Thyroxine in the Treatment of Chronic Hepatitis C Infection: A Case Report

Case Report

J Endocr Disord. 2014;1(3): 1015.

Thyroxine in the Treatment of Chronic Hepatitis C Infection: A Case Report

Huy A Tran1*, Elizabeth A Ianna2, Tracey L Jones2, Glenn EM Reeves1

1Hunter Area Pathology Service, University of Newcastle, Australia

2Hepatitis C Service, Gastroenterology Department, Australia

*Corresponding author: Huy A Tran, Hunter Area Pathology Service, University of Newcastle, John Hunter Hospital, Locked Bag Number 1, Hunter Mail Region Centre, Newcastle, New South Wales 2310, Australia

Received: September 25, 2014; Accepted: November 18, 2014; Published: November 20, 2014


Introduction: Chronic hepatitis C is a common and potentially fatal hepatic infection worldwide with an expected increase in incidence of complications including hepatoma, cirrhosis, portal hypertension and potential death. Current treatment regimen includes combination interferon-alpha, ribavirin and recently direct acting antiviral agents. Treated patients who are exposed to high endogenous thyroid hormone concentrations, commonly due to interferon-induced thyroiditis, achieve a better sustained virologic response. It is therefore plausible that thyroxine can be a potential adjuvant therapy in this setting with favorable outcomes.

Case Presentation: A 24 year-old woman with hypothyroidism and chronic hepatitis C, genotype 1, underwent routine treatment of interferon and ribavirin for 48 weeks. During the course of treatment and contrary to medical advice, she deliberately self-administered excessive thyroxine doses. Sustained virologic response was achieved at the completion of therapy despite her poor prognostic factors.

Conclusion: This is the first case report of self-treatment with high doses of thyroxine during treatment with Interferon and Ribavirin, which results in a sustained virologic response, averting potential hepatic related complications. This observation potentially offers an additional adjuvant option in the treatment of chronic hepatitis C infection.

Keywords: Thyroxine; Chronic hepatitis C; Ribavirin; Interferon; Virologic Response


IFN-α: Interferon-alpha; RBV: Ribavirin; SVR: Sustained Virologic Response; fT4: Free Tetra-iodothyronine; fT3: Free Tri-iodothyronine; HCV: Hepatitis C Virus; BMI: Body Mass Index; RR: Reference Range; TSH: Thyrotropin; RNA: Ribonuclei Acid; IL-28B: Interleukin-28B


Chronic hepatitis C is a worldwide epidemic with a prevalence of up to 8% [1]. Whilst the incidence has plateaued, HCV related complications are likely to continue to increase, especially cirrhosis, end-stage hepatic failure and hepatoma [2,3]. Current treatment regimen for this chronic infection includes pegylated-Interferon-alpha (IFN-α) and Ribavirin (RBV) [4]. With the addition of protease inhibitors, success rates of up to 85%, depending on the genotype, are achieved [5]. Previous reports indicated that exposure to high endogenous thyroid hormone concentrations in the presence of IFN-α and RBV contribute to a favorable treatment response [6,7]. The cause for this is uncertain and most data has been retrospective and anecdotal. Most responses are as a result of thyroiditis with a temporary exposure to supraphysiological levels of endogenous thyroid hormones [8]. The high endogenous concentrations of these hormones are thought to be virocidal and contribute to the relatively higher Sustained Virologic Response (SVR), indicating cure. We hereby report a first clinical case where unintentional and exogenous high dose of thyroxine supplements contributed to the eradication of chronic hepatitis C infection despite other unfavorable prognostic factors.

Case Presentation

A 24 year-old female Caucasian who was undergoing chronic hepatitis C treatment presented for an assessment of her thyroid status at the 12th week of treatment. She has a past medical history of intravenous drug abuse from which she contracted the viral infection, and reported primary hypothyroidism requiring regular thyroxine supplements. The cause of her hypothyroidism could not be ascertained. She has HCV genotype 1 and required 48 weeks of therapy with combination IFN-α and RBV. She has otherwise been well with no other health concern. Clinically she was obese with weight of 87.8kg, height of 1.58m, BMI~35kg/m2, blood pressure of 120/70 with prominent and multiple tattoos. There are no signs of chronic liver disease or portal hypertension. Her liver span was 16cm in the mid-clavicular line. No goiter was detected nor were there any signs of thyrotoxicosis. Laboratory investigations showed normal renal function and full blood count. Her alanine aminotransferase was 55 IU/L (Reference Range (RR), <50), alkaline phosphatase 128 IU/L (RR, <110), albumin 38gm/L (RR, 35-45). Her Thyrotropin (TSH) was <0.03 (RR: 0.4–4.0), fT4 32.8pmol/L (RR: 11.4–23.8), fT3 7.0pmol/L (RR: 3.3–6.2), consistent with over-replacement therapy. A thyroid ultrasound revealed a small thyroid with bilateral atrophic lobes. Her anti-thyroperoxidase and anti-thyroglobulin antibodies were undetectable. Her initial HCV Ribonucleic Acid (RNA) viral load was high at 6.5 log IU/mL. Her Interleukin-28B genotypes included RS12979860 CT and RS 8099917 GT. These constitute a poor predicted response rate of ~34.7% from the genetic contribution.

Because further information regarding the patient’s thyroid condition and the indication for thyroxine therapy could not be ascertained, the patient was advised to stop thyroxine pending a full revision of the diagnosis. However for unknown reasons, she declined medical advice and insisted on continuing with thyroxine. She completed the 48 weeks of ‘triple’ antiviral therapy including the prescribed thyroxine despite frequent reminders to stop. It was strongly suspected that she far exceeded the recommended amount. During this time, monthly thyroid function tests showed that her TSH levels were suppressed, with fT4 levels ranging between 27.8 and 47.7pmol/L and fT3 3.7 to 7.0pmol/L, Figure 1. She denied any thyrotoxic symptoms. Her HCV RNA was undetectable at 12 week therapy indicating an early viral response. Subsequently, her end of treatment and 24 week follow-up HCV RNA measurements were all undetected, consistent with cure. In spite of her unfavorable IL-28B genotype and other unfavorable prognostic factors, she managed to achieve SVR. This is consistent with our previous hypothesis that thyroid disease, especially the exposure to high fT4 concentration during treatment, carries a more favourable prognosis, above that of genetic propensity.

Citation: Tran HA, Ianna EA, Jones TL, Reeves GEM. Thyroxine in the Treatment of Chronic Hepatitis C Infection: A Case Report. J Endocr Disord. 2014;1(3): 1015. ISSN:2376-0133