Radioiodine Therapy For Graves Disease Research Articles

Ultrasound determination of pediatric thyroid mass.

Radioiodine therapy for Graves disease can be achieved with dosing based on estimated thyroid gland mass. Thyroid mass can be estimated using linear ultrasound measurements, and conversion factors for volume and density. The choice of conversion factors could impact estimated thyroid mass and thus administered radioiodine dose. The objective of this study was to define the relationship between thyroid mass estimated by ultrasound and measured thyroid mass following thyroidectomy. This was a retrospective, exempt study that included patients < 18 years of age with < 6 months between thyroid ultrasound and thyroidectomy January 2010-June 2020. Thyroid dimensions by ultrasound, thyroid mass at thyroidectomy and histopathological diagnosis were collected. Published conversion factors were used to estimate thyroid volume with conversion to mass using a density of 1.05g/cm3. Pearson correlations and Bland-Altman difference analyses were used to define the relationship between estimated mass and specimen weight. Linear regression was used to calculate an optimal conversion factor for estimating thyroid mass. We included 86 patients, 67 female (78%), with a mean age of 14.5 ± 3.15 years. Mass estimated using all tested conversion factors had similar strong, positive correlation with specimen weight (r = 0.95). The mean difference between thyroid mass estimated by ultrasound and measured mass ranged from - 0.34g (conversion factor = 0.523) to 1.69g (conversion factor = 0.554). The optimal simplified factor for estimation of thyroid mass for the study sample was 0.537. All published conversion factors for estimating thyroid mass based on linear ultrasound measurements produce good estimates of thyroid mass. Errors in estimated mass are less than 2g on average.

Utility of outpatient fractionated radioiodine therapy for Graves disease involving a large goiter measuring more than 100 mL in volume.

Contrary to large multinodular goiters, reports on 131I radioiodine therapy (RIT) for Graves disease (GD) involving a large goiter are scarce. We retrospectively reviewed a total of 71 consecutive patients (25 males, 46 females) with GD involving a large goiter (>100 mL) who had received RIT in our clinic. Patients with a history of thyroid surgery or with large thyroid nodules and those who had dropped out less than one year after the initial RIT session were excluded. A fixed 131I activity of 481 MBq was administered in most cases. RIT was repeated at intervals of 1-47 months, typically 3-6 months. The follow-up duration after the initial RIT session was 13-233 (median: 81) months. The thyroid volume was estimated using ultrasound. The number of 131I doses were 1 dose in 13 patients, 2 doses in 29, 3 doses in 17, 4 doses in 5, 5 doses in 5, 6 doses in 1, and 8 doses in 1. Sixty-six patients had remission from overt hyperthyroidism after RIT: overt hypothyroidism in 45 patients, subclinical hypothyroidism or euthyroidism in 13, and subclinical hyperthyroidism in 8. Their thyroid volume decreased from 101-481 (median: 126) mL to 1.4-37 (8.2) mL. Three patients still had overt hyperthyroidism under treatment with methimazole after one to three doses, and two dropped out less than six months after the third or sixth dose. Even in GD patients with a large goiter (>100 mL), repeated RIT with an activity of 481 MBq could sufficiently shrink goiters and remit overt hyperthyroidism.

Qualitative and Quantitative Impact of Protective Glucocorticoid Therapy on the Effective 131I Half-Life in Radioiodine Therapy for Graves Disease

This aim of this retrospective study was to determine the impact of glucocorticoid therapy on the effective (131)I half-life in radioiodine therapy for Graves disease. Three hundred fifteen consecutive Graves disease patients undergoing radioiodine therapy at our institution between August 2004 and January 2009 were enrolled. We investigated the influences of thyroid state (hypothyroidism, euthyroidism, hyperthyroidism), antithyroid drug dose before (131)I therapy, thyroid-stimulating hormone receptor antibody (TRAb) level, and qualitative and quantitative factors of prednisolone therapy on the effective (131)I half-life, applying univariate (paired t test) and multivariate (multiple-regression) analyses. Multivariate analyses revealed independent significant effects of the thyroid metabolic state (P = 0.004), antithyroid drugs (P < 0.001), presence of TRAb (P = 0.004), and glucocorticoids (P = 0.046) on thyroidal radioiodine half-life. Compared with euthyroidism, thyrotoxicosis and hypothyroidism reduced the effective half-life; high doses of antithyroid drugs and high TRAb levels had the same effect. Also, glucocorticoid therapy shortened the effective thyroidal radioiodine half-life in a dose-dependent manner. Pharmacologically, this effect is attributable to the prednisolone-induced increase of renal plasma (131)I clearance and the resulting reduction of plasma (131)I available for reuptake into the thyroid during radioiodine therapy. Oral treatment with prednisolone results in a reduction of effective thyroidal (131)I half-life in Graves disease, especially at higher doses.

Myopathy Associated with Acute Hypothyroidism following Radioiodine Therapy for Graves Disease in an Adolescent

Myopathy Associated with Acute Hypothyroidism following Radioiodine Therapy for Graves Disease in an Adolescent

Myopathy Associated with Acute Hypothyroidism following Radioiodine Therapy for Graves Disease in an Adolescent

We describe acute myopathy following I-131 treatment for hyperthyroidism due to Graves Disease (GD) in an adolescent. A 15 year-old diagnosed with GD required treatment with radioactive iodine (I-131) therapy. Six weeks post I-131, he developed generalized muscle cramps. The CK was 19.800 U/L, the total thyroxine was 2.3 mcg/dL (29.6 nmol/L SI) and the estimated free thyroxine (EFT) was 0.5 ng/dL (6.4 pmol/L SI). The ALT was 112 U/L and AST was 364 U/L (normal <35 U/L). The muscle cramps and CK elevation normalized five months after initiation of thyroid replacement therapy. This observation shows that acute myopathy can rarely occur in pediatric patients with GD following treatment with I-131.

Radioiodine treatment of juvenile Graves disease.

Ablation of the thyroid gland with radioactive iodine-I131 is an effective and safe method of therapy for older children and adolescents, as with adults, to treat hyperthyroidism of Graves disease (Graves-Basedow disease). The use of radioiodine as initial therapy or, as more often, the second line of therapy following antithyroid drug treatment is highly efficacious and rarely associated with short-term or long-term side effects. The indications for radioiodine therapy are failure of antithyroid drug therapy, idiosyncratic hypersensitivity reactions to antithyroid drugs, contraindications for surgical therapy including patients who refuse surgery, and the desirability to permanently prevent the development of hyperthyroidism. The treatment will induce permanent primary hypothyroidism within months after the use of ablative doses of radioiodine. The safety and simplicity of clinical management with L-thyroxine therapy for hypothyroidism favor radioiodine therapy for Graves disease over the potential risks from treatment with antithyroid drugs or surgery, and from untreated or relapsing hyperthyroidism. Radioiodine therapy is associated with the lowest morbidity and mortality among the currently available methods of therapy for Graves disease.

Radioiodine therapy for Graves disease as a risk factor of endocrine ophthalmopathy

In 1973 and 1976 2 cases of endocrine ophthalmopathy (EO)after external irradiation of the anterior surface of the neck due to a tumor (Hodgkin's lymphoma) was described. Further observations showed that treatment of Graves' disease (BG) with radioactive iodine (131I) can worsen the course of EO. So, L. De Groot et al., Observing 264 patients after exposure to 131I for BG, found progression of EO in 4% of patients after the 1st course of therapy and in 12% after subsequent sessions. Later the appearance or significant progression of EO in patients treated with 131I has been observed. Some studies have shown that the progression of EO after treatment with 131I without glucocorticoids administration can be observed in 18-30% of cases. Along with this, there is an opinion that 131I does not affect the incidence of clinical symptoms in the orbit and that hypothyroidism that occurs after it does not lead to the progression of eye symptoms. The relationship between treatment and the onset or progression of EO is not clear. Nevertheless, there is evidence of an adverse effect of an elevated level of antibodies to the thyroid stimulating hormone receptor in the blood serum after 131I training for EO.

Early Changes in Thyroid-Stimulating Antibody Activity following Radioiodine Therapy

Objective: The aim of this study was to determine whether or not the titre of thyroid-stimulating hormone receptor antibody with stimulating (TRAb-S) activity changes in patients with Graves’ disease (GD) or toxic multinodular goitres (TMNG) 3 months after treatment with sodium iodide (¹³¹I). Subjects and Methods: Serum specimens were obtained from 21 hyperthyroid patients (15 with GD and 6 with TMNG) at a median 0.5 months before and 3 months after ¹³¹I treatment using a standard ablative dose of 555 MBq. TRAb-S activity was measured in a sensitive and specific luminescent bioassay employing the lulu cell line and expressed as a stimulation index (SI; normal ≤1.5). Results: The mean TRAb-S in the GD patients was 2.72 SI (95% CI: 1.51–4.03) 0.5 months before administration of ¹³¹I and 3.98 SI (95% CI: 1.20–6.76) 3 months after administration of ¹³¹I. The difference was not statistically significant at p < 0.8. It was not elevated in the TMNG patients before (0.57 SI; 95% CI: 0.41– 0.73) and after (1.00 SI; 95% CI: 0.74–1.26) treatment either. Conclusions: Radioiodine therapy for GD or TMNG did not induce a significant change in TRAb-S activity at 3 months after treatment with ¹³¹I, probably due to effective antithyroid therapy or the timing of samples.