131I Therapy For Hyperthyroidism Research Articles

SUN-510 Prolonged RAIA Induced Thyroiditis After 131 I Therapy for Graves’ Hyperthyroidism

Radioactive iodine ablation (RAI) has been used for the treatment of Graves’ hyperthyroidism since 1946 and it is the primary recommended modality for Graves’ disease treatment in many countries. Acute painful radiation thyroiditis after radioiodine treatment for hyperthyroidism of Graves’ disease is considered uncommon. The prevalence is 1-5% in patients treated with 131I therapy for hyperthyroidism. Dose of RAI and thyroid volume can be precipitating factors for post radiation thyroiditis. The higher RAI dose increases the chance of RAI thyroiditis while the larger goiter size decreases the absorbed radiation dose in the thyroid gland. We present a 25-year-old Emirati male previously healthy, who was referred to our service for hyperthyroidism management. He presented with thyrotoxicosis in absence of goiter. All investigations revealed that graves’ disease is the primary cause of his hyperthyroidism. He was treated with RAI ablation 18.3 mCi. Day four after RAI, he presented with severe pain in the anterior neck associated with fatigue, tremor, palpitation and weight loss. Symptoms lasted for 6 weeks post RAI. There was laboratory evidence of thyrotoxicosis presented with further suppression of TSH and higher fT4 than the baseline. Acute radiation thyroiditis was diagnosed and has been commenced on propranolol 10mg BID. Symptoms completely resolved after 6 weeks of treatment and thyroid function returned to normal level. The patient has remained asymptomatic on continued follow up care till eventually became hypothyroid clinically and biochemically. Our case reflects that radioiodine thyroiditis can last for longer period and occur after larger doses of 131I treatment in absence of goiter. Our patient has RAIA induced thyroiditis lasted for 6 weeks post 18.3mCi of 131I, and has no goiter, which were both contributing factors for RAIA induced thyroiditis

131I therapy for hyperthyroidism and consequent appearing of anaplastic carcinoma of the thyroid: simple case-report or real pathophysiologic link?

BACKGROUND 131I is usually employed for the therapy of hyperfunctioning thyroid diseases. This β-emitting radioisotope acts releasing its radiations in small tissue volumes, but it is mandatory to consider, also for the small doses, the carcinogenic risk, well documented with the high 131I dosages used to cure differentiated thyroid cancers. METHODS We describe a case of anaplastic thyroid carcinoma appeared 4 years after therapy with 131I for Graves’ disease. The patient was treated both surgically and with thyonamides for Graves’ disease 20 years before; thereafter she underwent simple nephrectomy owing to Grawitz disease. After some years of well being, she was treated with 131I for a relapse of Graves’ disease. Four years later, she was treated with interleukin-2 and TNF-α, owing to distant metastases (pancreas, liver and lung) of Grawitz cancer. Some months later, because of a rapid enlargement of the thyroid gland, she was thyroidectomized and anaplastic thyroid cancer was histologically documented. DISCUSSION AND CONCLUSIONS It is very difficult to investigate the possible transformation of a benign thyroid lesion to a malignant one, and data from the literature are conflicting. Fractioned doses of 131I are known to induce less cancers than high doses: they allow DNA to repair. Nevertheless, in patients with altered or non valid genetic repair’s mechanisms (i.e. patients with p53 mutations) and, for this reason, prone to develop cancers, even low doses of 131I can induce carcinogenetic effects. In a patient with a history of cancer, who subsequently develops hyperthyroidism, even low doses of 131I can induce anaplastic thyroid cancer; in these subjects, therefore, other treatments than 131I could be preferred for the therapy of Graves’ disease. In our peculiar case, moreover, some studies have noteworthy demonstrated that certain cytokines (IL-1, TGF-β1 e TNF-α) can, rather than inhibit, induce anaplastic thyroid cancer cells to grow.

Clinical and biochemical changes following 131I therapy for hyperthyroidism in patients not pretreated with antithyroid drugs

Background: Radioiodine therapy (131I) for the treatment of hyperthyroidism has been shown to be effective and safe. Despite the extensive experience with radioiodine therapy, the necessity for pretreatment with antithyroid drugs is controversial. Pretreatment is partly based on the concept that antithyroid drugs deplete the thyroidal hormonal stores, thereby reducing the risk of a radioiodine-induced aggravation of hyperthyroidism or thyroid storm. Few data are available on the frequency of clinically significant exacerbations of hyperthyroidism following 131I therapy without prior treatment with antithyroid drugs. The aim of the present study was to determine prospectively the early clinical and biochemical changes after 131I therapy in patients who were not pretreated with antithyroid drugs.Methods: Patients with Graves’ disease (n=21), toxic multinodular goiter (n=11) or toxic adenoma (n=2) were studied before and after 131 I therapy. Clinical and biochemical parameters of thyroid function were investigated before and 1, 2, 8, 11, 18 and 25 days after 131I treatment. Patients were given no antithyroid drugs prior to 131I therapy, all patients received β-blocking agents for symptomatic relief.Results: In 19 of 34 patients, a transient increase in thyroid hormone levels was observed, predominantly in the first week following 131I therapy. None of these patients experienced worsening of thyrotoxic symptoms. This transient increase in thyroid hormone levels was demonstrated in all patients with toxic multinodular goiter, whereas it was found in only six of 21 patients with Graves’ disease. This difference could not readily be explained by differences in pretreatment thyroid hormone levels, administered dose or effectively absorbed dose of 131I.Conclusions:131I treatment of hyperthyroidism without pretreatment with antithyroid drugs may cause a transient increase in thyroid hormone levels. Clinically significant exacerbations of hyperthyroidism were, however, not observed in our study population. Increased hormone levels following 131I therapy were more often seen in patients with toxic multinodular goiter than in patients with Graves’ disease.

Use of radioiodine in the management of hyperthyroidism in the UK: development of guidelines.

Although 131I therapy for hyperthyroidism has been in use for more than 50 years, there are wide variations in every aspect of its administration to patients. A recent survey of physicists and clinicians in the UK documented variations in workloads, responsibility for prescribing, and selection for treatment. Wide variations also were noted in terminology, radioiodine preparations, and activities and doses administered. There was a wide range of comments and reasons given by clinicians for their choice of regimen. The use of antithyroid drugs and beta-blockers before or after 131I therapy also was variable. As a result of these findings, a multidisciplinary group was convened to produce recommended guidelines for the administration of 131I in the UK. The implementation of these guidelines will require consensus among clinicians and this will require further evaluation.

Incidence of hypothyroidism after 131I therapy for hyperthyroidism. Relation to pretherapy serum levels of T3, T4 and thyroid antibodies.

A correlation is reported between serum levels of triiodothyronine (S-T3) and thyroxine (S-T4) before treatment, as well as levels of thyroid antibodies before treatment, and the development of hypothyroidism following 131I therapy in 86 patients with hyperthyroidism. Patients with marked elevation of S-T3 or S-T4 had demonstrable antibodies to thyroid cytoplasmic antigen more often than those with normal or moderately elevated levels, and patients with markedly elevated levels of S-T3 also had a higher incidence of hypothyroidism after treatment. Patients with nodular thyroid glands and with markedly elevated levels of S-T3 required a larger number of 131I doses before no signs of hyperthyroidism persisted in comparison to those with moderately elevated levels.

Cure rate after 131I therapy for hyperthyroidism.

The cure rate of hyperthyroidism after 131I therapy was analysed in 4 473 patients, aged between 14 and 91 years, treated between 1951 and 1975. Despite unchanged treatment principles, the cumulative incidence of cure increased for each 5-year period. Within the first 4 months 34 per cent of the patients with diffuse thyroid glands treated during 1951-1955 were cured, as compared with 59 per cent of those treated 1971-1975, i.e. an increment by a factor of 1.7. The corresponding figures for patients with nodular thyroid glands were 23 and 54 per cent, respectively, or a factor of 2.3.

Effects of 131I therapy on blood borne leucocytes in hyperthyroid patients.

The different types of circulating leucocytes were examined in 54 patients before and 2 to 4 months after 131I therapy for hyperthyroidism. An absolute and differential percentage increase in the number of juvenile segmented neutrophils, eosinophilic and basophilic granulocytes was demonstrated in the patients free from signs of hyperthyroidism after therapy. This increase was statistically significant. No changes occurred in the 11 patients remaining hyperthyroid.

The role of surgery and 131-I therapy for hyperthyroidism in the etiology of thyroid carcinoma.

The role of surgery and 131-I therapy for hyperthyroidism in the etiology of thyroid carcinoma.

Hypoparathyroidism following 131-I therapy for hyperthyroidism

Hypoparathyroidism following 131-I therapy for hyperthyroidism

Hypoparathyroidism Following 131I Therapy for Hyperthyroidism

It is the purpose of this paper to report a patient who developed hypoparathyroidism following the administration of radioactive iodine ( 131 I) for treatment of hyperthyroidism. The medical literature will be reviewed and the pathogenesis of post 131 I hypoparathyroidism commented upon. Patient Summary A 58-year-old Negro man was admitted to Cook County Hospital on March 17, 1965, complaining of goiter and weight loss of 18.1 kg (40 lb) in spite of excellent appetite, generalized weakness, and nervousness of six months' duration. He also complained of ankle edema and dyspnea on exertion. A daughter had been treated for hyperthyroidism. Physical examination revealed a tall, thin, hyperkinetic man with a blood pressure of 120/70 mm Hg; pulse rate, 96 beats per minute; respiration, 22 breaths per minute; and temperature, 98.6 F (37 C). His skin was smooth, warm, and moist; his upper eyelids were retracted but he had no exophthalmos. The