D-dimer cut-off points and risk of venous thromboembolism in adult hospitalized patients with COVID-19

Choi, Justin; Wehmeyer, Graham T; Li, Han A; Alshak, Mark N.; Nahid, Musarrat; Rajan, Mangala; Liu, Bethina; Schatoff, Emma M.; Elahjji, Rahmi; Abdelghany, Youmna; D’Angelo, Debra; Crossman, Daniel J; Evans, Arthur T.; Steel, Peter; Pinheiro, Laura C.; Goyal, Parag; Safford, Monika M.; Mints, Gregory; DeSancho, Maria T.

doi:10.1016/j.thromres.2020.09.022

Cited by 52 publications

(57 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 123 COVID‐19 patients with VTE during hospitalization, D‐dimer was associated with the risk of VTE, with OR 1.09 (95%CI: 1.06−1.11) for every 1 μg/ml increase of D‐dimer. The OR for D‐dimer > 7.5 μg/ml was 4.1 (95%CI: 2.94−5.71) 191 . However, our previous study involving 127 severe COVID‐19 patients did not identify D‐dimer as a risk factor for mortality after adjusting according to age for each patient 3 …”

Section: Laboratory Indicatorsmentioning

confidence: 89%

Risk factors for severe and critically ill COVID‐19 patients: A review

Gao

Ding

Dong

et al. 2020

Allergy

1,161

864

View full text Add to dashboard Cite

The pandemic of coronavirus disease 2019 (COVID‐19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has caused an unprecedented global social and economic impact, and high numbers of deaths. Many risk factors have been identified in the progression of COVID‐19 into a severe and critical stage, including old age, male gender, underlying comorbidities such as hypertension, diabetes, obesity, chronic lung diseases, heart, liver and kidney diseases, tumors, clinically apparent immunodeficiencies, local immunodeficiencies, such as early type I interferon secretion capacity, and pregnancy. Possible complications include acute kidney injury, coagulation disorders, thoromboembolism. The development of lymphopenia and eosinopenia are laboratory indicators of COVID‐19. Laboratory parameters to monitor disease progression include lactate dehydrogenase, procalcitonin, high‐sensitivity C‐reactive protein, proinflammatory cytokines such as interleukin (IL)‐6, IL‐1β, Krebs von den Lungen‐6 (KL‐6), and ferritin. The development of a cytokine storm and extensive chest computed tomography imaging patterns are indicators of a severe disease. In addition, socioeconomic status, diet, lifestyle, geographical differences, ethnicity, exposed viral load, day of initiation of treatment, and quality of health care have been reported to influence individual outcomes. In this review, we highlight the scientific evidence on the risk factors of severity of COVID‐19.

show abstract

Section: Laboratory Indicatorsmentioning

confidence: 89%

Risk factors for severe and critically ill COVID‐19 patients: A review

Gao

Ding

Dong

et al. 2020

Allergy

1,161

864

View full text Add to dashboard Cite

show abstract

“…In early studies on COVID‐19, the most typical finding was a higher D‐dimer concentration on admission in patients with VTE than that in those without VTE 18,21,26 . Therefore, D‐dimer on admission was considered a diagnostic marker for VTE in COVID‐19 40 . Nevertheless, D‐dimer has a low specificity, and we have observed that many patients with a high D‐dimer level would not necessarily develop a symptomatic VTE if the level kept stable or increased slowly.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics and risk factors for symptomatic venous thromboembolism in hospitalized COVID‐19 patients: A multicenter retrospective study

Wang

Yin

et al. 2021

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

Background: High incidence of asymptomatic venous thromboembolism (VTE) has been observed in severe COVID-19 patients, but the characteristics of symptomatic VTE in general COVID-19 patients have not been described. Objectives: To comprehensively explore the prevalence and reliable risk prediction for VTE in COVID-19 patients. Methods/Results: This retrospective study enrolled all COVID-19 patients with a subsequent VTE in 16 centers in China from January 1 to March 31, 2020. A total of 2779 patients were confirmed with COVID-19. In comparison to 23,434 non-COVID-19 medical inpatients, the odds ratios (ORs) for developing symptomatic VTE in severe and non-severe hospitalized COVID-19 patients were 5.94 (95% confidence interval [CI] 3.91-10.09) and 2.79 (95% CI 1.43-5.60), respectively. When 104 VTE cases and 208 non-VTE cases were compared, pulmonary embolism cases had a higher rate for in-hospital death (OR 6.74, 95% CI 2.18-20.81). VTE developed at a median of 21 days (interquartile range 13.25-31) since onset. Independent factors for VTE were advancing age, cancer, longer interval from symptom onset to admission, lower fibrinogen and higher D-dimer on admission, and D-dimer increment (DI) ≥1.5-fold; of these, DI ≥1.5-fold had the most significant association (OR 14.18, 95% CI 6.25-32.18, p = 2.23 × 10 −10). A novel model consisting of three simple coagulation variables (fibrinogen and D-dimer levels on admission, and DI ≥1.5-fold) showed good prediction for symptomatic VTE (area under the curve 0.865, 95% CI 0.822-0.907, sensitivity 0.930, specificity 0.710). Conclusions: There is an excess risk of VTE in hospitalized COVID-19 patients. This novel model can aid early identification of patients who are at high risk for VTE.

show abstract

“…Vascular injury has been linked to COVID-19 acute respiratory distress syndrome (ARDS) (1,2), including the vascular complications of inflammation and thrombosis. Consistent with this, COVID-19 induced injury to the vascular compartment has been associated with complement activation and micro-thrombosis (3)(4)(5), systemic thrombosis (4,6), and to dysregulated immune responses (7)(8)(9). However, this focus on inflammation and thrombosis limits our insights into other disruptions associated with aberrant vascular activation.…”

Section: Introductionmentioning

confidence: 75%

The maladaptive vascular response in COVID-19 acute respiratory distress syndrome and recovery

Price

Benedetti

Hoffman

et al. 2021

Preprint

View full text Add to dashboard Cite

Vascular injury is a menacing element of acute respiratory distress syndrome (ARDS) pathogenesis. To better understand the role of vascular injury in COVID-19 ARDS, we used lung autopsy immunohistochemistry and blood proteomics from COVID-19 subjects at distinct timepoints in disease pathogenesis, including a hospitalized cohort at risk of ARDS development ("at risk", N=59), an intensive care unit cohort with ARDS ("ARDS", N=31), and a cohort recovering from ARDS ("recovery", N=12). COVID-19 ARDS lung autopsy tissue revealed an association between vascular injury and platelet-rich microthrombi. This link guided the derivation of a protein signature in the at risk cohort characterized by lower expression of vascular proteins in subjects who died, an early signal of vascular limitation termed the maladaptive vascular response. These findings were replicated in COVID-19 ARDS subjects, as well as when bacterial and influenza ARDS patients (N=29) were considered, hinting at a common final pathway of vascular injury that is more disease (ARDS) then cause (COVID-19) specific, and may be related to vascular cell death. Among recovery subjects, our vascular signature identified patients with good functional recovery one year later. This vascular injury signature could be used to identify ARDS patients most likely to benefit from vascular targeted therapies.

show abstract

D-dimer cut-off points and risk of venous thromboembolism in adult hospitalized patients with COVID-19

Cited by 52 publications

References 10 publications

Risk factors for severe and critically ill COVID‐19 patients: A review

Risk factors for severe and critically ill COVID‐19 patients: A review

Clinical characteristics and risk factors for symptomatic venous thromboembolism in hospitalized COVID‐19 patients: A multicenter retrospective study

The maladaptive vascular response in COVID-19 acute respiratory distress syndrome and recovery

Contact Info

Product

Resources

About