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Novel coronavirus pneumonia: abnormal coagulation parameters are associated with poor prognosis


Since December 2019, novel coronavirus pneumonia ( NCP ) cases have emerged in Wuhan, China, and the 2019 novel coronavirus ( 2019‐nCoV ) was confirmed as the cause of the novel coronavirus pneumonia.
The number of infected patients in China has increased rapidly.
In previous reports, the clinical characteristics of novel coronavirus pneumonia patients have been investigated, the reported mortalities were 4.3%, 11.0%, and 14.6%, respectively; organ dysfunction and coagulopathy were associated with high mortality.

However, the complete coagulation parameters of novel coronavirus pneumonia cases were not fully reported, which may have prognostic values and be important therapeutic targets.

A study has shown the coagulation parameters of consecutive NCP cases in Tongji hospital ( Huazhong University of Science and Technology, Wuhan, China ) and the differences between survivors and non‐survivors were investigated.

There were 183 patients ( 85 females and 98 males ) with novel coronavirus pneumonia enrolled into the study, and these patients had complete clinical information and the laboratory data required for this study.
The mean age at disease onset was 54.1 years ( range, 14‐94 years ).
Seventy‐five ( 41.0% ) patients had chronic diseases, including cardiovascular and cerebrovascular diseases, respiratory system disease, malignant tumor, chronic liver and kidney disease, and others.
All patients received antiviral and supportive therapies after diagnosis.

By the end of February 13, 78 ( 42.6% ) patients had been discharged and 21 ( 11.5% ) patients had died, the rest 84 ( 45.9% ) of the patients remained hospitalized in stable condition.

The coagulation parameters on admission between survivors and non‐survivors were compared.
The reportable range of D‐dimer and FDP were 0.22‐21.00 µg/mL and 4.0‐150.0 µg/mL, respectively.
The dynamic changes in coagulation parameters were tracked from day 1 to day 14 after admission at three‐day intervals.

According to the International Society on Thrombosis and Haemostasis ( ISTH ) diagnostic criteria for disseminated intravascular coagulation ( DIC ),15 ( 71.4% ) of the non‐survivors matched the grade of overt‐DIC ( greater than or equal to 5 points ) in later stages of novel coronavirus pneumonia, the median time from admission to DIC was 4 days ( range, 1‐12 days ).
On the contrary, only one ( 0.6% ) survivor matched the DIC criteria during hospital stay.

In the enrolled patients with novel coronavirus pneumonia, the non‐survivors revealed significantly higher D‐dimer and FDP levels, and longer PT compared to survivors on admission.
By the late hospitalization, the fibrinogen and AT levels were also significantly lower in non‐survivors; this suggested that conventional coagulation parameters during the course of novel coronavirus pneumonia were significantly associated with prognosis.

DIC appeared in most of the deaths. Patients presenting with a virus infection may develop into sepsis associated with organ dysfunction.
Sepsis is well established as one of the most common causes of DIC; development of DIC results when monocytes and endothelial cells are activated to the point of cytokine release following injury, with expression of tissue factor and secretion of von Willebrand factor.
Circulation of free thrombin, uncontrolled by natural anticoagulants, can activate platelets and stimulate fibrinolysis.
At the late stages of novel coronavirus pneumonia, levels of fibrin‐related markers ( D‐dimer and FDP ) moderately or markedly elevated in all deaths, which suggested a common coagulation activation and secondary hyperfibrinolysis condition in these patients.

In a previous study, Gralinski et al ( mBio 2013 ) investigated viral pathogenesis and identified a novel host pathway involved in severe acute respiratory syndrome ( SARS )‐coronavirus disease progression.
The data have suggested that dysregulation of the urokinase pathway during SARS‐coronavirus infection contributes to more severe lung pathology and that plasminogen activator inhibitor‐1 plays a protective role following infection.
In addition, Fatma Berri et al ( PLoS Pathog 2013 ) reported that plasminogen contributes to inflammation caused by influenza through fibrinolysis, and 6‐aminocaproic acid can protect against influenza.
Presumably, fibrinolysis may also be induced following severe 2019‐nCoV infection.

The limitations of this report included that, as a relatively small, single‐center study, the mortality and characteristics of enrolled patients may not be representative; these findings should be confirmed in an adequately powered clinical study. ( Xagena )

Tang N et al, J Thromb Haemost 2020;18:844-847

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