ABSTRACT
Immune thrombocytopenia (ITP) is an autoimmune disease which is characterized by antibody-mediated destruction of platelets by the reticuloendothelial system. The rate of ITP is 3.3 per 100,000 adults per year with a prevalence of 9.5 per 100,000 adults. Pregnancy does not increase the frequency or severity of ITP, but ITP can significantly affect pregnancy and cause bleeding in women. Pregnancy requires regular control of the number of platelets: monthly in the I and II trimesters, every 2 weeks – in the III trimester, and weekly control near the delivery date. Indications for treatment are determined by the pregnant woman condition, not the fetus, since it has not been proven that the treatment reduces the risks of thrombocytopenia in newborns with the development of cerebral hemorrhage. The drug of the first line of treatment of such pathology is prednisolone at a dose of 1 mg/kg orally once a day. An increase in the number of platelets is usually observed within 3-7 days, the maximum response is determined after 2-3 weeks. If necessary, the dose can be increased. When the required level of platelets is reached, the dose can be gradually reduced by 10-20 % to the minimum dose necessary to maintain the number of platelets at an acceptable level. Thrombocytopathy can be the cause of primary hemostasis disorders, even if the number of platelets in the blood is normal. For diagnosis, tests are carried out to detect the aggregation ability of platelets. In addition, flow cytometry can be used, which makes it possible to detect the defects of surface membrane receptors, as well as defects of the end point of secretion. ITP is a common cause of thrombocytopenia after viral infections. The onset of this pathology is more often detected in the second and third weeks after the onset of COVID-19. The treatment aim is to prevent the significant bleeding in patients with COVID-19. The article presents a clinical case of a pregnant woman with ITP and thrombocytopathy, whose pregnancy was complicated by COVID-19. The patient complained on bleeding gums, the appearance of hematomas on the skin. Medical treatment of the main disease included prednisolone, eltrombopag, intravenous human immunoglobulin, transfusion of platelet concentrate. At 34–35 weeks of pregnancy alive boy was born with a body weight of 2800 g, length of 49 cm, 7–8 points on the Apgar scale. © The Author(s) 2023.
ABSTRACT
The increase in the frequency of COVID-19 is closely related to the fact that the number of patients in Russia who have had COVID-19 is currently increasing every day. At the same time, many of them continue to experience symptoms after an acute infection regardless of its severity, which is of concern to the entire medical community. In this context, it is important to remem-ber that COVID-19 is characterized not only by lesions of the respiratory system, but also by damage to the heart and blood ves-sels, hemostasis disorders, which aggravate the course of the infection and lead to a significant number of complications both in the acute and subacute phase of the disease, and in the long-term follow-up period. Early detection, diagnosis, as well as prevention and treatment of cardiovascular complications in patients who have undergone COVID-19 will be key to reducing the risk of further adverse health outcomes. The use of low-dose acetylsalicylic acid (ASA) in patients with cardiovascular disease and high cardiovascular risk patients without cardiovascular disease in the post-COVID-19 period is currently considered as one of the main directions of prevention of arterial cardiovascular complications. In this regard, this article discusses the pathogenetic basis of ASA use in patients who have undergone COVID-19, the position of ASA in current clinical guidelines, and the optimal dose and form of ASA for patients who have undergone COVID-19. © 2022, Media Sphera Publishing Group. All rights reserved.
ABSTRACT
Coronavirus disease 2019 (COVID-19) induces a hypercoagulatory state that frequently leads to thromboembolic complications. Whereas anticoagulation is associated with reduced mortality, the role of antiplatelet therapy in COVID-19 is less clear. We retrospectively analyzed the effect of anticoagulation and antiplatelet therapy in 578 hospitalized patients with COVID-19 and prospectively monitored 110 patients for circulating microthrombi and plasma markers of coagulation in the first week of admission. Moreover, we determined platelet shape change and also thrombi in postmortem lung biopsies in a subset of patients with COVID-19. We observed no association of antiplatelet therapy with COVID-19 survival. Adverse outcome in COVID-19 was associated with increased activation of the coagulation cascade, whereas circulating microthrombi did not increase in aggravated disease. This was in line with analysis of postmortem lung biopsies of patients with COVID-19, which revealed generally fibrin(ogen)-rich and platelet-low thrombi. Platelet spreading was normal in severe COVID-19 cases; however, plasma from patients with COVID-19 mediated an outcome-dependent inhibitory effect on naïve platelets. Antiplatelet medication disproportionally exacerbated this platelet impairment in plasma of patients with fatal outcome. Taken together, this study shows that unfavorable outcome in COVID-19 is associated with a profound dysregulation of the coagulation system, whereas the contribution of platelets to thrombotic complications is less clear. Adverse outcome may be associated with impaired platelet function or platelet exhaustion. In line, antiplatelet therapy was not associated with beneficial outcome.
ABSTRACT
Thromboembolic complications are frequently observed in Coronavirus disease 2019 (COVID-19). While COVID-19 is linked to platelet dysregulation, the association between disease outcome and platelet function is less clear. We prospectively monitored platelet activation and reactivity in 97 patients during the first week of hospitalization and determined plasma markers of platelet degranulation and inflammation. Adverse outcome in COVID-19 was associated with increased basal platelet activation and diminished platelet responses, which aggravated over time. Especially GPIIb/IIIa responses were abrogated, pointing toward impeded platelet aggregation. Moreover, platelet-leukocyte aggregate formation was diminished, pointing toward abrogated platelet-mediated immune responses in COVID-19. No general increase in plasma levels of platelet-derived granule components could be detected, arguing against platelet exhaustion. However, studies on platelets from healthy donors showed that plasma components in COVID-19 patients with unfavorable outcome were at least partly responsible for diminished platelet responses. Taken together this study shows that unfavorable outcome in COVID-19 is associated with a hypo-responsive platelet phenotype that aggravates with disease progression and may impact platelet-mediated immunoregulation.