Table 3: Distribution of the thrombophilic mutations identified in our study cohort.

APCMutations identified/subjects testedFrequency from the subset of subjects tested in each group (*1) (*2), (*3).Frequency from the total cohort 𝑛 = 9 0 7 Thrombophilic mutations identified

(*1) 𝑛 = 1 4 0 Positive APCR (inherited and acquired)

67/14047.8%7.3%MTHFR-C677T (54ht13hom)
3 /1402.1%0.3%ht prothrombin G20210A
16/14011.4%1.7%ht (H) R2
29/14020.7%3.1%ht FV Leiden
1/1400.7%0.1%ht Cambridge
48/14031.4%3.9%no mutation

(*2) 𝑛 = 1 0 5 Positive APCR (acquired)

51/10548.5%5.6%MTHFR -C677T (38ht13hom)
3/1052.8%0.3%ht Prothrombin G20210A
16/10515.2%1.7%ht(H) R2
44/10541.9%4.8%no mutations

(*3) 𝑛 = 3 1 Negative APCR

5/3116.1%0.6%ht (H) R2
13/3141.9%1.7%MTHFR-C677T
13/3141.9%1.7%No mutation

(*1) 𝑛 = 1 4 0 are subjects with total APCR (acquired +modified).
(*2) 𝑛 = 1 0 5 are subjects with acquired APCR, without inherited FVL.
(*3) 𝑛 = 3 1 are negative APCR subjects tested out of 767.
𝑛 : Number of subjects; ht: Heterozygotes; hom: Homozygotes; H: Haplotype.
Subjects identified with more than one mutation simultaneously:
in the total APCR group, (inherited plus acquired) They had 13 subjects with MTHFR+FVL; 1subject with MTHFR + FVL + Cambridge; 7 subjects with MTHFR + HR2; 1 subject with prothrombin G20210A + HR2; and 1 subject with prothrombin G20210A + MTHFR; in the acquired APCR group, They had 7 subjects with MTHFR+HR2; 1 subject with prothrombin G20210A + HR2; 1 subject with prothrombin G20210A + MTHFR.