2025 Korean Thyroid Association Management Guidelines for Radioactive Iodine Therapy in Patients with Hyperthyroidism

Kyeong Jin Kim; Eyun Song; Mijin Kim; Hyemi Kwon; Eu Jeong Ku; Hyun Woo Kwon; Jee Hee Yoon; Eun Kyung Lee; Won Woo Lee; Young Joo Park; Dong-Jun Lim; Sun Wook Kim; Ho-Cheol Kang; Jae Hoon Chung; Tae Yong Kim; Sin Gon Kim; Dong Gyu Na; Jee Soo Kim

doi:10.3803/EnM.2025.2464

Articles

Page Path: HOME > Endocrinol Metab > Volume 40(3); 2025 > Article

Review Article Thyroid 2025 Korean Thyroid Association Management Guidelines for Radioactive Iodine Therapy in Patients with Hyperthyroidism Keypoint -The Korean Thyroid Association has developed and published evidence-based recommendations for the use of radioactive iodine therapy in patients with hyperthyroidism including clinical indications and contraindications. -A fixed dose of 10–15 mCi is recommended, with dose selection based on goiter size and clinical context. -Routine low-iodine diets are not required, but iodine-rich foods should be avoided within 1 week before treatment. -Antithyroid drugs should be discontinued 3–7 days before radioactive iodine and restarted selectively after treatment. -The guideline provides detailed recommendations for the use of prophylactic steroids based on the activity and severity of thyroid eye disease and associated risk factors.: Kyeong Jin Kim¹, Eyun Song², Mijin Kim³, Hyemi Kwon⁴, Eu Jeong Ku⁵, Hyun Woo Kwon⁶, Jee Hee Yoon⁷, Eun Kyung Lee⁸, Won Woo Lee⁹, Young Joo Park¹⁰, Dong-Jun Lim¹¹, Sun Wook Kim¹², Ho-Cheol Kang⁷, Jae Hoon Chung¹², Tae Yong Kim¹³, Sin Gon Kim¹, Dong Gyu Na¹⁴, Jee Soo Kim¹⁵; Endocrinology and Metabolism 2025;40(3):342-356.
DOI: https://doi.org/10.3803/EnM.2025.2464
Published online: June 24, 2025

¹Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Korea

²Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Korea

³Department of Internal Medicine, Pusan National University Hospital, Pusan National University School of Medicine, Busan, Korea

⁴Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea

⁵Department of Internal Medicine, Seoul National University Hospital Healthcare System Gangnam Center, Seoul National University College of Medicine, Seoul, Korea

⁶Department of Nuclear Medicine, Korea University College of Medicine, Seoul, Korea

⁷Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea

⁸Department of Internal Medicine, Center for Thyroid Cancer, National Cancer Center, Goyang, Korea

⁹Department of Nuclear Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea

¹⁰Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea

¹¹Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea

¹²Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

¹³Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

¹⁴Department of Radiology, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea

¹⁵Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea

Corresponding authors: Tae Yong Kim. Division of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul 05505, Korea Tel: +82-2-3010-3249, Fax: +82-2-3010-6962, E-mail: tykim@amc.seoul.kr

Sin Gon Kim. Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, 73 Goryeodae-ro, Seongbuk-gu, Seoul 02841, Korea Tel: +82-2-920-5767, Fax: +82-2-920-5880, E-mail: k50367@korea.ac.kr

• Received: May 20, 2025 • Revised: May 26, 2025 • Accepted: June 5, 2025

This guideline has been originally written in Korean and published in the International Journal of Thyroidology 2025;18(1):65-79.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

642 Views
72 Download

prev next

Full Article

Download PDF

ABSTRACT
INTRODUCTION
DEVELOPMENT PROCESS OF THE KTA CLINICAL PRACTICE GUIDELINE FOR RAI THERAPY IN PATIENTS WITH HYPERTHYROIDISM
EFFICACY AND SAFETY OF RAI THERAPY IN HYPERTHYROIDISM
Section 1. Indications for RAI therapy in patients with hyperthyroidism
Section 2. Determination of the RAI dose in patients with hyperthyroidism
Section 3. Need for a low-iodine diet before RAI therapy in patients with hyperthyroidism
Section 4. Appropriate discontinuation period of ATD before and after RAI therapy
Section 5. Use of glucocorticoid before RAI therapy to reduce the development or progression of thyroid eye disease
Section 6. Intervals for thyroid function test after RAI therapy
CONCLUSIONS
Article information
References

ABSTRACT

Hyperthyroidism is a condition marked by excessive thyroid hormone production, most commonly due to Graves’ disease. Treatment options include antithyroid drugs (ATD), radioactive iodine (RAI) therapy, and thyroidectomy. To develop standardized clinical recommendations for RAI therapy with a focus on safety, efficacy, and monitoring, the Korean Thyroid Association formed a task force to create evidence-based guidelines. Six key clinical questions were identified through expert consensus, and a systematic literature review from 2013 to 2022 was conducted. Clinical indications for RAI therapy were categorized into three groups: strongly recommended, may be considered, and not recommended. A fixed dose of 10 to 15 mCi is recommended. Although a strict low-iodine diet is unnecessary, iodine-rich foods should be avoided for at least 1 week before treatment. ATD should be stopped 3 to 7 days before RAI and may be resumed in select cases. Prophylactic glucocorticoids are recommended for patients with mildly active thyroid eye disease and may be considered for others at risk. Thyroid function should be monitored at 4–6 weeks post-treatment, every 2–3 months until stabilized, and then every 6–12 months. These guidelines highlight recent advances and underscore the importance of individualized treatment based on clinical features, comorbidities, and patient preferences in Korea.
Keywords: Hyperthyroidism; Graves disease; Radioactive iodine; Practice guideline; Korean Thyroid Association

INTRODUCTION

Hyperthyroidism is a clinical condition characterized by the excessive production of thyroid hormones, resulting in thyrotoxicosis, with Graves’ disease being the most common underlying cause [1-3]. In Korea, the age-standardized incidence of hyperthyroidism has increased from 42.23 per 100,000 persons in 2004 to 105.13 in 2018, with the highest incidence observed in women in their 50s and 60s [4]. Treatment modalities include antithyroid drug (ATD), radioactive iodine (RAI) therapy, and thyroidectomy [5-7]. ATD maintain euthyroidism by suppressing thyroid hormone production, while RAI therapy and thyroidectomy treat hyperthyroidism by ablating or removing thyroid tissue, thereby eliminating the source of hormone excess [5-7]. Each treatment option has distinct advantages and disadvantages, and the choice of therapy should be individualized based on clinical factors, such as patient age, goiter size, symptom severity, and treatment adherence, as well as non-clinical factors, including socioeconomic conditions, accessibility to RAI treatment facilities, patient preferences, and the national healthcare system. Treatment preferences for hyperthyroidism vary by country. In Korea, RAI therapy is used less frequently than in Europe and the United States [4]. According to the Korean Thyroid Association (KTA) Fact Sheet [8] and National Health Insurance Service data, 97.3% of Korean patients with hyperthyroidism receive ATDs as a first-line treatment. The proportion of patients receiving RAI therapy decreased from 5.46% in 2003 to 2.66% in 2018, whereas the rate of thyroidectomy increased slightly from 1.43% to 1.95% over the same period [4].

The KTA published a consensus statement on the diagnosis and management of hyperthyroidism in 2013 [9], followed by guidelines from the American Thyroid Association in 2016 [5], the European Thyroid Association in 2018 [6], and the National Institute for Health and Care Excellence in 2019 [7]. However, the direct application of international guidelines to Korean clinical settings is limited by practical constraints. Moreover, the 2013 KTA consensus requires revision to reflect current clinical realities in Korea and to provide more explicit criteria for appropriate treatment selection. In particular, the low utilization of RAI therapy in Korea underscores the need for updated guidelines detailing its indications, procedures, and follow-up protocols. In response to these needs, the present guideline provides evidence-based recommendations derived from a systematic review of literature or from an experts’ consensus. Key points in each section are presented within a framework that includes specific recommendations and levels of evidence. This guideline has been published in the official journal of the KTA, the International Journal of Thyroidology, and is also available on the KTA website (www.thyroid.kr).

Composition of the guideline development task force and process for recommendations: The KTA convened a multidisciplinary task force in 2022, comprising experts in internal medicine and nuclear medicine, to develop revised clinical practice guidelines for RAI therapy in patients with hyperthyroidism. A total of 10 meetings were held by the task force to formulate key clinical questions, assess the relevant evidence, and derive corresponding recommendations. A comprehensive literature review was performed using database such as PubMed and Embase, with ‘hyperthyroidism’ and ‘Graves’ disease’ as the primary keywords, covering publications from 2013 to 2022. Additional studies published during the manuscript preparation were also included. The selected literature was reviewed, and relevant evidence was extracted to formulate the recommendations.; This guideline provides evidence-based recommendations for the use of RAI therapy in adult patients with suspected or confirmed hyperthyroidism, with a focus on autoimmune hyperthyroidism and the exclusion toxic nodular disease. It is intended to support clinical decision-making regarding RAI therapy for healthcare professionals managing patients with hyperthyroidism across various medical settings. Other treatment options, such as ATD therapy and surgery, are beyond the scope of this guideline and are not discussed in detail.; The draft guidelines were presented at the KTA Spring Scientific Meeting in March 2024 to solicit feedback. They were subsequently revised based on comments from the KTA Board of Directors and advisory committees comprising representatives from five related academic societies: the Korean Endocrine Society, the Korean Society of Nuclear Medicine, the Korean Association of Endocrine Surgeons, the Korean Society of Head and Neck Surgery, and the Korean Society of Thyroid Radiology. Final approval was obtained through member feedback collected via the KTA website and formal endorsements from these same five societies.
Levels of recommendation and summary: Table 1 outlines the grading of recommendations, based on the framework previously used in the KTA guidelines to ensure consistency. Recommendations regarding the RAI therapy for patients with hyperthyroidism are summarized in Table 2.
Survey on the use of RAI therapy for hyperthyroidism: To better understand the current practice patterns regarding RAI therapy in Korea, the KTA task force conducted a survey of its members from January 24 to February 4, 2024. A total of 169 respondents completed a 15-item questionnaire. Among them, 77% (130/169) of respondents had experience administering RAI therapy, and only 16% (27/169) had selected it as the initial treatment for newly diagnosed hyperthyroidism.; The most frequently reported challenge in managing patients treated with RAI was concern about treatment-related complications, such as exacerbation of ophthalmopathy, sialadenitis, and the potential risk of secondary malignancies (113 respondents, 66.9%). Other commonly reported barriers included the considerable time required to explain RAI therapy to patients (108 respondents, 63.9%) and concerns about social stigma and other negative perceptions associated with RAI treatment (102 respondents, 60.4%). Of note, 89% (151/169) of respondents indicated that explaining RAI therapy required more time than explaining ATD therapy. Differences in perception were observed according to the respondents’ experience with RAI treatment. For instance, concern about post-treatment hypothyroidism was reported by 45.5% of those without prior experience, compared to 15.4% of those with experience. Similarly, concerns regarding adverse effects were more prevalent among respondents without experience (45.9% vs. 26.2%).; When asked about the management of patients maintained on low-dose ATD for more than 5 years without achieving remission, 71% (120/169) of respondents reported that they would not consider RAI therapy. Likewise, 51% (85/169) responded that they would not choose RAI therapy for patients with relapse after ATD treatment. These findings indicate that RAI therapy is not actively considered in Korea, even in situations where ATD treatment has failed—unlike the treatment patterns commonly observed in the United States and Europe. In response to these findings, the task force formulated six key clinical questions to guide the appropriate use of RAI therapy, which served as the basis for this updated guideline.

EFFICACY AND SAFETY OF RAI THERAPY IN HYPERTHYROIDISM

Successful treatment of hyperthyroidism is defined as the elimination of excessive thyroid hormone production, resulting in either euthyroidism or hypothyroidism. In patients receiving RAI therapy, remission is achieved in approximately 50%–90% of cases within 3–12 months. A Korean study reported remission rates of 62.8% at 1 year and 76.8% at 2 years following the initial RAI treatment [10]. In contrast, the 2-year remission rate after ATD therapy was 41%, suggesting that RAI therapy offers a higher likelihood of long-term remission [11]. As RAI therapy is intended to cure hyperthyroidism with a single administration, the dose used is often sufficient to induce hypothyroidism [5-7]. Consequently, many patients who achieve remission after RAI therapy require lifelong thyroid hormone replacement. The incidence of hypothyroidism within the first year after treatment ranges from 24% to 87%, with higher rates observed a higher RAI doses [12,13]. Even among patients who initially maintain normal thyroid function, hypothyroidism subsequently develops at an annual rate of approximately 3% to 5% [14,15].

RAI therapy may lead to both short- and long-term adverse effects. The short-term complications include transient pain, swelling, and sialadenitis, while long-term risks involve permanent hypothyroidism and a potential increased in secondary malignancies. However, evidence regarding the risk of secondary malignancies remains inconclusive. Although some studies have reported an elevated risk [16,17], a recent meta-analysis involving 479,452 patients with hyperthyroidism found no significant difference in overall cancer incidence between those treated with RAI and those who were not (risk ratio, 1.02; 95% confidence interval [CI], 0.95 to 1.09) [18]. A Korean study comparing 10,737 patients treated with RAI therapy to 53,003 untreated patients also found no significant increase in overall cancer risk (hazard ratio [HR], 0.96; 95% CI, 0.83 to 1.10) [19]. Moreover, recent evidence suggests that RAI therapy may be associated with lower all-cause and cardiovascular mortality compared to ATD therapy [20,21]. Some studies have further reported a lower risk of cardiovascular event in patients undergoing thyroidectomy than in those treated with RAI therapy [22,23]. In addition, early remission of hyperthyroidism has been linked to reduced cardiovascular mortality [21], highlighting the clinical importance of the timely restoration of euthyroidism. Collectively, these findings support the efficacy and safety of RAI therapy as a valid therapeutic option for the management of hyperthyroidism.

1.1. RAI therapy should be considered in the following clinical situation: 1.1.1. When the patient prefers an initial treatment option with a high likelihood of cure. [Recommendation level 1]; 1.1.2. When serious adverse events occur during ATD therapy. [Recommendation level 1]; 1.1.3. In patients who experience recurrent hyperthyroidism after remission with ATD therapy and desire a definitive cure. [Recommendation level 1]; 1.1.4. When thyroid function remains poorly controlled despite appropriate ATD therapy. [Recommendation level 1]; Comparative studies of ATD, RAI therapy, and surgery in patients with Graves’ disease have reported relapse rates of 34%–42%, 21%, and 3%–8%, respectively [24]. ATDs is generally associated with lower remission rates (approximately 50%) and higher relapse rates, while RAI therapy achieves initial success rate of 75% to 81% [25-27]. Therefore, for patients who prioritize definitive treatment, RAI therapy or thyroidectomy should be considered as a first-line option. Although thyroidectomy offers the highest cure rate, it is associated with potential risks such as surgical scarring, complications related to general anesthesia, hypocalcemia, and vocal cord palsy. Therefore, in patients with high surgical risk or limited access to experienced surgeons, RAI therapy may be the preferred option.; RAI therapy is also indicated for patients who experience serious complications related to ATD therapy, such as agranulocytosis, hepatotoxicity, or vasculitis; those who relapse after achieving remission with ATD; and those whose hyperthyroidism remains uncontrolled despite adequate ATD treatment [28,29]. Due to the risk of cross-reactivity among ATDs, switching to another ATD is generally not recommended in cases of severe adverse effects. Notably, patients who develop agranulocytosis and subsequently receive RAI therapy have shown high remission rates (88.8%) [30].; The standard duration of ATD therapy is typically 12 to 18 months. Patients whose thyroid function remains unstable after 12 to 18 months of adequate ATD therapy, or those who relapse following discontinuation, should be considered for definitive treatment with RAI or surgery [5,6]. A meta-analysis of 3,388 patients from 26 randomized controlled trials demonstrated that extending ATD therapy beyond 18 months did not significantly improve remission rates [31]. Prolonged or inadequately controlled hyperthyroidism is known to be associated with increased mortality [20,32]. In addition, the remission rate with ATD retreatment after relapse is approximately 23%, which is lower than that of initial treatment [33]. Korean study involving 247 patients with Graves’ disease, the success rate of RAI therapy as a second-line treatment was reported to be approximately 62.8% [10]. Therefore, in patients whose thyroid function remains unstable despite sufficient use of ATD for the standard treatment duration, definite therapy such as RAI or surgery should be considered.
1.2. RAI therapy may be considered in the following clinical situation: 1.2.1. In patients with poor adherence to ATD therapy. [Recommendation level 2]; 1.2.2. In patients with comorbidities that may lead to clinical instability if hyperthyroidism worsens (e.g., uncontrolled arrhythmia or heart failure). [Recommendation level 2]; 1.2.3. In patients requiring prolonged high-dose ATD therapy to maintain euthyroidism (particularly in women planning pregnancy in the next 6 months or beyond). [Recommendation level 3]; Although a 12- to 18-month course of ATD therapy is generally required to achieve remission in patients with Graves’ disease [31], extended treatment durations are frequently needed in real clinical practice [34,35]. Therefore, in patients requiring long-term therapy who demonstrate poor adherence to ATD, RAI therapy may be considered as a definitive treatment option. Nevertheless, as RAI-induced hypothyroidism also necessitates lifelong thyroid hormone replacement, clinicians should carefully assess the patient’s adherence to both ATDs and thyroid hormone therapy before selecting a treatment strategy.; Fluctuating or inadequately controlled thyroid hormone levels are associated with an increased risk of cardiovascular diseases, such as arrhythmia and heart failure [36,37]. In a retrospective cohort study of 4,189 patients with newly diagnosed Graves’ disease, outcomes were compared across three groups: those treated with ATD, those who achieved remission after RAI therapy, and those in whom hyperthyroidism persisted after RAI therapy. Compared with the ATD group, the RAI remission group showed significantly lower risks of major cardiovascular events (HR, 0.59; 95% CI, 0.38 to 0.92) and all-cause mortality (HR, 0.50; 95% CI, 0.29 to 0.85). In contrast, patients in whom hyperthyroidism persisted after RAI therapy had an increased risk of major cardiovascular events (HR, 1.51; 95% CI, 1.01 to 2.28), while no statistically significant difference in mortality was observed (HR, 1.51; 95% CI, 0.96 to 2.37) [21]. Notably, patients with subnormal thyroid stimulating hormone (TSH) levels 1 year after diagnosis exhibited higher rates of major cardiovascular events and mortality. Therefore, RAI therapy may be considered in patients with underlying conditions—such as uncontrolled arrhythmia or heart failure—in whom worsening hyperthyroidism could lead to clinical instability.; RAI therapy may also be considered in patients requiring sustained high-dose ATD therapy (e.g., >15–20 mg/day of methimazole or >150–300 mg/day of propylthiouracil) to maintain euthyroidism. Recent studies have reported that the risk of serious adverse events, such as agranulocytosis and toxic hepatitis, increases with higher ATD dosages [38-40]. In particular, for women with hyperthyroidism who are planning to conceive in more than 6 months and required ongoing high-dose ATD therapy, RAI therapy may be a reasonable option. However, because TSH receptor antibody (TRAb) levels may be transiently increase following RAI therapy [41], it is advisable to delay pregnancy until thyroid function stabilized—typically for at least 6 months after RAI therapy. In male patients, considering the spermatogenesis cycle, deferring conception for 3 to 4 months after RAI therapy is also recommended [5,42].; In women treated for hyperthyroidism, pregnancy is recommended after thyroid function has been stable within the normal range for at least two consecutive measurements under a stable treatment regimen [43,44]. For those planning pregnancies within 6 months, surgical treatment may be considered as the first treatment option. As current evidence is insufficient to recommend a single optimal treatment approach for women with hyperthyroidism planning pregnancy, it is essential to carefully evaluate the benefits and potential risks of each option in the context of the patient’s clinical status. Shared decision-making with the patient is crucial in determining the most appropriate treatment strategy.
1.3. RAI therapy is not recommended in the following clinical situation: 1.3.1. Pregnant or breastfeeding women. [Recommendation level 1]; 1.3.2. Patients with active moderate-to-severe thyroid eye disease. [Recommendation level 1]; 1.3.3. Patients with coexisting thyroid cancer. [Recommendation level 1]; Radioactive isotope freely crosses the placenta and can accumulate in the fetal thyroid gland, posing a risk of fetal hypothyroidism and impaired neurodevelopment. Therefore, RAI therapy is strictly contraindicated during pregnancy [42]. In addition, RAI is excreted in breast milk, making it contraindicated in breastfeeding women as well [42]. To prevent radiation exposure, breastfeeding must be discontinued before treatment. Pregnancy must be excluded by testing within 48 hours before RAI administration.; RAI therapy is not recommended in patients with moderate-to-severe active thyroid eye disease (TED), as it may worsen ophthalmopathy [5,45-47]. In patients with hyperthyroidism and mild TED, prophylactic corticosteroid may be considered to reduce the risk of TED progression when RAI therapy is selected (see Part V for detailed guidance). In patients with coexisting thyroid cancer, RAI therapy is not recommended for treating hyperthyroidism.; Although the following are not absolute contraindications, they are associated with a higher risk of RAI treatment failure: (1) large goiter, and (2) high titers of TRAb. In addition, RAI therapy may increase the risk of adverse events in patients with severe thyrotoxicosis with markedly elevated thyroid hormone levels.; A retrospective study of 388 patients with Graves’ disease who received RAI therapy identified that the presence of a large goiter, defined as a visible cervical swelling consistent with thyroid enlargement on palpation [48], and elevated TRAb levels at the time of RAI administration were observed to be significant predictors of decreased treatment success [49]. Other studies have also reported that TRAb levels greater than 40 U/L at diagnosis or at the time of treatment are associated with lower rates of treatment success [50]. In such cases, surgical thyroidectomy may be a more appropriate treatment option than RAI therapy, particularly when rapid resolution of hyperthyroidism is required. Although a thyroid storm following RAI therapy is very rare [51,52], transient increases in the serum thyroid hormone levels may occur immediately after treatment [53,54]. Therefore, in patients with markedly elevated pretreatment thyroid hormone levels, ATD therapy should be used to achieve euthyroidism prior to RAI administration. In cases where ATD use is not feasible and rapid control of thyroid function is required, alternative approaches such as inorganic iodine [55], lithium [56,57], or therapeutic plasma exchange [58-60] have been suggested. Inorganic iodine should be used only for a short duration (7 to 10 days) due to the risk of the escape phenomenon, and should be discontinued at least 1 to 2 weeks before RAI therapy, as it can interfere with RAI uptake. In addition, the use of lithium is limited in clinical practice due to its potential toxicity, which necessitates regular serum level monitoring. Therefore, its application remains restricted in current Korean clinical settings. Detailed guidance on the use of ATD before and after RAI therapy is provided in part IV.

Section 2. Determination of the RAI dose in patients with hyperthyroidism

2.1. A fixed dose of RAI (10–15 mCi) sufficient to induce hypothyroidism is recommended when determining the appropriate RAI dose. [Recommendation level 2]

The goal of RAI therapy is to cure hyperthyroidism by administering a sufficient dose to induce hypothyroidism [5-7]. The determination of RAI dosage can follow either a fixed-dose approach—typically 10 to 15 mCi—or a calculated-dose approach, which considers individual factors such as thyroid gland size and RAI uptake. In a study of 88 patients with hyperthyroidism, participants were assigned to either a fixed-dose group were (low dose: 6.3 mCi; high dose: 9.5 mCi) or a calculated-dose group (adjusted low doses and adjusted high doses). No significant differences in clinical outcomes were observed between the two groups during the median follow-up of 63 months [61]. Similarly, a meta-analysis comparing the rates of euthyroidism or hypothyroidism found no difference between fixed-dose and calculated-dose approaches. In fact, the calculated-dose method was associated with a higher rate of persistent or recurrent hyperthyroidism [7], suggesting that it does not offer greater clinical benefit than the fixed-dose method. Another meta-analysis, however, reported that maintaining euthyroidism was more likely when the absorbed radiation dose was within the range of 120 to 180 Gy, and that the risk of hypothyroidism or recurrence increased when the dose was outside this range [62], indicating the potential utility of calculated dosing when euthyroidism is the treatment goal. Nevertheless, considering the limited feasibility of applying calculated-dose methods in current Korean clinical practice and the lack of domestic studies, this guideline recommends the use of a fixed-dose approach. Future evidence evaluating the clinical applicability and effectiveness of calculated dosing in Korean settings may help inform recommendations supporting individualized dosing strategies.

The success rates of RAI therapy vary according to the administered dose: 61% with 5.4 mCi [63], 69% with 8.2 mCi [64], 69%–74% with 10 mCi [15,26], 75%–81% with 15 mCi [13], and 86% with 15.7 mCi [13]. However, many of these studies were conducted in patients without prior use of ATD, and there remains insufficient evidence to determine the optimal dose for successful treatment. Therefore, this guideline recommends a minimum dose of 10 mCi and supports the use of a sufficient fixed dose of 10 to 15 mCi, considering factors such as prior ATD use [65]. In patients with large goiters, a dose higher than 15 mCi may be considered; however, close monitoring is required due to the potential risk of transient thyroiditis following treatment.

A significant reduction in thyroid volume, one of the advantages of RAI therapy, is typically observed beginning around 6 months after treatment, with an average decrease of more than 50% to 70%. In a multicenter prospective study, the median reduction in thyroid volume was 57% at 6 months and 71% at 12 months post-treatment [66]. Similarly, a recent ultrasound-based study reported a mean thyroid volume of 43.01 cm³ before treatment, which decreased to 11.58 cm³ at 6 months, corresponding to an average reduction of approximately 73% [67].

Section 3. Need for a low-iodine diet before RAI therapy in patients with hyperthyroidism

3.1. A low-iodine diet is not routinely recommended before RAI therapy for hyperthyroidism; but iodine-rich foods should be avoided for at least 1 week prior to treatment. [Recommendation level 3]

A low-iodine diet is generally not recommended for patients with hyperthyroidism undergoing RAI therapy. However, the intake of iodine-rich supplements, health products, and seaweed may interfere with treatment efficacy; therefore, discontinuation of such products at least 1 week prior to therapy should be considered [5].

Due to geographic and environmental factors, as well as traditional dietary habits, seaweed consumption (e.g., laver, kelp, and sea mustard) is common in Korea. According to the Korea National Health and Nutrition Examination Survey (2013–2017), the average daily iodine intake among Koreans was 416.5 μg/day (median, 129.0 μg/day), nearly three times the recommended daily intake of 150 μg/day for adults [68]. Therefore, RAI therapy administered following a typical Korean diet may result in reduced treatment efficacy.

In a single-arm study involving 21 patients with hyperthyroidism, a low-iodine diet was prescribed to limit daily iodine intake to below 400 μg/day starting 1 week prior to RAI therapy. As a result, urinary iodine excretion significantly decreased from a baseline of 511 to 41 μg/gCr. Moreover, patients with urinary iodine excretion levels below 100 μg/gCr showed a significant increase in RAI uptake [69]. However, there is insufficient evidence to conclude that strict low-iodine diets improve the efficacy of RAI therapy. In a small randomized study comparing the effects of a low-iodine diet with a regular diet, patients in the low-iodine group (n=31) showed a significant reduction in urinary iodine levels compared to the control group (n=36)—by 23% at 1 week and 42% at 2 weeks. However, there was no significant difference in the cure rate of hyperthyroidism between the two groups at 6 months after RAI therapy [70]. Therefore, given the lack of clear evidence that strict low-iodine diets enhance the efficacy of RAI therapy, routine prescription of a low-iodine diet prior to treatment is not recommended. However, excessive iodine intake may interfere with the efficacy of RAI therapy. Given the high average dietary iodine intake among Koreans, it is recommended to avoid iodine-rich foods—such as seaweed (e.g., laver, kelp, sea mustard) and high-dose iodine-containing supplements—for at least 1 week prior to treatment. In addition, when RAI therapy is being considered for patients who have recently used or are currently taking agents known to affect iodine uptake—such as iodine contrast media or amiodarone—the potential impact of these substances should be carefully evaluated. Inorganic iodine should be discontinued at least 1 to 2 weeks before RAI therapy.

Section 4. Appropriate discontinuation period of ATD before and after RAI therapy

4.1. Discontinuation of ATD for 3 to 7 days before RAI therapy is recommended. [Recommendation level 1]

4.2. Resumption of ATD within 3–7 days after RAI therapy may be considered in patients who received ATD prior to treatment or are at high risk of clinical deterioration due to worsening hyperthyroidism. [Recommendation level 2]

A meta-analysis of 14 randomized controlled trials involving a total of 1,306 patients found that the use of ATD up to the time of RAI therapy was associated with a reduced risk of post-treatment hypothyroidism (relative risk [RR], 0.68; 95% CI, 0.53 to 0.87; P=0.006), but an increased risk of treatment failure (RR, 1.28; 95% CI, 1.07 to 1.52; P=0.006) [52]. The ATD used in the included studies were propylthiouracil (50–300 mg/day), methimazole (5–30 mg/day), and carbimazole (20–30 mg/day). In the withdrawal groups, ATD were discontinued 3 to 7 days prior to RAI therapy. Compared to patients who did not receive ATDs before RAI therapy, those who did had a significantly higher risk of treatment failure (RR, 1.48; 95% CI, 1.09 to 2.00). Similarly, the post-treatment use of ATD was also associated with a significantly increased risk of treatment failure (RR, 1.32; 95% CI, 1.04 to 1.68) [52].

Several studies have reported that propylthiouracil may reduce the efficacy of RAI therapy due to its radioprotective effects [71,72]. Based on these findings, the European Association of Nuclear Medicine recently recommended discontinuing propylthiouracil for at least 2 weeks prior to RAI therapy [73]. However, based on the literature review, there is currently insufficient evidence to support extending the ATD withdrawal period beyond 1 week. Therefore, this guideline recommends discontinuing ATDs for 3 to 7 days before RAI therapy.

A transient increase in thyroid hormone levels may be observed following RAI therapy [51-54,74]. Although rare, thyroid storm can occur and is associated with an increased risk of severe cardiovascular and cerebrovascular events [51]. Therefore, in patients with severe hyperthyroidism, advanced age, or comorbidities that lead to clinical deterioration in the event of thyroid storm—such as atrial fibrillation, heart failure, pulmonary hypertension, renal failure, infection, trauma, poorly controlled diabetes, cerebrovascular disease, or pulmonary disease—thyroid function and underlying conditions should be adequately controlled with ATD before initiating RAI therapy.

A transient increase in serum thyroid hormone levels may occur after RAI therapy, even in patients pretreated with ATD or those with normalized thyroid function prior to treatment. Therefore, thyroid hormone levels should be closely monitored following RAI therapy. In a randomized study of 42 patients, those who received ATD pretreatment showed post-RAI increases in free thyroxine (T4) and triiodothyronine (T3) by 52.4% and 61.8%, respectively, whereas the control group (no pretreatment) showed decreases of 32.4% and 32.9%, with only two of 21 patients (9.5%) showing hormone elevation [54]. Another randomized controlled trial reported that patients who did not receive ATD pretreatment exhibited a significant decline in thyroid hormone levels beginning on day 5 after RAI, with stabilization observed by day 30. In contrast, the ATD group showed a 70% increase in free T4 on day 7 (peaking at 107% on day 14), and an 85% increase in T3 on day 2, followed by a gradual decline between days 14 and 30 [75].

Based on these findings, ATD should be discontinued 3 to 7 days before RAI therapy, as continuing ATD up to the time of treatment has been associated with transient elevations in serum thyroid hormone levels. However, in elderly patients or those at high risk of complications from worsening thyrotoxicosis, resumption of ATD within 3 to 7 days after RAI therapy may be considered [51,54,75]. Following treatment, thyroid hormone levels should be monitored regularly to determine the need for continued ATD therapy.

Section 5. Use of glucocorticoid before RAI therapy to reduce the development or progression of thyroid eye disease

5.1. RAI therapy is not recommended in patients with active moderate-to-severe TED. [Recommendation level 1]

5.2. Prophylactic corticosteroid therapy is recommended when RAI therapy is administered to patients with active mild TED. [Recommendation level 1]

5.3. In patients with inactive moderate-to-severe TED, prophylactic corticosteroid therapy may be considered during RAI treatment when additional risk factors—such as high TSH receptor antibody levels or smoking—are present. [Recommendation level 2]

5.4. Prophylactic corticosteroid therapy is not recommended during RAI treatment in patients with inactive mild TED when additional risk factors—such as high TSH receptor antibody levels or smoking—are not present. [Recommendation level 1]

Approximately one-third of patients with Graves’ disease exhibit signs and symptoms of TED, with about 5% experiencing moderate-to-severe forms [76]. Therefore, assessing the severity and activity of TED is essential for appropriate treatment decision-making in patients with hyperthyroidism [5]. In patients with moderate-to-severe TED or sight-threatening manifestations such as optic neuropathy or corneal ulceration, prompt treatment of hyperthyroidism is required. In these cases, ATD therapy or thyroidectomy is generally preferred over RAI treatment [5].

In patients with moderate-to-severe TED, rapid normalization of thyroid function with ATD therapy is effective in preventing progression of TED. Long-term use of ATD is also considered a safe and effective option for inducing remission of TED [34]. Thyroidectomy has also shown efficacy; in a study of 44 patients with active moderate-to-severe TED who underwent thyroidectomy, all patients demonstrated improvement in TED within 3 years postoperatively [77]. This finding suggests that thyroidectomy not only does not exacerbate TED, but may also contribute to symptomatic improvement in selected patients.

In contrast, RAI therapy has been associated with a 3.2- to 5.8-fold higher risk of worsening TED compared to ATD therapy [78,79]. A recent randomized controlled trial also reported a higher incidence of new-onset TED in the RAI group than in the ATD group (38.7% vs. 21.3%; RR, 1.8) [80].

In patients with mild and inactive TED, prophylactic low-dose oral glucocorticoids have been shown to be effective in preventing the development or progression of TED following RAI therapy [45,79,81-83]. A meta-analysis of 850 patients demonstrated that oral glucocorticoids significantly reduced the risk of worsening TED with a risk ratio of 0.14 (95% CI, 0.06 to 0.35; P<0.01) [82]. Therefore, in patients with mild active TED undergoing RAI therapy, oral glucocorticoids may be safely administered for prophylaxis, unless contraindicated. Common adverse effects include worsening of diabetes, hypertension, osteoporosis, psychiatric symptoms, increased risk of infection, and reactivation of viral hepatitis [5]. However, standard prophylactic dosing with oral prednisone (initial dose of 0.1 to 0.4 mg/kg with gradual tapering) is generally considered safe [84]. A recent retrospective cohort study reported that short-term, low-dose oral prednisone (0.1 to 0.2 mg/kg, tapered over 6 weeks) was as effective as higher-dose regimens (0.3 to 0.5 mg/kg) [85]. Although low-dose intravenous regimens have also been proposed, their requirement for weekly hospital visits over 4-week period limits their practical feasibility [83].

In patients with inactive TED, the risk of disease progression or reactivation after RAI therapy is low [82]. In one study, none of the 72 patients with inactive TED experienced disease progression after receiving RAI therapy without steroid prophylaxis [86]. A recent study from Japan comparing 295 patients with no TED or inactive TED found no significant difference in the risk of TED progression between those who received prophylactic steroids and those who did not. Among patients without risk factors, the progression rate was as low as 4.2% [87]. Furthermore, steroid prophylaxis conferred no additional benefit in patients without TED [5]. Therefore, prophylactic steroid therapy is not recommended for patients with inactive TED and no risk factors, or for those without TED. Recommendations for steroid use during RAI therapy, based on TED severity, activity, and the presence of risk factors, are summarized in Table 3 [88].

Section 6. Intervals for thyroid function test after RAI therapy

6.1. Thyroid function test, including TSH and free T4, may be considered within 4 to 6 weeks after RAI therapy. [Recommendation level 2]

6.2. Thyroid function can be monitored every 2 to 3 months for up to 6 months after RAI therapy or until TSH levels normalize. [Recommendation level 2]

6.3. Thyroid function test may be repeated every 6 to 12 months, once thyroid function has been confirmed to be stable and within the normal range on at least two consecutive assessments. [Recommendation level 2]

6.4. Thyroid function test is recommended when symptoms of hyperthyroidism or hypothyroidism are suspected. [Recommendation level 2]

An initial thyroid function test is recommended within 4 to 6 weeks after RAI therapy. During this period, serum TSH levels may remain suppressed even in the presence of hypothyroidism due to delayed recovery of TSH secretion [89]. Therefore, both TSH and free T4 levels should be measured to ensure accurate assessment of thyroid function [90].

Changes in thyroid function typically emerge between 2 and 6 months following RAI therapy; however, hypothyroidism may develop as early as 4 weeks post-treatment. While uncommon, transient hypothyroidism may develop around 2 months post-treatment and persists for 1 to 4 months [89]. At 8 weeks post-treatment, approximately 40% of patients developed hypothyroidism, with the incidence increasing to over 80% by 16 weeks [91]. In another report, 80% to 90% of patients reached either euthyroidism or hypothyroidism within 6 months [92]. Additionally, a separate study reported that 50% to 90% of patients reached stable thyroid function between 3 and 12 months after RAI therapy [93]. Therefore, thyroid function tests can be monitored every 2–3 months for 6–12 months following RAI therapy, or until TSH levels normalize.

After the first year following RAI therapy, an additional 3% to 5% of patients may develop hypothyroidism annually [14]. In a prospective study, the cumulative incidence of hypothyroidism in patients with Graves’ disease was 24% at 1 year, 59% at 10 years, and 82% at 25 years after RAI therapy—substantially higher than in patients with toxic multinodular goiter, whose corresponding rates were 4%, 15%, and 32%, respectively [12]. These findings indicate that hypothyroidism following RAI therapy is relatively common and tends to increase over time. Therefore, long-term and regular monitoring of thyroid function may be recommended to ensure timely detection and management of hypothyroidism after RAI therapy. Even after thyroid function has stabilized, annual testing is recommended, with additional tests performed when thyroid dysfunction is clinically suspected.

CONCLUSIONS

This guideline is an updated version of the 2013 KTA consensus statement on the diagnosis and treatment of hyperthyroidism, specifically focusing on RAI therapy. Treatment options for hyperthyroidism include ATD, RAI therapy, and thyroidectomy. The choice of therapy should be made through shared decision-making, considering the patient’s clinical condition, comorbidities, treatment efficacy, and potential side effects. This guideline provides detailed clinical recommendations regarding indications for RAI therapy—particularly in cases where it is preferred or contraindicated—pre- and post-treatment management, and the use of prophylactic steroids in patients with coexisting TED. Given the relatively low utilization of RAI therapy in Korea, further research is warranted to assess the long-term outcomes of prolonged ATD therapy and post-RAI thyroid function, including the incidence of hypothyroidism and the maintenance of euthyroidism. These studies will contribute to a more systematic evaluation of the efficacy and safety of RAI therapy and strengthen the evidence base for future treatment guidelines.

Article information

CONFLICTS OF INTEREST

Young Joo Park is an editor-in-chief and Eun Kyung Lee is an associate editor (chief) of the journal. But they were not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.

ACKNOWLEDGMENTS

This research was supported by a grant from the Korean Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health and Welfare, South Korea (grant number: HC21C0078). The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or the decision to submit the manuscript for publication.

Table 1.

Korean Thyroid Association Recommendation Levels for Clinical Strategies, Diagnostic Testing, or Treatment in Patient Care

Grade	Level	Definition
1	Strongly recommend for/against	Sufficient and objective evidence exists that performing (or avoiding) the recommended action leads to significant health benefits or harms.
2	Conditionally recommend for/against	Evidence suggests important health benefits or harms, but the evidence is uncertain or indirect, making a uniform recommendation difficult.
3	Expert consensus recommendation	In the absence of strong clinical evidence, the recommendation is based on expert consensus and patient-specific considerations.
4	Inconclusive	Insufficient or conflicting evidence exists regarding significant health benefits or harms; no definitive recommendation for or against the action can be made.

Table 2.

Summary of 2025 Korean Thyroid Association Guidelines Statements for Radioactive Iodine Therapy in Patients with Hyperthyroidism

Section 1. Indications for RAI therapy in patients with hyperthyroidism
1.1. RAI therapy should be considered in the following clinical situation.
1.1.1. When the patient prefers an initial treatment option with a high likelihood of cure. [Recommendation level 1]
1.1.2. When serious adverse events occur during ATD therapy. [Recommendation level 1]
1.1.3. In patients who experience recurrent hyperthyroidism after remission with ATD therapy and desire a definitive cure. [Recommendation level 1]
1.1.4. When thyroid function remains poorly controlled despite appropriate ATD therapy. [Recommendation level 1]
1.2. RAI therapy may be considered in the following clinical situation.
1.2.1. In patients with poor adherence to ATD therapy. [Recommendation level 2]
1.2.2. In patients with comorbidities that may lead to clinical instability if hyperthyroidism worsens (e.g., uncontrolled arrhythmia or heart failure). [Recommendation level 2]
1.2.3. In patients requiring prolonged high-dose ATD therapy to maintain euthyroidism (particularly in women planning pregnancy in the next 6 months or beyond). [Recommendation level 3]
1.3. RAI therapy is not recommended in the following clinical situation.
1.3.1. Pregnant or breastfeeding women. [Recommendation level 1]
1.3.2. Patients with active moderate-to-severe thyroid eye disease. [Recommendation level 1]
1.3.3. Patients with coexisting thyroid cancer. [Recommendation level 1]
Section 2. Determination of the RAI dose in patients with hyperthyroidism
2.1. A fixed dose of RAI (10–15 mCi) sufficient to induce hypothyroidism is recommended when determining the appropriate RAI dose. [Recommendation level 2]
Section 3. Need for a low-iodine diet before RAI therapy in patients with hyperthyroidism
3.1. A low-iodine diet is not routinely recommended before RAI therapy for hyperthyroidism; but iodine-rich foods should be avoided for at least 1 week prior to treatment. [Recommendation level 3]
Section 4. Appropriate discontinuation period of ATD before and after RAI therapy
4.1. Discontinuation of ATD for 3 to 7 days before RAI therapy is recommended. [Recommendation level 1]
4.2. Resumption of ATD within 3–7 days after RAI therapy may be considered in patients who received ATD prior to treatment or are at high risk of clinical deterioration due to worsening hyperthyroidism. [Recommendation level 2]
Section 5. Use of glucocorticoid before RAI therapy to reduce the development or progression of TED
5.1. RAI therapy is not recommended in patients with active moderate-to-severe TED. [Recommendation level 1]
5.2. Prophylactic corticosteroid therapy is recommended when RAI therapy is administered to patients with active mild TED. [Recommendation level 1]
5.3. In patients with inactive moderate-to-severe TED, prophylactic corticosteroid therapy may be considered during RAI treatment when additional risk factors—such as high TSH receptor antibody levels or smoking—are present. [Recommendation level 2]
5.4. Prophylactic corticosteroid therapy is not recommended during RAI treatment in patients with inactive mild TED when additional risk factors—such as high TSH receptor antibody levels or smoking—are not present. [Recommendation level 1]
Section 6. Intervals for thyroid function test after RAI therapy
6.1. Thyroid function test, including TSH and free T4, may be considered within 4 to 6 weeks after RAI therapy. [Recommendation level 2]
6.2. Thyroid function can be monitored every 2 to 3 months for up to 6 months after RAI therapy or until TSH levels normalize. [Recommendation level 2]
6.3. Thyroid function test may be repeated every 6 to 12 months, once thyroid function has been confirmed to be stable and within the normal range on at least two consecutive assessments. [Recommendation level 2]
6.4. Thyroid function test is recommended when symptoms of hyperthyroidism or hypothyroidism are suspected. [Recommendation level 2]

RAI, radioactive iodine; ATD, antithyroid drug; TED, thyroid eye disease; TSH, thyroid stimulating hormone; T4, thyroxine.

Table 3.

Recommendations for RAI Therapy and Prophylactic Steroid Use Based on TED Severity, Activity, and Risk Factors

TED activity	Severity
	Mild		Moderate-to-severe
	No risk factors	With risk factors	No risk factors	With risk factors
Inactive	No steroid prophylaxis required	Consider steroid prophylaxis	No steroid prophylaxis required	Steroid prophylaxis recommended
Active	Consider steroid prophylaxis	Steroid prophylaxis recommended	RAI therapy not recommended	RAI therapy not recommended

Active TED: TED is considered active when the Clinical Activity Score (CAS) is ≥3 out of 7. The CAS includes the following signs: spontaneous retrobulbar pain, pain on attempted upward or downward gaze, redness of the eyelids, redness of the conjunctiva, swelling of the caruncle or plica, swelling of the eyelids, and conjunctival edema (chemosis) [88]. Mild TED: Defined as TED that has little impact on daily life and does not require immunosuppressive therapy. Typical features include lid retraction <2 mm, mild exophthalmos, and intermittent or no diplopia that can be managed with lubricating eye drops [88]. Moderate-to-severe TED: Characterized by TED that does not threaten vision but significantly affects daily functioning and justifies the risk of immunosuppression (if active) or surgical treatment (if inactive). It usually presents with ≥2 of the following: lid retraction ≥2 mm, moderate-to-severe soft-tissue involvement, exophthalmos ≥3 mm above normal, or constant/inconstant diplopia [88]. Risk factors: smoking and high titers of thyrotropin receptor antibodies (TRAb).

RAI, radioactive iodine; TED, thyroid eye disease.

References

1. Bartalena L. Diagnosis and management of Graves disease: a global overview. Nat Rev Endocrinol 2013;9:724–34.Article PubMed PDF
2. Smith TJ, Hegedus L. Graves’ disease. N Engl J Med 2016;375:1552–65.Article PubMed
3. Chung JH. Antithyroid drug treatment in Graves’ disease. Endocrinol Metab (Seoul) 2021;36:491–9.Article PubMed PMC PDF
4. Ahn HY, Cho SW, Lee MY, Park YJ, Koo BS, Chang HS, et al. Prevalence, treatment status, and comorbidities of hyperthyroidism in Korea from 2003 to 2018: a nationwide population study. Endocrinol Metab (Seoul) 2023;38:436–44.Article PubMed PMC PDF
5. Ross DS, Burch HB, Cooper DS, Greenlee MC, Laurberg P, Maia AL, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid 2016;26:1343–421.Article PubMed
6. Kahaly GJ, Bartalena L, Hegedus L, Leenhardt L, Poppe K, Pearce SH. 2018 European Thyroid Association guideline for the management of Graves’ hyperthyroidism. Eur Thyroid J 2018;7:167–86.Article PubMed PMC PDF
7. National Institute for Health and Care Excellence. Thyroid disease: assessment and management: NICE guideline. London: NICE; 2019 [cited 2025 June 7]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK550859.
8. Korean Thyroid Association. Thyroid disease fact sheet 2021 [Internet]. Seoul: KTA; 2021 [cited 2025 June 7]. Available from: https://www.thyroid.kr/board/list.html?num=573&start =0&sort =top%20desc,num%20desc&code =notice&key=&keyword=.
9. Yi KH, Moon JH, Kim IJ, Bom HS, Lee J, Chung WY, et al. The diagnosis and management of hyperthyroidism consensus: report of the Korean Thyroid Association. J Korean Thyroid Assoc 2013;6:1–11.Article
10. Park H, Kim HI, Park J, Park SY, Kim TH, Chung JH, et al. The success rate of radioactive iodine therapy for Graves’ disease in iodine-replete area and affecting factors: a single-center study. Nucl Med Commun 2020;41:212–8.Article PubMed
11. Kim KJ, Choi J, Shin SM, Kim JA, Kim KJ, Kim SG. Treatment patterns and preferences for Graves’ disease in Korea: insights from a nationwide cohort study. Endocrinol Metab (Seoul) 2024;39:659–63.Article PubMed PMC PDF
12. Metso S, Jaatinen P, Huhtala H, Luukkaala T, Oksala H, Salmi J. Long-term follow-up study of radioiodine treatment of hyperthyroidism. Clin Endocrinol (Oxf) 2004;61:641–8.Article PubMed
13. Braga M, Walpert N, Burch HB, Solomon BL, Cooper DS. The effect of methimazole on cure rates after radioiodine treatment for Graves’ hyperthyroidism: a randomized clinical trial. Thyroid 2002;12:135–9.Article PubMed
14. Nygaard B, Hegedus L, Gervil M, Hjalgrim H, Hansen BM, Soe-Jensen P, et al. Influence of compensated radioiodine therapy on thyroid volume and incidence of hypothyroidism in Graves’ disease. J Intern Med 1995;238:491–7.Article PubMed
15. Peters H, Fischer C, Bogner U, Reiners C, Schleusener H. Radioiodine therapy of Graves’ hyperthyroidism: standard vs. calculated 131iodine activity: results from a prospective, randomized, multicentre study. Eur J Clin Invest 1995;25:186–93.Article PubMed
16. Kitahara CM, Berrington de Gonzalez A, Bouville A, Brill AB, Doody MM, Melo DR, et al. Association of radioactive iodine treatment with cancer mortality in patients with hyperthyroidism. JAMA Intern Med 2019;179:1034–42.Article PubMed PMC
17. Metso S, Auvinen A, Huhtala H, Salmi J, Oksala H, Jaatinen P. Increased cancer incidence after radioiodine treatment for hyperthyroidism. Cancer 2007;109:1972–9.Article PubMed
18. Shim SR, Kitahara CM, Cha ES, Kim SJ, Bang YJ, Lee WJ. Cancer risk after radioactive iodine treatment for hyperthyroidism: a systematic review and meta-analysis. JAMA Netw Open 2021;4:e2125072.Article PubMed PMC
19. Kim KJ, Choi J, Kim KJ, Song E, Yu JH, Kim NH, et al. Cancer risk in Graves disease with radioactive 131i treatment: a nationwide cohort study. J Nucl Med 2024;65:693–9.Article PubMed
20. Boelaert K, Maisonneuve P, Torlinska B, Franklyn JA. Comparison of mortality in hyperthyroidism during periods of treatment with thionamides and after radioiodine. J Clin Endocrinol Metab 2013;98:1869–82.Article PubMed
21. Okosieme OE, Taylor PN, Evans C, Thayer D, Chai A, Khan I, et al. Primary therapy of Graves’ disease and cardiovascular morbidity and mortality: a linked-record cohort study. Lancet Diabetes Endocrinol 2019;7:278–87.Article PubMed
22. Giesecke P, Frykman V, Wallin G, Lonn S, Discacciati A, Torring O, et al. All-cause and cardiovascular mortality risk after surgery versus radioiodine treatment for hyperthyroidism. Br J Surg 2018;105:279–86.Article PubMed PDF
23. Ryodi E, Metso S, Huhtala H, Valimaki M, Auvinen A, Jaatinen P. Cardiovascular morbidity and mortality after treatment of hyperthyroidism with either radioactive iodine or thyroidectomy. Thyroid 2018;28:1111–20.Article PubMed
24. Torring O, Tallstedt L, Wallin G, Lundell G, Ljunggren JG, Taube A, et al. Graves’ hyperthyroidism: treatment with antithyroid drugs, surgery, or radioiodine: a prospective, randomized study. Thyroid Study Group. J Clin Endocrinol Metab 1996;81:2986–93.Article PubMed
25. Sundaresh V, Brito JP, Thapa P, Bahn RS, Stan MN. Comparative effectiveness of treatment choices for Graves’ hyperthyroidism: a historical cohort study. Thyroid 2017;27:497–505.Article PubMed PMC
26. Santos RB, Romaldini JH, Ward LS. A randomized controlled trial to evaluate the effectiveness of 2 regimens of fixed iodine (¹³¹I) doses for Graves disease treatment. Clin Nucl Med 2012;37:241–4.PubMed
27. Sundaresh V, Brito JP, Wang Z, Prokop LJ, Stan MN, Murad MH, et al. Comparative effectiveness of therapies for Graves’ hyperthyroidism: a systematic review and network meta-analysis. J Clin Endocrinol Metab 2013;98:3671–7.Article PubMed PMC
28. Wing SS, Fantus IG. Adverse immunologic effects of antithyroid drugs. CMAJ 1987;136:121–7.PubMed PMC
29. Meyer-Gessner M, Benker G, Lederbogen S, Olbricht T, Reinwein D. Antithyroid drug-induced agranulocytosis: clinical experience with ten patients treated at one institution and review of the literature. J Endocrinol Invest 1994;17:29–36.Article PubMed PDF
30. Yang J, Zhu YJ, Zhong JJ, Zhang J, Weng WW, Liu ZF, et al. Characteristics of antithyroid drug-induced agranulocytosis in patients with hyperthyroidism: a retrospective analysis of 114 cases in a single institution in China involving 9690 patients referred for radioiodine treatment over 15 years. Thyroid 2016;26:627–33.Article PubMed
31. Abraham P, Avenell A, McGeoch SC, Clark LF, Bevan JS. Antithyroid drug regimen for treating Graves’ hyperthyroidism. Cochrane Database Syst Rev 2010;2010:CD003420.Article PubMed PMC
32. Lillevang-Johansen M, Abrahamsen B, Jorgensen HL, Brix TH, Hegedus L. Duration of hyperthyroidism and lack of sufficient treatment are associated with increased cardiovascular risk. Thyroid 2019;29:332–40.Article PubMed
33. Sjolin G, Holmberg M, Torring O, Bystrom K, Khamisi S, de Laval D, et al. The long-term outcome of treatment for Graves’ hyperthyroidism. Thyroid 2019;29:1545–57.Article PubMed
34. Laurberg P, Berman DC, Andersen S, Bulow Pedersen I. Sustained control of Graves’ hyperthyroidism during long-term low-dose antithyroid drug therapy of patients with severe Graves’ orbitopathy. Thyroid 2011;21:951–6.Article PubMed
35. Azizi F, Amouzegar A, Tohidi M, Hedayati M, Khalili D, Cheraghi L, et al. Increased remission rates after long-term methimazole therapy in patients with Graves’ disease: results of a randomized clinical trial. Thyroid 2019;29:1192–200.Article PubMed
36. Brandt F, Green A, Hegedus L, Brix TH. A critical review and meta-analysis of the association between overt hyperthyroidism and mortality. Eur J Endocrinol 2011;165:491–7.Article PubMed
37. Biondi B, Kahaly GJ. Cardiovascular involvement in patients with different causes of hyperthyroidism. Nat Rev Endocrinol 2010;6:431–43.Article PubMed PDF
38. Yoshimura Noh J, Inoue K, Suzuki N, Yoshihara A, Fukushita M, Matsumoto M, et al. Dose-dependent incidence of agranulocytosis in patients treated with methimazole and propylthiouracil. Endocr J 2024;71:695–703.Article PubMed
39. Watanabe N, Narimatsu H, Noh JY, Yamaguchi T, Kobayashi K, Kami M, et al. Antithyroid drug-induced hematopoietic damage: a retrospective cohort study of agranulocytosis and pancytopenia involving 50,385 patients with Graves’ disease. J Clin Endocrinol Metab 2012;97:E49–53.Article PubMed
40. Wang MT, Lee WJ, Huang TY, Chu CL, Hsieh CH. Antithyroid drug-related hepatotoxicity in hyperthyroidism patients: a population-based cohort study. Br J Clin Pharmacol 2014;78:619–29.Article PubMed PMC
41. Laurberg P, Wallin G, Tallstedt L, Abraham-Nordling M, Lundell G, Torring O. TSH-receptor autoimmunity in Graves’ disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study. Eur J Endocrinol 2008;158:69–75.Article PubMed
42. Gorman CA. Radioiodine and pregnancy. Thyroid 1999;9:721–6.Article PubMed
43. Yi KH, Ahn HY, Kim JH, Park SY, Yoo WS, Jung KY, et al. 2023 Revised Korean Thyroid Association guidelines for the diagnosis and management of thyroid disease during pregnancy and postpartum. Int J Thyroidol 2023;16:51–88.Article
44. Alexander EK, Pearce EN, Brent GA, Brown RS, Chen H, Dosiou C, et al. 2017 Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid 2017;27:315–89.PubMed
45. Bartalena L, Marcocci C, Bogazzi F, Panicucci M, Lepri A, Pinchera A. Use of corticosteroids to prevent progression of Graves’ ophthalmopathy after radioiodine therapy for hyperthyroidism. N Engl J Med 1989;321:1349–52.Article PubMed
46. Bahn Chair RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid 2011;21:593–646.Article PubMed
47. Gontarz-Nowak K, Szychlinska M, Matuszewski W, Stefanowicz-Rutkowska M, Bandurska-Stankiewicz E. Current knowledge on Graves’ orbitopathy. J Clin Med 2020;10:16.Article PubMed PMC
48. World Health Organization; International Council for Control of Iodine Deficiency Disorders & United Nations Children’s Fund (UNICEF). Indicators for assessing iodine deficiency disorders and their control through salt iodization. Geneva: WHO; 1994 [cited 2025 Jun 7]. Available from: https://iris.who.int/handle/10665/70715.
49. Tay WL, Chng CL, Tien CS, Loke KS, Lam WW, Fook-Chong SM, et al. High thyroid stimulating receptor antibody titre and large goitre size at first-time radioactive iodine treatment are associated with treatment failure in Graves’ disease. Ann Acad Med Singap 2019;48:181–7.Article PubMed
50. Aung ET, Zammitt NN, Dover AR, Strachan MW, Seckl JR, Gibb FW. Predicting outcomes and complications following radioiodine therapy in Graves’ thyrotoxicosis. Clin Endocrinol (Oxf) 2019;90:192–9.Article PubMed PDF
51. McDermott MT, Kidd GS, Dodson LE Jr, Hofeldt FD. Radioiodine-induced thyroid storm: case report and literature review. Am J Med 1983;75:353–9.PubMed
52. Walter MA, Briel M, Christ-Crain M, Bonnema SJ, Connell J, Cooper DS, et al. Effects of antithyroid drugs on radioiodine treatment: systematic review and meta-analysis of randomised controlled trials. BMJ 2007;334:514.Article PubMed PMC
53. Shafer RB, Nuttall FQ. Acute changes in thyroid function in patients treated with radioactive iodine. Lancet 1975;2:635–7.Article PubMed
54. Burch HB, Solomon BL, Cooper DS, Ferguson P, Walpert N, Howard R. The effect of antithyroid drug pretreatment on acute changes in thyroid hormone levels after (131)I ablation for Graves’ disease. J Clin Endocrinol Metab 2001;86:3016–21.Article PubMed
55. Wartofsky L, Ransil BJ, Ingbar SH. Inhibition by iodine of the release of thyroxine from the thyroid glands of patients with thyrotoxicosis. J Clin Invest 1970;49:78–86.Article PubMed PMC
56. Bogazzi F, Giovannetti C, Fessehatsion R, Tanda ML, Campomori A, Compri E, et al. Impact of lithium on efficacy of radioactive iodine therapy for Graves’ disease: a cohort study on cure rate, time to cure, and frequency of increased serum thyroxine after antithyroid drug withdrawal. J Clin Endocrinol Metab 2010;95:201–8.PubMed
57. Turner JG, Brownlie BE, Rogers TG. Lithium as an adjunct to radioiodine therapy for thyrotoxicosis. Lancet 1976;1:614–5.Article PubMed
58. Min SH, Phung A, Oh TJ, Han KS, Kim MJ, Kim JM, et al. Therapeutic plasmapheresis enabling radioactive iodine treatment in a patient with thyrotoxicosis. J Korean Med Sci 2015;30:1531–4.Article PubMed PMC PDF
59. Cherniauskas V, Santos AL, Carvalho DD, Olivato MC, de Prado Padovani R, Kawabata NK, et al. Plasmapheresis as an effective treatment for thyroid storm in critical patients: case reports and systematic literature review. J Endocr Soc 2021;5(Supplement 1):A947–8.Article PDF
60. Ozdemir Baser O, Cetin Z, Catak M, Koseoglu D, Berker D. The role of therapeutic plasmapheresis in patients with hyperthyroidism. Transfus Apher Sci 2020;59:102744.Article PubMed
61. Leslie WD, Ward L, Salamon EA, Ludwig S, Rowe RC, Cowden EA. A randomized comparison of radioiodine doses in Graves’ hyperthyroidism. J Clin Endocrinol Metab 2003;88:978–83.Article PubMed
62. Taprogge J, Gape PM, Carnegie-Peake L, Murray I, Gear JI, Leek F, et al. A systematic review and meta-analysis of the relationship between the radiation absorbed dose to the thyroid and response in patients treated with radioiodine for Graves’ disease. Thyroid 2021;31:1829–38.Article PubMed PMC
63. Kung AW, Yau CC, Cheng AC. The action of methimazole and L-thyroxine in radioiodine therapy: a prospective study on the incidence of hypothyroidism. Thyroid 1995;5:7–12.Article PubMed
64. Bonnema SJ, Bennedbaek FN, Veje A, Marving J, Hegedus L. Propylthiouracil before 131I therapy of hyperthyroid diseases: effect on cure rate evaluated by a randomized clinical trial. J Clin Endocrinol Metab 2004;89:4439–44.PubMed
65. Shalaby M, Hadedeya D, Toraih EA, Razavi MA, Lee GS, Hussein MH, et al. Predictive factors of radioiodine therapy failure in Graves’ disease: a meta-analysis. Am J Surg 2022;223:287–96.Article PubMed
66. Vija Racaru L, Fontan C, Bauriaud-Mallet M, Brillouet S, Caselles O, Zerdoud S, et al. Clinical outcomes 1 year after empiric 131I therapy for hyperthyroid disorders: real life experience and predictive factors of functional response. Nucl Med Commun 2017;38:756–63.PubMed
67. Santos TA, Marui S, Watanabe T, Lima N, Ozaki CO, Cerri GG, et al. Color duplex Doppler US can follow up the response of radioiodine in Graves’ disease by evaluating the thyroid volume and peak systolic velocity. Ultraschall Med 2020;41:658–67.Article PubMed
68. Lee J, Yeoh Y, Seo MJ, Lee GH, Kim CI. Estimation of dietary iodine intake of Koreans through a Total Diet Study (TDS). Korean J Community Nutr 2021;26:48–55.Article PDF
69. Tsuruhara R, Tamura M, Nakada K, Beniko M, Mizukoshi T, Satou Y, et al. Does low iodine diet improve radioiodine uptake in hyperthyroidism? J Nucl Med 2013;54(supplement 2):41.
70. Santarosa VA, Orlandi DM, Fiorin LB, Kasamatsu TS, Furuzawa GK, Kunii IS, et al. Low iodine diet does not improve the efficacy of radioiodine for the treatment of Graves’ disease. Arch Endocrinol Metab 2015;59:501–6.Article PubMed
71. Santos RB, Romaldini JH, Ward LS. Propylthiouracil reduces the effectiveness of radioiodine treatment in hyperthyroid patients with Graves’ disease. Thyroid 2004;14:525–30.Article PubMed
72. Hancock LD, Tuttle RM, LeMar H, Bauman J, Patience T. The effect of propylthiouracil on subsequent radioactive iodine therapy in Graves’ disease. Clin Endocrinol (Oxf) 1997;47:425–30.Article PubMed PDF
73. Campenni A, Avram AM, Verburg FA, Iakovou I, Hanscheid H, de Keizer B, et al. The EANM guideline on radioiodine therapy of benign thyroid disease. Eur J Nucl Med Mol Imaging 2023;50:3324–48.Article PubMed PMC PDF
74. Akamizu T, Satoh T, Isozaki O, Suzuki A, Wakino S, Iburi T, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid 2012;22:661–79.Article PubMed PMC
75. Andrade VA, Gross JL, Maia AL. Effect of methimazole pretreatment on serum thyroid hormone levels after radioactive treatment in Graves’ hyperthyroidism. J Clin Endocrinol Metab 1999;84:4012–6.Article PubMed
76. Laurberg P, Berman DC, Bulow Pedersen I, Andersen S, Carle A. Incidence and clinical presentation of moderate to severe Graves’ orbitopathy in a Danish population before and after iodine fortification of salt. J Clin Endocrinol Metab 2012;97:2325–32.Article PubMed PMC
77. Jarhult J, Rudberg C, Larsson E, Selvander H, Sjovall K, Winsa B, et al. Graves’ disease with moderate-severe endocrine ophthalmopathy-long term results of a prospective, randomized study of total or subtotal thyroid resection. Thyroid 2005;15:1157–64.Article PubMed
78. Tallstedt L, Lundell G, Torring O, Wallin G, Ljunggren JG, Blomgren H, et al. Occurrence of ophthalmopathy after treatment for Graves’ hyperthyroidism. The Thyroid Study Group. N Engl J Med 1992;326:1733–8.Article PubMed
79. Bartalena L, Marcocci C, Bogazzi F, Manetti L, Tanda ML, Dell’Unto E, et al. Relation between therapy for hyperthyroidism and the course of Graves’ ophthalmopathy. N Engl J Med 1998;338:73–8.Article PubMed
80. Traisk F, Tallstedt L, Abraham-Nordling M, Andersson T, Berg G, Calissendorff J, et al. Thyroid-associated ophthalmopathy after treatment for Graves’ hyperthyroidism with antithyroid drugs or iodine-131. J Clin Endocrinol Metab 2009;94:3700–7.PubMed
81. Acharya SH, Avenell A, Philip S, Burr J, Bevan JS, Abraham P. Radioiodine therapy (RAI) for Graves’ disease (GD) and the effect on ophthalmopathy: a systematic review. Clin Endocrinol (Oxf) 2008;69:943–50.Article PubMed
82. Shiber S, Stiebel-Kalish H, Shimon I, Grossman A, Robenshtok E. Glucocorticoid regimens for prevention of Graves’ ophthalmopathy progression following radioiodine treatment: systematic review and meta-analysis. Thyroid 2014;24:1515–23.Article PubMed
83. Vannucchi G, Covelli D, Campi I, Curro N, Dazzi D, Rodari M, et al. Prevention of orbitopathy by oral or intravenous steroid prophylaxis in short duration Graves’ disease patients undergoing radioiodine ablation: a prospective randomized control trial study. Thyroid 2019;29:1828–33.Article PubMed
84. Rosetti S, Tanda ML, Veronesi G, Masiello E, Premoli P, Gallo D, et al. Oral steroid prophylaxis for Graves’ orbitopathy after radioactive iodine treatment for Graves’ disease is not only effective, but also safe. J Endocrinol Invest 2020;43:381–3.Article PubMed PDF
85. Lai A, Sassi L, Compri E, Marino F, Sivelli P, Piantanida E, et al. Lower dose prednisone prevents radioiodine-associated exacerbation of initially mild or absent Graves’ orbitopathy: a retrospective cohort study. J Clin Endocrinol Metab 2010;95:1333–7.Article PubMed
86. Perros P, Kendall-Taylor P, Neoh C, Frewin S, Dickinson J. A prospective study of the effects of radioiodine therapy for hyperthyroidism in patients with minimally active Graves’ ophthalmopathy. J Clin Endocrinol Metab 2005;90:5321–3.Article PubMed
87. Watanabe N, Noh JY, Kozaki A, Iwaku K, Sekiya K, Kosuga Y, et al. Radioiodine-associated exacerbation of Graves’ orbitopathy in the Japanese population: randomized prospective study. J Clin Endocrinol Metab 2015;100:2700–8.Article PubMed
88. Bartalena L, Kahaly GJ, Baldeschi L, Dayan CM, Eckstein A, Marcocci C, et al. The 2021 European Group on Graves’ orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves’ orbitopathy. Eur J Endocrinol 2021;185:G43–67.PubMed
89. Sawers JS, Toft AD, Irvine WJ, Brown NS, Seth J. Transient hypothyroidism after iodine-131 treatment of thyrotoxicosis. J Clin Endocrinol Metab 1980;50:226–9.Article PubMed
90. Uy HL, Reasner CA, Samuels MH. Pattern of recovery of the hypothalamic-pituitary-thyroid axis following radioactive iodine therapy in patients with Graves’ disease. Am J Med 1995;99:173–9.Article PubMed
91. Stan MN, Durski JM, Brito JP, Bhagra S, Thapa P, Bahn RS. Cohort study on radioactive iodine-induced hypothyroidism: implications for Graves’ ophthalmopathy and optimal timing for thyroid hormone assessment. Thyroid 2013;23:620–5.Article PubMed
92. Holm LE, Lundell G, Dahlqvist I, Israelsson A. Cure rate after 131I therapy for hyperthyroidism. Acta Radiol Oncol 1981;20:161–6.Article PubMed
93. Bonnema SJ, Hegedus L. Radioiodine therapy in benign thyroid diseases: effects, side effects, and factors affecting therapeutic outcome. Endocr Rev 2012;33:920–80.Article PubMed PDF

Figure & Data

References

Citations

Citations to this article as recorded by

PubReader
ePub Link

Cite

Cite: export Copy Download Format; Close

Download Citation

Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.

Format:

RIS — For EndNote, ProCite, RefWorks, and most other reference management software
BibTeX — For JabRef, BibDesk, and other BibTeX-specific software

Include:

Citation for the content below
Citation and abstract for the content below

2025 Korean Thyroid Association Management Guidelines for Radioactive Iodine Therapy in Patients with Hyperthyroidism

Endocrinol Metab. 2025;40(3):342-356. Published online June 24, 2025

DOI: https://doi.org/10.3803/EnM.2025.2464

XML Download

Related articles

2025 Korean Thyroid Association Management Guidelines for Radioactive Iodine Therapy in Patients with Hyperthyroidism

Grade	Level	Definition
1	Strongly recommend for/against	Sufficient and objective evidence exists that performing (or avoiding) the recommended action leads to significant health benefits or harms.
2	Conditionally recommend for/against	Evidence suggests important health benefits or harms, but the evidence is uncertain or indirect, making a uniform recommendation difficult.
3	Expert consensus recommendation	In the absence of strong clinical evidence, the recommendation is based on expert consensus and patient-specific considerations.
4	Inconclusive	Insufficient or conflicting evidence exists regarding significant health benefits or harms; no definitive recommendation for or against the action can be made.

Section 1. Indications for RAI therapy in patients with hyperthyroidism
1.1. RAI therapy should be considered in the following clinical situation.
1.1.1. When the patient prefers an initial treatment option with a high likelihood of cure. [Recommendation level 1]
1.1.2. When serious adverse events occur during ATD therapy. [Recommendation level 1]
1.1.3. In patients who experience recurrent hyperthyroidism after remission with ATD therapy and desire a definitive cure. [Recommendation level 1]
1.1.4. When thyroid function remains poorly controlled despite appropriate ATD therapy. [Recommendation level 1]
1.2. RAI therapy may be considered in the following clinical situation.
1.2.1. In patients with poor adherence to ATD therapy. [Recommendation level 2]
1.2.2. In patients with comorbidities that may lead to clinical instability if hyperthyroidism worsens (e.g., uncontrolled arrhythmia or heart failure). [Recommendation level 2]
1.2.3. In patients requiring prolonged high-dose ATD therapy to maintain euthyroidism (particularly in women planning pregnancy in the next 6 months or beyond). [Recommendation level 3]
1.3. RAI therapy is not recommended in the following clinical situation.
1.3.1. Pregnant or breastfeeding women. [Recommendation level 1]
1.3.2. Patients with active moderate-to-severe thyroid eye disease. [Recommendation level 1]
1.3.3. Patients with coexisting thyroid cancer. [Recommendation level 1]
Section 2. Determination of the RAI dose in patients with hyperthyroidism
2.1. A fixed dose of RAI (10–15 mCi) sufficient to induce hypothyroidism is recommended when determining the appropriate RAI dose. [Recommendation level 2]
Section 3. Need for a low-iodine diet before RAI therapy in patients with hyperthyroidism
3.1. A low-iodine diet is not routinely recommended before RAI therapy for hyperthyroidism; but iodine-rich foods should be avoided for at least 1 week prior to treatment. [Recommendation level 3]
Section 4. Appropriate discontinuation period of ATD before and after RAI therapy
4.1. Discontinuation of ATD for 3 to 7 days before RAI therapy is recommended. [Recommendation level 1]
4.2. Resumption of ATD within 3–7 days after RAI therapy may be considered in patients who received ATD prior to treatment or are at high risk of clinical deterioration due to worsening hyperthyroidism. [Recommendation level 2]
Section 5. Use of glucocorticoid before RAI therapy to reduce the development or progression of TED
5.1. RAI therapy is not recommended in patients with active moderate-to-severe TED. [Recommendation level 1]
5.2. Prophylactic corticosteroid therapy is recommended when RAI therapy is administered to patients with active mild TED. [Recommendation level 1]
5.3. In patients with inactive moderate-to-severe TED, prophylactic corticosteroid therapy may be considered during RAI treatment when additional risk factors—such as high TSH receptor antibody levels or smoking—are present. [Recommendation level 2]
5.4. Prophylactic corticosteroid therapy is not recommended during RAI treatment in patients with inactive mild TED when additional risk factors—such as high TSH receptor antibody levels or smoking—are not present. [Recommendation level 1]
Section 6. Intervals for thyroid function test after RAI therapy
6.1. Thyroid function test, including TSH and free T4, may be considered within 4 to 6 weeks after RAI therapy. [Recommendation level 2]
6.2. Thyroid function can be monitored every 2 to 3 months for up to 6 months after RAI therapy or until TSH levels normalize. [Recommendation level 2]
6.3. Thyroid function test may be repeated every 6 to 12 months, once thyroid function has been confirmed to be stable and within the normal range on at least two consecutive assessments. [Recommendation level 2]
6.4. Thyroid function test is recommended when symptoms of hyperthyroidism or hypothyroidism are suspected. [Recommendation level 2]

TED activity	Severity
	Mild		Moderate-to-severe
	No risk factors	With risk factors	No risk factors	With risk factors
Inactive	No steroid prophylaxis required	Consider steroid prophylaxis	No steroid prophylaxis required	Steroid prophylaxis recommended
Active	Consider steroid prophylaxis	Steroid prophylaxis recommended	RAI therapy not recommended	RAI therapy not recommended

Table 1. Korean Thyroid Association Recommendation Levels for Clinical Strategies, Diagnostic Testing, or Treatment in Patient Care

Table 2. Summary of 2025 Korean Thyroid Association Guidelines Statements for Radioactive Iodine Therapy in Patients with Hyperthyroidism

RAI, radioactive iodine; ATD, antithyroid drug; TED, thyroid eye disease; TSH, thyroid stimulating hormone; T4, thyroxine.

Table 3. Recommendations for RAI Therapy and Prophylactic Steroid Use Based on TED Severity, Activity, and Risk Factors

RAI, radioactive iodine; TED, thyroid eye disease.

Articles

ABSTRACT

INTRODUCTION

DEVELOPMENT PROCESS OF THE KTA CLINICAL PRACTICE GUIDELINE FOR RAI THERAPY IN PATIENTS WITH HYPERTHYROIDISM

EFFICACY AND SAFETY OF RAI THERAPY IN HYPERTHYROIDISM

Section 1. Indications for RAI therapy in patients with hyperthyroidism

Section 2. Determination of the RAI dose in patients with hyperthyroidism

Section 3. Need for a low-iodine diet before RAI therapy in patients with hyperthyroidism

Section 4. Appropriate discontinuation period of ATD before and after RAI therapy

Section 5. Use of glucocorticoid before RAI therapy to reduce the development or progression of thyroid eye disease

Section 6. Intervals for thyroid function test after RAI therapy

CONCLUSIONS

Article information

References

Figure & Data

References

Citations

Table 1.

Table 2.

Table 3.