Telaprevir- and boceprevir-based tritherapies in real practice for F3-F4 pretreated hepatitis C virus patients

Table 2 Factors associated with sustained virological response n (%)

	No sustained virological responsen = 49	Sustained virological responsen = 73	P valueunivariate analysis	P valuemultivariate analysisOR(95%CI)
Protease inhibitor
Telaprevir	30 (34.1)	58 (65.9)	0.0276	NS1
Boceprevir	19 (55.9)	15 (44.1)
Gender
Male	27 (34.2)	52 (65.8)	0.0675	NS1
Female	22 (51.2)	21 (48.8)
HCV genotype 1 subtype
1a	17 (45.9)	20 (54.1)	0.8051	-
1b	26 (37.1)	44 (62.9)
IL28B genotype, rs12979860, n (%)
C/C	4 (25)	12 (75)	0.4420	-
C/T or T/T	40 (45.5)	48 (54.5)
Response to prior therapy				0.008
Null-responders	40 (52.6)	36 (47.4)	0.0004	1.0
Relapsers	9 (20)	36 (80)		3.9 (1.4-10.6)
Grade of liver fibrosis
Metavir F3	11 (31.4)	24 (68.6)	0.2118	-
Metavir F4	38 (43.7)	49 (56.3)
Liver stiffness value (kPa)
Median, kPa (IQR)	17.3 (11.5-28.8)	13.9 (9.4-19.7)	0.0296	0.001
< 21.3 kPa	21 (30)	49 (70)	0.002	8.2 (2.3-29.5)
≥ 21.3 kPa	14 (66.7)	7 (33.3)		1
Rapid virological response	18 (23.7)	58 (76.3)	≤ 0.0001	≤ 0.001
No rapid virological response	26 (68.4)	12 (31.6)		6.9 (2.6-18.2) 1.0
Decrease of ribavirin dosage	18 (37.5)	30 (62.5)	0.6287	-
No decrease of ribavirin dosage	31 (41.9)	43 (58.1)

Sustained virological response (SVR) was analyzed 24 wk after triple therapy withdrawal for 122 patients. Rapid virological response (RVR) under triple therapy was defined as undetectable HCV RNA levels following 4 wk of antiviral triple therapy (i.e., week 4 in the TPV group and week 8 in the BOC treatment group)1. These factors were initially included in the multivariate model (P value < 0.2 in the univariate analysis) and were not independently associated with SVR in the final multivariate model.