Thyroid dysfunction induced by peginterferon alfa-2b (Peg-2b)/Ribavirin (Rbv) is associated with higher SVR rates in patients with HCV Genotype 1 (G1) infection due to improved early virologic response at week 4 and week 12
Aims: Recently, we have shown that patients (pts) who developed thyroid dysfunction during treatment of HCV G1 infection with peginterferon alfa-2b and ribavirin yielded higher SVR rates. In order to better understand this beneficial effect we investigated the impact of thyroid dysfunction on early virologic response.
Methods: Data from pts treated for G1 (N = 1923) infection with Peg2b 1.5 µg/kg/wk + weight-based RBV (800 – 1200 mg/day) for up to 48 wks in a large observational real-life study at 285 sites in Germany were retrospectively analyzed. Thyroid dysfunction was estimated by serum TSH levels. TSH levels below or above the normal range were classified as abnormal.
Results: 1436 pts with G1 infection had normal TSH levels at baseline and at least one TSH measurement during therapy. After starting treatment abnormal TSH values became apparent in 304 pts (21.2%). Significantly higher SVR rates were achieved by pts with abnormal than by pts with normal TSH values (44.0% vs. 53.6%). Higher SVR rates were attributed to significantly lower non-response rates (34.9% vs. 24.7%, p = 0.007) in pts with thyroid dysfunction while relapse rates were similar (22.2 vs. 18.9%, p = 0.3223). Development of thyroid dysfunction was associated with a significant reduction in week 4 and week 12 null-response rates. While 37% (172/464) of pts with normal TSH values had a week 4 null-response < 1log10, only 27% (36/134) of pts with abnormal TSH values achieved < 1log10 decline (p = 0.0289) in week 4. In week 12, 28% (258/909) and 21% (54/252) of pts with normal/abnormal TSH values yielded < 2log10 decline in viral load (p = 0.0289).
Conclusions: Thyroid dysfunction triggered by Peg2b/RBV treatment predicts high SVR and low non-response rates in pts with HCV G1 infection. This is attributed to an improved early virologic response in week 4 and week 12.