Table 3.
CYP2C19 | CYP3A4*18a | CYP3A5*3b | MDR1-3435c | |||||
---|---|---|---|---|---|---|---|---|
Genotype (n) |
T/T |
T/C |
G/G |
A/G |
A/A |
C/C |
C/T |
T/T |
HomEM: n = 102 (%) |
93 (91.2) |
9 (8.8) |
55 (53.9) |
35 (34.3) |
12 (11.8) |
39 (38.2) |
51 (50.0) |
12 (11.8) |
D: n = 56 (%) |
50 (53.8) |
6 (66.7) |
32 (58) |
17 (48.6) |
7 (58.3) |
23 (59) |
29 (56.9) |
4 (33.3) |
R: n = 46 (%) |
43 (46.2) |
3 (33.3) |
23 (42) |
18 (51.4) |
5 (41.7) |
16 (41) |
22 (43.1) |
8 (66.7) |
HetEM: n = 130 (%) |
127 (97.7)d |
3 (2.3)d# |
65 (50.0) |
54 (41.5) |
11 (8.5) |
52 (40) |
64 (49.2) |
14 (10.8) |
D: n = 58 (%) |
58 (45.7) |
0 (0) |
30 (46.2) |
26 (48) |
2 (18.2) |
22 (42.3) |
32 (50) |
4 (28.6) |
R: n = 72 (%) |
69 (54.3) |
3 (100) |
35 (53.8) |
28 (52) |
9 (81.8) |
30 (57.7) |
32 (50) |
10 (71.4) |
PM: n = 34 (%) |
30 (88.2)d |
4 (11.8)d |
14 (41.2) |
20 (58.8) |
|
16 (47.1) |
16 (47.1) |
2 (5.9) |
D: n = 19 (%) |
16 (53.3) |
3 (75) |
9 (64.3) |
10 (50) |
0 |
11 (68.8) |
6 (37.5) |
2 (100) |
R: n = 15 (%) | 14 (46.7) | 1 (25) | 5 (35.7) | 10 (50) | 5 (31.2) | 10 (62.5) | 0 (0) |
D, donor; HetEM, heterozygous extensive metabolizers; HomEM, homozygous extensive metabolizers; PM, poor metabolizers; R: recipient.; aCYP3A4*18 (exon 10; T878C).
bCYP3A5*3 (intron 3; A6986G).
cMDR1-3435 (exon 26; C3435T).
dP < 0.05. There was no statistically significant difference between the haplotypes of CYP3A4*18 (T/T and T/C), CYP3A5*3 (G/G, A/G, and A/A), and MDR1-3435 (C/C, C/T, and T/T) and also between the different CYP2C19 genotypes (HomEM, HetEM, and PM) between healthy donors and recipients with end stage liver disease. There were independent isoenzymes and no correlation of genetic interaction between CYP2C19 and CYP3A4*18, CYP3A5*3, or MDR1-3435 not only, but also the variant haplotypes or genotypes.