|Year : 2013 | Volume
| Issue : 3 | Page : 96-99
Radioactive iodine therapy for hyperthyroidism: Our experience
Subodh Banzal, Abhishek Singhai, Jamal Asaraf, DC Tiwary, Padmnabh Sharma, Pragya Jain
Department of Medicine, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India
|Date of Web Publication||6-Aug-2013|
Department of Medicine, Sri Aurobindo Medical College, Indore, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
Context: Radioactive iodine (RAI) therapy for hyperthyroidism is safe and definitive, although, post-treatment hypothyroidism and the need for life-long thyroxine are to be expected. The optimal dose of I-131 for hyperthyroidism is still debated. Aims: The aim of this study is to evaluate the response rate of hyperthyroidism to RAI treatment, optimum effective dose, effect of pre-treatment with anti-thyroid medications, ophthalmopathy, and hypothyroidism incidence post RAI therapy. Subjects and Methods: A prospective study was conducted in a tertiary care center to look at the therapeutic practice of use of RAI in the treatment of hyperthyroidism, to determine whether the expected or desired therapeutic outcome is achieved. Seventy consecutive subjects of hyperthyroidism, treated with RAI were followed-up. Results: Grave's disease was the most common cause of hyperthyroidism. The dose of RAI ranged from 4 mCi to 17.5 mCi. Over 95% cure rate achieved with RAI dose 4-7 mCi. Hypothyroidism occurred in 52.17% cases with this dose. Goiter size significantly decreased with RAI therapy. No deterioration of eye signs observed with RAI therapy. Pre-treatment with anti-thyroid drugs had no influence on outcome. Conclusions: RAI treatment is an effective modality for definitive treatment of hyperthyroidism with long-term cure approaching 95%. Its efficacy, safety and low cost made it the preferred definitive treatment for most patients with hyperthyroidism.
Keywords: Hyperthyroidism, hypothyroidism, radioactive iodine
|How to cite this article:|
Banzal S, Singhai A, Asaraf J, Tiwary D C, Sharma P, Jain P. Radioactive iodine therapy for hyperthyroidism: Our experience. Thyroid Res Pract 2013;10:96-9
|How to cite this URL:|
Banzal S, Singhai A, Asaraf J, Tiwary D C, Sharma P, Jain P. Radioactive iodine therapy for hyperthyroidism: Our experience. Thyroid Res Pract [serial online] 2013 [cited 2017 Jul 26];10:96-9. Available from: http://www.thetrp.net/text.asp?2013/10/3/96/116134
| Introduction|| |
Hyperthyroidism is a common endocrine disease. The essential goal in the management of hyperthyroidism is to reduce the hyper secretion of thyroid hormones. Of the three forms of therapy available, the use of radioactive iodine (RAI) as the first-line of treatment has gradually, but steadily been increasing over the years and is presently considered to be the treatment of choice for most patients beyond adolescent years because of its effectiveness, simplicity, and relatively low cost. Pregnancy and breast feeding are absolute contraindications. However, there is yet no uniformity in the application and some controversies still exist in some aspects of RAI Therapy. Different approaches of RAI therapy have varied, from repeated low doses in order to reduce the incidence of hypothyroidism to high dose ablative therapy with consequent hypothyroidism. Hypothyroidism may occur weeks, months or even years after RAI therapy. In this study, we evaluated 70 cases of hyperthyroidism that were treated with different doses over a period of 5 years. The results of RAI therapy were evaluated and compared with studies in literature in respect to cure rate (remission of hyperthyroidism) and incidence of hypothyroidism.
| Materials and Methods|| |
Total 70 cases received RAI therapy over 5 years period. Out of these, 3 did not complete follow-up criteria therefore, not calculated for final outcome. Remaining Seventy cases of hyperthyroidism treated with RAI were analyzed.
The diagnosis of hyperthyroidism was based on clinical grounds, biochemically on raised levels of total/free Triiodothyronine T3 (> 3.5-6.5 pmol/L/0.9-2.8 nmol/L), total/free Thyroxine T4 (58-161 nmol/L/10-23 pmol/L) and suppressed serum Thyroid Stimulating Hormone (TSH) (< 0.1-0.3) using immune assay and in most of the cases increased uptake of Tc99 on thyroid scintigraphy (uptake more than 4%). Patients on anti-thyroid drugs at the time of examinations were considered hyperthyroid. The size and type of goiter at the time of diagnosis was determined on the basis of physical examination: None (non-palpable or normal size gland), small (palpable but not visible, around <30 g), moderate to large (palpable and visible, around 30-60 g) and large (> 60 g). Thyroid ophthalmopathy was defined as per NO-SPECS classification. Following demographic factors were retrieved from hospital record : g0 ender, age at the time of diagnosis, presence of eye signs, size and shape of goiter, serum concentration of Total/Free T3T/FT3, Total/Free T4(T/FT4 and TSH. 44 cases were receiving anti-thyroid drugs before RAI therapy. All anti-thyroid drugs were stopped 3 days prior to I-131 dose. The RAI dose was calculated arbitrarily in most cases; often by an empirical fixed dose based on the goiter size and Tc99 uptake values. The patients were reviewed at 3 monthly intervals for at least 1 year. During each follow-up, clinical examination and laboratory measures of serum T4, T3 and TSH were carried out. Patient was considered euthyroid if serum Free T3 and Free T4 were normal in spite of suppressed TSH. Hypothyroidism was diagnosed if a patient had TSH>10 IU/l with low serum T4. Patients who were found to have developed hypothyroidism were given appropriate therapy; those with persisting hyperthyroidism were either followed-up on beta blockers or were given anti-thyroid drugs. Some patients were given another dose of RAI patient clinically and biochemically remained thyrotoxic, but not before 6 months of the previous RAI therapy.
Statistical analyses were performed using SPSS for Windows 7 13.0 (SPSS, Chicago, Ill). The Chi-square test was used to determine statistical significance between two categorical variables. P value <0.05 was considered statistically significant.
| Results|| |
[Table 1], [Table 2], [Table 3] and [Table 4] summarizes the demographic and clinical characteristics of 70 subjects. Out of 70 cases of thyrotoxicosis, 54 cases were diagnosed to have Grave's disease, 10 cases diagnosed as toxic multi-nodular goiter (TMG), 3 cases diagnosed as toxic adenoma and 3 cases had mixed disease (toxic nodular goiter and Grave's disease). All cases were treated with I-131 dose varied from 4 mCi to 17.5 mCi.
Mean age of patients with Grave's Disease was 35.66 ± 14.02 years, TMG was 44.4 ± 10.17 years, toxic adenoma was 37.5 ± 7.5 years and mixed disease was 34.33 ± 10.8 years. Mean serum T4 level in Graves's disease was 301.77 ± 102.3 nmol/L as compared to 265.44 ± 67.3 nmol/L in TMG.
Goiter was present in all cases with Grave's disease and TMNG with 50% of patients having moderate to large sized goiter. Additional findings included atrial fibrillation (six patients) rheumatic valvular disease (one patient) and hypokalemic paralysis (one patient).
RAI dose regime was divided into four group: Group A (4-7 mCi), Group B (7.1-10 mCi), Group C (10.1-12 mCi) and Group D (> 12 mCi). Three Patients needed two doses and one patient remained thyrotoxic in spite of 3 doses (30 mCi) and then lost follow up.
Cure rate at the end of 12 months was 95.65%, 73.33%, 57.14% and 57.14% in Group A, B, C and D respectively [Figure 1]. Forty-one cases (58.57%) were taking anti-thyroid drug before RAI therapy and it had no relationship with response to RAI. Incidence of hypothyroidism was 52.17%, 46.66%, 42.85% and 14.28% in Group A, B, C and D respectively. Thyroid-associated orbitopathy remained stable in 54 cases (77.14%), improved in 15 cases (21.42%) and worsened in only one case (1.42%). Goiter disappeared in 29 cases (41.42%); size decreased in 38 cases (54.28%) and remained same in 3 cases (4.28%)
| Discussion|| |
The idea of using radioiodine as a diagnostic and therapeutic tool was mooted by Karl Compton in 1936.  Robley Evans used a random beryllium mixture to produce small quantities of 128I for experimental work. Saul Hertz and Arthur Roberts were the first to use radioiodine 131 for the treatment of hyperthyroidism on 31 March 1941. 
Over the last 3 decades, investigators have been trying to determine suitable regimens of radioiodine doses to achieve euthyroidism. These included fixed low and high doses of radioiodine and doses calculated on the basis of thyroid gland size and Tc99 uptake. Since several studies have shown comparable results of both fixed and calculated doses, we prefer to use a fixed-dose regimen as it has the advantage of being more convenient with lower cost. Given the importance of preventing persistent hyperthyroidism and the high probability of eventual hypothyroidism after any regimen of RAI therapy, we decided that our goal of therapy was to induce euthyroidism or hypothyroidism within 1 year of treatment with a single dose of I-131. Our results confirmed the effectiveness of this regimen, with 95% of the patients became euthyroid or hypothyroid 1 year after treatment.
Nordyke and Gilbert analyzed a series of 605 patients treated with RAI to find out the optimal dose to achieve cure. They concluded that cure was directly related to the dose of I-131 administered and there was no significant relation between cure and age, gender, and >30% RAI uptake. The study also concluded that the optimal I-131 dose for curing hyperthyroidism is approximated by starting with 10 mCi and increasing it for unusually large glands or for special patient circumstances.  In our study optimal dose of RAI was 4-7 mCi.
The Royal College of Physicians in their guidelines for the use of RAI in the management of hyperthyroidism recommend a dose in the range of 10 mCi or more for a "standard" case of Graves' hyperthyroidism. 
Hypothyroidism is an inevitable consequence of the treatment of Graves' hyperthyroidism with RAI and almost certainly would occur in all patients if they lived long enough. , Hypothyroidism that occurs in the 1 st year following RAI therapy is related to dose, while the subsequent occurrence is due to a combination of radiation-mediated injury and underlying autoimmunity. Hence current practice guidelines, recommend large single dose because attempting to achieve permanent euthyroidism with RAI is nearly impossible. , Gopinath et al.  on the basis of their experience in Indian population observed that the dose of radioiodine in the treatment of Graves' hyperthyroidism should be such that to achieve rapid control of hyperthyroidism and the long term incidence of hypothyroidism should not be a deterrent in deciding on the dose. In another study reported from Mumbai,  only 16% of the subjects (20/79) who received a 5 mCi fixed dose radioiodine for treatment of thyrotoxicosis were hypothyroid at the end of 1 year after therapy. This study also noticed that age, sex and pre-treatment thyroid hormone values had no influence on outcome, but size of goiter had a direct relationship, larger goiters were associated with higher treatment failure. While in our study, hypothyroidism developed in over 95% cases even with 4-7 mCi RAI dose and size of goiter had no relationship with response rate. Adjunctive drug therapy requires higher doses of RAI due to the induction of radio-resistance by anti-thyroid drugs. ,, While in our study, prior treatment with anti-thyroid drugs had no influence on response to RAI. The use of anti-thyroid drug prior to and/or following RAI therapy has to be individualized based on the age of the patient, the severity of thyrotoxicosis and other comorbid conditions.
| Conclusion|| |
RAI treatment is an effective modality for definitive treatment of hyperthyroidism with long-term cure approaching 95%. Its efficacy, safety, and low-cost made it the preferred definitive treatment in most patients with hyperthyroidism although, post-treatment hypothyroidism and the need for life-long T4 are to be expected.
| References|| |
|1.||Becker DV, Sawin CT. Radioiodine and thyroid disease: The beginning. Semin Nucl Med 1996;26:155-64. |
|2.||Sawin CT, Becker DV. Radioiodine and the treatment of hyperthyroidism: The early history. Thyroid 1997;7:163-76. |
|3.||Nordyke RA, Gilbert FI Jr. Optimal iodine-131 dose for eliminating hyperthyroidism in Graves' disease. J Nucl Med 1991;32:411-6. |
|4.||Lazarus JH. Guidelines for the use of radioiodine in the management of hyperthyroidism: A summary. Prepared by the Radioiodine Audit Subcommittee of the Royal College of Physicians Committee on Diabetes and Endocrinology, and the Research Unit of the Royal College of Physicians. J R Coll Physicians Lond 1995;29:464-9. |
|5.||Alevizaki CC, Alevizaki-Harhalaki MC, Ikkos DG. Radioiodine-131 treatment of thyrotoxicosis: Dose required for and some factors affecting the early induction of hypothyroidism. Eur J Nucl Med 1985;10:450-4. |
|6.||Cevallos JL, Hagen GA, Maloof F, Chapman EM. Low-dosage 131-I therapy of thyrotoxicosis (diffuse goiters). A five-year follow-up study. N Engl J Med 1974;290:141-3. |
|7.||Solomon B, Glinoer D, Lagasse R, Wartofsky L. Current trends in the management of Graves' disease. J Clin Endocrinol Metab 1990;70:1518-24. |
|8.||Gopinath PG, Kumari KM, Padhy AK, Aggarwal SL. Thyroid status 10 years after I-131 therapy for toxic diffuse goiter. Indian J Nucl Med 1989;4:8-10. |
|9.||Nair N. Results of a single 5 mCi dose of radioactive iodine in thyrotoxicosis. Indian J Nucl Med 1991;6:6-11. |
|10.||Dunn JT. Choice of therapy in young adults with hyperthyroidism of Graves' disease. A brief, case-directed poll of fifty-four thyroidologists. Ann Intern Med 1984;100:891-3. |
|11.||Lundell G, Holm LE, Ljunggren JG, Wasserman J. Incidence of hypothyroidism after 131I therapy for hyperthyroidism. Relation to pretherapy serum levels of T3, T4 and thyroid antibodies. Acta Radiol Oncol 1981;20:225-30. |
|12.||Lundell G, Holm LE. Hypothyroidism following 131I therapy for hyperthyroidism in relation to immunologic parameters. Acta Radiol Oncol 1980;19:449-54. |
[Table 1], [Table 2], [Table 3], [Table 4]