Platelet reactivity, inflammation and endothelial dysfunction during and after exacerbation in chronic obstructive pulmonary disease (COPD) patients

Platelet reactivity, inflammation and endothelial dysfunction during and after exacerbation in chronic obstructive pulmonary disease (COPD) patients - IMPROVE study

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

NL-OMON

Registry ID

NL-OMON46302

Enrollment

Registered

2018-10-23

Start date

2018-11-20

Completion date

Unknown

Last updated

2024-04-15

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Chronic Obstructive Pulmonary Disease COPD

Interventions

None listed

Eligibility

Age

18 Years to 99 Years

Inclusion criteria

Inclusion criteria: * Acute exacerbation of COPD, defined as an as an acute worsening of respiratory symptoms that results in additional therapy (COPD Gold 2018) * >40 years oud * Moderate to severe (>Gold 2) airflow limitation detected by spirometry (FEV1/FVC ratio

Exclusion criteria

Exclusion criteria: * Suspected or proven alternative diagnosis for the acute deterioration in symptoms such as pneumonia, pulmonary embolism or heart failure * Use of anti-coagulants, aspirin or other platelet function inhibitors * Use of statins or ACE inhibitors * Concomitant diagnosis of asthma or other respiratory disease * Diagnosis of hepatic and/or renal failure * Chronic inflammatory diseases, such as rheumatoid arthritis, psoriasis, inflammatory bowel diseases, systemic lupus erythematous (SLE), diabetes mellitus (DM) * Malignancies (excluding basal cell carcinoma of the skin)

Design outcomes

Primary

Measure	Time frame
The primary study outcome is platelet activation/reactivity, expressed as the membrane expression of the platelet activation markers CD62P (P-selectin) and activation of integrin IIb3, following ex vivo stimulation with platelet agonists ADP, CRP and TRAP.	—

Secondary

Measure	Time frame
Secondary study parameters: * Platelet-monocyte complexes (PMCs) and monocyte MAC-1 expression (MAC-1 supports interaction with platelets) * Soluble (plasma) markers of endothelial dysfunction: vWF antigen (vWF:Ag), vWF ristocetin cofactor activity (vWF:RCo), vWF propeptide (vWF:pp), active vWF (vWF:act) * Soluble (plasma) markers of inflammation (leukocyte count, IL-6, IL-1B, CRP, fibrinogen) and hypoxemia (VEGF) * Plasmatic coagulation: Thrombin generation, stimulated by 0, 1, 5 pM TF and thrombomodulin (TM), described by the three main parameters lag time (clotting time), peak (max thrombin generation) and endogenous thrombin potential (ETP, area under the thrombin-time curve). Coagulation factor VIII (FVIII) and D-dimer. * Clinical parameters; hypoxemia at presentation (i.e. SO2	—

Measure

Time frame

Secondary study parameters: * Platelet-monocyte complexes (PMCs) and monocyte MAC-1 expression (MAC-1 supports interaction with platelets) * Soluble (plasma) markers of endothelial dysfunction: vWF antigen (vWF:Ag), vWF ristocetin cofactor activity (vWF:RCo), vWF propeptide (vWF:pp), active vWF (vWF:act) * Soluble (plasma) markers of inflammation (leukocyte count, IL-6, IL-1B, CRP, fibrinogen) and hypoxemia (VEGF) * Plasmatic coagulation: Thrombin generation, stimulated by 0, 1, 5 pM TF and thrombomodulin (TM), described by the three main parameters lag time (clotting time), peak (max thrombin generation) and endogenous thrombin potential (ETP, area under the thrombin-time curve). Coagulation factor VIII (FVIII) and D-dimer. * Clinical parameters; hypoxemia at presentation (i.e. SO2

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Countries

Netherlands

Outcome results