Background: Several studies have evaluated the direct effect of antiphospholipid antibodies in isolated platelets from healthy volunteers, but the literature is scarce about platelet activity obtained from patients with APS.

Aims: To evaluate platelet aggregation from patients with primary APS with thrombosis (t-PAPS) or healthy volunteers with no history of diabetes, hypertension or dyslipidemia.

Methods: Twenty-four patients with t-PAPS (66.6% females, mean age: 38 years) and fifty-three healthy volunteers (58.5% females, mean age: 33 years) were included. Firstly, platelet-rich plasma (PRP) was obtained and stimulated with adenosine diphosphate (ADP, 3 or 10 µM), collagen (1 µg/ml) or arachidonic acid (AA, 300 µM). Next, PRP was pre-incubated with platelets inhibitors, as nitric oxide donor, sodium nitroprusside (SNP, 3 or 10 µM) or the stable analogue of prostacyclin, (iloprost, 3 or 10 nM) and then stimulated with ADP or collagen.

Results: Effect of agonists and inhibitors on platelet-rich plasma (PRP). Platelets from patients with thrombotic primary antiphospholipid syndrome (t-PAPS) or healthy volunteers were stimulated with ADP (3 or 10 µM) (A), collagen (1 µg/mL) or AA (300 µM) (B). Panel C: in another set of experiments, PRP from both groups was pre-incubated with SNP (3 or 10 µM, 3 minutes) or iloprost (3 or 10 nM, 3 minutes) and then stimulated with ADP (3 µM). Data represent the mean ± DP, N=24 (ADP, 3 or 10 µM), 20 (collagen 1 µg/mL), 15 (AA, 300 µM) or 21 (ADP 3 µM with SNP or iloprost) for t-PAPS and N=48 (ADP, 3 or 10 µM), 44 (collagen 1 µg/mL), 32 (AA, 300 µM), 40 (ADP 3 µM with SNP) or 37 (ADP 3 µM with iloprost) for control. For statistical analysis, unpaired t test with Welch’s correction was performed. P<0.05 was considered statistically significant. *P<0.05; **P<0.01.

ADP-induced platelet aggregation was significantly higher in t-PAPS group than in controls (3 µM: 70% ± 26.4% vs 55.5% ± 23.3%, P=0.02; 10 µM: 82% ± 21.3% vs 70% ± 13.4%, P=0.02). No difference in AA- (49.7% ± 37.3% vs 49% ± 29.4%, P=0.95) or collagen- (72% ± 20.9% vs 68.2% ± 18.6%, P=0.51) -induced aggregation was seen between groups. The aggregation inhibition induced by SNP (3 µM: 26.4% ± 40.2% vs 50% ± 26.1%, P=0.001; 10 µM: 50.5% ± 36.5% vs 71.1% ± 20.2%, P=0.004) or iloprost (3 nM: 59.5% ± 39.8% vs 80.7% ± 22.9%, P=0.01) was less prominent in platelets from t-PAPS than in healthy volunteers.  

Conclusions: Our results showed that ADP-induced aggregation was increased and the inhibition induced by endothelial mediators was reduced in platelets from t-PAPS patients when compared to controls. Our findings suggest that platelets activity is increased in t-PAPS and point towards a possible role of the ADP signaling pathway in the thrombotic event seen in these patients.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/platelet-activity-from-antiphospholipid-syndrome-aps-patients-is-enhanced-possible-role-of-the-adp-signaling-pathway/