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Chronic hepatitis C infection and sex hormone levels: effect of disease severity and recombinant interferon-α therapy

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Abstract Background:

We aimed to investigate the associations between androgen status and markers of liver disease severity and to determine the effect of interferon-α (IFN-α) treatment on sex hormone levels in the context of hepatitis C infection. Methods:

We audited liver biopsy and sex hormone data from 35 men with chronic hepatitis C and a separate group of 11 men with hepatitis C who received IFN-α treatment at Fremantle Hospital. Results:

We found that men with low fibrosis scores (0–2) on the modified Knodell histological activity index were more likely to have lower sex hormone–binding globulin (SHBG) levels (38.2 ± 13.2 vs 66.6 ± 43.3 nmol/L, P < 0.001) and higher free testosterone levels (380.4 ± 102.0 vs 255.9 ±83.0 pmol/L, P = 0.01) than those with higher fibrosis scores (3–6). SHBG directly correlated with fibrosis scores (r = 0.37, P = 0.032). Free testosterone levels inversely correlated with liver fibrosis scores (r = −0.43, P = 0.011). A transient reduction in total testosterone of 5.7 ± 4.2 nmol/L (P = 0.014) occurred within the first 6 months of IFN-α therapy although free testosterone was unaffected. Conclusion:

More severe liver disease was associated with lower free testosterone and higher SHBG. IFN-α therapy reduced total testosterone but not to hypogonadal levels, with no decline in free testosterone. These data suggest that liver disease in hepatitis C infection modulates androgen status indirectly via increased SHBG. Screening for androgen deficiency in the context of hepatitis C infection should selectively target men with more severe liver disease or documented higher grade fibrosis.
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Keywords: free testosterone; hepatitis C; interferon alpha; liver disease; sex hormone–binding globulin

Document Type: Research Article

Affiliations: 1: Endocrinology 2: School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia

Publication date: June 1, 2006

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