Enhanced thrombin formation and fibrinolysis during acute Puumala hantavirus infection

Laine, Outi; Mäkelä, Satu; Mustonen, Jukka; Huhtala, Heini; Szántó, Tímea; Vaheri, Antti; Lassila, Riitta; Joutsi‐Korhonen, Lotta

doi:10.1016/j.thromres.2010.05.025

Cited by 71 publications

(93 citation statements)

References 24 publications

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“…HFRS patients have abnormal coagulation with elevated thrombosis and fibrinolysis 9 and disseminated intravascular coagulopathy. 10 Additionally, hantavirus infection seems to have a negative impact on heart functions; cardiac disturbances have been observed in more than half of the HFRS patients.…”

Section: Discussionmentioning

confidence: 99%

Increased Risk of Acute Myocardial Infarction and Stroke During Hemorrhagic Fever With Renal Syndrome

et al. 2014

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G lobally, cardiovascular diseases (CVDs) are the leading cause of death and a major source of disability. The majority of these are caused by ischemic heart disease such as acute myocardial infarction (AMI), stroke, and other cerebrovascular diseases.1 Several factors, including infectious diseases, have been associated with increased risk for CVD. [2][3][4][5][6] The host inflammatory response to infection often results in release of proinflammatory cytokines and activation of platelets, leukocytes, and endothelial cells that can activate procoagulant pathways and can inhibit anticoagulant pathways. 2,3 This can tip the balance of hemostasis toward a prothrombotic state, laying the foundation for acute cardiovascular events such as AMI and stroke. 2,3 Clinical Perspective on p 1302Viral hemorrhagic fevers are characterized by fever, hemorrhages, and shock. Abnormal coagulation and vascular dysfunction are common observations during viral hemorrhagic fevers, 7 which could be risk factors for CVD. Four viral families contain members that cause viral hemorrhagic fevers: Bunyaviridae, Flaviviridae, Filoviridae and Arenaviridae. Pathogenic hantaviruses in the Bunyaviridae family cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus cardiopulmonary syndrome in the Americas.8 HFRS caused by Puumala virus is considered a mild viral hemorrhagic fever 7 characterized by thrombocytopenia, enhanced coagulation and fibrinolysis, 9 and disseminated intravascular coagulopathy. 10In a highly endemic area for Puumala virus in Northern Sweden, we observed a tendency of HFRS patients to develop acute cardiovascular events. Furthermore, we have recently shown that CVD is a common cause of death during acute HFRS in Sweden.11 Together, these findings suggest a possible association between acute HFRS and CVD. Therefore, we decided to investigate in more detail whether HFRS is a risk factor for CVD. To test this, we compared the incidence of AMI and stroke Background-We recently observed that cardiovascular causes of death are common in patients with hemorrhagic fever with renal syndrome (HFRS), which is caused by hantaviruses. However, it is not known whether HFRS is a risk factor for the acute cardiovascular events of acute myocardial infarction (AMI) and stroke. Methods and Results-Personal identification numbers from the Swedish HFRS patient database (1997-2012; n=6643) were cross-linked with the National Patient Register from 1987 to 2011. Using the self-controlled case series method, we calculated the incidence rate ratio of AMI/stroke in the 21 days after HFRS against 2 different control periods either excluding (analysis 1) or including (analysis 2) fatal AMI/stroke events. The incidence rate ratios for analyses 1 and 2 for all AMI events were 5.53 (95% confidence interval [CI], 2.6-11.8) and 6.02 (95% CI, 2.95-12.3) and for first AMI events were 3.53 (95% CI, 1.25-9.96) and 4.64 (95% CI, 1.83-11.77). The incidence rate ratios for analyses 1 and 2 for all stroke events were 12.93 (95% CI, 5.62-29.74)...

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Section: Discussionmentioning

confidence: 99%

Increased Risk of Acute Myocardial Infarction and Stroke During Hemorrhagic Fever With Renal Syndrome

et al. 2014

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“…Increased thrombin formation together with remarkable fibrinolysis and decreased natural anticoagulants has been documented. [10] Platelet ligands von Willebrand factor, fibrinogen, and fibronectin are also altered. [11] These findings support the role of activated platelets and endothelium in the pathogenesis of hantavirus infections.…”

Section: Introductionmentioning

confidence: 99%

Thrombocytopenia associates with the severity of inflammation and variables reflecting capillary leakage in Puumala Hantavirus infection, an analysis of 546 Finnish patients

Outinen

Laine

Mäkelä

et al. 2016

Infectious Diseases

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“…PTX3 could be involved in the pathogenesis of thrombocytopenia in NE through the activation of the complement system, which, in turn, activates the coagulation system and leads to thrombocytopenia through the consumption of the platelets [38]. Recently, it has been shown that thrombin formation and fibrinolysis are enhanced in NE [20].…”

Section: Discussionmentioning

confidence: 99%

“…We have also previously studied complement activation in NE in the same cohort of 61 patients [11]. Furthermore, 19 of the patients in the present study were also included in a study that examined the activation of coagulation and fibrinolysis in NE [20].…”

Section: Patientsmentioning

confidence: 93%

High pentraxin-3 plasma levels associate with thrombocytopenia in acute Puumala hantavirus-induced nephropathia epidemica

Outinen

Mäkelä

Huhtala

et al. 2011

Eur J Clin Microbiol Infect Dis

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Our aim was to investigate whether plasma levels of the long pentraxin-3 (PTX3) associate with the severity of Puumala hantavirus-induced nephropathia epidemica (NE). Sixty-one prospectively identified consecutively hospitalized NE patients were examined. Plasma PTX3, interleukin (IL)-6, terminal complement complex SC5b-9, complement component C3, C-reactive protein (CRP), creatinine, sodium, kynurenine, and tryptophan levels, as well as the blood cell count, were determined for up to five consecutive days after hospitalization. Receiver operating characteristic (ROC) analysis revealed that the maximum PTX3 level >101.6 ng/ml (high PTX3) showed a sensitivity of 71% and a specificity of 89% for detecting platelet level <50 × 10(9)/l, with an area under the curve (AUC) value of 0.78 (95% confidence interval [CI] 0.63-0.94). High PTX3 level was also associated with several other variables reflecting the severity of the disease: patients with high PTX3 level had higher maximum blood leukocyte (16.1 vs. 9.7 × 10(9)/l, p < 0.001), plasma IL-6 (16.9 vs. 9.0 pg/ml, p = 0.007), and creatinine (282 vs. 124 μmol/l, p = 0.007) levels than patients with low maximum PTX3 level. They also had longer hospital stays (8 vs. 5 days, p = 0.015) compared to patients with low PTX3 level. High plasma PTX3 levels are associated with thrombocytopenia and the overall severity of NE.

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Enhanced thrombin formation and fibrinolysis during acute Puumala hantavirus infection

Cited by 71 publications

References 24 publications

Increased Risk of Acute Myocardial Infarction and Stroke During Hemorrhagic Fever With Renal Syndrome

Increased Risk of Acute Myocardial Infarction and Stroke During Hemorrhagic Fever With Renal Syndrome

Thrombocytopenia associates with the severity of inflammation and variables reflecting capillary leakage in Puumala Hantavirus infection, an analysis of 546 Finnish patients

High pentraxin-3 plasma levels associate with thrombocytopenia in acute Puumala hantavirus-induced nephropathia epidemica

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