No abstract

Autoimmune thyroid disease is a common side-effect of interferon-a (IFN-a) treatment of viral hepatitis C. We have described three patients with hepatitis C for whom IFN-a and ribavirin were prescribed and who developed two successive phases of silent thyroiditis followed by hyperthryroidism relapse due to Graves' disease. These three men had no known history of familial or personal thyroid disease. Destructive thyrotoxicosis appeared 4-6 months after starting IFN-a, followed by Graves' hyperthyroidism within 8 to11 months. The thyrotropin (TSH) level was normal before IFN-a was started. The diagnosis of destructive thyroiditis was confirmed by anti-TSH receptor antibody (TSHRAb) negativity and the absence of radionuclide ( 123 I or 99 Tc) uptake on thyroid scintiscans. Eight to eleven months after starting treatment, TSHRAb positivity and intense scintigraphic uptake confirmed the appearance of Graves' disease. IFN-a was continued in only one patient. Hence, hyperthyroidism induced by IFN-a could correspond to the first phase of silent thyroiditis, to Graves' disease or to the succession of both. Rigorous diagnostic procedures with repeated scintiscans and TSHRAb titering are necessary to avoid a false diagnosis and inappropriate therapy.

In this monocentric population of CHC, dysthyroidism, especially hyperthyroidism, developed in 10% of patients. Low fibrosis was found to be a predictive factor of dysthyroidism. Thyroid disorder recovered in 16/30 patients (53%) and recovery was better in the non-autoimmune form.

No abstract

Fifteen patients with advanced hematopoietic and other malignancies were treated with recombinant DNA produced Alpha 2 Interferon (IFN) (Schering) by intravenous (IV) and intramuscular (IM) routes at weekly intervals in escalating doses from 1 X 10(6) IU to 100 X 10(6) IU in order to determine the tolerance and pharmacokinetics. The most common side effects included fever, chills, myalgia, and arthralgia. At doses of 60 X 10(6) or above, severe but reversible hypotension was observed in five patients receiving interferon by intravenous route. Patients receiving interferon by intramuscular route had fever, chills, and myalgias but did not develop hypotension at the same dosage. Two patients with non-Hodgkin lymphoma showed objective evidence of regression. Our data suggest a biphasic pattern of elimination with terminal half-life ranging from 1.9 to 2.9 hours and peak titer of 16,000 units and under for IV interferon, and terminal half-life of 6 hours with peak titers of 600 units for intramuscular interferon. However, interpatient variability precludes a definite conclusion. Although the areas under the serum concentration vs time curves were similar, the intravenous route provided higher but unsustained levels of interferon than the intramuscular route.