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Increased thromboxane formation in patients with antiphospholipid syndrome
L Arfors1, O Vesterqvist, H Johnsson
1Department of Rheumatology, Karolinska Hospital, Stockholm, Sweden.
European Journal of Clinical Investigation
|December 1, 1990
Summary
Patients with IgG antibodies to cardiolipin (ACLA) show significantly increased thromboxane A2 (TxA2) production, indicating platelet activation. This heightened TxA2 may drive thrombosis risk in ACLA patients, suggesting aspirin therapy.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Thrombosis Research
Background:
- Immunoglobulin G (IgG) antibodies to cardiolipin (ACLA) are associated with an increased risk of arterial and venous thrombosis.
- The precise mechanisms linking ACLA to thrombosis are not fully understood, but platelet activation is suspected.
Purpose of the Study:
- To investigate the in vivo formation of thromboxane A2 (TxA2) and prostacyclin (PGI2) in patients with IgG ACLA.
- To determine the pathophysiological relevance of TxA2 and PGI2 production in ACLA-associated thrombosis.
Main Methods:
- Measurement of urinary metabolites of TxA2 (2,3-dinor-TxB2) and PGI2 (2,3-dinor-6-keto-PGF1 alpha) in 31 ACLA patients and healthy controls.
- Utilized gas chromatography-mass spectrometry for precise metabolite quantification.
Main Results:
- Patients with IgG ACLA exhibited a highly significant increase in TxA2 biosynthesis compared to controls (807 +/- 163 vs. 230 +/- 15 pg mg-1 creatinine, P = 0.0000005).
- A significant, though less pronounced, increase in PGI2 formation was also observed in ACLA patients (189 +/- 23 vs. 125 +/- 11 pg mg-1 creatinine, P = 0.03).
Conclusions:
- Elevated TxA2 formation in IgG ACLA patients reflects significant platelet activation.
- The increased TxA2 biosynthesis is likely a key factor in the thrombotic tendency observed in these patients.
- Prophylactic treatment with thromboxane A2 formation inhibitors, such as aspirin, should be considered for patients with IgG ACLA.