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. 2019 Oct 14;25(38):5826–5837. doi: 10.3748/wjg.v25.i38.5826

Table 2.

APOE allele distribution among the study population and stages of fibrosis in chronic hepatitis C patients, n (%)

HCV-patients
Fibrosis stage in CHC patients4
Chronic (n = 206) Clearance (n = 93) P value F1-F2 (n = 49) F3-F4 (n = 38) P value
Genotypes
ε2ε2 2 (1.0) 0 - 0 0 -
ε2ε3 15 (7.4) 8 (8.6) 0.691 5 (10.5) 2 (5.3) 0.400
ε2ε4 2 (1.0) 0 - 0 0 -
ε3ε3 160 (77.5) 64 (68.8) 0.102 29 (59.2) 34 (89.5) 0.001
ε3ε4 26 (12.7) 19 (20.4) 0.080 14 (28.6) 1 (2.6) 0.001
ε4ε4 1 (0.5) 2 (2.2) 0.181 1 (2) 1 (2.6) 0.969
Alleles
ε2 21 (5.1) 8 (4.3) 0.674 4 (5.1) 2 (2.6) 0.603
ε3 361 (87.6) 155 (83.3) 0.158 78 (78.6) 70 (93.4) 0.0222
ε4 30 (7.3) 23 (12.4) 0.0421 16 (16.3) 4 (4) 0.0233
HWE 0.438 0.892 - 0.910 0.286 -
1

ε4 allele was associated with SC OR = 0.55, 95%CI: 0.31-0.98, P = 0.042.

2

ε3 allele was associated with severe fibrosis (F3-F4) OR = 2.99, 95%CI: 1.13-7.87, P = 0.021.

3

ε4 allele was associated with mild fibrosis (F1-F2) OR = 0.091, 95%CI: 0.01-0.75, P = 0.020.

4

Liver damage was assessed in 87 chronic hepatitis C patients. CHC: Chronic hepatitis C; HWE: Hardy-Weinberg Equilibrium.