Structural features of the lower limb deep vein remodeling as a morphologic component in the pathogenesis of pulmonary thromboembolism in cancer patients
Oncological patients are at high risk of developing thromboembolic complications, which is a manifestation of a complex set of symptoms – cancer. At the same time, the analysis of the literature shows that the question of the involvement of structural changes of the vascular wall in the pathogenesis of possible primary thrombus formation in cancer patients remains open. The aim of the study – to study the structural features of remodeling of the deep vein of the lower extremity as a morphological link of pathogenesis of pulmonary embolism in cancer patients. Retrospective analysis of 54 protocols of autopsy of deaths from cardiopulmonary shock caused by pulmonary embolism in 2014-2018 was performed. In parallel, all patients were determined the number of free-circulating endothelial cells in the citrate blood by Hladovez J. method, in modification of Sivak V.V. and co-authors (2007). Statistical processing of digital data was performed using the software “Excel” and “STATISTICA” 6.0. In retrospective analysis of autopsy protocols, the highest proportion of pulmonary embolism was report in patients with cancer of the uterus and colon. Morphological changes of the deep vein of the lower extremities in cancer patients were manifested by endothelium desquamation and circular and focal muscular-fibrous hyperplasia of the intima, which caused disturbances of laminar flow of blood; muscular-fibrous atrophy with neovascularization of the middle membrane and sclerosis of vasa vasorum vessels of adventitia. The process of remodeling was also manifest by the inflammatory transformation of the vascular wall, the formation of obstructing and floating blood clots with their subsequent organization, vascularization and recanalization. The cause of intimal thickening, atrophy, and sclerosis with midbrain neovascularization is most likely a hypoxic mechanism of activation of transforming connective tissue growth factors that stimulate collagenogenesis and neoangiogenesis. Desquamation of endothelial cells can also be considered as a significant contributor to thrombus formation. Endothelial cells have a protective function aimed at eliminating damage to the vascular wall by thrombus formation and the development of fibrous intima hyperplasia. In addition, tumor cells are themselves capable of producing excess platelet growth factor, which causes intima proliferation. So, a component of pathomorphogenesis of pulmonary artery thromboembolism in cancer patients is a complex structural reconstruction of the wall of the deep vein of the lower extremity, which causes the development of its thrombosis. Deep vein remodeling in cancer patients is characterized by endothelial cell desquamation, intima and middle-membrane thickening and sclerosis in combination with vasa vasorum fibrous degeneration and perforant vein thrombosis. In response to hemodynamic disorders, compensatory remodeling develops: the combination of leiomyocyte atrophy with their hypertrophy and neovascularization of the middle membrane.
 Akhmetzianov, F. Sh., & Kamalov, I. A. (2017). Pulmonary thromboembolism and cancer. Volga Oncology Bulletin, 2(29), 4-7.
 Bodnar, Ya. Ya., & Datsko, T. V. (2012). Clinical pathohistology: a textbook. Ternopil: Ternopil State Medical University. “Ukrmedgnyga”.
 Gryshanov, S. I. (2015). Epidemiology of pulmonary embolism according to autopsy. Smolensk Medical Almanac, 1(1), 19-20.
 Hillen, H. F. (2000). Thrombosis in cancer patients. Annals of oncology: official journal of the European Society for Medical Oncology, 11, 273-276. doi: 10.1023/a:1011191205274
 Kakkar, A. K., Haas, S., Walsh, D., & Encke, A. (2001). Prevention of perioperative venous thromboembolism: outcome after cancer and noncancer surgery. British Journal of Surgery, 88(S1).
 Karnabeda, O. A. (2012). Venous thromboembolism in patients with cancer. Clinical Oncology, 5(1), 109-114. (4)
 Magnus, N., D’Asti, E., Meehan, B., Garnier, D., & Rak, J. (2014). Oncogenes and the coagulation system–forces that modulate dormant and aggressive states in cancer. Thrombosis Research, 133, S1-S9. doi: 10.1016/S0049-3848(14)50001-1
 Okhotnikova, O. M., Ponochevna, O. V., & Mellina, K. V. (2017). Endothelial dysfunction as a factor in the development, severe course and prognosis of systemic vasculitis in children. Clinical immunology. Allergology. Infectology, 2(99), 46-52.
 Prandoni, P., Falanga, A., & Piccioli, A. (2005). Cancer and venous thromboembolism. The Lancet Oncology, 6(6), 401-410. doi: 10.1016/S1470-2045(05)70207-2
 Rozanov, I. D., Rozanova, E. A., Shyrykov, E. I., Balkanov, A. S., Hahanov, L. E., & Stepanova, E. A. (2016). Pulmonary embolism in breast cancer: etiology, pathogenesis and treatment options. Clinical Medicine Almanac, 44(5), 580-586. https://doi.org/10.18786/2072-0505-2016-44-5-580-586
 Rozanov, I. D., Semashkova, A. E., Balkanov, A. S., Terpyhorev, S. A., & Stepanova, E. A. (2015). Pulmonary thromboembolism: some issues of epidemiology and treatment in cancer patients. Clinical Medicine Almanac, 41, 97-102. https://doi.org/10.18786/2072-0505-2015-41-97-102
 Sciacca, F. L., Ciusani, E., Silvani, A., Corsini, E., Frigerio, S., Pogliani, S., ... Salmaggi, A. (2004). Genetic and plasma markers of venous thromboembolism in patients with high grade glioma. Clinical Cancer Research, 10(4), 1312-1317. doi: 10.1158/1078-0432.ccr-03-0198
 Sivak, V. V. (2007). A method of determining free-circulating endothelial cells in the blood. Patent 25012 U, Ukraine.
 Verso, M., & Agnelli, G. (2014). New strategies of VTE prevention in cancer patients. Thrombosis research, 133, S128-S132. doi: 10.1016/S0049-3848(14)50022-9
 Vlenterie, M., Desar, I. M., van Herpen, C. M., & Tol, J. (2014). Fatal microscopic pulmonary tumour embolisms in patients with breast cancer: necessary knowledge for future medical practice. Neth. J. Med., 72(1), 28-31. PMID: 24457436
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