OBJECTIVE Hypothyroidism can occur after radioiodine treatment for Graves' disease. It may happen precociously and transiently in the first year after treatment. The purpose of this study was to understand the mechanisms responsible for precocious hypothyroidism. METHODS 36 patients treated for Graves disease by radiodiodine were prospectively studied; The following variables were included in the analysis: age, gender, attendance for Graves' orbitopathy (GO), delay before radioiodine treatment, number of recurrences, previous treatments, corticosteroid therapy, thyroid mass, and (131)I dose. The titres of free T4 (FT4), thyroid-stimulating hormone (TSH), anti-TSH receptor antibodies (TRAb), anti-thyroid peroxydase antibodies (TPOAb) and anti-thyroglobulin antibodies (TGAb) were monitored. Thyroid stimulating (TSAb) and blocking (TBAb) antibodies were determined and (123)I uptake was measured when hypothyroidism occurred. RESULTS 23 patients became precociously hypothyroid (group A) while 13 patients did not (group B). The initial TGAb titre was higher in group A (p=0.0024), and corticosteroid therapy was used more frequently to avoid aggravating GO in group B (p=0.0276). TPOAb and TGAb titres increased significantly only in group A (p=0.0112 and p=0.0202, respectively). When hypothyroidism occurred, TBAb was present in 13 patients. Transient hypothyroidism due to TBAb was observed in 1 patient. No iodide organification impairment was disclosed by the perchlorate test. CONCLUSIONS Radioinduced thyroiditis appears to be the main mechanism involved in the pathogenesis of precocious hypothyroidism. A higher TGAb titre before treatment is associated with precocious hypothyroidism, suggesting the prognostic value of TGAb. Transient hypothyroidism directly due to TBAb remains rare.