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Neutrophils and deep venous thrombosis
1Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pa 19140.
Haemostasis
|March 1, 1993
Summary
Polymorphonuclears (PMN) play a role in venous thrombosis. Inhibiting PMN adhesion may prevent deep venous thrombosis (DVT), offering a new therapeutic strategy.
Area of Science:
- Vascular biology
- Hematology
- Immunology
Background:
- Polymorphonuclears (PMN) are implicated in the initiation and progression of venous thrombosis.
- Leukocyte adhesion to veins is observed in animal models at sites of thrombus formation.
- PMN interaction with platelets in thrombi may promote coagulation and thrombus development.
Purpose of the Study:
- To explore the role of PMN in venous thrombosis.
- To investigate potential therapeutic strategies targeting PMN adhesion in deep venous thrombosis (DVT).
Main Methods:
- Review of animal models demonstrating leukocyte adhesion to veins.
- Analysis of clinical data on lidocaine's effect on DVT incidence post-hip replacement.
- Examination of studies on adhesive receptors (integrins, ICAMs, selectins) and monoclonal antibody interventions.
- Consideration of PMN and platelet adhesion to fibrin.
Main Results:
- Lidocaine and derivatives inhibited leukocyte adhesion in canine models.
- Lidocaine reduced DVT incidence in patients after hip replacement.
- Monoclonal antibodies against beta 2-integrins decreased leukocyte adhesion and injury in animal models.
- Selectin ligands suggest potential for small molecule inhibitors of PMN adhesion.
Conclusions:
- PMN adhesion is a key factor in venous thrombosis.
- Targeting PMN adhesion mechanisms, particularly involving integrins and selectins, presents a promising avenue for DVT prevention.
- Further research into PMN-fibrin interactions could yield novel therapeutic targets.