scholarly journals Calcification Patterns in Papillary Thyroid Carcinoma are Associated with Changes in Thyroid Hormones and Coronary Artery Calcification

2018 ◽  
Vol 7 (8) ◽  
pp. 183
Author(s):  
Jeonghoon Ha ◽  
Jeongmin Lee ◽  
Kwanhoon Jo ◽  
Jeong-Sun Han ◽  
Min-Hee Kim ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Coronary Artery Calcification ◽  
Close Association ◽  
Papillary Thyroid ◽  
Free T4 ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

Recent studies suggested that a lower serum thyroid hormone level is associated with more vascular calcification. However, it has been rarely evaluated whether lower thyroid hormone levels affect the calcification of thyroid cancer and there is a relationship between calcification patterns of papillary thyroid carcinoma (PTC) and coronary artery calcification (CAC). The study was divided into two groups: First, we retrospectively reviewed 182 PTC patients and examined the correlation between PTC calcification patterns and CAC by coronary computed tomography (CT). Second, the correlation between the calcification pattern of PTC and thyroid hormone concentration was investigated (n = 354). The calcification pattern of PTC was evaluated by thyroid ultrasonography and classified into four groups: no-calcification, microcalcification, macrocalcification, and mixed-calcification. In PTC patients with microcalcification and mixed calcification, more CAC was observed and coronary calcium score (CCS) was higher. Lower free T4 and higher thyroid-stimulating hormone (TSH) levels were associated with microcalcification and mixed calcification, not with macrocalcification and no calcification. PTC with microcalcification and mixed calcification showed more aggressive phenotypes like lymph node metastasis and more advanced TNM (tumor, node, and metastasis) stage than those with no calcification and macrocalcification. Calcification patterns of PTC showed close association with thyroid hormone levels and CAC. Further research is needed to determine how these findings are related to cardiovascular risk and disease-specific mortality.

scholarly journals Thyroid Hormone Resistance With Concurrent Papillary Thyroid Cancer

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A961-A962
Author(s):  
Dhivya Pahwa ◽  
Michael Howard Shanik
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Thyroid Hormone Receptor ◽  
Hormone Resistance ◽  
Papillary Thyroid ◽  
Free T4 ◽  
Thyroid Hormone Resistance ◽  
History Of

Abstract Introduction: Thyroid hormone resistance is a genetic mutation resulting in decreased receptor responsiveness. We present a case of thyroid hormone resistance with concurrent papillary thyroid cancer. Clinical Case: A 34-year-old man with a history of papillary thyroid carcinoma status post total thyroidectomy and radioactive iodine. He had transferred his care after moving to our area. He presented with persistently elevated TSH despite ongoing treatment with Levothyroxine 400 mcg daily. Upon presentation the patient reported intermittent palpitations and tremor. Vital signs revealed height of 74 inches, weight of 235 pounds, blood pressure of 112/64, and heart rate of 48. Physical examination revealed a well -healed scar on the neck without palpable lymphadenopathy. Bloodwork revealed TSH of 15.28 mIU/L and Free T4 of 2.8 ng/dL. The patient was maintained on Levothyroxine 400 mcg daily and educated on proper administration of the medication. Two months later, bloodwork revealed a TSH of 9.22 mIU/L with a Free T4 of 3.3 ng/dL. MRI of the pituitary revealed a 4mm hyper-intensity which likely represented a microadenoma. Resistance Thyroid Hormone (RTH) Mutation analysis was ordered which revealed a heterozygous mutation for the Thyroid Hormone Receptor (THR)-Beta gene. The mutation was detected at pArg438His indicating a single nucleotide substitution leading to the replacement of arginine by histidine at the p.438 of the translated protein on exon 10. The patient was maintained on Levothyroxine at 400 mcg daily. Discussion: Thyroid hormone resistance describes a constellation of symptoms from decreased tissue responsiveness to thyroid hormones. Literature reveals the prevalence of THR to be 1 in 40,000 individuals. It occurs due to mutation on the thyroid hormone receptor, most often found on the alpha or beta subunit. Frequently patients present with tachycardia and hyperactivity but it can also present with symptoms suggestive of hypothyroidism and goiter. Risk factors include family history of RTH mutation often with an autosomal dominant inheritance pattern. Patients with an elevated Free T4 with a non-suppressed TSH should be investigated with a genetic analysis of Resistance Thyroid hormone. A positive mutation would confirm the diagnosis. Close monitoring of symptoms as well as thyroid function tests should guide treatment. The concurrent diagnosis of thyroid hormone resistance in conjunction with papillary thyroid carcinoma in our patient is unique and makes management a challenge. The literature reveals few cases reported. Reference: DynaMed. (2018, November 30). Thyroid Hormone Resistance. Retrieved October 2, 2020, from https://www-dynamed-com.arktos.nyit.edu/topics/dmp~AN~T912485 Igata M, et al. Coexistence of resistance to thyroid hormone and papillary thyroid carcinoma. Endocrinol Diabetes Metab Case Rep. 2016;2016:160003. doi:10.1530/EDM-16-0003

scholarly journals MON-472 A Case of Resistance to Thyroid Hormone with Concurrent Hashimoto’s Thyroiditis and Post-Surgical Hypothyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Julie Bernthal ◽  
Sarah Kim ◽  
Shira Grock
Keyword(s):  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Hashimoto's Thyroiditis ◽  
Papillary Thyroid ◽  
Free T4 ◽  
Resistance To Thyroid Hormone ◽  
The Right

Abstract Introduction: Resistance to thyroid hormone (RTH) is a rare defect that results in impaired sensitivity to thyroid hormone. While most commonly caused by mutations in the thyroid hormone receptor beta (THRβ) gene, in 15% of patients with the RTH phenotype, no mutation is identified.1 This entity is known as non-thyroid hormone receptor RTH (nonTR-RTH). Patients with RTH have an increased risk of autoimmune thyroid disease with a reported odds ratio of 2.36.2 Hashimoto’s thyroiditis or other etiologies of hypothyroidism add a layer of complexity to RTH as such individuals may require high doses of levothyroxine to overcome hormone resistance. Clinical Case: A 36-year-old male was referred for abnormal thyroid function tests. He denied symptoms of thyroid dysfunction. Physical examination was notable for a goiter. Weight was 83 kg. Initial labs revealed TSH 6.8 mcIU/mL (0.3-4.7 mcIU/mL), free T4 2.0 ng/dL (0.8-1.7 ng/dL), free T3 491 pg/dL (222-383 pg/dL), and thyroid peroxidase antibody >600 IU/mL (≤20 IU/mL). Additional work-up demonstrated elevated free T4 by equilibrium dialysis 2.5ng/dL (0.9-2.2 ng/dL) and elevated TSH with HAMA treatment 5.96 mIU/L (0.40-4.50 mIU/L), thereby ruling out familial dysalbuminemic hyperthyroxinemia and HAMA interference. Alpha-subunit of 0.30 ng/mL (<0.55 ng/mL) and normal pituitary MRI did not support a TSH-secreting adenoma. Quest Diagnostics RTH Gene Sequencing was negative for a mutation in the THRβ gene. The patient was subsequently diagnosed with nonTR-RTH. Thyroid ultrasound showed multiple thyroid nodules, including a 1.8 cm hypoechoic, complex nodule in the left inferior gland and a 1.7 cm isoechoic nodule in the right inferior gland. Fine needle aspiration of the left nodule was suspicious for papillary thyroid carcinoma and the right nodule showed lymphocytic thyroiditis. The patient underwent total thyroidectomy and pathology demonstrated a benign left nodule and an incidental 0.3 cm right papillary thyroid carcinoma. The patient started levothyroxine 150 mcg daily (1.8 mcg/kg) post-operatively with subsequent TSH of 18.1 mcIU/mL. His dose was increased to 200 mcg daily (2.4 mcg/kg) and TSH was still elevated at 11.7 mcIU/mL. His levothyroxine dose was subsequently increased to 250 mcg daily (3 mcg/kg) and TSH is outstanding. Conclusions: This case highlights the diagnostic challenge in nonTR-RTH. It also demonstrates the complex management of patients with RTH and concurrent hypothyroidism. Such patients need close monitoring and aggressive titration of levothyroxine to achieve desired hormone levels. 1. Dumitrescu AM, Refetoff S. The syndromes of reduced sensitivity to thyroid hormone. Biochim Biophys Acta 2013;1830:3987-4003. 2. Barkoff MS, Kocherginsky M, Anselmo J, Weiss RE, Refetoff S. Autoimmunity in patients with resistance to thyroid hormone. J Clin Endocrinol Metab 2010;95:3189-93.

scholarly journals Rescue pre-operative treatment with Lugol’s solution in uncontrolled Graves’ disease

2017 ◽  
Vol 6 (4) ◽  
pp. 200-205 ◽  
Author(s):  
Jan Calissendorff ◽  
Henrik Falhammar
Keyword(s):  
Heart Rate ◽  
Thyroid Hormone ◽  
Side Effects ◽  
Definitive Treatment ◽  
Graves Disease ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Adherence To Medication ◽  
Thyroid Hormone Levels

Background Graves’ disease is a common cause of hyperthyroidism. Three therapies have been used for decades: pharmacologic therapy, surgery and radioiodine. In case of adverse events, especially agranulocytosis or hepatotoxicity, pre-treatment with Lugol’s solution containing iodine/potassium iodide to induce euthyroidism before surgery could be advocated, but this has rarely been reported. Methods All patients hospitalised due to uncontrolled hyperthyroidism at the Karolinska University Hospital 2005–2015 and treated with Lugol’s solution were included. All electronic files were carefully reviewed manually, with focus on the cause of treatment and admission, demographic data, and effects of iodine on thyroid hormone levels and pulse frequency. Results Twenty-seven patients were included. Lugol’s solution had been chosen due to agranulocytosis in 9 (33%), hepatotoxicity in 2 (7%), other side effects in 11 (41%) and poor adherence to medication in 5 (19%). Levels of free T4, free T3 and heart rate decreased significantly after 5–9 days of iodine therapy (free T4 53–20 pmol/L, P = 0.0002; free T3 20–6.5 pmol/L, P = 0.04; heart rate 87–76 beats/min P = 0.0007), whereas TSH remained unchanged. Side effects were noted in 4 (15%) (rash n = 2, rash and vomiting n = 1, swelling of fingers n = 1). Thyroidectomy was performed in 26 patients (96%) and one was treated with radioiodine; all treatments were without serious complications. Conclusion Treatment of uncontrolled hyperthyroidism with Lugol’s solution before definitive treatment is safe and it decreases thyroid hormone levels and heart rate. Side effects were limited. Lugol’s solution could be recommended pre-operatively in Graves’ disease with failed medical treatment, especially if side effects to anti-thyroid drugs have occurred.

scholarly journals A Brief Exposure to Moderate Passive Smoke Increases Metabolism and Thyroid Hormone Secretion

2007 ◽  
Vol 92 (1) ◽  
pp. 208-211 ◽  
Author(s):  
Giorgos S. Metsios ◽  
Andreas D. Flouris ◽  
Athanasios Z. Jamurtas ◽  
Andres E. Carrillo ◽  
Demetrios Kouretas ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Passive Smoking ◽  
Repeated Measures ◽  
Hormone Secretion ◽  
Free T4 ◽  
Hormone Levels ◽  
Urine Cotinine ◽  
The Mean ◽  
Thyroid Hormone Levels ◽  
Serum And Urine

Abstract Context: Active smoking influences normal metabolic status and thyroid function. Objective: The objective was to assess experimentally the effects of 1 h of moderate passive smoking in a controlled simulated bar/restaurant environment on the metabolism and thyroid hormone levels in healthy nonsmokers. Participants: Eighteen (nine females, nine males) healthy individuals (mean ± sd: age, 25.3 ± 3.1 yr; height, 174.0 ± 10.1 cm; weight, 65.2 ± 13.7 kg) participated in the study. Design: In repeated-measures randomized blocks, participants visited the laboratory on 2 consecutive days. In the experimental condition, they were exposed to 1 h of moderate passive smoking at a carbon monoxide concentration of 23 ± 1 ppm in an environmental chamber, whereas in the control condition participants remained in the same chamber for 1 h breathing normal atmospheric air. Main Outcome Measures: In both conditions, cotinine serum and urine levels, resting energy expenditure (REE), as well as concentration of T3, free T4, and TSH were assessed before participants entered the chamber and immediately after their exit. Heart rate and blood pressure were tested in 10-min intervals during all REE assessments. Results: The mean ± sd difference of serum and urine cotinine levels (−0.27 ± 3.94 vs. 14.01 ± 6.54 and 0.05 ± 2.07 vs. 7.23 ± 3.75, respectively), REE (6.73 ± 98.06 vs. 80.58 ± 120.91) as well as T3 and free T4 (0.05 ± 0.11 vs. 0.13 ± 0.12 and 0.02 ± 0.15 vs. 0.22 ± 0.20) were increased in the experimental compared with the control condition at baseline and follow-up (P < 0.05). No statistically significant variation was observed in the mean difference of the remaining parameters (P > 0.05). Serum and urine cotinine values were linearly associated with REE (P < 0.05). Conclusion: One hour of passive smoking at bar/restaurant levels is accompanied by significant increases in metabolism and thyroid hormone levels.

scholarly journals Hyponatremia after Thyroid Hormone Withdrawal in a Patient with Papillary Thyroid Carcinoma

2014 ◽  
Vol 29 (1) ◽  
pp. 77 ◽  
Author(s):  
Hyo Jin Jo ◽  
Yong Hyun Kim ◽  
Dong Hyun Shin ◽  
Mi Jeoung Kim ◽  
Sang Jin Lee ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Papillary Thyroid ◽  
Thyroid Hormone Withdrawal

scholarly journals Coexistence of resistance to thyroid hormone and papillary thyroid carcinoma

2016 ◽  
Vol 2016 ◽  
Author(s):  
Motoyuki Igata ◽  
Kaku Tsuruzoe ◽  
Junji Kawashima ◽  
Daisuke Kukidome ◽  
Tatsuya Kondo ◽  
...  
Keyword(s):  
Lymph Node ◽  
Thyroid Hormone ◽  
Thyroid Carcinoma ◽  
Total Thyroidectomy ◽  
Close Association ◽  
Papillary Thyroid ◽  
Node Metastases ◽  
Tsh Suppression Therapy ◽  
Tsh Levels

Summary Resistance to thyroid hormone (RTH) is a syndrome of reduced tissue responsiveness to thyroid hormones. RTH is majorly caused by mutations in the thyroid hormone receptor beta (THRB) gene. Recent studies indicated a close association of THRB mutations with human cancers, but the role of THRB mutation in carcinogenesis is still unclear. Here, we report a rare case of RTH with a papillary thyroid carcinoma (PTC). A 26-year-old woman was referred to our hospital due to a thyroid tumor and hormonal abnormality. She had elevated serum thyroid hormones and non-suppressed TSH levels. Genetic analysis of THRB identified a missense mutation, P452L, leading to a diagnosis of RTH. Ultrasound-guided fine-needle aspiration biopsy of the tumor and lymph nodes enabled the cytological diagnosis of PTC with lymph node metastases. Total thyroidectomy and neck lymph nodes dissection were performed. Following surgery, thyroxine replacement (≥500 μg) was necessary to avoid the symptoms of hypothyroidism and to maintain her TSH levels within the same range as before the operation. During the follow-up, basal thyroglobulin (Tg) levels were around 6 ng/ml and TSH-stimulated Tg levels were between 12 and 20 ng/ml. Up to present, the patient has had no recurrence of PTC. This indicates that these Tg values are consistent with a biochemical incomplete response or an indeterminate response. There is no consensus regarding the management of thyroid carcinoma in patients with RTH, but aggressive treatments such as total thyroidectomy followed by radioiodine (RAI) and TSH suppression therapy are recommended. Learning points There are only a few cases reporting the coexistence of RTH and thyroid carcinoma. Moreover, our case would be the first case presenting one with lymph node metastases. Recent studies indicated a close association of THRB mutations with human cancers, but the role of THRB mutation in carcinogenesis is still unclear. When total thyroidectomy is performed in patients with RTH, a large amount of thyroxine is needed to maintain their thyroid function. There is no consensus regarding the management of thyroid carcinoma in patient with RTH, but effective treatments such as total thyroidectomy followed by RAI and TSH suppression therapy are recommended.

scholarly journals Thyroid Hormone Receptor β (THRB) Is a Major Target Gene for Micro-RNAs Deregulated in Papillary Thyroid Carcinoma (PTC)

2011 ◽  
Vol 25 (2) ◽  
pp. 373-373
Author(s):  
Krystian Jazdzewski ◽  
Joanna Boguslawska ◽  
Jaroslaw Jendrzejewski ◽  
Sandya Liyanarachchi ◽  
Janusz Pachucki ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Hormone Receptor ◽  
Untranslated Region ◽  
Normal Tissue ◽  
Thyroid Hormone Receptor ◽  
Papillary Thyroid ◽  
Down Regulation ◽  
Micro Rnas

Context: Loss of the thyroid hormone receptor is common in tumors. In mouse models, a truncated THRB gene leads to thyroid cancer. Previously, we observed up-regulation of the expression of eight micro-RNAs (miR) in papillary thyroid carcinoma (PTC) tumors. Objective: Our objective was to determine whether THRB might be inhibited by miR up-regulated in PTC. Design: The potential binding of miR to the 3′-untranslated region of THRB was analyzed in silico. Direct inhibition by miR binding to the cloned 3′-untranslated region of THRB was evaluated using luciferase assays. Inhibition of endogenous THRB and its target genes (DIO1 and APP) was examined in cell lines transfected by pre-miR. The impact on thyroid hormone response elements (TRE) was evaluated in promoter assays. Correlations between the expression of THRB and miR was evaluated in 13 PTC tumor/normal tissue pairs. Results: THRB contains binding sites for the top seven miR up-regulated in PTC (P = 0.0000002). Direct interaction with THRB was shown for miR-21 and miR-146a. We observed lower levels of THRB transcripts in cell lines transfected with miR-21, −146a, and −221 (down-regulation of 37–48%; P < 0.0001), but not with miR-181a. THRB protein was suppressed down to 10–28% by each of four miR. Concomitant expression of DIO1 and APP was affected (down-regulation of 32–66%, P < 0.0034 and up-regulation of 48–57%, P < 0.0002, respectively). All four miR affected TRE activity in promoter assays. Down-regulation of luciferase occurred after transfection with pTRE-TK-Luc construct and each of four miR. The analysis of tumor/normal tissue pairs revealed down-regulation of THRB in 11 of 13 pairs (1.3- to 9.1-fold), and up-regulation of miR-21, −146a, −181a, and −221 in almost all pairs. Conclusions: MiR up-regulated in PTC tumors directly inhibit the expression of THRB, an important tumor suppressor gene.

scholarly journals Thyroid Autoantibodies Are Rare in Nonhuman Great Apes and Hypothyroidism Cannot Be Attributed to Thyroid Autoimmunity

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4896-4907 ◽  
Author(s):  
Holly Aliesky ◽  
Cynthia L. Courtney ◽  
Basil Rapoport ◽  
Sandra M. McLachlan
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Autoimmunity ◽  
Great Apes ◽  
Normal Serum ◽  
Thyroid Peroxidase ◽  
Thyroid Autoantibodies ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Thyroid Hormone Levels

The great apes include, in addition to Homo, the genera Pongo (orangutans), Gorilla (gorillas), and Pan, the latter comprising two species, P. troglodytes (chimpanzees) and P. paniscus (bonobos). Adult-onset hypothyroidism was previously reported in 4 individual nonhuman great apes. However, there is scarce information on normal serum thyroid hormone levels and virtually no data for thyroid autoantibodies in these animals. Therefore, we examined thyroid hormone levels and TSH in all nonhuman great ape genera including adults, adolescents, and infants. Because hypothyroidism in humans is commonly the end result of thyroid autoimmunity, we also tested healthy and hypothyroid nonhuman great apes for antibodies to thyroglobulin (Tg), thyroid peroxidase (TPO), and the TSH receptor (TSHR). We established a thyroid hormone and TSH database in orangutans, gorillas, chimpanzees, and bonobos (447 individuals). The most striking differences are the greatly reduced free-T4 and free-T3 levels in orangutans and gorillas vs chimpanzees and bonobos, and conversely, elevated TSH levels in gorillas vs Pan species. Antibodies to Tg and TPO were detected in only 2.6% of adult animals vs approximately 10% in humans. No animals with Tg, TPO, or TSHR antibodies exhibited thyroid dysfunction. Conversely, hypothyroid nonhuman great apes lacked thyroid autoantibodies. Moreover, thyroid histology in necropsy tissues was similar in euthyroid and hypothyroid individuals, and lymphocytic infiltration was absent in 2 hypothyroid animals. In conclusion, free T4 and free T3 are lower in orangutans and gorillas vs chimpanzees and bonobos, the closest living human relatives. Moreover, thyroid autoantibodies are rare and hypothyroidism is unrelated to thyroid autoimmunity in nonhuman great apes.

scholarly journals The Effect of Antithyroid Drug Pretreatment on Acute Changes in Thyroid Hormone Levels after 131I Ablation for Graves’ Disease1

2001 ◽  
Vol 86 (7) ◽  
pp. 3016-3021 ◽  
Author(s):  
H. B. Burch ◽  
B. L. Solomon ◽  
D. S. Cooper ◽  
P. Ferguson ◽  
N. Walpert ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Radioiodine Therapy ◽  
Antithyroid Drug ◽  
Antithyroid Drugs ◽  
Free T4 ◽  
Hormone Levels ◽  
Free T3 ◽  
Average Decrease ◽  
Thyroid Hormone Levels ◽  
Acute Changes

Acute changes in thyroid hormone levels before and after radioiodine therapy for Graves’ disease were compared in 42 patients randomized to receive either antithyroid drug pretreatment or no pretreatment. Five patients (11.9%), including 3 in the pretreatment arm and 2 in the no pretreatment arm experienced a late exacerbation of thyrotoxicosis after radioiodine therapy. The majority (19 of 21, 90.5%) of pretreated patients experienced a transient increase in free T4 and free T3 after discontinuation of antithyroid drugs, with little further elevation after radioiodine therapy. After stopping antithyroid drugs and before radioiodine administration, mean serum free T4 values rose from 14.7 ± 6.9 to 21.6 ± 12.1 pmol/L, representing a 46.9% increase, whereas serum free T3 levels rose from 4.9± 1.7 to 8.1 ± 6.3 pmol/L, representing a 65.3% increase. The average pretreated patient experienced a 52.4% increase [95% confidence interval (CI), +26.4% to +78.5%] in free T4 and a 61.8% increase (95% CI, +23.5% to +100.0%) in free T3. Conversely, the majority (19 of 21, 90.5%) of nonpretreated patients experienced a rapid decline in thyroid hormone levels after radioiodine treatment. Over the 14 days after radioiodine therapy mean free T4 values in nonpretreated patients fell from 85.8 ± 60.4 to 58.0 ± 76.5 pmol/L, representing a 32.4% decrease, whereas mean free T3 levels fell from 16.1 ± 8.0 to 10.8 ± 11.1 pmol/L, representing a 32.9% decrease. The average nonpretreated patient experienced a 20.6% decrease (95% CI, −47.3% to +7.0%) in free T4 and a 24.3% decrease (95% CI, −1.2% to −47.4%) in free T3 during this time period. Excluding 2 patients with a late exacerbation after radioiodine, 19 nonpretreated patients experienced a decrease in mean free T4 values from 76.8 ± 46.6 to 36.6 ± 19.8 pmol/L, representing a 52.3% decrease, whereas mean free T3 levels fell from 15.5 ± 7.7 to 7.8 ± 3.6 pmol/L, representing a 49.7% decrease. The average decrease in free T4 levels among this subgroup of patients was 30.1% (95% CI, −4.6% to −55.6%), whereas the average decrease in free T3 was 34.4% (95% CI, −13.7% to −55.1%). High levels of TSH receptor autoantibodies at diagnosis were associated with an acute worsening of thyrotoxicosis after stopping antithyroid drug pretreatment. We conclude that pretreatment with antithyroid drugs does not protect against worsening thyrotoxicosis after radioiodine, but may allow such patients to start from a lower baseline level should an aggravation in thyrotoxicosis occur. The findings support the recommendation that most patients with Graves’ disease do not require antithyroid drug pretreatment before receiving radioiodine.

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