Introduction: The parameters that influence the success of radioiodine therapy (RIT) in the treatment of hyperthyroidism due to Graves' disease (GD) still remain controversial and an object of several studies.
Objective: To identify factors that may influence the outcome of thyroid function in patients with GD after RIT.
Materials and methods: One hundred and thirty six patients (110 females and 26 males) with Graves' disease were studied, with a mean age of 42.5 +/- 12.2 years. Exophthalmia was present in 86 (63.2%) and absent in 50 (36.8%) patients; 113 patients were under treatment with methimazole and 23 with propylthiouracil; 61 patients (44.9%) remained with anti-thyroid drugs (ATD) during the RIT and 75 (55.1%) discontinued the medication 2 to 30 days prior to treatment. The mean thyroid uptake of 99mTc-pertechnetate before RIT was 13.1 +/- 10.6%; 82 (60.3%) patients were treated with 10 mCi, 33 (24.2%) with 12 mCi and 21 (15.5%) with 15 mCi of 131I-iodide.
Results: Twenty three (16.9%) patients remained euthyroid; 72 (52.9%) became hypothyroid and 41 (30.1%) persisted with hyperthyroidism during the follow-up. There was no significant statistical association between clinical outcome and gender; age at the diagnosis; presence of exophthalmia; serum levels of free-T4; TSH; TPOAb and TgAb before RIT; ATD utilized and time without ATD before treatment. The administration of 15 mCi of 131I-iodide led to a significant lower failure rate (p=0.0468*) than the doses of 10 and 12 mCi. The multivariate logistic regression analysis demonstrated that patients with 99mTc-pertechnetate uptake values above 15% had a chance of failure 4.5 times higher than those with uptake values under 15% (p<0.0001*;OR=4.513; CI 95% 1.377-14.793).
Conclusion: Fixed doses of 15 mCi of 131I-iodide show a greater success rate of RIT than doses of 10 or 12 mCi. High 99mTc-pertechnetate uptake values before RIT may be indicative of greater risk of treatment failure, especially when above 15%, possibly due to increased turn-over or the presence of a hormone synthesis defect in these glands.