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J Infect Dis. 2015 Oct 1;212(7):1061-9. doi: 10.1093/infdis/jiv161. Epub 2015 Mar 11.

Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients.

Author information

1
Infectious Diseases, Department of Clinical Microbiology.
2
Infectious Diseases, Department of Clinical Microbiology Clinical Chemistry, Department of Medical Biosciences, Umeå University, Sweden.
3
Clinical Chemistry, Department of Medical Biosciences, Umeå University, Sweden.
4
Clinical Research Centre, Royal College of Surgeons in Ireland, Dublin.
5
Department of Clinical and Experimental Medicine, Linköping University, Sweden.

Abstract

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.

KEYWORDS:

disseminated intravascular coagulation; hantavirus; hemorrhagic fever with renal syndrome; platelets; thrombosis; viral hemorrhagic fever

PMID:
25762786
DOI:
10.1093/infdis/jiv161
[Indexed for MEDLINE]
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