The addition of ribavirin to interferon-α therapy in patients with hepatitis C virus-related chronic hepatitis does not modify the thyroid autoantibody pattern but increases the risk of developing hypothyroidism

Carlo Carella, Gherardo Mazziotti, Filomena Morisco, Mario Rotondi, Michele Cioffi, Concetta Tuccillo, Francesca Sorvillo, Nicola Caporaso, Giovanni Amato

Research output: Contribution to journalArticle

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Abstract

Objective: The aim of this study was to investigate whether the addition of ribavirin (RIBA) to interferon-α (IFN-α) therapy increases the risk of developing thyroid autoimmunity and/or dysfunction. Design and Methods: The study group (group A) included 72 patients undergoing treatment with IFN-α (3-6 million units three times weekly) plus RIBA (1.0-1.2g/day) for chronic hepatitis C (CHC), as first line therapy (30 cases) or as a second therapeutic attempt after a previous ineffective IFN-α treatment (42 cases). The control group (group B) encompassed 75 age- and sex-matched patients affected by CHC, undergoing treatment with IFN-α alone as first line therapy (35 cases) or as a second therapeutic attempt (40 cases). Thyroid autoimmunity and function were retrospectively evaluated on frozen aliquots, drawn before, after 6 months, and at the end of the antiviral treatment. In patients receiving two antiviral treatments (42 cases in group A and 40 cases in group B) thyroid parameters were also assayed on serum samples drawn before and at the end of the first IFN-α therapy. Results: Thyroid autoimmunity rate (17/72 for group A and 17/75 for group B) as well as anti-thyroglobulin antibodies (TgAb) and anti-thyroid peroxidase antibodies (TPOAb) serum levels were comparable between the two groups. Similarly, in patients undergoing two consecutive antiviral treatments (42 cases in group A and 40 cases in group B) the percentage of positivity for thyroid autoantibodies did not change significantly from the first to the second therapeutic schedules in both groups, with no significant increase of median TgAb and TPOAb levels. By the same token, all but one patient negative for thyroid autoantibodies at the end of the first treatment remained so also during the subsequent treatment. In group A patients, the rate of hypothyroidism (11/72) was significantly higher than that observed in group B (3/75). Similarly, in patients undergoing two consecutive antiviral treatments the percentage of hypothyroidism increased significantly from the first to the second therapeutic schedule in group A (from 4.8% to 19.0% P

Original languageEnglish
Pages (from-to)743-749
Number of pages7
JournalEuropean Journal of Endocrinology
Volume146
Issue number6
Publication statusPublished - 2002

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Ribavirin
Chronic Hepatitis
Hypothyroidism
Hepacivirus
Autoantibodies
Interferons
Thyroid Gland
Therapeutics
Antiviral Agents
Autoimmunity
Iodide Peroxidase
Chronic Hepatitis C
Antibodies
Appointments and Schedules
Thyroglobulin
Serum

ASJC Scopus subject areas

  • Endocrinology

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The addition of ribavirin to interferon-α therapy in patients with hepatitis C virus-related chronic hepatitis does not modify the thyroid autoantibody pattern but increases the risk of developing hypothyroidism. / Carella, Carlo; Mazziotti, Gherardo; Morisco, Filomena; Rotondi, Mario; Cioffi, Michele; Tuccillo, Concetta; Sorvillo, Francesca; Caporaso, Nicola; Amato, Giovanni.

In: European Journal of Endocrinology, Vol. 146, No. 6, 2002, p. 743-749.

Research output: Contribution to journalArticle

Carella, Carlo ; Mazziotti, Gherardo ; Morisco, Filomena ; Rotondi, Mario ; Cioffi, Michele ; Tuccillo, Concetta ; Sorvillo, Francesca ; Caporaso, Nicola ; Amato, Giovanni. / The addition of ribavirin to interferon-α therapy in patients with hepatitis C virus-related chronic hepatitis does not modify the thyroid autoantibody pattern but increases the risk of developing hypothyroidism. In: European Journal of Endocrinology. 2002 ; Vol. 146, No. 6. pp. 743-749.
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abstract = "Objective: The aim of this study was to investigate whether the addition of ribavirin (RIBA) to interferon-α (IFN-α) therapy increases the risk of developing thyroid autoimmunity and/or dysfunction. Design and Methods: The study group (group A) included 72 patients undergoing treatment with IFN-α (3-6 million units three times weekly) plus RIBA (1.0-1.2g/day) for chronic hepatitis C (CHC), as first line therapy (30 cases) or as a second therapeutic attempt after a previous ineffective IFN-α treatment (42 cases). The control group (group B) encompassed 75 age- and sex-matched patients affected by CHC, undergoing treatment with IFN-α alone as first line therapy (35 cases) or as a second therapeutic attempt (40 cases). Thyroid autoimmunity and function were retrospectively evaluated on frozen aliquots, drawn before, after 6 months, and at the end of the antiviral treatment. In patients receiving two antiviral treatments (42 cases in group A and 40 cases in group B) thyroid parameters were also assayed on serum samples drawn before and at the end of the first IFN-α therapy. Results: Thyroid autoimmunity rate (17/72 for group A and 17/75 for group B) as well as anti-thyroglobulin antibodies (TgAb) and anti-thyroid peroxidase antibodies (TPOAb) serum levels were comparable between the two groups. Similarly, in patients undergoing two consecutive antiviral treatments (42 cases in group A and 40 cases in group B) the percentage of positivity for thyroid autoantibodies did not change significantly from the first to the second therapeutic schedules in both groups, with no significant increase of median TgAb and TPOAb levels. By the same token, all but one patient negative for thyroid autoantibodies at the end of the first treatment remained so also during the subsequent treatment. In group A patients, the rate of hypothyroidism (11/72) was significantly higher than that observed in group B (3/75). Similarly, in patients undergoing two consecutive antiviral treatments the percentage of hypothyroidism increased significantly from the first to the second therapeutic schedule in group A (from 4.8{\%} to 19.0{\%} P",
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T1 - The addition of ribavirin to interferon-α therapy in patients with hepatitis C virus-related chronic hepatitis does not modify the thyroid autoantibody pattern but increases the risk of developing hypothyroidism

AU - Carella, Carlo

AU - Mazziotti, Gherardo

AU - Morisco, Filomena

AU - Rotondi, Mario

AU - Cioffi, Michele

AU - Tuccillo, Concetta

AU - Sorvillo, Francesca

AU - Caporaso, Nicola

AU - Amato, Giovanni

PY - 2002

Y1 - 2002

N2 - Objective: The aim of this study was to investigate whether the addition of ribavirin (RIBA) to interferon-α (IFN-α) therapy increases the risk of developing thyroid autoimmunity and/or dysfunction. Design and Methods: The study group (group A) included 72 patients undergoing treatment with IFN-α (3-6 million units three times weekly) plus RIBA (1.0-1.2g/day) for chronic hepatitis C (CHC), as first line therapy (30 cases) or as a second therapeutic attempt after a previous ineffective IFN-α treatment (42 cases). The control group (group B) encompassed 75 age- and sex-matched patients affected by CHC, undergoing treatment with IFN-α alone as first line therapy (35 cases) or as a second therapeutic attempt (40 cases). Thyroid autoimmunity and function were retrospectively evaluated on frozen aliquots, drawn before, after 6 months, and at the end of the antiviral treatment. In patients receiving two antiviral treatments (42 cases in group A and 40 cases in group B) thyroid parameters were also assayed on serum samples drawn before and at the end of the first IFN-α therapy. Results: Thyroid autoimmunity rate (17/72 for group A and 17/75 for group B) as well as anti-thyroglobulin antibodies (TgAb) and anti-thyroid peroxidase antibodies (TPOAb) serum levels were comparable between the two groups. Similarly, in patients undergoing two consecutive antiviral treatments (42 cases in group A and 40 cases in group B) the percentage of positivity for thyroid autoantibodies did not change significantly from the first to the second therapeutic schedules in both groups, with no significant increase of median TgAb and TPOAb levels. By the same token, all but one patient negative for thyroid autoantibodies at the end of the first treatment remained so also during the subsequent treatment. In group A patients, the rate of hypothyroidism (11/72) was significantly higher than that observed in group B (3/75). Similarly, in patients undergoing two consecutive antiviral treatments the percentage of hypothyroidism increased significantly from the first to the second therapeutic schedule in group A (from 4.8% to 19.0% P

AB - Objective: The aim of this study was to investigate whether the addition of ribavirin (RIBA) to interferon-α (IFN-α) therapy increases the risk of developing thyroid autoimmunity and/or dysfunction. Design and Methods: The study group (group A) included 72 patients undergoing treatment with IFN-α (3-6 million units three times weekly) plus RIBA (1.0-1.2g/day) for chronic hepatitis C (CHC), as first line therapy (30 cases) or as a second therapeutic attempt after a previous ineffective IFN-α treatment (42 cases). The control group (group B) encompassed 75 age- and sex-matched patients affected by CHC, undergoing treatment with IFN-α alone as first line therapy (35 cases) or as a second therapeutic attempt (40 cases). Thyroid autoimmunity and function were retrospectively evaluated on frozen aliquots, drawn before, after 6 months, and at the end of the antiviral treatment. In patients receiving two antiviral treatments (42 cases in group A and 40 cases in group B) thyroid parameters were also assayed on serum samples drawn before and at the end of the first IFN-α therapy. Results: Thyroid autoimmunity rate (17/72 for group A and 17/75 for group B) as well as anti-thyroglobulin antibodies (TgAb) and anti-thyroid peroxidase antibodies (TPOAb) serum levels were comparable between the two groups. Similarly, in patients undergoing two consecutive antiviral treatments (42 cases in group A and 40 cases in group B) the percentage of positivity for thyroid autoantibodies did not change significantly from the first to the second therapeutic schedules in both groups, with no significant increase of median TgAb and TPOAb levels. By the same token, all but one patient negative for thyroid autoantibodies at the end of the first treatment remained so also during the subsequent treatment. In group A patients, the rate of hypothyroidism (11/72) was significantly higher than that observed in group B (3/75). Similarly, in patients undergoing two consecutive antiviral treatments the percentage of hypothyroidism increased significantly from the first to the second therapeutic schedule in group A (from 4.8% to 19.0% P

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