Introduction: Hashimotos thyroiditis (HT) and Graves disease (GD) are two auto-immune diseases. They have different phenotypes and are generally believed to share a number of common etiological factors but the mechanisms leading to their dichotomy are unknown. An unusual outcome of HT is the conversion to GD.
A mechanism that might be hypothesized to account for the change from HT to GD is the alteration in the biological activity of TSH receptor Abs from predominantlythyroid-blocking antibodies during the hypothyroid phase to thyroid-stimulating antibodies when GD manifests itself.
Case report: A 14-year-old girl, B H, was seen complaining of clinical hypothyriodism manifestation with enlargement of thyroid gland. The result of thyroid function was, FT4=5.6 pg/ml (normal=6.520.5), TSHs=113 μUI/ml (normal=0.15.0), and anti-microsomal antibody titer was high. She takes levothyroxine 75 μg/day.
6 years after she develops clinical hyperthyroidism manifestation and laboratory tests revealed thyrotoxicosis:TSH<0.001 and FT4=30 pg/ml. The biological hyperthyroidism remain without levothyroxine and TRAb was high confirming the diagnostic of Graves disease. She was treated with neomercazole for 6 months and afterward her thyroid function remained normal without medication.
Conclusion: Graves disease rarely succeded to Hashimoto thyroiditis and the mecanism leading to this state remain unclear.