GRAVES DISEASE WITH TRANSITORY HYPOTIROIDISM DEVELOPED DURING THE THERAPY WITH PEGINTERFERON α 2A 180 μg /WEEK AND RIBAVIRIN 1200 μg/DAY IN THE TREATMENT OF THE CHRONIC ACTIVE VCH HEPATITES
Abstract:
We present the case of a patient with active chronic hepatitis with C virus, in treatment with
Peginterferon α 2A 180 μg / week, whose tiroidian function was modified from hypertiroidism initially to
transitory hypotiroidism and next to hypertiroidism. The patient of 45 years began his treatment with
Peginterferon α 2A 180 μg / week for chronic active hepatitis with hepatitic virus C in february 2005.
The thyroid’s function at the beginning of the treatment was normal, the antibodies anti-thyroid were
absent. There weren’t any pathological or heredo collateral personal antecedents of a thyroidal or
autoimmune pathology. The patient develops hyperthyroidism at 3 months from the beginning of the
therapy with Peg interferon α 2A, with the positivation of the antithyroid antibodies. The thyroidal
scintigraphy reveals a value of 1,07% (Normal values = 0,5 – 3%). Later, the patient develops transitory
hypothyroidism in 8 months from the beginning of the treatment and the intercurrence of the
hyperthyroidism in January 2006. The transitory status of the hypothyroidism may be explained through
two possible mechanisms: the complications induced by the destructive thyroiditis in the therapy with
Peg interferon α 2A, respectively the variations between the levels of the anti-thyroid antibodies. A
possible mechanism of passing in the phase of transitory hypothyroidism during the therapy with Peg
interferon α 2A could be the complications in the distructive tiroiditis. The thyroid gland modifications
appeared in the patient in the lack of an historical of thyroid gland pathology or positive antithyroid
antibodies during the therapy with Peg interferon α 2A are rare. This aspect as well as the biphasic
evolution of passing from hyperthyroidism in hypothyroidism and later back to hyperthyroidism
represents the particularity of the presented case. Other studies will need the precise elucidation of the
pathogenetic mechanism induced by the Interferon at the level of the thyroid.
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