The evolution of Graves' disease following auto immune hypothyroidism appears to be rather infrequent. We present seven female patients with autoimmune thyroiditis, 2 with goiter and 5 with hypothyroidism who, after a few months or years, presented signs of Graves'. Therefore it is usefull to carefully monitor TSH in patients treated for autoimmune thyroiditis to detect a possible evolution towards Graves' disease. This should be mostly true in patients with TBII positive antibodies autoimmune thyroiditis. During hyperthyroidism, 123 lodine uptake is much lower than usually observed in Graves' nevertheless, it is always increased compared to the uptake measured during hypothyroidism. This could be in favor of residual functional capacity of these often small thyroid glands. The alternate action of blocking or stimulating antibodies upon the TSH receptor would probably explained the switch from hypo to hyperthyroidism, even if there is usually no correlation between antibodies levels and clinical signs.