Graves' Disease: Can It Be Cured?

Whether or not Graves' hyperthyroidism can be really cured, depends on the definition of “cure.” If eradication of thyroid hormone excess suffices for the label “cure,” then all patients can be cured because total thyroidectomy or high doses of 1¹³¹I will abolish hyperthyroidism albeit at the expense of creating another disease (hypothyroidism) requiring lifelong medication with levothyroxine. I would not call this a “cure,” which I would like to define as a state with stable thyroid stimulating hormone (TSH), free thyroxine, and triiodothyronine serum concentrations in the normal range in the absence of any thyroid medication. Surgery and radioiodine are unlikely to result in so-defined cures, as their preferable aim as stated in guidelines is to cause permanent hypothyroidism. Discontinuation of antithyroid drugs is followed by 50% recurrences within 4 years; before starting therapy the risk of recurrences can be estimated with the Graves' Recurrent Events After Therapy (GREAT) score. At 20-year follow-up about 62% had developed recurrent hyperthyroidism, 8% had subclinical hypothyroidism, and 3% overt hypothyroidism related to TSH receptor blocking antibodies and thyroid peroxidase antibodies. Only 27% was in remission, and might be considered cured. If the definition of “cure” would also include the disappearance of thyroid antibodies in serum, the proportion of cured patients would become even lower.

Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients

ABSTRACT Objective: The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clinical and biological variables in a series of patients switching from Hashimoto's thyroiditis to Grave's disease. Subjects and methods: Retrospective case study of 24 patients with Hashimoto's thyroiditis followed during 48 ± 36 months that developed later Graves' disease (GD). These variables were analysed in the hypo and hyperthyroid phase: age, sex, initial TSH, free triiodothyronine (fT3), free thyroxine (fT4), anti-TPO, TBII antibodies, parietal cell autoantibodies, time between hypo and hyperthyroidism, thyroid volume and levothyroxine doses (LT). Results: In HT, mean TSH was 9.4 ± 26.1 UI/L and levothyroxine treatment was 66.2 ± 30.8 µg/day. The switch to GD was observed 38 ± 45 months after HT diagnosis. As expected, we found significant differences on TSH, FT3, FT4 and TBAb levels. Three out of 14 patients had parietal cell autoantibodies. In two of these three cases there was an Helicobacter pylori infection. There were no significant differences between HT and GD groups with respect to thyroid volume. Conclusions: To our knowledge, large series documenting the conversion of HT to GD are scarce. Although rare, this phenomenon should not be misdiagnosed. Suspicion should be raised whenever thyroxine posology must be tapered down during the follow-up of HT patients. Further immunological and genetic studies are needed to explain this unusual autoimmune change.

131I therapy effect on medium and large goiter with goiter with hyperthyroidism / 中国综合临床

Objective To evaluate the effect of 131 iodine(131I) therapy in medium and large goiter with hyperthyroidism in order to investigate the influence of pretreatment with antithyroid drugs (ATD) methimazole(MMI) and propylthiouracide (PTU) on 131I therapy.Methods A total of 338 hyperthyroidism patients (136 cases for male,202 cases for female) with thyroid mass greater than 40 grams were treated with 131I in the People's Hospital of Sichuan Province.Thyroid function,thyroid 131I uptake ratio and thyroid imaging were measured before treatment were measured 1-3 months later after administration of 131I,and they were followed up for 6 months to 4 years.Results There were statistical difference between pretreatment and 3 months later of 131I therapy in terms of free triiodothyronine (FT3),(Free thyroxine) FT4.The level of FT3 decreased from (31.9 ± 16.2) pmol/L to (7.8 ±8.5) pmol/L(t =23.9,P =0.000) and level of FT4 decreased from (58.8 ± 22.2) pmol/L to (19.4 ± 16.9) pmol/L(t =25.4,P =0.000).Among 338 patients,109 patients (32.2％) were developed hypothyroidism,and 91 patients (26.9％) were cured,91patients (26.9％) with improved state,20 patients(5.9％) with ineffective and 27 patients(8.0％) with relapse after administration of 131I.The total effective rate was 94.1％ (318/338).Thyroid weight,levels of FT3,FT4,thyroglobulin antibody(TGA),thyroid microsomal antibody(MCA) in effective group were (49.8 ± 9.97) g,(32.5 ± 16.3) pmol/L,(59.5 ± 22.2) pmol/L,(43.6 ± 35.3) ％,(30.1 ± 22.6) ％ respectively,and were (56.9±15.7) g,(22.8 ± 12.8) pmol/L,(47.9 ±20.3) pmol/L,(22.8±30.0)％,(15.3 ±20.5)％ respectively in ineffective group.There were statistically significant differences between the ineffective group and effective group (t =2.932,2.602,2.287,2.501,2.766 ; P =0.000,0.010,0.023,0.013,0.006).Logistic regression analysis was showed that weight of thyroid and serum FT3 were the most important factors in affecting 1131 therapy.Conclusion 131 I therapy for medium and large-sized goiter with hyperthyroidism is safe and effective.ATD may not reduce the effectiveness of subsequent 131I of hyperthyroidism.Thyroid weight and FT3 are the key influential factors in affecting 131I.