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Treatment with one of a number of cytokines, interferon-a, interferon-gamma, interleukin-1,
interleukin-2, tumour necrosis factor and granulocyte colony stimulating factor have been associated
with hypothyroidism or thyrotoxicosis; these abnormalities are often transient, with resolution over
several months after treatment is ceased (Baudin et al, 1993). Abnormal thyroid function may be
accompanied by increase in titres of thyroid autoantibodies, which suggests that the changes are
autoimmune, but in vitro these agents can also influence thyroid cell growth, thyroglobulin
production and hormone release. In addition to these longterm effects, treatment of healthy
volunteers with a single injection of interferon-a resulted in a prompt decrease in serum T3
and TSH and an increase in serum reverse T3 - changes that closely resemble the so-called "sick
euthyroid syndrome" (Corssmit et al. 1995).
Both hypothyroidism and thyrotoxicosis are described during treatment of chronic active hepatitis C with interferon-a, with an estimated incidence of hypothyroidism in about 6%, although positive anti-peroxidase antibodies occur in up to one fifth of cases (Koh et al, 1997). Risk factors for hypothyroidism include female sex, higher dose, longer duration of treatment, positive autoantibodies before treatment and associated use of interleukin-2. In over half of the reported cases, hypothyroidism has resolved spontaneously after cessation of treatment. Thyrotoxicosis is less common than hypothyroidism. A recent report of monoclonal antibody treatment for multiple sclerosis documented a striking incidence of subsequent persistent autoimmune thyroid dysfunction (Coles et al, 1999). Six to 30 months after treatment, one third of previously euthyroid patients who received a five day course of the humanized anti-CD52 monoclonal antibody, developed antibodies against the TSH receptor, associated with carbimazole-responsive thyrotoxicosis. In most cases, ablative treatment was required because the thyrotoxicosis tended to relapse after withdrawal of carbimazole. Transient primary hypothyroidism with a duration of 6 months to 2 years, perhaps of autoimmune origin, has been described in association with hypersensitivity reactions to phenytoin, carbamazepine and sulphonamides; in vitro studies suggested a possible immune interaction with thyroid peroxidase (Gupta et al, 1992). |
