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Decreased fibrinolytic activity in juvenile chronic arthritis
L Mussoni1, G Pintucci, G Romano
1Istituto di Ricerche, Farmacologiche Mario Negri, Milan, Italy.
Insights
Children with juvenile chronic arthritis (JCA) exhibit reduced fibrinolytic activity and increased plasminogen activator inhibitor. Systemic JCA may involve endothelial cell dysfunction, indicated by elevated tissue-type plasminogen activator levels.
Area of Science:
- Rheumatology
- Hematology
- Pediatrics
Background:
- Juvenile chronic arthritis (JCA) is a significant autoimmune condition in children.
- Fibrinolytic system dysregulation may play a role in inflammatory diseases.
Purpose of the Study:
- To investigate basal fibrinolytic activity in children with active JCA.
- To explore differences in fibrinolysis among JCA subtypes.
Main Methods:
- Assessed plasma fibrinolytic activity in 17 children with active JCA.
- Measured levels of plasminogen activator inhibitor (PAI).
- Quantified circulating tissue-type plasminogen activator (t-PA) and endothelial cell protein.
Main Results:
- Patients with JCA showed decreased fibrinolytic activity.
- Systemic JCA demonstrated a marked increase in plasminogen activator inhibitor.
- Systemic JCA patients had elevated circulating tissue-type plasminogen activator and endothelial cell protein.
Conclusions:
- Children with JCA, especially the systemic form, have impaired fibrinolysis.
- Increased PAI suggests a prothrombotic tendency in JCA.
- Elevated t-PA and endothelial markers in systemic JCA point to potential endothelial cell involvement.
Abstract:
The basal fibrinolytic activity in 17 children with active juvenile chronic arthritis (JCA) was investigated. It was found that patients with JCA, and particularly those with the systemic form, show decreased plasma fibrinolytic activity and a marked increase in plasminogen activator inhibitor. Additionally, it was found that patients with systemic JCA, but not those with the polyarticular or pauciarticular form, have increased circulating levels of tissue-type plasminogen activator, and endothelial cell protein, suggesting possible endothelial cell participation in systemic JCA.