Abstract
Background: Hantaviruses cause hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS) in humans. Hantavirus infections are characterized by thrombocytopenia. Our objective was to assess the association of thrombocytopenia with disease severity in HFRS induced by Puumala hantavirus (PUUV).
Methods: Altogether 546 patients treated for acute serologically confirmed PUUV infection during 1982–2013 at Tampere University Hospital, Finland, were examined. Blood platelet count was determined daily and analysed in relation to different variables reflecting disease severity. The patients were divided into two groups according to the minimum platelet count: severe thrombocytopenia (<69 × 109/L, i.e. below median) and no severe thrombocytopenia (≥69 × 109/L).
Results: Thrombocytopenia (platelet count <150 × 109/L) was detected in 90% of patients, and in 28% of patients platelet count was <50 × 109/L. Patients with severe thrombocytopenia had longer stay (8 versus 7 days, p = 0.002) and greater weight gain (2.8 versus 2.0 kg, p < 0.001) at the hospital, higher blood leukocyte count (11.2 × 109/L versus 9.6 × 109/L, p < 0.001), plasma C-reactive protein (81 versus 59 mg/L, p < 0.001), maximum hematocrit (0.44 versus 0.42, p < 0.001), urinary protein excretion (1.7 versus 1.1 g/24 h, p = 0.002), and lower plasma albumin concentration (27 versus 32 g/L, p < 0.001) than patients without severe thrombocytopenia (comparisons between medians). Maximum creatinine concentration did not differ between patients with or without severe thrombocytopenia (median 235 versus 214 μmol/L, p = 0.217).
Conclusions: The severity of thrombocytopenia associates with the degree of inflammation and variables reflecting capillary leakage, but not with the severity of acute kidney injury in PUUV infected Finnish patients.
Acknowledgements
The skilful technical assistance of Ms Katriina Ylinikkilä, Ms Reeta Kulmala and Ms Eini Eskola is greatly appreciated.
Disclosure statement
The authors declare that they have no competing interests.
Funding information
This study was financially supported by the Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital (9P031), European Commission Project “Diagnosis and control of rodent-borne viral zoonoses in Europe” (QLK2-CT-2002-01358), Tampere Tuberculosis Foundation, Sigrid Juselius Foundation, and the Finnish Kidney Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.