Figure 1
Figure 1. AnxA5 resistance in relation to aPL antibodies with different specificities. To determine the effects of different plasma samples on AnxA5 activity, a 2-stage PT reagent-phospholipid coagulation assay was used. The coagulation times, in the presence and absence of AnxA5 were measured; the anticoagulant activity of AnxA5 was calculated as follows: AnxA5 anticoagulant ratio = (coagulation time in the presence of AnxA5/coagulation time in the absence of AnxA5) × 100%. (A) The absolute coagulation times found with or without AnxA5 specified for the 4 groups. Horizontal bars indicate the mean ratio of the patients in different groups. (B) The AnxA5 anticoagulant ratio was significantly lower for patients who displayed a β2GPI-dependent LAC (group A: mean, 157%) compared to patients displaying a β2GPI-independent LAC (group B: mean, 235%; P < .001), patients without LAC (group C: mean, 232%; P < .001), or healthy controls (group D: mean, 247%: P < .001).

AnxA5 resistance in relation to aPL antibodies with different specificities. To determine the effects of different plasma samples on AnxA5 activity, a 2-stage PT reagent-phospholipid coagulation assay was used. The coagulation times, in the presence and absence of AnxA5 were measured; the anticoagulant activity of AnxA5 was calculated as follows: AnxA5 anticoagulant ratio = (coagulation time in the presence of AnxA5/coagulation time in the absence of AnxA5) × 100%. (A) The absolute coagulation times found with or without AnxA5 specified for the 4 groups. Horizontal bars indicate the mean ratio of the patients in different groups. (B) The AnxA5 anticoagulant ratio was significantly lower for patients who displayed a β2GPI-dependent LAC (group A: mean, 157%) compared to patients displaying a β2GPI-independent LAC (group B: mean, 235%; P < .001), patients without LAC (group C: mean, 232%; P < .001), or healthy controls (group D: mean, 247%: P < .001).

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