Radioiodine-induced Hypothyroidism Research Articles

6537 Recurrent Graves Thyrotoxicosis After Prolonged Radioiodine-Induced Hypothyroidism

Abstract Disclosure: H.K. Deveaux: None. A. Gundeti: None. K. Mitrollari: None. A.P. Calimag: None. T. Yasmeen: None. Radioactive iodine (I-131) ablation (RAI) is one of the effective therapies for Graves’ disease (GD). Successful treatment is indicated by sustained, irreversible hypothyroidism requiring lifelong replacement for which recurrence of disease rarely develops. Recurrent hyperthyroidism is a rare development without apparent predisposition. Here, we describe a case of recurrent thyrotoxicosis after 36 years of RAI.70-year-old female PMH atrial fibrillation (AFib) on apixaban s/p cardioversion, HTN, HFpEF, Pulmonary HTN, and Graves’ Disease s/p RAI ablation 36 years ago with RAI-induced hypothyroidism. The patient was initially on levothyroxine for post-ablative hypothyroidism and stopped taking levothyroxine around 2019. NM scintigraphy done in 2019 showed an abnormal I-123 thyroid uptake and scan with the five-hour radioiodine thyroid uptake showed mildly hyperthyroid. On the thyroid scan, there is a note of a prominent pyramidal lobe with some thyroid gland asymmetry. In 2022, the patient was admitted for new-onset AFib and was noted to have subclinical hyperthyroidism with TSH 0.157, fT4 1.4, TrAb>40, and TSI 34.8. The patient was started on methimazole, which she stopped one month later. During this admission, the patient presented secondary to a mechanical fall and was found to be in AFib with a rapid ventricular rate. Her labs were significant for TSH<0.008 fT4 4.2, TrAb >40. Methimazole was restarted with maximal doses of diltiazem and metoprolol for rate control. Thyroid ultrasound demonstrated an enlarged, heterogeneous thyroid gland with increased vascularity and multiple bilateral TR3 thyroid nodules.Hyperthyroidism affects approximately 1.2% of the population. GD involves autoantibodies activating the thyrotropin receptor, increasing synthesis and release of thyroid hormone and is for 50-60% of cases with a 5-to-10-fold preference for females. RAI ablation is preferred, being inexpensive, with a cure rate approaching 100%. The incidence of transient hypothyroidism post-RAI varies from 9-17%. Retrospective studies have observed hyperthyroidism within the first 12 months post-RAI; however, some cases have seen a resurgence as late as 22 years later. Recurrent hyperthyroidism is an uncommon occurrence with various postulated aetiologies, such as inadequate dosing/incomplete ablation with residual cells remaining viable and regenerating in the setting of increased TSIiv, Marine-Lenhart syndrome (MLS), or an unclear mechanism associated with autoimmunity in the presence of TSI. Hyperthyroidism rarely recurs in GD after successful post-ablative treatment with RAI. Our case, while an uncommon presentation and underlying aetiology yet to be determined, illustrates the importance of continued surveillance, even after successful treatment.‌ Presentation: 6/3/2024

Neonatal Thyrotoxicosis in Infants of Mothers with Graves' Disease Treated for Radioiodine-Induced Hypothyroidism: A Literature Review.

Fetal and neonatal thyrotoxicosis occurs in up to 5% of pregnancies in mothers with Graves' disease (GD). This condition is caused by stimulating antibodies against the thyrotropin receptor (TRAbs) that cross the placenta and may stimulate the fetal thyroid, typically in the second half of pregnancy. GD is often treated with radioiodine, resulting in hypothyroidism in most patients, but TRAbs can persist for several years. Even if a pregnant mother is hypothyroid after radioiodine therapy or surgery, her TRAbs can still, although rarely, induce fetal hyperthyroidism. In this review, we first present two cases of neonatal hyperthyroidism in mothers with GD who became hypothyroid after prior radioiodine therapy, identified through a 10-year analysis of the National Perinatal System in Slovenia. Based on these cases, we provide an overview of existing data on this rare clinical condition in neonates. We also discuss the underlying mechanisms and clinical outcomes based on currently available data. In conclusion, our review highlights the importance of careful monitoring during pregnancy in all women with GD, even in those well managed after radioiodine therapy or surgery.

Treatment of subclinical hyperthyroidism in patients older than 50 years: A randomized controlled study.

Subclinical hyperthyroidism (SCH) is common and associated with atrial fibrillation (AF) risk in the elderly. Current guidelines rely on a low level of evidence. Randomized clinical trial including patients 50 years and older, with TSH <0.4 mU/L and normal thyroid hormone concentrations. All patients showed autonomy on thyroid scan. They were randomized either to receive radioiodine (I131) or to be monitored and treated only if they underwent AF or evolved towards overt hyperthyroidism. Primary outcome was the onset of new AF. Secondary outcomes were treatment-induced hypothyroidism rate and health-related quality of life. 144 patients (mean age 65.3±8.9y, 76% female) were randomized, 74 to surveillance and 70 to treatment. Four patients in the surveillance group and one in the treatment group developed AF (p=0.238). However, the patient who developed AF in the treatment group maintained TSH <0.4 mU/L at AF onset. A post-hoc analysis was carried out and showed that when normalization of TSH was considered, the risk of AF was significantly reduced (p=0.0003). In the surveillance group, several patients showed no classical characteristics associated with AF risk, including age>65y or TSH<0.1mU/L. Of 94 patients treated using radioiodine, 25% developed hypothyroidism during follow-up. Due to recruitment difficulties this study failed to demonstrate that SCH treatment can reduce significantly the incidence of AF in patients older than 50 years with thyroid autonomy even if all the patients who developed AF maintained TSH <0.4 mU/L. This result must be balanced with the increased risk of radioiodine-induced hypothyroidism.

FGF21 Is Released During Increased Lipogenesis State Following Rapid-Onset Radioiodine-Induced Hypothyroidism.

BackgroundFGF21 pharmacological treatment reverses fatty liver and lowers serum triglyceride concentration but FGF21 serum level is increased in hepatic steatosis. FGF21 secretion is induced by thyroid hormones in vitro.PurposeTo determine the influence of thyroid hormones and metabolic changes secondary to thyroid dysfunction on FGF21 secretion in humans.Materials and MethodsThis was a case-control study. 82 hyperthyroid and 15 hypothyroid patients were recruited together with 25 healthy controls. Of those with hyperthyroidism, 56 received radioiodine treatment and 42 of them achieved hypothyroidism and then euthyroidism within one year following therapy. Radioiodine-induced hypothyroidism developed abruptly within a six week interval between clinic visits. FGF21 serum levels were determined with an ELISA method.ResultsSerum FGF21 levels did not differ in hyper- and hypothyroid patients in comparison to controls [median 103.25 (interquartile range, 60.90-189.48) and 86.10 (54.05-251.02) vs 85.20 (58.00-116.80) pg/mL P=0.200 and 0.503, respectively]. In hyperthyroid patients treated with radioiodine, serum FGF21 levels increased significantly in rapid-onset hypothyroidism in comparison to the hyperthyroid and euthyroid phase [median 160.55 (interquartile range, 92.48 - 259.35) vs 119.55 (67.78-192.32) and 104.43 (55.93-231.93) pg/mL, P=0.034 and 0.033, respectively]. The rising serum FGF21 level correlated positively with serum triglycerides (Spearman coefficient rs=0.36, P=0.017) and inversely with serum SHBG (rs=-0.41, P=0.007), but did not correlate with thyroid hormone levels.ConclusionsThere was a transient increase in FGF21 serum level during rapid-onset hypothyroidism following radioiodine treatment. There was no association between FGF21 serum level and thyroid hormones. In radioiodine-induced hypothyroidism, the rising serum FGF21 concentration correlated positively with rising serum triglycerides and negatively with falling SHBG, reflecting increased hepatic lipogenesis.

Serum Thyroid Hormone Balance in Levothyroxine Monotherapy-Treated Patients with Atrophic Thyroid After Radioiodine Treatment for Graves' Disease

Background: Some studies reported that among athyreotic patients on levothyroxine (LT4) after total thyroidectomy, patients with normal serum thyrotropin (TSH) levels had mildly low serum free triiodothyronine (fT3) levels, whereas patients with mildly suppressed serum TSH levels had normal serum fT3 levels. The reduction of the thyroid volume (TV) after radioiodine treatment for Graves' disease is well known; however, a few studies evaluated thyroidal function including serum triiodothyronine (T3) levels of hypothyroid patients on LT4 after radioiodine treatment in detail.Methods: We retrospectively studied 446 patients treated with LT4 for radioiodine-induced hypothyroidism and who had undergone ultrasonography. We compared serum fT4 and fT3 levels in hypothyroid patients on LT4 who presented an atrophic thyroid change after radioiodine treatment, with those in the euthyroid matched control group with intact thyroids. We also stratified patients with normal TSH levels according to TV and evaluated serum thyroid hormone levels.Results: In 356 of 446 (80%) patients, TV was lower than the lower limit of the 95% reference range of controls. Excluding 43 patients with high serum TSH levels, we assessed thyroid function test results in 313 patients with atrophic thyroid glands. Of these cases, eight patients with strongly suppressed TSH levels had serum fT3 levels that were significantly higher than those in controls (p < 0.001). Overall, 27 patients with mildly suppressed TSH levels had serum fT3 levels equivalent to those in controls (p = 0.386), whereas 278 patients with normal TSH levels had serum fT3 levels that were significantly lower than those in controls (p < 0.001). We also assessed fT3 levels relative to TV in 326 patients with normal TSH levels. Of these cases, in 267 patients with TV less than 5 mL and in 46 patients with TV between 5 and 10 mL, serum fT3 levels were significantly lower than those in controls (p < 0.001). In 13 patients with TV more than 10 mL, serum fT3 levels were equivalent to those in controls (p = 0.844).Conclusions: Serum thyroid hormone balance in most patients on LT4 after radioiodine treatment for Graves' disease was similar to that in athyreotic patients on LT4. Mild TSH suppression with LT4 is needed to achieve normal fT3 levels in such patients.

Patients Treated for Hyperthyroidism are at Increased Risk of Becoming Obese: A Large Prospective Cohort Study

Background: The most commonly reported symptom of hyperthyroidism is weight loss but successful treatment increases weight. It is not clear if represents replenishment of premorbid weight or overshoot beyond expected regain. Moreover, if there is excessive weight gain, it is unclear whether this is associated with the applied treatment modality. Methods: We analysed 1373 patients with overt hyperthyroidism seen in a secondary care setting. We compared body mass index at initial and discharge visits with the age-sex-matched background population. We modelled longitudinal weight data in relation to treatment modality and thyroid function. Findings: During treatment of hyperthyroidism, men gained 8·0kg (SD±7·5) and women 5·5kg (±6·8). At discharge, there was a significantly increased risk of obesity in male (OR=1·7, 95%CI 1·3¬-2·2, P 10 mIU/L; 0·5kg, 0·3-0·7, P<0·001) or free thyroxine was reduced (fT≤10 pmol/L; 0·3kg, 0·1-0·4, P<0·001) during follow-up. Initiation of levothyroxine was associated with further weight gain (0·4kg, 0·2-0·6, P<0·001) and the predicted excess weight gain in radioiodine-induced hypothyroidism was 1·8kg. Interpretation: Treatment for hyperthyroidism is associated with significant risks of becoming obese. Radioiodine treatment and subsequent development of hypothyroidism were associated with small but significant amounts of excess weight gain compared with antithyroid drugs alone. Funding: Institutional (higher education) Declaration of Interest: All authors declare no conflict of interest. Ethical Approval: The project was 95 approved and registered by the University Hospitals Birmingham NHS Foundation Trust (CARMS-96 11842).

Recurrent Graves' hyperthyroidism after prolonged radioiodine-induced hypothyroidism.

Radioactive iodine (RAI) is the most cost effective therapy for Graves' disease (GD). Patients with GD who have become hypothyroid after therapeutic RAI, rarely develop recurrence of disease. Herein we describe a case of recurrence of thyrotoxicosis after 2 years of hypothyroidism. We present the clinical features, laboratory findings, imaging and management of an unusual case of recurrent hyperthyroidism. A 48-year-old male presented to the emergency room with a 2-day history of palpitation, chest discomfort and 30 pounds of weight loss. Examination was remarkable for rapid and irregular pulse, diffuse thyromegaly and brisk deep tendon reflexes but no eye changes or tremors. Laboratory tests showed thyroid-stimulating hormone (TSH) of <0.004 (0.3-5.6 mIU/ml), free thyroxine (FT4) 4.96 (0.9-1.8 ng/dl), free triiodothyronine (FT3) >20 (1.8-4.7 pg/ml), total thyroxine >800 (80-200 ng/dl). Electrocardiogram showed atrial fibrillation with rapid ventricular response. RAI uptake and scan showed a homogenous gland with 54% uptake in 6 h and 45% in 24 h. He was treated with propranolol and propylthiouracil with some clinical improvement. He subsequently underwent RAI therapy and developed hypothyroidism after 8 weeks. Hypothyroidism was treated with levothyroxine. At 2 years after RAI ablation, he again developed symptoms of hyperthyroidism and had suppressed TSH. The levothyroxine dose was stopped, 3 weeks after discontinuing levothyroxine, he remained hyperthyroid with TSH of 0.008 and FT4 of 1.62 and FT3 of 4.8. RAI uptake demonstrated 17% uptake at 24 h. Recurrent hyperthyroidism in GD is uncommon after development of post-ablative hypothyroidism. Our case illustrates the need for continued surveillance.

Comparison of Mortality in Hyperthyroidism During Periods of Treatment With Thionamides and After Radioiodine

Hyperthyroidism is common, but opinions regarding optimal therapy with antithyroid drugs or radioiodine (131-I) differ. There are no randomized trials comparing these options in terms of mortality. The aim of the study was to determine whether mortality associated with hyperthyroidism varies with treatment administered or other factors. We conducted a prospective observational population-based study of 1036 subjects aged ≥ 40 years presenting to a single specialist clinic from 1989-2003 with a first episode of hyperthyroidism who were followed until June 2012. Antithyroid drugs or radioiodine (131-I) were administered. We compared causes of death with age-, sex-, and period-specific mortality in England and Wales and used within-cohort analysis of influence of treatment modality, outcome, disease etiology, severity and control, and comorbidities. In 12 868 person-years of follow-up, 334 died vs 290.6 expected (standardized mortality ratio [SMR], 1.15 [95% confidence interval (CI),1.03-1.28]; P = .01). Increased all-cause mortality largely reflected increased circulatory deaths (SMR, 1.20 [95% CI, 1.01-1.43]; P = .04). All-cause mortality was increased for the person-years accumulated during thionamide treatment (SMR, 1.30 [95% CI, 1.05-1.61]; P = .02) and after 131-I not associated with hypothyroidism (SMR, 1.24 [95% CI, 1.04-1.46]; P = .01) but not during T₄ replacement for 131-I-induced hypothyroidism (SMR, 0.98 [95% CI, 0.82-1.18]; P = .85). Within-cohort analysis comparing mortality during thionamide treatment showed a similar hazard ratio (HR) for all-cause mortality when 131-I did not result in hypothyroidism (HR, 0.95 [95% CI, 0.70-1.29]), but reduced mortality with 131-I-induced hypothyroidism (HR, 0.70 [95% CI, 0.51-0.96]). Reduced mortality associated with hypothyroidism was seen only in those without significant comorbidities and not in those with other serious diseases. Atrial fibrillation at presentation (P = .02) and an increment of 10 pmol/L in serial free T₄ concentration during follow-up (P = .009) were independently associated with mortality. Among hyperthyroid subjects aged 40 years or older, mortality was increased during periods of thionamide treatment and after radioiodine not resulting in hypothyroidism, but not during follow-up after radioiodine-induced hypothyroidism. Independent associations of mortality with atrial fibrillation and incomplete biochemical control during treatment indicate potential causative links with poor outcome.

Radioiodine Thyroid Ablation in Graves′ Hyperthyroidism: Merits and Pitfalls

Ablative approaches using radioiodine are increasingly proposed for the treatment of Graves′ disease (GD) but their ophthalmologic and biological autoimmune responses remain controversial and data concerning clinical and biochemical outcomes are limited. The aim of this study was to evaluate thyroid function, TSH-receptor antibodies (TRAb) and Graves′ ophthalmopathy (GO) occurrence after radioiodine thyroid ablation in GD. We reviewed 162 patients treated for GD by iodine-131 (131I) with doses ranging from 370 to 740 MBq, adjusted to thyroid uptake and sex, over a 6-year period in a tertiary referral center. Collected data were compared for outcomes, including effectiveness of radioiodine therapy (RIT) as primary endpoint, evolution of TRAb, and occurrence of GO as secondary endpoints. The success rate was 88.3% within the first 6 months after the treatment. The RIT failure was increased in the presence of goiter (adjusted odds ratio = 4.1, 95% confidence interval 1.4–12.0, P = 0.010). The TRAb values regressed with time (r = −0.147; P = 0.042) and patients with a favorable outcome had a lower TRAb value (6.5 ± 16.4 U/L) than those with treatment failure (23.7 ± 24.2 U/L, P < 0.001). At the final status, 48.1% of patients achieved normalization of serum TRAb. GO occurred for the first time in 5 patients (3.7%) who were successfully cured for hyperthyroidism but developed early and prolonged period of hypothyroidism in the context of antithyroid drugs (ATD) intolerance (P = 0.003) and high TRAb level (P = 0.012). On the basis the results of this study we conclude that ablative RIT is effective in eradicating Graves’ hyperthyroidism but may be accompanied by GO occurrence, particularly in patients with early hypothyroidism and high pretreatment TRAb and/or ATD intolerance. In these patients, we recommend an early introduction of LT4 to reduce the duration and the degree of the radioiodine-induced hypothyroidism.

Recurrent Graves' Disease after Successful Radioiodine Therapy Induced Hypothyroidism: A Rare Occurrence

ABSTRACT One of the three principal therapies of Graves' disease is radioiodine treatment. Hypothyroidism is considered as a treatment end point of successful radioiodine treatment for Graves' disease. The radioiodine-induced hypothyroidism is mostly irreversible. Though, early recurrences can be due to treatment failure, inadequate radioiodine dose or rarely due to Marine-Lenhart syndrome. Here, we report a rare case of recurrent Graves' disease, 3 years after successful radioiodine therapy induced hypothyroidism in a 50-year-old lady.

Thyroid Function and Mortality in Patients Treated for Hyperthyroidism

Hyperthyroidism has been reported to cause excess all-cause and circulatory mortality. Whether this can be reversed is unknown, as is the influence of mild persisting thyroid dysfunction and treatment-induced hypothyroidism. To determine whether radioiodine treatment is associated with increased mortality and to determine the influences of mild thyroid dysfunction and the development of overt hypothyroidism treated with thyroxine (T(4)). A population-based study of 2668 individuals aged 40 years or older treated for overt hyperthyroidism with radioiodine in the West Midlands region of England from 1984-2002. Cause of death compared with age- and period-specific mortality in England and Wales and assessment of the influence of T(4) therapy for radioiodine-induced hypothyroidism and subclinical thyroid dysfunction on mortality. In 15,968 person-years of follow-up, 554 died vs 487 expected deaths (standardized mortality ratio [SMR], 1.14; 95% confidence interval [CI], 1.04-1.24, P=.002). Increased risks of all-cause and circulatory deaths vs age- and period-specific mortality were observed in follow-up in those not requiring, or prior to, T(4) therapy. These increased risks were not observed during follow-up on T(4) therapy (circulatory disease SMR prior to T(4), 1.33; 95% CI, 1.14-1.53 vs SMR, 0.91; 95% CI, 0.70-1.17 during T(4)). Patients receiving T(4) had decreased risk of mortality vs risk in the period not requiring, or prior to, T(4) therapy (all-cause mortality hazard ratio [HR], 0.65; 95% CI, 0.54-0.79; circulatory mortality HR, 0.65; 95% CI, 0.48-0.87). Increased all-cause mortality vs the background population was observed in the period prior to T(4) therapy in follow-up associated with low, normal, and high serum thyrotropin. The SMR for ischemic heart disease increased slightly when analyzed by serum thyrotropin, high serum thyrotropin being the highest SMR (low thyrotropin SMR, 1.06; 95% CI, 0.75-1.45; normal thyrotropin SMR, 1.17; 95% CI, 0.76-1.71; high thyrotropin SMR, 1.48; 95% CI, 0.86-2.37). Comparison within the cohort showed that mild hypothyroidism prior to T(4) therapy was associated with increased risk of mortality from ischemic heart disease vs biochemical euthyroidism (HR, 2.08; 95% CI, 1.04-4.19). Patients treated with radioiodine for hyperthyroidism had increased mortality vs age- and period-specific mortality in England and Wales, a finding no longer evident during T(4) therapy. This supports treating hyperthyroidism with doses of radioiodine sufficient to induce overt hypothyroidism. The association within the cohort of mortality from ischemic heart disease with subclinical hypothyroidism suggests T(4) replacement should be considered should this biochemical abnormality develop after radioiodine therapy.

Effect of replacement doses of thyroxine on bone mineral density

Hyperthyroidism is associated with a reduction in bone mineral density (BMD). Suppressive doses of thyroxine (T4), inducing subclinical hyperthyroidism, have been reported by some investigators to reduce BMD. Little work has been done on replacement doses of T4. The aim was to investigate the effect of replacement doses of T4 on BMD. Cross-sectional study of hypothyroid patients on long-term T4 replacement doses, comparing those who had primary hypothyroidism with those who were previously hyperthyroid. Fifty women on replacement doses of T4 for more than 5 years were recruited. Twenty-five were treated for primary (group 1) and 25 for radioiodine-induced hypothyroidism (group 2). They were well matched for age, menstrual status, smoking history, body mass index (BMI), dose and duration of T4 replacement as well as thyroid status. BMD was assessed by dual energy X-ray absorptiometry. Free T4 (FT4), FT3 as well as ultrasensitive TSH assays were used to assess thyroid status. The two groups showed no difference in BMD (g/cm2) of the lumbar spine (1.008 vs. 0.957, P = 0.25), femoral neck (0.745 vs. 0.735, P = 0.79) and total hip (0.878 vs. 0.837, P = 0.24). When the two groups were pooled, there was no significant difference between the patients and a reference population with femoral neck and total hip BMD expressed as a standard deviation (Z) score. However, the lumbar spine mean Z score was significantly greater than zero. For each site, there was a negative correlation of BMD with age in at least one group but, in general, BMI, FT4, FT3 and duration of T4 replacement did not correlate with BMD. T4 dose, however, had a consistent positive correlation with BMD in the spine, femoral neck and the hip (P = 0.01, 0.04 and 0.02, respectively) in group 2 but not group 1. In this study, there is no evidence for a difference in bone mineral density in patients receiving replacement doses of thyroxine irrespective of the aetiology of their hypothyroidism. The reduced bone mineral density associated with hyperthyroidism appears to be restored, maintained and in some cases possibly improved while on long-term thyroxine replacement post-radioiodine.

Hyperthyroidism. Current treatment guidelines.

Hyperthyroidism is common and affects approximately 2% of women and 0.2% of men. The most common cause of hyperthyroidism is Graves' disease, an autoimmune disorder associated with circulating immunoglobulins that bind to and stimulate the thyrotropin (TSH) receptor, resulting in sustained thyroid overactivity. Toxic nodular goitres cause hyperthyroidism due to autonomous hyperfunctioning of localised areas of the thyroid. There are 3 recognised modalities of treatment for hyperthyroidism: antithyroid drugs, surgery and radioiodine. All are effective but no single method offers an absolute cure. Patients with Graves' disease may be prescribed antithyroid drugs over a period of 12 to 18 months with a view to inducing a long term remission. These drugs are also often given for a short period to render the patient euthyroid before definitive therapy with radioiodine or thyroidectomy. However, antithyroid drugs will not 'cure' hyperthyroidism associated with a toxic nodular goitre. The use of radioiodine as a first-line therapy for hyperthyroidism is growing. It is well tolerated, with the only long term sequelae being the risk of developing radioiodine-induced hypothyroidism. Radioiodine can be used in all age groups other than children, although it should also be avoided in pregnancy and during lactation. Pregnancy should be avoided for 4 months following its administration. Radioiodine may cause a deterioration in Graves' ophthalmopathy and corticosteroid cover may reduce the risk of this complication. The treatment of choice for toxic nodular goitre hyperthyroidism is radioiodine. Surgery, either subtotal or near-total thyroidectomy, has limited but specific roles to play in the treatment of hyperthyroidism: this approach is rarely used in patients with Graves' disease unless radioiodine has been refused or there is a large goitre causing symptoms of compression in the neck. The goal of surgery is to cure the underlying pathology while leaving residual thyroid tissue to maintain postoperative euthyroidism.

Recurrent Hyperthyroidism After Radioiodine-Induced Hypothyroidism: Report of Two Cases and Literature Review

The practice at the Mayo Clinic in treating Graves' disease with radioiodine (131 I) is to achieve a hypothyroid state. Less than 10% of the patients need more than one dose. Although cases of transient hypothyroidism have been reported after treatment with 131 I, the recurrence of hyperthyroidism is unusual after hypothyroidism has been induced with 131 I. We studied two cases seen at our institution in the past year in which the circumstances behind the recurrence have never been reported previously. The first case illustrates a recurrence of hyperthyroidism after the patient had received 38.5 mCi of 131 I. The second patient had recurrence of hyperthyroidism after 22 years of replacement therapy with levothyroxine. Both patients had increased levels of thyroid-stimulating immunoglobulin. We believe that the recurrence of the hyperthyroid state in these two patients was due to incomplete ablation of the thyroid. Apparently 131 I caused hypothyroidism, but residual cells remained viable and under continuous stimulation of thyroid-stimulating immunoglobulin produced recurrent thyrotoxicosis.

Changes in Serum Thyroid Hormone Autoantibody Concentrations during Pregnancy: A Case Report

A 29-year-old female patient with Graves' disease who developed thyroid hormone autoantibodies (THAA) under treatment with methimazole is presented. THAA were identified as IgG-kappa. During a first pregnancy that ended by miscarriage in the 3rd month, the titer of anti-thyroxine autoantibodies decreased by about 30%. Relapse of Graves' disease occurred 2 months later and an increase in serum THAA concentration to the initial titer was observed. THAA titer remained unchanged during treatment with methimazole and afterwards during thyroxine supplementation for radioiodine-induced hypothyroidism. During a second pregnancy, a decrease in anti-thyroxine autoantibody titer reached 45% at the time of delivery and an increase by 20% was noted 5 months later. A similar decline in THAA concentration was shown during a third pregnancy. The changes in THAA concentrations observed during pregnancy suggest an immunological influence of pregnancy on the THAA production, as previously demonstrated in other autoimmune diseases, like Hashimoto's thyroiditis.

On the choice of treatment for hyperthyroidism.

Article1 February 1956ON THE CHOICE OF TREATMENT FOR HYPERTHYROIDISME. PERRY MCCULLAGH, M.D., F.A.C.P.E. PERRY MCCULLAGH, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-44-2-292 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDuring the last 50 years there have been repeated sweeping changes in the management of hyperthyroidism. The changes have veered from emphasis on radical surgery to conservative surgery, away from surgery altogether and toward medicine, and away from medicine toward radioactive iodine. The emphasis probably will continue to shift until the etiology of hyperthyroidism has been established and the disease can be attacked specifically at its origin or, better still, prevented.It was in 1869 that Cheadle1reported excellent results in the treatment of hyperthyroidism with iodine, but the medical world was unconvinced. For many years recognized authorities warned against...Bibliography1. Cheadle WB: Exophthalmic goiter, St. George's Hosp. Rep. 4: 175-192, 1869. Google Scholar2. ChevalleyMcGavackKenigsbergPearson JTHSS: A four-year study of the treatment of hyperthyroidism with methimazole, J. Clin. Endocrinol. and Metabolism 14: 948-960 (Aug.) 1954. CrossrefGoogle Scholar3. Davidson LA: Clinical trial of methimazole in treatment of thyrotoxicosis, Brit. M. J. 2: 1300-1303 (Dec. 12) 1953. CrossrefMedlineGoogle Scholar4. SpechtBoehme NWEJ: Death due to agranulocytosis induced by methimazole therapy, J. A. M. A. 149: 1010-1011 (July 12) 1952. CrossrefMedlineGoogle Scholar5. 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Author, Article, and Disclosure InformationAffiliations: Cleveland, Ohio*Presented at the Thirty-sixth Annual Session of the American College of Physicians, Philadelphia, Pennsylvania, April 26, 1955.From the Department of Endocrinology, The Cleveland Clinic Foundation, and The Frank E. Bunts Educational Institute, Cleveland, Ohio. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRecurrent Hyperthyroidism After Radioiodine-Induced Hypothyroidism: Report of Two Cases and Literature ReviewDie Strahlentherapie gutartiger Erkrankungen innersekretorischer DrüsenDie Strahlentherapie gutartiger Erkrankungen innersekretorischer DrüsenTHE TREATMENT OF TOXIC NODULAR GOITER WITH RADIOACTIVE IODINE: 10 YEARS' EXPERIENCE WITH 436 CASES*MILTON ELLER, M.D., SOLOMON SILVER, M.D., F.A.C.P., STEPHEN B. YOHALEM, M.D., F.A.C.P., ROBERT L. SEGAL, M.D.Treatment of Toxic Nodular Goitre with Radioactive IodineChapter I: Physical Growth 1 February 1956Volume 44, Issue 2Page: 292-301KeywordsAdenomasEndocrinologyEtiologyHyperthyroidismLesionsPregnancySurgeryThyroid ePublished: 1 December 2008 Issue Published: 1 February 1956 PDF downloadLoading ...