; 2005. 328 p. Russian.
  2. Torimoto K, Okada Y, Mori H, Tanaka Y. Relationship between fluctuations in glucose levels measured by continuous glucose monitoring and vascular endothelial dysfunction in type 2 diabetes mellitus. Cardiovasc Diabetol. 2013;13:18-24.
  3. Woodman PG, Futter CE. Multivesicular bodies: coordinated progression to maturity. Curr Opin Cell Biol. 2008;20:408-14.
  4. Blair P. Platelet α-granules: Basic biology and clinical correlates. Blood Rev. 2009;23(4):177-89.
  5. Demirtunc R, Duman D, Basar M. The relationship between glycemic control and platelet activity in type 2 diabetes mellitus. J Diabetes Complications. 2009;23(2):89-94.
  6. Barkis GL. Pathogenesis of hypertension in diabetes. Diabetes Rev. 1995;3:460-76.
  7. Mathewkutty S, McGuire DK. Platelet perturbations in diabetes: implications for cardiovascular disease risk and treatment. Expert Rev Cardiovasc Ther. 2009;7(5):541-9.
  8. Vaskina EA, Tsirendorzhiev DD, Demina LM. Rol neytrofilov i prooksidantnogo potentsiala krovi v razvitii endotelialnoy disfunktsii pri arterialnoy gipertenzii [Role of neutrophils and pro-oxidant capacity of the blood in the development of endothelial dysfunction in hypertension]. Bulletin SO RAMN. 2003;2:107-12. Russian.
  9. Sowers JR, Sowers PS, Peuler JD. Role of insulin resistance and hyperinsulinemia in development of hypertension and atherosclerosis. J Lab Clin Med. 1994;23:647-52.
  10. Italiano JE, Richardson JL, Patel-Hett S. Angiogenesis is regulated by a novel mechanism: pro- and antiangiogenic proteins are organized into separate platelet alpha-granules and differentially released. Blood. 2008;111:1227-33.
  11. Sawatzke CL, Solomons CC. Fixation and embedding of small volumes of platelets for transmission electron microscopy. J Clin Pathol. 1980;33(6):600-2.
  12. Mironov AA, Komissarchik YuYa, Mironov VA. Metodyi elektronnoy mikroskopii v biologii i meditsine: Metodicheskoe rukovodstvo. [Electron microscopy methods in biology and medicine : Methodological Guide]. St. Petersburg: Science; 1994. 400 p. Russian.
  13. Kuo J. Electron microscopy: methods and protocols. Totowa, New Jersey: Humana Press Inc. 2007. 608 p.
  14. Medvedev IV, Kumova TA. Oslablenie agregatsionnoy sposobnosti trombotsitov u bolnyih arterialnoy gipertoniey pri metabolicheskom sindrome na fone lozartana. [Weakening aggregability platelets in hypertensive patients with metabolic syndrome on a background of losartan]. Russ J Cardiol. 2008;5:53-5. Russian.
  15. Lakin GF. Biometriya [Biometrics: 4th ed.]. Moscow : Vysshaya shkola; 1990. 352 p. Russian.

Downloads

How to Cite

Pertseva, N. O. (2015). Morphological substrate of platelet hemostasis damage in patients with type 2 diabetes mellitus and hypertension. Морфологія / Morphologia / Morfologìâ, 9(4), 57–65. https://doi.org/10.26641/1997-9665.2015.4.57-65

Issue

Vol. 9 No. 4 (2015)

Section

Статті

License

Copyright (c) 2018 Morphologia

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

 The authors reserve the right to authorship of their work and transfer to the Journal the right to the first publication of this work under the terms of a license Creative commons Attribution 4.0 International (CC BY 4.0), which allows other people to freely distribute the published work with a mandatory reference to the authors of the original work and the first publication of the work in this journal.
        By submitting a manuscript to the editorial office of the Journal ‘Morphologia’ authors agree to transfer the rights to protect and use the manuscript (all supplemental materials, particularly protected objects such as photos, drawings, diagrams, tables, etc.), including the reproduction in the press and distribution via the Internet; translation of the manuscript into any language; export and import of journal copies with the Authors’ article in order to make it available for public. Authors convey the rights mentioned above to the editorial office without any temporal or territorial limitation all over the world. 
        The Authors guarantee that they have the exclusive rights to use the material transferred to editorial office. Editors are not responsible to third parties for contraventions of warranty given by the Authors. The considered rights are transferred to the editorial office since the moment when the current issue is signed for publishing. Reproduction of materials published in the Journal by other individuals and legal entities is possible only with the consent of Editorial office, with the obligatory indication of the full bibliographic reference of the primary publication. The Authors reserve the right to use the published material, its fragments and parts for teaching materials, oral presentations, dissertation thesis prepararion with obligatory bibliographic citation of the original paper. Electron copy of the published article, downloaded from official journal web-site in .pdf format may be put by authors on the official web-site of their institutions, any other official resources with open access.