Three methods--spontaneous aggregation, ADP-induced aggregation and levels of circulating platelet aggregates--were used to test for platelet hyperaggregation in 87 adult patients divided into three groups. Group A comprised 26 patients with severe arterial diseases, including cerebral vascular accidents (16) and peripheral thrombosis (10) ; group B consisted of 31 patients with venous conditions, including deep phlebitis (22) and recurrent thrombo-embolic disease (9) ; group C, which served as control, comprised 30 patients with various non-vascular disorders. Spontaneous aggregation and enhanced reactivity to ADP correlated well with each other and were more frequent in patients with vascular diseases. However, one-third of patients in group C had pathological results, while one-third of patients in groups A and B had normal results, independently of any clinical particularity or therapeutic regimen. There were no significant differences between the three groups with regard to circulating platelet aggregates. These tests, therefore, appear to be of statistical and epidemiological interest, but of questionable practical value.
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Background: Research on heart injury caused by COVID-19 is limited to large observational and retrospective cohort studies using imaging or pathological data. Reported changes in the levels of myocardial markers in severe diseases have been limited, with few studies on mild infections. The effects of COVID-19 on cardiac function and changes in myocardial marker levels have not yet been reported.
View Article and Find Full Text PDFThromb Haemost
January 2025
Hemostasis and Erythropathology Laboratory, Hematopathology, Pathology Department, Centre de Diagnòstic Biomèdic (CDB), Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Background: V617F-mutated myeloproliferative neoplasms (MPN) exhibit abnormal proliferation of bone marrow progenitors and increased risk of thrombosis, specifically in splanchnic veins (SVT). The contribution of the endothelium to the development of the prothrombotic phenotype was explored.
Material And Methods: Plasma and serum samples from V617F MPN patients with (n=26) or without (n=7) thrombotic debut and different treatments, were obtained (n=33).
Nat Commun
January 2025
Division of Virology, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Microthrombus formation is associated with COVID-19 severity; however, the detailed mechanism remains unclear. In this study, we investigated mouse models with severe pneumonia caused by SARS-CoV-2 infection by using our in vivo two-photon imaging system. In the lungs of SARS-CoV-2-infected mice, increased expression of adhesion molecules in intravascular neutrophils prolonged adhesion time to the vessel wall, resulting in platelet aggregation and impaired lung perfusion.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Hemostasis and Hemostatic Disorders, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.
COVID-19 and post-COVID (long COVID) are associated with thromboembolic complications; however, it is still not clear whether platelets play a leading role in this phenomenon. The platelet hyperreactivity could result from the direct interaction between platelets and viral elements or the response to inflammatory and prothrombotic factors released from blood and vessel cells following infection. The existing literature does not provide clear-cut answers, as the results determining platelet status vary according to methodology.
View Article and Find Full Text PDFJ Transl Med
January 2025
Scientia Clinical Research and Prince of Wales Clinical School, University of New South Wales, Sydney, NSW, 2052, Australia.
Background: A novel anti-human epidermal growth factor receptor 2 (HER2) antibody-drug conjugate (ADC) GQ1001 was assessed in patients with previously treated HER2 positive advanced solid tumors in a global multi-center phase Ia dose escalation trial.
Methods: In this phase Ia trial, a modified 3 + 3 study design was adopted during dose escalation phase. Eligible patients were enrolled, and GQ1001 monotherapy was administered intravenously every 3 weeks.
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