Ignite Creation Date:
2025-12-25 @ 2:12 AM
Ignite Modification Date:
2025-12-27 @ 12:20 PM
Study NCT ID:
NCT05380960
Status:
UNKNOWN
Last Update Posted:
2022-05-19
First Post:
2022-05-14
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Blood Hpercoagublity in Copd
Sponsor:
Assiut University
Organization:
Study Overview
Official Title:
A Study on the State of Coagulability in Patients With Chronic Obstructive Disease Admitted to Assiut University Hospital
Status:
UNKNOWN
Status Verified Date:
2022-05
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
"The objective of this study is to evaluate the blood coagulability state in patients with COPD admitted at Assiut University Hospital"
Detailed Description:
Chronic Obstructive Pulmonary Disease (COPD) is a chronic debilitating lung disease with a high prevalence of approximately 380 million cases worldwide \[1\]. It is currently the third leading cause of death, responsible for approximately 6% of the world's total deaths (approximately 3.3 million annually) \[2\]. In addition to the known devastating respiratory consequences, a large number of studies support the hypothesis that COPD increases the risk for both venous thromboembolism (VTE) and cardiovascular disease (CVD) Although the observed association of COPD with CVD and VTE can be partially explained by comorbidities and shared risk factors, there is strong evidence that COPD increases the risk for cardiovascular morbidity and mortality independently of age, gender, and smoking history \[3,4\]. It is of note that up to 63.5% of patients with COPD die of comorbid circulatory system diseases \[5\].
Increased thrombin formation \[6\] , reflected by elevated thrombin-antithrombin com- plexes \[7\] , tissue factor procoagulant activity \[8\] and activated factor XI \[9\] , increased d-dimers \[10\] , and FI \[11\] , FII and FX \[12\] levels in the serum of COPD patients support the theory that a hypercoagulable state occurs in patients with COPD and might contribute to the incidence of atherothrombotic events and VTE, increasing disease related morbidity and mortality.
Potential pathways illustrating pathogenetic mechanisms of increased risk of CVD and VTE in COPD are imprecise. Evidence illustrates four possible synergistic mechanisms: systemic inflammation \[13\], platelet activation \[14\] , oxidative stress \[15\], and hypoxia, either sustained in severe COPD or intermittent during exercise and sleep \[16,17\]
Increased thrombin formation \[6\] , reflected by elevated thrombin-antithrombin com- plexes \[7\] , tissue factor procoagulant activity \[8\] and activated factor XI \[9\] , increased d-dimers \[10\] , and FI \[11\] , FII and FX \[12\] levels in the serum of COPD patients support the theory that a hypercoagulable state occurs in patients with COPD and might contribute to the incidence of atherothrombotic events and VTE, increasing disease related morbidity and mortality.
Potential pathways illustrating pathogenetic mechanisms of increased risk of CVD and VTE in COPD are imprecise. Evidence illustrates four possible synergistic mechanisms: systemic inflammation \[13\], platelet activation \[14\] , oxidative stress \[15\], and hypoxia, either sustained in severe COPD or intermittent during exercise and sleep \[16,17\]
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: