CASE REPORTS
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Effects and clinical significance of exogenous thyroxine therapy in patients with circulating thyroid hormone autoantibodies.

The effects of exogenous L-thyroxine therapy (0.2-0.3 mg/day) on spontaneously occurring thyroid hormone autoantibodies (THAA) and on serum levels of thyroxine (T4), triiodothyronine (T3) and reverse triiodothyronine (rT3) are described in a boy with lymphocytic thyroiditis. Prior to T4 medication, THAA bound virtually all thyroid hormones as noted by serum gamma globulin binding of tracer hormones. During T4 therapy, however, gamma globulin binding of tracer thyroid hormones decreased markedly. T4 and T3 levels as determined by radioimmunoassay (RIA) were grossly distorted prior to thyroxine therapy and bore no relation to clinical status, the single antibody technics yielding falsely low values whereas the double antibody procedures spuriously exaggerating serum hormone concentration. That spontaneously occurring THAA interfered in RIA hormone measurements was clearly shown by the lack of inconsistencies in laboratory and clinical evaluation when hormone determinations were performed in protein free serum extracts (to remove circulating THAA), or when RIAs were carried out in sera during thyroxine therapy when THAA were saturated by exogenous hormones. The thyroid stimulating hormone (TSH) level prior to therapy was 300 microunits/ml which decreases to less than 3 microunits/ml during T4 medication (0.3 mg/day). There was a gross inverse correlation between TSH secretion and T4 antibody saturation. The marked inhibition of antibody binding of tracer thyroid hormones observed during therapy suggested possible masking of thyroid hormone antibody activity during T4 treatment; experiments involving addition of tracer thyroid hormones to hormone stripped serums from thyroxine treated patients confirmed the hypothesis in two cases of hypothyroidism--one of which was diagnosed in the boy with chronic thyroiditis and the other a woman with postradioactive iodine-induced hypothyroidism. The pathophysiologic significance of thyroid hormone autoantibodies in the transport of thyroid hormones is briefly discussed.

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