Outi Laine1, Lotta Joutsi-Korhonen2, Riitta Lassila3, Tomi Koski4, Heini Huhtala5, Antti Vaheri6, Satu Mäkelä7, Jukka Mustonen8. 1. Department of Internal Medicine, Tampere University Hospital, PO Box 2000, 33521 Tampere, Finland; School of Medicine, University of Tampere, 33014 Tampere, Finland. Electronic address: outi.laine@staff.uta.fi. 2. Coagulation Disorders Unit, Clinical Chemistry, HUSLAB Laboratory Services, Helsinki University Hospital, PO Box 372, 00029 Helsinki, Finland. Electronic address: lotta.joutsi-korhonen@hus.fi. 3. Coagulation Disorders Unit, Department of Hematology, Comprehensive Cancer Center, Helsinki University, and Helsinki University Hospital, PO Box 372, 00029 Helsinki, Finland. Electronic address: riitta.lassila@hus.fi. 4. Fimlab Medical Laboratories, Tampere University Hospital, PO Box 66, 33101 Tampere, Finland. Electronic address: tomi.koski@fimlab.fi. 5. School of Health Sciences, University of Tampere, 33014 Tampere, Finland. Electronic address: heini.huhtala@uta.fi. 6. Department of Virology, Faculty of Medicine, University of Helsinki, PO Box 21, 00014 Helsinki, Finland. Electronic address: antti.vaheri@helsinki.fi. 7. Department of Internal Medicine, Tampere University Hospital, PO Box 2000, 33521 Tampere, Finland. Electronic address: satu.marjo.makela@uta.fi. 8. Department of Internal Medicine, Tampere University Hospital, PO Box 2000, 33521 Tampere, Finland; School of Medicine, University of Tampere, 33014 Tampere, Finland. Electronic address: jukka.mustonen@uta.fi.
Abstract
INTRODUCTION: We evaluated the mechanisms of thrombocytopenia encountered in hantavirus disease by studying platelet production together with platelet aggregation and deposition to collagen surface. PATIENTS AND METHODS: The study group consisted of 31 prospectively recruited, consecutive, hospitalized patients having acute Puumala hantavirus infection. Blood samples were collected acutely and at the control visit and subjected to analysis in Sysmex® XE-5000 to capture mean platelet volume (MPV) and immature platelet fraction (IPF%). Platelet aggregation under low shear rate conditions was assessed with impedance aggregometry Multiplate®, whereas platelet function analyzer (PFA)-100® was applied under blood flow of high shear forces. RESULTS: IPF% was 3.1-fold higher acutely compared with the control (median 7.4%, range 2.0-23.8% vs. median 2.4%, range 1.4%-5.2%, p<0.001) tightly associating with the low platelet count (r=-0.76, p<0.001). Accordingly, acute MPV was high (median 11.4f l, range 9.4-13.1 fl vs. median 10.5 fl, range 9.0-12.0 fl, p=0.003). Acute platelet aggregation in Multiplate® was decreased to all agonists compared with the later control (p<0.05 for all agonists). Aggregation capacity associated with thrombocytopenia (for all agonists r ≥ 0.81, p<0.001), but impaired aggregation occurred also among patients with a nearly normal platelet count. Triggered by collagen, 20% of values were below reference range, while 73% of responses were low with thrombin receptor activating peptide. Significantly, under high shear platelet deposition to collagen surface was normal despite thrombocytopenia. CONCLUSIONS: During acute hantavirus disease, platelet aggregation is impaired especially when induced with thrombin. Platelet adhesive mechanisms on collagen are intact despite thrombocytopenia while thrombopoiesis is active.
INTRODUCTION: We evaluated the mechanisms of thrombocytopenia encountered in hantavirus disease by studying platelet production together with platelet aggregation and deposition to collagen surface. PATIENTS AND METHODS: The study group consisted of 31 prospectively recruited, consecutive, hospitalized patients having acute Puumala hantavirus infection. Blood samples were collected acutely and at the control visit and subjected to analysis in Sysmex® XE-5000 to capture mean platelet volume (MPV) and immature platelet fraction (IPF%). Platelet aggregation under low shear rate conditions was assessed with impedance aggregometry Multiplate®, whereas platelet function analyzer (PFA)-100® was applied under blood flow of high shear forces. RESULTS: IPF% was 3.1-fold higher acutely compared with the control (median 7.4%, range 2.0-23.8% vs. median 2.4%, range 1.4%-5.2%, p<0.001) tightly associating with the low platelet count (r=-0.76, p<0.001). Accordingly, acute MPV was high (median 11.4f l, range 9.4-13.1 fl vs. median 10.5 fl, range 9.0-12.0 fl, p=0.003). Acute platelet aggregation in Multiplate® was decreased to all agonists compared with the later control (p<0.05 for all agonists). Aggregation capacity associated with thrombocytopenia (for all agonists r ≥ 0.81, p<0.001), but impaired aggregation occurred also among patients with a nearly normal platelet count. Triggered by collagen, 20% of values were below reference range, while 73% of responses were low with thrombin receptor activating peptide. Significantly, under high shear platelet deposition to collagen surface was normal despite thrombocytopenia. CONCLUSIONS: During acute hantavirus disease, platelet aggregation is impaired especially when induced with thrombin. Platelet adhesive mechanisms on collagen are intact despite thrombocytopenia while thrombopoiesis is active.
Authors: Sirpa Koskela; Satu Mäkelä; Tomas Strandin; Antti Vaheri; Tuula Outinen; Lotta Joutsi-Korhonen; Ilkka Pörsti; Jukka Mustonen; Outi Laine Journal: Viruses Date: 2021-08-06 Impact factor: 5.048
Authors: Johanna Tietäväinen; Outi Laine; Satu Mäkelä; Heini Huhtala; Ilkka Pörsti; Antti Vaheri; Jukka Mustonen Journal: Viruses Date: 2021-11-13 Impact factor: 5.048
Authors: Marlene Tarvainen; Satu Mäkelä; Outi Laine; Ilkka Pörsti; Sari Risku; Onni Niemelä; Jukka Mustonen; Pia Jaatinen Journal: Viruses Date: 2021-09-13 Impact factor: 5.048