International journal of laboratory hematology
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Review
Laboratory testing for suspected COVID-19 vaccine-induced (immune) thrombotic thrombocytopenia.
COVID-19 (coronavirus disease 2019) represents a pandemic, and several vaccines have been produced to prevent infection and/or severe sequelae associated with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection. There have been several reports of infrequent post vaccine associated thrombotic events, in particular for adenovirus-based vaccines. These have variously been termed VIPIT (vaccine-induced prothrombotic immune thrombocytopenia), VITT (vaccine-induced [immune] thrombotic thrombocytopenia), VATT (vaccine-associated [immune] thrombotic thrombocytopenia), and TTS (thrombosis with thrombocytopenia syndrome). ⋯ In suspected VITT, there is a generally highly elevated level of D-dimer, thrombocytopenia, and PF4 antibodies can be identified by ELISA-based assays, but not by other immunological assays typically positive in HITT. In addition, in some functional platelet activation assays, standard doses of heparin have been identified to inhibit activation in suspected VITT, but they tend to augment activation in HITT. Conversely, it is also important to not over-diagnose VITT, given that not all cases of thrombosis post vaccination will have an immune basis and not all PF4-ELISA positive patients will be VITT.
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There are many preanalytical variables (PAV) that are known to affect coagulation testing. The more commonly acknowledged PAV addressed by the clinical laboratory tend to start with their influence on blood collection, but realistically coagulation PAV starts with the patient, where the laboratory has less influence or control. ⋯ Laboratory oversight of sample transportation, processing and storage will assure sample integrity until testing can be facilitated. The purpose of this document is to review common PAV that should be taken into consideration when ordering, performing and interpreting a coagulation test result, with additional attention to the effect of direct oral anticoagulants (DOACs).
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The ongoing COVID-19 pandemic has had a profound worldwide impact on the laboratory hematology community. Nevertheless, the pace of COVID-19 hematology-related research has continued to accelerate and has established the role of laboratory hematology data for many purposes including disease prognosis and outcome. The purpose of this scoping review was to assess the current state of COVID-19 laboratory hematology research. ⋯ Despite the major improvements in our understanding of the role of coagulation, automated hematology, and cell morphology in COVID-19, there are gaps in the literature, including biosafety and the laboratory role in screening and prevention of COVID-19. There is a gap in the publication of papers focused on guidelines for the laboratory. Our findings suggest that, despite the large number of publications related to laboratory data and their use in COVID-19 disease, many areas remain unexplored or under-reported.
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The ongoing COVID-19 pandemic originated in Wuhan, Hubei Province, China, in December 2019. The etiologic agent is a novel coronavirus of presumed zoonotic origin with structural similarity to the viruses responsible for severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). ⋯ In addition to its central role in the diagnosis of COVID-19 infection, the clinical laboratory provides critical information to clinicians regarding prognosis, disease course, and response to therapy. The purpose of this review is to (a) provide background context about the origins and course of the pandemic, (b) discuss the laboratory's role in the diagnosis of COVID-19 infection, (c) summarize the current state of biomarker analysis in COVID-19 infection, with an emphasis on markers derived from the hematology laboratory, (d) comment on the impact of COVID-19 on hematology laboratory safety, and (e) describe the impact the pandemic has had on organized national and international educational activities worldwide.
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Several clinical conditions, in particular those associated with a systemic inflammatory response, can cause some degree of activation of coagulation but when the procoagulant stimulus is sufficiently severe and overcomes the natural anticoagulant mechanisms of coagulation, disseminated intravascular coagulation (DIC) may occur. The clinical manifestations of DIC encompass multiorgan dysfunction caused by fibrin-platelet clots in the microcirculation, and bleeding caused by consumption of platelets and coagulation factors. Molecular mechanisms that play a role in inflammation-induced effects on coagulation have been recognized in much detail. ⋯ In addition, more sophisticated tests for activation of individual factors or pathways of coagulation may point to specific involvement of these components in the pathogenesis of the disorder. A combination of readily available tests is usually sufficient in establishing the diagnosis of DIC, and for this purpose, several scoring algorithms have been developed. Some specific clinical situations may elicit coagulation responses that can be distinguished from DIC or may occur in combination with DIC, including dilutional coagulopathy, liver failure-related coagulation derangement, and thrombotic microangiopathies.