umu.sePublications
Change search
ReferencesLink to record
Permanent link

Direct link
Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology. Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry. Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases.
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Infectious Diseases. (Arcum)
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
Show others and affiliations
2015 (English)In: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, no 7, 1061-1069 p.Article in journal (Refereed) Published
Abstract [en]

Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation. Methods. Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications. Results. The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

Place, publisher, year, edition, pages
Oxford University Press, 2015. Vol. 212, no 7, 1061-1069 p.
Keyword [en]
disseminated intravascular coagulation, hantavirus, hemorrhagic fever with renal syndrome, platelets, thrombosis, viral hemorrhagic fever
National Category
Public Health, Global Health, Social Medicine and Epidemiology Infectious Medicine
Identifiers
URN: urn:nbn:se:umu:diva-111492DOI: 10.1093/infdis/jiv161ISI: 000363191300007PubMedID: 25762786OAI: oai:DiVA.org:umu-111492DiVA: diva2:875966
Available from: 2015-12-02 Created: 2015-11-13 Last updated: 2016-05-24Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

Search in DiVA

By author/editor
Connolly-Andersen, Anne-MarieSundberg, ErikAhlm, ClasHultdin, JohanBaudin, MariaLarsson, JohannaNilsson, Sofie
By organisation
VirologyInfectious DiseasesClinical chemistry
In the same journal
Journal of Infectious Diseases
Public Health, Global Health, Social Medicine and EpidemiologyInfectious Medicine

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 40 hits
ReferencesLink to record
Permanent link

Direct link