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Thromb Haemost. Author manuscript; available in PMC 2012 October 26.
Published in final edited form as:
Thromb Haemost. 2003 July; 90(1): 108–115.
doi: 10.1267/THRO03010108

Table 5

Association of the number of different aPL present, and aPL profiles, with thrombosis for the pooled population (N = 415).

OR (95% CI)
Number of aPL antibodies present (per 1-antibody difference)1.46 (0.93 to 2.27)1.69 (1.14 to 2.50)1.70 (1.16 to 2.51)
 aCL only1.89 (0.55 to 6.46)3.02(1.11 to 8.23)3.13 (1.24 to 7.90)
 LAC only2.43 (0.68 to 8.67)1.63 (0.43 to 6.20)1.99 (0.67 to 5.92)
 aCL + LAC1.05(0.21 to 5.35)6.32 (1.86 to 21.45)3.33 (0.90 to 12.25)
 aCL + aβ2GPI8.20 (0.66 to 102.60)NI2.61 (0.22 to 30.49)
 aCL + LAC + aβ2GPI3.20 (0.60 to 17.18)2.47 (0.45 to 13.40)3.11 (0.65 to 15.04)
*ATE = arterial thrombotic events; VTE = venous thrombotic events; TE = arterial or venous thrombotic events. N = 409, 406, and 409 for the models with ATE, VTE, and TE as the outcomes, respectively.
ATE models are adjusted for study group, family history, sex, hypertension, and age; VTE models are adjusted for study group; and TE models are adjusted for study group, family history, sex, and hypertension.
The reference category was the absence of all three antibodies. NI = not included in the model. The categories “aβ2GPI only” and “LAC + aβ2GPI” were not included in any of the regression models, as none of the subjects with only aβ2GPI had any thrombotic events, and no one had the LAC + aβ2GPI antibody combination. The category “aCL + aβ2GPI” was not included in the model with VTE as the outcome due to a lack of thrombotic events.