Logistic regression analyses of inhibitor risk
| . | Race* . | INH(−) . | INH(+)† . | Adjusted OR‡ . | 95% CI . | P . |
|---|---|---|---|---|---|---|
| Model 1: 347 AA + W subjects,§age 4+ y | ||||||
| H3 + H4 + H5 | AA + W | 19 | 11 | 1.2 | 0.5-2.8 | .7 |
| H1 + H2 | AA + W | 224 | 93 | |||
| Potentially exposed to “sequence-mismatched” FVIII¶ | AA + W | 198 | 92 | 2.3 | 1.1-4.8 | .03 |
| Not exposed to “sequence-mismatched” FVIII | AA + W | 45 | 12 | |||
| Intron-22 inversion (+) | AA | 30 | 25 | 2.3 | 1.1-5.0 | .04 |
| Intron-22 inversion (+) | W | 67 | 24 | |||
| Intron-22 inversion (−) | AA | 57 | 25 | 1.4 | 0.7-3.0 | .3 |
| Intron-22 inversion (−) | W | 65 | 18 | |||
| Intron-22 inversion (unknown) | AA | 20 | 8 | 0.3 | 0.07-1.7 | .2 |
| Intron-22 inversion (unknown) | W | 4 | 4 | |||
| Model 2: 165 AA subjects, age 4+ y | ||||||
| H3 + H4 + H5 | AA | 18 | 11 | 1.3 | 0.5-3.1 | .6 |
| H1 + H2 | AA | 89 | 47 | |||
| Potentially exposed to “sequence-mismatched” FVIII | AA | 81 | 51 | 2.9 | 1.1-7.5 | .026 |
| Not exposed to “sequence-mismatched” FVIII | AA | 26 | 7 | |||
| Intron-22 inversion (+) | AA | 30 | 25 | 2.5 | 1.0-7.0 | .7 |
| Intron-22 inversion (−) | AA | 57 | 25 | 1.2 | 0.4-3.0 | .7 |
| Intron-22 inversion (unknown) | AA | 20 | 8 |
| . | Race* . | INH(−) . | INH(+)† . | Adjusted OR‡ . | 95% CI . | P . |
|---|---|---|---|---|---|---|
| Model 1: 347 AA + W subjects,§age 4+ y | ||||||
| H3 + H4 + H5 | AA + W | 19 | 11 | 1.2 | 0.5-2.8 | .7 |
| H1 + H2 | AA + W | 224 | 93 | |||
| Potentially exposed to “sequence-mismatched” FVIII¶ | AA + W | 198 | 92 | 2.3 | 1.1-4.8 | .03 |
| Not exposed to “sequence-mismatched” FVIII | AA + W | 45 | 12 | |||
| Intron-22 inversion (+) | AA | 30 | 25 | 2.3 | 1.1-5.0 | .04 |
| Intron-22 inversion (+) | W | 67 | 24 | |||
| Intron-22 inversion (−) | AA | 57 | 25 | 1.4 | 0.7-3.0 | .3 |
| Intron-22 inversion (−) | W | 65 | 18 | |||
| Intron-22 inversion (unknown) | AA | 20 | 8 | 0.3 | 0.07-1.7 | .2 |
| Intron-22 inversion (unknown) | W | 4 | 4 | |||
| Model 2: 165 AA subjects, age 4+ y | ||||||
| H3 + H4 + H5 | AA | 18 | 11 | 1.3 | 0.5-3.1 | .6 |
| H1 + H2 | AA | 89 | 47 | |||
| Potentially exposed to “sequence-mismatched” FVIII | AA | 81 | 51 | 2.9 | 1.1-7.5 | .026 |
| Not exposed to “sequence-mismatched” FVIII | AA | 26 | 7 | |||
| Intron-22 inversion (+) | AA | 30 | 25 | 2.5 | 1.0-7.0 | .7 |
| Intron-22 inversion (−) | AA | 57 | 25 | 1.2 | 0.4-3.0 | .7 |
| Intron-22 inversion (unknown) | AA | 20 | 8 |
The study cohort consisted of all F8-haplotyped severe HA subjects plus 7 intron-22 inversion subjects with reported mild or moderate severity HA.
Relative risks of developing an inhibitor were evaluated for the indicated subgroups of African American (AA) and white (W) HA subjects.
Positive inhibitor status (INH(+)) indicates the clinical record showed at least 1 measured inhibitor titer of ≥0.6 BU/mL.
The multivariate logistic analyses adjusted for age (under or over age 18), F8 haplotype, family relationships, and potential exposure to “sequence-mismatched” FVIII. P values <.05 were considered significant.
Subjects age 4 y and over were considered to be multiply infused with FVIII.
Subjects potentially exposed to “sequence-mismatched” FVIII included all who had been exposed to blood products, for example, blood transfusions or Factor Eight Inhibitor Bypass Agent to control bleeding. The risk factors calculated for this subgroup should be interpreted with caution due to possible confounding from clinical conditions requiring treatment with blood-derived products. Comparisons of individual (eg, H2 vs H1) and alternatively grouped (eg, H1 vs H3 + H4 + H5) F8 haplotypes (not shown) showed no statistically significant differences in inhibitor risk.