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Advances in Avascular Necrosis of the Hip joint
Published in K. Mohan Iyer, Hip Joint in Adults: Advances and Developments, 2018
Different reasons have been suggested for the basic cause of the necrosis. Various studies have been carried out about the relationship between the genetic background and hypercoagulation. Hereditary thrombophilia, impaired fibrinolysis, antiphospholipid antibodies, mutation of Factor V Leiden and lack of proteins S and C have been suggested in different studies [23–26].
Direct Oral Anticoagulants: New Options
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
The major indications of the VKA are primary and secondary stroke prevention in patients with atrial fibrillation (SPAF), therapy and secondary prevention of VTE, i.e., deep vein thrombosis (DVT) and pulmonary embolism (PE), prophylactic anticoagulation of patients with prosthetic heart valves and of patients with severe thrombophilia.
Understanding the role of genetic susceptibility (ACE2 and TMPRSS2) in COVID-19
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Abdullahi Tunde Aborode, Sherifdeen Bamidele Onigbinde, Khadijah Omoshalewa Sanusi, Noah Alaba, Aderinola H. Rasaq-Lawal, Babatunde Samuel Obadawo, Allison Olatoyosi, Saidat Omowunmi Adeniran-Obey, Victor Onwukwe, Uchenna Asogwa, Ridwan Iyanu Arinola, Seun Idowu Imani, Ayoola S. Fasawe, Ibukunoluwa Sodiya, Sherif Babatunde Adeyemi, Gaber El-Saber Batiha
Children are less likely to have thrombosis because of coagulation, unbalance, inherited, or acquired thrombophilia, so there is a low prevalence among them [13]. The more rare disseminated intravascular coagulation (DIC) and microthromboembolic events or cardiac injury in the more severe elderly patients may be partly explained by this fact, strongly substantiating heparin-based anticoagulant treatments in selected severe cases [9,13,29,31]. The severity of COVID-19 increases with advancing age in male and female sexes, possibly due to deregulated immune responses, differences in sex hormones at older ages, or a significant imbalance in coagulation and fibrinolysis with advancing age [28].
Computational modeling of hypercoagulability in COVID-19
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Ge Zhu, Susree Modepalli, Mohan Anand, He Li
There are several limitations related to our simulation results. In this study, we mainly focus on the abnormal coagulation factors in COVID-19 that promote the thrombus formation and did not consider their impact on the fibrinolysis process. For example, COVID-19 patients present with elevated fibrin degradation products, especially D-dimers, a fibrin degradation product and this could be an indication of excessive thrombosis in the patients body. Since we are employing the ODE models, we did not consider the impact of blood flow on the coagulation process. Flowing blood can deliver inactive factors, such as factors II and V, to thrombogenic sites to continuously supply the coagulation reactions. On the other hand, it can also transport the generated active factors, such as f-IIa, downstream. Therefore, the overall coagulation reactions could be dictated by the rate of coagulation reactions as well as blood flow rate (Shen et al. (2008)). Investigation of the blood flow rates on the coagulation requires more sophisticated models that integrate the coagulation kinetics with the blood flow dynamics (Anand et al. (2003); Fogelson and Guy (2008); Fogelson and Tania (2005); Leiderman and Fogelson (2011, 2013); Li et al. (2022a,b, 2020); Yazdani et al. (2021, 2018, 2017)). Moreover, elevated levels of proinflammatory cytokines, such as Interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and Interleukin 1 (IL-1), due to viral invasion could also elicit potent thrombosis (thromboinflammation) through regulating the level of TF (Connors and Levy (2020); Iba et al. (2020); Jose and Manuel (2020); Lazzaroni et al. (2021)), a key mediator for the inflammation-induced coagulation (Esmon (2005); Levi and van der Poll (2010); Levi et al. (2004); Petäjä (2011)). Detailed simulation of these immune thrombotic processes requires more comprehensive kinetics models that combine aspects of coagulation with the complement system, which is not covered in the current study. In addition, integration of the mathematical models of biochemical reactions with biophysical models of thrombosis (Bouchnita et al. (2021); Xu et al. (2008); Zheng et al. (2020)) or hemorheology (Deng et al. (2022); Javadi et al. (2022); Li et al. (2017); Liu et al. (2021)) could be important topics to further explore the COVID-19-induced thrombophilia and hemorheological abnormalities.