Peginterferon-α

Reactions 1114 - 12 Aug 2006 Peginterferon-α Thyroid disorders: 3 case reports Three men developed thyroiditis, progressing to Graves’ disease, during treatment with peginterferon-α [dosages not stated] for hepatitis C. A 41-year-old man started receiving peginterferon-α plus ribavirin. After about 4 months, he presented with asthenia, palpitations, 9kg weight loss and nervousness. On examination, he had a painless, small, firm, non-vascularised goitre with no palpable nodule or adenopathy. Laboratory investigations confirmed hyperthyroidism. Carbimazole was prescribed. Results of further investigations, including positive anti-thyroglobin antibodies (TgAbs) and the presence of a homogenous hypoechogenic goitre on ultrasound, were typical of destructive hyperthyroidism. Carbimazole was stopped after 15 days and he started treatment with a β- adrenoceptor antagonist. His thyroid stimulating hormone (TSH) levels normalised within 2 weeks, but his free thyroxine (FT4) level was 4.9 ng/L (normal 9.3–17). Fifteen days later, hypothyroidism was detected, and he started taking levothyroxine sodium. Over 2 months later, he experienced a recurrence of hyperthyroidism. Levothyroxine was discontinued and treatment with a β-adrenoceptor antagonist resumed. His clinical condition worsened, he lost 10kg in 1 month, his FT4 and free tri-iodithyronine (FT3) levels became elevated, and he started receiving prednisolone. A repeat ultrasound revealed hypervascularisation of the thyroid gland parenchyma. At this time, he had positive anti-thyroperoxidase (TPOAbs) and anti-TSH antibodies and positive TgAbs. Prednisolone was discontinued and carbimazole was reinitiated. Within 6 weeks, his thyroid function normalised, and evolution was unremarkable under treatment. A 39-year-old man started treatment with peginterferon-α and ribavirin. After 4 months, low TSH levels were detected. Investigations showed that he had a moderately sized, painless hypoechogenic goitre without nodules. About 2 months later, laboratory investigations revealed asymptomatic hypothyroidism. One month later, his FT4 and TSH levels had nearly normalised. Hyperthyroidism recurred about 1 month later, and findings from investigations were highly suggestive of Graves’ disease. Interferon-α was stopped and carbimazole and levothyroxine treatment initiated. His evolution was unremarkable. A 47-year-old man started receiving peginterferon-α and ribavirin and, after 6 months, experienced hyperthyroidism. He had a painless, homogeneous goitre and elevated TPOAbs. Peginterferon-α was discontinued and, 2 months later, he developed subclinical hypothyroidism. After about 4 months, his hyperthyroidism recurred with a picture consistent with Graves’ disease. Carbimazole was started and he showed an unremarkable evolution. Author comment: "[Interferon-α] is able to induce all kinds of thyroid autoimmune disease. . . treatment with [interferon-α] has led us to report this new clinical form of thyrotoxicosis that fluctuates between silent thyroiditis and Graves’ disease." Bohbot NL, et al. Interferon-alpha-induced hyperthyroidism: a three-stage evolution from silent thyroiditis towards Graves’ disease. European Journal of Endocrinology 154: 367-372, No. 3, Mar 2006 - France 801043064 1 Reactions 12 Aug 2006 No. 1114 0114-9954/10/1114-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

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Transcript of Peginterferon-α

Reactions 1114 - 12 Aug 2006

Peginterferon-αThyroid disorders: 3 case reports

Three men developed thyroiditis, progressing to Graves’disease, during treatment with peginterferon-α [dosages notstated] for hepatitis C.

A 41-year-old man started receiving peginterferon-α plusribavirin. After about 4 months, he presented with asthenia,palpitations, 9kg weight loss and nervousness. Onexamination, he had a painless, small, firm, non-vascularisedgoitre with no palpable nodule or adenopathy. Laboratoryinvestigations confirmed hyperthyroidism. Carbimazole wasprescribed. Results of further investigations, including positiveanti-thyroglobin antibodies (TgAbs) and the presence of ahomogenous hypoechogenic goitre on ultrasound, weretypical of destructive hyperthyroidism. Carbimazole wasstopped after 15 days and he started treatment with a β-adrenoceptor antagonist. His thyroid stimulating hormone(TSH) levels normalised within 2 weeks, but his free thyroxine(FT4) level was 4.9 ng/L (normal 9.3–17). Fifteen days later,hypothyroidism was detected, and he started takinglevothyroxine sodium. Over 2 months later, he experienced arecurrence of hyperthyroidism. Levothyroxine wasdiscontinued and treatment with a β-adrenoceptor antagonistresumed. His clinical condition worsened, he lost 10kg in1 month, his FT4 and free tri-iodithyronine (FT3) levels becameelevated, and he started receiving prednisolone. A repeatultrasound revealed hypervascularisation of the thyroid glandparenchyma. At this time, he had positive anti-thyroperoxidase(TPOAbs) and anti-TSH antibodies and positive TgAbs.Prednisolone was discontinued and carbimazole wasreinitiated. Within 6 weeks, his thyroid function normalised,and evolution was unremarkable under treatment.

A 39-year-old man started treatment with peginterferon-αand ribavirin. After 4 months, low TSH levels were detected.Investigations showed that he had a moderately sized, painlesshypoechogenic goitre without nodules. About 2 months later,laboratory investigations revealed asymptomatichypothyroidism. One month later, his FT4 and TSH levels hadnearly normalised. Hyperthyroidism recurred about 1 monthlater, and findings from investigations were highly suggestiveof Graves’ disease. Interferon-α was stopped and carbimazoleand levothyroxine treatment initiated. His evolution wasunremarkable.

A 47-year-old man started receiving peginterferon-α andribavirin and, after 6 months, experienced hyperthyroidism.He had a painless, homogeneous goitre and elevated TPOAbs.Peginterferon-α was discontinued and, 2 months later, hedeveloped subclinical hypothyroidism. After about 4 months,his hyperthyroidism recurred with a picture consistent withGraves’ disease. Carbimazole was started and he showed anunremarkable evolution.

Author comment: "[Interferon-α] is able to induce allkinds of thyroid autoimmune disease. . . treatment with[interferon-α] has led us to report this new clinical form ofthyrotoxicosis that fluctuates between silent thyroiditis andGraves’ disease."Bohbot NL, et al. Interferon-alpha-induced hyperthyroidism: a three-stageevolution from silent thyroiditis towards Graves’ disease. European Journal ofEndocrinology 154: 367-372, No. 3, Mar 2006 - France 801043064