Thyroid-stimulating Immunoglobulin Research Articles

FRI568 Hashimoto’s Thyroiditis With Negative Antibodies In Association With Common Variable Immunodeficiency

Abstract Disclosure: I.C. Ebrahim: None. K.F. Brown: None. N.O. Vietor: None. T.D. Hoang: None. M.K. Shakir: None. Introduction: Common variable immunodeficiency (CVID) is associated with several autoimmune manifestations including Hashimoto’s thyroiditis (HT). We report a 47-year-old male with CVID and HT with negative thyroid antibodies (Abs). Case Report: A 47-year-old male, while undergoing coronary calcium scan in 2021, was found to have scattered lung nodules. Follow-up Ct scans showed interval increase in size of lung nodules and a PET scan confirmed bilateral lung nodules which demonstrated hypermetabolic activity and scattered hypermetabolic lymph nodes, suggesting infectious or inflammatory processes. PET scan also revealed thyromegaly with diffusely increased uptake, suggesting thyroiditis. Serum immunoglobulins were measured: IgA < 5 mg/dL (normal 70-400), IgG 334 mg/dL (normal 700-1600), and IgM < 25 mg/dL (normal 40-230). Serum immunoglobulins levels from depository serum samples collected in 2005 also showed similarly low values. CBC was normal, excluding any bone marrow disorders. There was no family history of immunodeficiency or thyroid disorders. On review of systems patients did not have any symptoms of hypothyroidism. Exam: thyroid 50-gms diffusely enlarged with no palpable nodules; heart and lung exam was normal. Laboratory tests including comprehensive metabolic panel, serum complement CH 50, leukemia/lymphoma panel, T/B - lymphocyte/Natkiller, CRP were all normal. Thyroid functions: TSH 5.6 mc1U/mL (0.27-4.2), Free T4 1.20 ng/dL (0.93-1.71), TPO Ab < 9 IU/mL (0-34), TG Ab < 1.0 1U/mL (0.0-0.9), thyrotropin receptor Ab < 0.3 IU/L (<1.0), thyroid stimulating immunoglobulin < 0.10 1U/L (0.06-0.55). Serum thyroid Ab levels from depository samples collected in 2005 also showed normal values. FNA of thyroid showed atypical lymphoid infiltrates and an excision biopsy of the thyroid isthmus confirmed lymphocytic thyroiditis. A PET avid right inguinal lymph node biopsy showed a reactive lymph node. Additional lab evaluation also showed low post vaccination pneumococcal titers. With pan-hypoglobulinemia and low vaccine response, a diagnosis of CVID was made. Patient preferred watchful waiting than iv immunoglobulin therapy. Additionally, the patient has HT with negative thyroid Abs and although patient had mild subclinical hypothyroidism patient elected no treatment. Common variable immunodeficiency (CVID) is the most frequent symptomatic primary immunodeficiency in adults. Autoimmune manifestations occur in 22% of CVID patients and these include autoimmune cytopenia, pernicious anemia, rheumatoid arthritis, vitiligo, and/or HT. Interestingly, our patient did not manifest any thyroid Abs thus it may be postulated that thyroid follicles destruction in HT is mediated predominantly by thyroid-specific B and T cells rather than by thyroid antibodies. Presentation: Friday, June 16, 2023

FRI549 The See-Saw Theory - Hypothyroidism Due To Hashimoto's Thyroiditis Followed By Hyperthyroidism Due To Graves' Disease

Abstract Disclosure: P. Sharma: None. Introduction: Hashimoto's thyroiditis is an autoimmune disorder characterized by chronic inflammation of the thyroid gland that leads to hypothyroidism due to formation of autoantibodies against thyroid antigens such as thyroid peroxidase (TPO Ab). Graves' disease is caused by stimulating TSH-receptor antibodies (TRAb) that cause hypertrophy of the thyroid gland leading to hyperthyroidism. While the transformation of Graves' disease to Hashimoto's thyroiditis has been reported, flipping from Hashimoto's thyroiditis to Graves' disease is uncommon. Case Report: A 62 year old female with 20 year history of hypothyroidism secondary to Hashimoto's thyroiditis presented to establish care. She had run out of levothyroxine refills one year prior during COVID-19 pandemic restrictions. She had tachycardia, diarrhea, fatigue, tremors, hair loss, dysphagia, and weight gain. Thyroid panel testing showed hyperthyroidism with an undetectable TSH (normal range 0.45-4.5uIU/ml) and elevated free T4 (2.84, normal 0.82-1.77ng/ml). Patient denied recent infections, iodine intake or iodine contrast exposure. Repeat labs confirmed hyperthyroidism with undetectable TSH with elevated free T4 (3.17ng/ml). Antibody testing comfirmed hyperthyroidism secondary to Graves disease (TRAb 20.7, normal <1.75IU/L). Patient has been on methimazole with fluctuating response and is reviewing definitive therapy options. Discussion: We demonstrate the rare phenomenon of thyroid function transformation from long-standing inhibition to stimulation after 20 years. Hashimoto's thyroiditis is characterized by chronic inflammation due to autoantibodies against TPO, thyroglobulin and the TSH receptor with gradual gland destruction and hypothyroidism. Stimulating autoantibodies to the TSH receptor (thyroid stimulating immunoglobulin (TSIg), TRAb) in Graves' disease lead to hyperthyroidism from gland hypertrophy. The flip from underactivity to overactivity can be explained by recovery of the gland from Hashimoto's thyroiditis injury which gradually leads to an overt response to TSIg, causing a hyperfunctioning gland. An imbalance between the inhibitory and stimulating antibodies can also lead to this transformation. Age, pregnancy and immunomodulating drugs such as alemtuzumab are also thought to play a role. The recovery theory is unlikely in our patient with a 20 year history of Hashimoto's thyroiditis. We believe that she had a high inhibitory antibody titre initially and now has higher titre of stimulating antibodies later, leading to Graves' disease. Luckily, she ran out of levothyroxine otherwise the additive effect of levothyroxine and intrinsic gland activity could have led to worse symptoms. This case highlights that autoimmune hypothyroidism and hyperthyroidism are conditions in the same spectrum, rather than two distinct entities as previously thought. Presentation: Friday, June 16, 2023

SAT579 Newly Diagnosed Graves' Disease With Complete Heart Block In Elderly Patient. A Case Report

Abstract Disclosure: M.M. Eid: None. T. Zahra: None. J. Vargas-Jerez: None. Introduction: Hypothyroidism is the most common thyroid disorder in elderly. The prevalence of hyperthyroidism in elderly is 0.5-3% and mainly caused by toxic thyroid nodules. Graves’ disease is an autoimmune disorder mediated by TSH receptor antibody (TSHR AB), presents commonly with hyperthyroidism in middle age female(1). Complete heart block in elderly can be due to conduction system fibrosis, Ischemic/structural heart diseases, medications, electrolyte disturbance and hypothyroidism(2). Case 72yo, Female with history of DM and HTN. Denied smoking, alcohol, drug and allergy. Irrelevant family history. Medications include amlodipine, metformin and atorvastatin. She was referred to endocrinology clinic for low TSH (was normal last year). Review of system was negative, denied tremor, palpitation, anxiety, weight loss, bowel movement/mood/sleep change, vision/swallowing problem. Physical examination: ABP150/80, Heart Rate(HR) 75/min. Mild lid lag, no exophthalmos. No tremor. Thyroid gland: diffusely enlarged non tender, no bruit. Normal cardiopulmonary and abdomen examination. Laboratory work up TSH less than 0.01 normal 0.2 to 4.20 uIU/ml , FT4 3.5 normal 0.9 to1.8 ng/dl, FT3 6 normal 2 to 4.4 pg/ml. Repeat lab confirmed TSH suppression and high FT4 ,FT3. TSHR antibody 7.66 normal less than 1.75 IU/L, Thyroid stimulating immunoglobulin 5.05 normal less than 0.5 IU/L ,HBA1C 6.6, Normal liver and kidney function tests and Complete blood count. She was diagnosed with Graves’ disease, kept on Methimazole 10mg/day. 2 weeks later, she presented to the ED after syncope at home. Initial EKG showed complete heart block HR 35/min and right bundle branch block (RBBB), ABP 110/65. Hours later EKG showed transient first degree heart block HR 75/min, RBBB and left axis deviation, then complete heart block with HR 30/min. Normal Troponin, potassium 4.2 mmol/L, sodium 141 mmol/L, calcium 9.2mg/dl, TSH 0.015 uIU/ml,FT4 3 ng/dl. Negative Anti-Lyme IgG and IgM. Normal Echocardiogram. She underwent uneventful Dual chamber pacemaker implantation with close endocrinology follow up. Conclusion: Graves’ Disease has variable presentations in elderly. Hyperthyroidism causes tachyarrhythmia due to the positive chronotropic effect of thyroid hormones. Bradyarrhythmia in our case is most likely due to conduction system fibrosis and could be related to the inhibitory effect of TSHR AB in elderly in contrary to the simulating effect in young patients. It is still rare to diagnose symptomatic bradyarrhythmia with uncontrolled hyperthyroidism(1).

THU661 Marine-Lenhart Syndrome: An Unusual Presentation Of Hyperthyroid Disease

Abstract Disclosure: B. Ji: None. O. Adeniran: None. L. Soni: None. Background: Marine-Lenhart syndrome, also known as nodular Graves’ disease, is defined as the coexistence of functioning thyroid nodules and Graves’ disease. It is a rare syndrome, with a prevalence of approximately 0.8-2.7%. The two diseases may coexist or present at different times [1]. Treatment options include high doses of antithyroid medications or radioactive iodine and thyroidectomy in selected cases [2]. Clinical Case: A 72-year-old female with a medical history of right-sided breast cancer treated with lumpectomy and radiation therapy in 2012 on anastrozole was referred for multinodular goiter (MNG) evaluation in 2018. She was clinically and biochemically euthyroid. Her thyroid ultrasound demonstrated two isoechoic right lobe nodules measuring 2.1cm and 1.3cm, respectively. An isoechoic rounded isthmus nodule measures 2.1cm. Three isoechoic nodules in the left lobe measuring 2.6cm, 2.2cm, and 1.7cm. She underwent fine needle aspiration (FNA) of two nodules in 2019, and both demonstrated benign follicular nodules with Bethesda II classification. At a follow-up visit in 2021, she reported unintentional weight loss but denied any other symptoms of hyperthyroidism, including heat intolerance, palpitation, tremor, or diarrhea. Physical examination was significant for exophthalmos, lid retraction, and diffusely enlarged thyroid with non-tenderness to palpation. Thyroid function tests revealed subclinical hyperthyroidism with TSH of <0.01uIU/mL (0.27-4.2uIU/ml) and FT4 of 1.5ng/dL(0.9-1.8ng/mL). Thyroid stimulating immunoglobulin (TSI) was 3.98IU/L (0.00-0.55IU/L), and TSH receptor antibody was 7.64 IU/L (0.00-1.75 IU/L). She was started on low-dose methimazole therapy. Thyroid uptake scan showed markedly elevated radioactive iodine uptake with 63.46% in 24 hours and focal nodular regions of increased uptake of the bilateral thyroid lobes compatible with toxic multinodular goiter. Repeated thyroid ultrasound in 2022 revealed stable-sized nodules with at least two new sub-centimeter nodules in both lobes. The patient was also seen by ophthalmology and plans to start teprotumumab treatment. At her most recent follow-up visit in January 2023, she has been continued on methimazole 2.5mg daily. Conclusion: The criteria for diagnosing Marine-Lenhart syndrome have not been well established. The possibility of Marine-Lenhart syndrome should be considered in hyperthyroid patients with positive antibodies and nodular goiter. In this case, she was initially asymptomatic with an enlarged multinodular goiter; three years later, she developed subclinical hyperthyroidism due to Graves’ disease and toxic multinodular goiter. Her symptom and thyroid function are well-controlled with low-dose methimazole. Presentation: Thursday, June 15, 2023

SAT473 First Case Of Diffuse Thyroid Lipomatosis With Amyloid Deposits Presenting With Hyperthyroidism

Abstract Disclosure: A.M. Gonzalez Gil: None. M.A. Ruiz Santillan: None. H. Quadri: None. B.K. Force: None. R. Gaba: None. Background: Diffuse thyroid lipomatosis (DTL) is an exceedingly rare entity of unknown etiology which can be associated with amyloidosis. It generally presents with euthyroidism but very few cases with hyperthyroidism have been reported. Clinical Case: A 64-year-old woman from Pakistan with a several-year history of a non-tender goiter presented to the emergency department with an upper respiratory and gastrointestinal viral syndrome in the context of several weeks of progressively worsening fatigue. She also reported unintentional weight loss over several years. She denied other hyperthyroid or compressive symptoms. Her exam was notable for resting sinus tachycardia and an approximately 100 gm painless goiter. Laboratory evaluation was notable for a markedly elevated creatinine with nephrotic range proteinuria. She was declared to have end stage renal disease (ESRD) and hemodialysis was initiated. She was also found to have a suppressed TSH (<0.01 uIU/mL, NR=0.45-5.33) and elevated FT4 (2.17 ng/dl, NR=0.64-1.42). Total T3 was low (42 ng/dl, NR=87-178), which was attributed to hypoalbuminemia and altered peripheral thyroid hormone metabolism with underlying ESRD. Further evaluation revealed elevated ESR, CRP and thyroglobulin levels (625.9 ng/mL, NR=1.5-38.5), while thyroid stimulating immunoglobulin, thyroid receptor antibodies and thyroid peroxidase antibodies were undetectable. A thyroid ultrasound revealed an enlarged fatty thyroid consistent with DTL. A radioactive iodine uptake scan revealed normal 24-hour uptake (14.1%, NR=7-32%) in a slightly heterogeneous thyroid with no aberrant functioning thyroid tissue. She was started on atenolol, with significant improvement in her tachycardia, but her FT4 continued to increase. Methimazole was initiated. Dose uptitration and administration after dialysis resulted in near-normalization of FT4 levels. She subsequently underwent renal and thyroid biopsies, both of which showed apple green birefringence under polarized light with Congo Red stain, indicating amyloidosis. Core thyroid biopsy additionally showed benign adipose tissue with entrapped thyroid follicles, confirming concomitant DTL. Although other authors have found thyroid amyloid deposits in DTL, and yet others have reported hyperthyroidism in DTL without amyloidosis, this is the first reported case of hyperthyroidism in a patient with DTL with amyloid deposits. Interestingly, chronic hypoxia in amyloid goiters has been hypothesized to cause fibroblast-to-adipocyte metaplasia leading to DTL. We speculate that excess thyroid hormone release could also be mediated by follicular cells’ response to hypoxia induced by amyloid and fatty infiltration of the thyroid. Conclusion: To the best of our knowledge, this is the first reported case of diffuse thyroid lipomatosis with amyloid deposits to be associated with concurrent hyperthyroidism. Presentation Date: Saturday, June 17, 2023

SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption

Abstract Disclosure: M.K. Shakir: None. K.F. Brown: None. J.S. Hatfield: None. N.O. Vietor: None. T.D. Hoang: None. Introduction: In iodine-replete countries, iodine-induced thyrotoxicosis may occasionally develop after ingestion or therapy with high doses of iodine. Recently, Himalayan salt has become very popular to bridge iodine deficiency, control hypothyroidism, and improve thyroid function. We report a patient with a history of treated Graves’ disease (GD) who developed acute thyrotoxicosis following the use of Himalayan salt. Case report: A 58-year-old woman presented with symptoms of heat intolerance, and unexpected 18-lbs weight loss over 3 months. Physical examination: HR 108 bpm, BP 110/70 mm Hg, normal eye examination, thyroid 45 gms, diffusely enlarged. Examinations of the heart, lungs and abdomen were normal. Lab tests: TSH 0.01 IU/mL, free T4 3.8 ng/dL, T3 308 pg/dL, thyrotropin receptor Ab 4.2 IU/L (<1.0), and thyroid stimulating immunoglobulin 1.89 1U/L (0.06-0.55). The I131 uptake was 60% at 4 hours and the thyroid scan revealed diffuse homogenous uptake confirming GD. She was treated with methimazole (MMI) for 2 years and remission was achieved. MMI was stopped and she remained euthyroid. Twelve months later, she developed hyperthyroid symptoms with a 15-lb weight loss, palpitations, and anxiety. Examination confirmed a 50-gram diffuse goiter and other physical findings consistent with hyperthyroidism. She admitted that she had been taking Himalayan salt (approximately 10 grams daily) in place of regular salt for the past 6 months. Lab tests confirmed recurrent GD: TSH <0.01 IU/mL, FT4 4.1 ng/dL, total T3 278 pg/dL, and I131 uptake was 55% at 24 hours. A 24-hours urine iodine was 898 mcg (normal 100-199) and plasma iodine level was 484 mcg/L (normal 52-109). A diagnosis of iodine-induced recurrence of GD was made, and she was treated with MMI and low iodine diet. After 3 months, she improved significantly and was able to discontinue the MMI by 6 months. A follow- up urine iodine was 189 mcg/L with a plasma iodine level of 78 mcg/L. Subsequently she remained euthyroid for an additional 18 months of follow-up without any treatment. Conclusion: The recommended daily dietary allowance for iodine in adults is 150mcg. Himalayan rock salt may provide a rich source of iodine and consumption of large amounts can lead to iodine excess. However, the available studies do not provide the iodine content in commercially available Himalayan salt preparations. Although the Himalayan salt is advertised to have beneficial effects in patients with thyroid disorders, this food supplement may have deleterious effects in susceptible patients who do not have iodine deficiency, have GD, or are at risk for thyrotoxicosis. Indeed, Himalayan salt use exacerbated GD in our patient, as evidenced by iodine overdose during acute exacerbation and resolution of GD with iodine normalization and low dose MMI. We recommend that patients with thyroid disorders be educated regarding Himalayan salt use. Presentation Date: Saturday, June 17, 2023

SAT476 A Case of Thyroid Hemiagenesis

Abstract Disclosure: P. Kachhadia: None. S. Khan: None. S. Aldasouqi: None. A. Abu Limon: None. Introduction: Thyroid hemiagenesis is congenitally rare, in which one side of the thyroid does not develop. Hemiagenesis is more common with an absent left thyroid lobe, at a 4:1 ratio. Though prevalence is sited at 0.05%, actual incidence of hemiagenesis amongst the population is unknown as most patients are euthyroid and asymptomatic. We present a case of a patient who was referred to our clinic for unilateral thyroid enlargement on physical exam. Thyroid Ultrasound (US) was done which showed an absent left thyroid lobe along with enlarged right thyroid lobe and hypervascularity. There was also an incidental thyroid nodule noted on US. Case Presentation: Patient is a 38 year old female who presented to the clinic 4 years prior for enlarged thyroid nodule noted on ultrasound. With symptoms of dysphagia and a visibly enlarged gland, an US with labs was prompted by her primary physician. US showed absent left thyroid lobe and right lobe enlargement with hypervascularity and incidental subcentimeter nodule. Clinically and biochemically, the patient was euthyroid. Singular right lobe was verified on clinic real time ultrasound and on NM uptake scan. The 24 hour uptake was at 30.5%, with the upper limit of normal being 30%. With increased uptake and hypervascularity, thyroid stimulating immunoglobulin and thyrotropin receptor antibodies were checked and were not detected. It was thought that the right thyroid gland enlargement and hypervascularity were compensatory due to the left hemiagenesis. The thyroid nodule was monitored, and within 3 years of original imaging, it enlarged to 0.98 x 0.59 x 0.39 cm, with TI-RADS 5 assessment per ACR criteria. Patient chose to undergo thyroid biopsy which showed Bethesda III, Follicular Lesion of Undetermined Significance (FLUS). Microscopy showed follicular cells arranged in microfollicles and crowded groups with round, enlarged, irregular nuclei and overlapping nucleoli. Intranuclear chromatin clearing and intranuclear grooves are present. Background is hemorrhagic with minimal colloid. Molecular Thyroseq testing was at 5-10% chance of malignancy or noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP). Genetic markers were only positive for copy number alterations. Discussion: Thyroid Hemiagenesis, though rare, has been associated with other thyroid pathologies such as hypothyroidism, hyperthyroidism and thyroid malignancies. Genetic studies have not found a common background within cases reported. As these patients are more likely to incur additional thyroid pathologies, questions still remain as to the clinical management and outcome of such patients. Due to concerning cytological features for PTC, the patient was offered right thyroidectomy and will be looking to make a decision in the near future. Presentation Date: Saturday, June 17, 2023

FRI486 Overactive Thyroid And Overactive Mind - An Intervened Relationship

Abstract Disclosure: S. Bilichodu Rangappa: None. S. Avula: None. Z.A. Anderson: None. A. Kumar: None. Introduction: Traditionally, psychiatric symptoms were thought to be common manifestation of hypothyroidism. However, in the recent times the trend has changed. Various studies have shown a strong association of hyperthyroidism and psychosis. Thyrotoxicosis is associated with various psychiatric symptoms such as anxiety, restlessness, emotional liability, depression, mania, and rarely acute psychosis. Association between thyroid and mental health is a long-known entity but poorly understood pathophysiology. Here we present a case of graves disease presenting as acute psychosis as initial presentation. Clinical Case: A 45-year-old male with no significant past medical history was brought to emergency department (ED) by police after he was found to be walking in front of a shopping mall and was severely agitated. On arrival to ED, he was found to be very restless, irritable, and aggressive. Patient was found to have persecutory delusions and auditory hallucinations. His blood pressure was elevated, and he had tachycardia. He was given Haloperidol to calm down. Patient was evaluated with blood work and urine toxicology. Blood work up showed thyroid stimulating hormone (TSH) of <0.01m IU/L, Free T4 of 4 ng/dl and Total T3 of 380 ng/dl. Patient was started on Methimazole and propranolol. On further work up for thyrotoxicosis there was elevated thyroid stimulating immunoglobulin (TSI) which was consistent with Grave’s disease. Ultrasound thyroid revealed diffuse enlarged thyroid with increased vascularity. Once the patient was stable, he was further interviewed, he gave a history of palpitations, increased anxiety, and weight loss for two months, but he didn’t seek any medical attention. By the time of discharge, he symptomatically improved and his Free T4 and total T3 trended down. Patient was discharged on methimazole 10 mg daily along with propranolol. Conclusion: Graves’s disease can mimic psychosis. Psychosis may develop in the wake of thyroid hormone excess. Future research is warranted to find out the relation between psychotic disorders and excess thyroid hormone and the pathological process involved. It also helps in having clear treatment guidelines which will reduce the morbidity and improves the quality of life. Identifying somatic causes for psychiatric issues will help in treating them and might lead to complete recovery and not needing any further psychiatric medications. Presentation: Friday, June 16, 2023

FRI553 ICI-induced Thyroid Ophthalmopathy With De Novo Graves’ Disease

Abstract Disclosure: S.I. Moctezuma: None. J. Perlman: None. J.S. Mammen: None. Background: Immune checkpoint inhibitors frequently target the thyroid gland. However, immune checkpoint inhibitor (ICI)-induced Graves’ disease (GD) is rare. To our knowledge, there are no reported cases of thyroid eye disease after immune checkpoint inhibitor therapy in patients with newly positive anti-thyroid antibodies. Clinical Case: An 81-year-old man developed thyroiditis within three weeks of a single dose of ipilimumab/nivolumab for the treatment of metastatic cholangiocarcinoma. ICI therapy was discontinued for cardiotoxicity. He presented one year later with onset of periorbital edema, pain with downgaze, redness, irritation and progressive proptosis with diplopia. He did not have a prior history of thyroid disease. Thyroid function tests before the start of ICI therapy revealed euthyroidism [TSH 2.982 uIU/mL (0.55 - 4.78)]. Symptoms of palpitations, weight loss, and hyper-defecation that characterized his initial presentation with thyroiditis were absent at the time of onset of eye disease. At presentation of thyrotoxicosis his TSH was <0.01 uIU/mL, free T4 3.6 ng/dL (0.89 - 1.76) total T3 190 ng/dL (60-180) Thyroid-peroxidase autoantibodies (TPOAb) and thyroid-stimulating immunoglobulin (TSI) were negative. When his visual symptoms appeared, TPOAb remained negative while a repeat TSI antibody was positive [0.64 IU/L (0.00 - 0.55)]. Thyroid ultrasound at the time of thyroiditis revealed a heterogeneous gland without discrete nodules and a normal vascular flow. Most cases of ICI-induced GD have been reported at the start of therapy, particularly in the first 6 weeks, although thyrotoxicosis has been described to occur as late as 224 days after starting PD-1 inhibitor. GD is more frequently reported with combination anti-CTLA-4 and anti-PD-1 therapy. Patients with thyroid ICI-induced adverse events experience either isolated hypothyroidism or thyroiditis spontaneously evolving towards hypothyroidism. However, ICI-induced GD is more likely to have a relapsing-remitting disease. In 2021, Peiffert et al. described the antibody profile for 243 patients with ICI-induced thyrotoxicosis. In this case series, 5 patients developed thyrotoxicosis with positive thyrotropin-receptor antibodies (TRAb). Only 2 patients had a typical clinical presentation of GD. TSI antibodies were not reported. Furthermore, none of the patients with positive TRAb had Graves’ ophthalmopathy. Conclusion: Our case demonstrates the acquisition of auto-antibodies capable of mediating Graves’ disease, and raises the possibility that thyroid eye disease-like orbital inflammation may occur as a side effect of immune checkpoint inhibitor therapy. These symptoms developed as late as one year after initiation of therapy. As with sporadic cases, this can occur in the absence of clinically significant hyperthyroidism. Presentation: Friday, June 16, 2023

THU655 Methimazole Desensitization As An Effective Alternative To Ablation Therapy In Patients With Graves’ Disease Experiencing Thionamide-induced Type IV Hypersensitivity Reactions

Abstract Disclosure: J. Arguinchona: None. A. Mahajan: None. A. Gonzalez-Estrada: None. E. De Filippis: None. Introduction: Patients with newly diagnosed Graves’ disease often choose treatment with methimazole (MMI) over traditional ablation therapies. However, MMI can result in adverse reactions including skin rash, pruritus, and urticaria. We present a case of Graves’ thyrotoxicosis with a type IV hypersensitivity reaction while on MMI. The patient was successfully treated with a novel, individualized, 27-day desensitization protocol which resulted in tolerance of MMI with subsequent improvement in thyroid indices. Clinical Case: A 42-year-old female presented for abnormal thyroid studies with associated insomnia, heat intolerance, palpitations, resting tremor, and weight loss. Lab work revealed a thyroid-stimulating hormone <0.005 (0.450-4.500 μIU/mL), free thyroxine 3.28 (0.82-1.77 ng/dL), triiodothyronine 310 (71-180 ng/dL), thyroid peroxidase antibody (Ab) 62 (0-34 IU/mL), thyroid-stimulating immunoglobulin 0.67 (0.00 -0.55 IU/L), and thyrotropin receptor Ab of 6.00 (0.00-1.75 IU/L). She was started on MMI, 10 mg daily for Graves’ disease. Three weeks later, T3 and T4 remained elevated prompting an increase in MMI dose to 10 mg twice daily. Two weeks later, she developed a diffuse, pruritic maculopapular exanthema over her trunk, neck, and extremities. Methimazole was discontinued while prednisone was initiated that subsided her rash. Unfortunately, the patient’s symptoms recurred upon repeat MMI exposure. The patient declined propylthiouracil due to concerns of hepatotoxicity and elected to avoid ablation therapy with iodine or surgery. With the assistance of an allergist, a novel, 10-step, 27-day desensitization protocol was developed specifically for her reaction to MMI with plans to taper prednisone once desensitization was completed. The patient underwent desensitization with development of mild lower extremity exanthema that was successfully treated with high dose antihistamines. Three months later, she was tolerating MMI at 15 mg daily without further adverse reactions and tapered off prednisone. While on MMI, her immune titers normalized with euthyroid clinical and biochemical restoration. Conclusion: Many patients and clinicians initially prefer medical management over definitive ablation therapies in the treatment of Graves’ disease. This case demonstrates with the assistance of an allergist, desensitization to MMI is a viable option in the setting of a known hypersensitivity reaction when it is the first line treatment and no equally efficacious alternatives exist. In addition, patient’s preferences should also be considered during medical decision making. Previous literature has offered various rapid desensitization protocols for MMI for immediate type hypersensitivity reactions. However, in non-immediate, type IV hypersensitivity reactions, a slower desensitization protocol can be considered, as demonstrated in this case. Presentation: Thursday, June 15, 2023

THU665 Unilateral Graves’ Disease In A Bilobar Thyroid Gland: Unusual Cause Of Hyperthyroidism

Abstract Disclosure: K.H. Alaybaa: None. O. Alhuzaim: None. Introduction: Graves' disease (GD) is an autoimmune condition that affects both thyroid gland lobes. GD patients with unilateral thyroid scan uptake are rare. These patients present with classic Graves' symptoms, occasionally with Graves' ophthalmopathy characteristics and increased thyroid hormones, and scintigraphic assessment reveals radiotracer uptake in only one lobe of the thyroid gland. Patient Findings: In this case, a 48-year-old female presented with symptoms and signs indicative of thyrotoxicosis. Lab results revealed that thyroid-stimulating hormone (TSH) was undetectable, while free thyroxine (T4) and free triiodothyronine (T3) were in the high-normal range. Positive results were observed for both thyroid-stimulating immunoglobulin and TSH receptor antibodies. Ultrasonography of the thyroid gland revealed an enlarged left lobe with heterogeneous echotexture and a hyperemic gland without any focal lesions, distinct nodules, or cysts. The NM TC-99M thyroid scintigraphy revealed enlarged and increased radioisotopes uptake in the left thyroid lobe and decreased uptake in the right thyroid lobe, with no hot or cold nodules. The calculated thyroid uptake is 4.5 percent (normal range: 0.5% to 3.5 percent). The most likely diagnosis was unilateral GD. The patient was administered carbimazole and within eight weeks had improved clinically and biochemically. Summary: This patient has thyrotoxicosis symptoms and positive autoantibodies. Tc99m uptake was increased in the left thyroid lobe and decreased in the right thyroid lobe. The left thyroid lobe was hypervascular and enlarged on ultrasonography, indicating the presence of unilateral GD. Unilateral GD is a rare disease with a poorly understood pathophysiology. Presentation: Thursday, June 15, 2023

FRI466 Toxic Retrosternal Goiter Following SARS-CoV-2 Vaccination

Abstract Disclosure: J. Schipper: None. Z. Abdul Sater: None. Since the outbreak of the SARS-CoV-2 pandemic, there have been reports of autoimmune thyroid diseases related to COVID inflection and SARS-CoV-2 vaccination. We report a case of SARS-CoV-2 mRNA vaccination (mCoVvax)-induced Graves with retrosternal extension. A 21-year-old Hispanic male with no previous history of thyroid illness presented with a 4-month history of tachycardia, tremors, agitation, unintentional weight loss, night sweats, low-grade fever, and orthopnea that developed 62 days after receiving the first dose of mCoVvax. His physical examination was significant for sinus tachycardia, hypertension, a resting tremor, brisk deep tendon reflexes, and diffuse nonpruritic maculopapular rash. His thyroid gland was diffusely enlarged with an unpalpable lower margin and positive Pemberton sign. TSH was undetectable with elevated Free T4 and Total T3 [11.0 (NL 0.8-1.8 ng/dL) and 800 (76-181 ng/dL), respectively]. Thyroid-stimulating immunoglobulin (TSI) was 337% (NL<140%), and thyroid peroxidase antibody was 653 IU/mL (NL < 9 IU/mL). Thyroid ultrasound showed a diffusely enlarged thyroid gland with diffusely increased thyroid uptake on technetium thyroid scan (95% and 85% uptake after 6 and 24 hrs, respectively), consistent with Graves’ disease. CT scan of the neck and chest confirmed retrosternal Goiter without tracheal deviation. He was treated with high-dose of Methimazole, Atenolol, and Prednisone. A literature search revealed five cases of Graves’ disease after mCOVvax, all of which did not have a retrosternal extension of the thyroid. Our case represents a rare complication of mCoVvax. Clinicians should consider retrosternal goiter in patients with thyrotoxicosis and orthopnea after mCoVvax exposure. Presentation: Friday, June 16, 2023

FRI561 The Thyroid Trifecta

Abstract Disclosure: P. Kachhadia: None. S. Khan: None. A. Abu Limon: None. S. Aldasouqi: None. Introduction: Autoimmune Hashimoto’s Thyroiditis (HT) and Graves’ Disease (GD) may co-exist or may occur alternatingly, known in many case reports as Graves’s Alternans. Hyperfunctioning (Toxic, hot) thyroid nodules (TN) may also co-exist with GD, a rare condition called Marine-Lenhart syndrome. However, the co-existence of HT, GD and TN is perceivably rarer. Case Presentation: The patient is a 45 year old female with a prior history of HT for 20 years, who presented to the clinic with symptoms of minimal eye pain, tremors, fatigue, diarrhea and anxiety. She was not on thyroid replacement, with normal thyroid function tests (TFTs). Physical exam showed bilateral proptosis, a moderate goiter, hand tremors, mild anxiety and tachycardia. Labs showed high TPO (3995.0 IU/mL, n <18 IU/mL), Thyrotropin receptor antibody (5.25 IU/L, n<1.75 IU/L), and Thyroid-stimulating immunoglobulins (1.8 TSI index, n<1.3 TSI index) with low-normal TSH of 0.42 uIU/mL (0.35-4.01 uIU/mL) , mid-range free triiodothyronine (FT3) at 3.6 pg/mL (2.8-4.4 pg/mL) and normal free thyroxine (FT4) at 0.80 NG/dL (0.61-1.37 NG/dL). Thyroid US showed a 2.4 cm left lobe inferior nodule classified as TI-RADS 3. Fine needle aspiration of this nodule was benign. Radioactive Iodine-123 Uptake Scan showed a hot nodule in the left inferior lobe and with visible uptake in the rest of the gland (uptake was mid-normal). She was started on methimazole 5mg once daily and propranolol 10mg BID with improvement in her symptoms. Subsequent TFTs showed stable T4 and T3 and normalization of TSH to 1.78 uIU/mL (0.35-4.01 uIU/mL). Discussion: Marine-Lenhart syndrome was described in 1911 by surgeons David Marine and Carl Lenhart. Graves’ Alternans has been described in the literature, with variable time separation. Though thyroid nodules occur in up to 35% of those with GD, only 1-4.1% are deemed functional nodules. Nuclear medicine imaging via Tc-99m pertechnetate or I-123 iodine at diagnosis of GD generally shows such nodules as cold nodules lacking uptake, while the rest of the gland has diffuse uptake. However, with normalization of TSH through treatment, these cold nodules may alternate uptake and present as hot nodules. Conclusion: In conclusion, this case presents the co-existence of HT, GD and HN, a term we are calling “Thyroid Trifecta”. It is imperative that HNs should be identified if RAI treatment is planned in such patients. Literature review portrays cases in which if thyrotoxicosis persists post RAI treatment for GD, careful examination and repeat RAIU may show a hot nodule consistent with Marine-Lenhart Syndrome. These patients may benefit instead from thyroidectomy. In the case of our patient, definitive treatment options have been discussed and she has been referred for thyroidectomy due to the presence of the TN. RAI ablation will be avoided in view of mild but active thyroid eye disease. Presentation: Friday, June 16, 2023

FRI557 Don’t Forget The Incidental Thyroid Nodule In Graves’ Disease. A Case of Marine-Lenhart Syndrome

Abstract Disclosure: K.N. Andino-Lebrón: None. A. Martinó-Morales: None. J.M. Colón-Castellano: None. Marine-Lenhart syndrome (MLS) was initially described by Charkes in 1972 as he observed patients with Graves’ disease (GD) and incidental functioning thyroid nodules. He named the disease Marine-Lenhart syndrome based on a paper published by Marine and Lenhart in 1911. MLS is a variant of GD now described as the coexistence of GD and autonomous functional thyroid nodules (AFTN); thus, patients present with thyrotoxicosis due to GD and AFTN. MLS is very rare, and prevalence is estimated to be around 0.8%-2.7%. Here, we present a case of MLS in a 79-year-old female. A 79-year-old Hispanic woman with history of breast metaplasia s/p chemoprevention with tamoxifen for 5 years, atrial premature contractions on metoprolol, among other medical conditions was referred to Endocrinology clinics by her primary care physician (PCP) because of abnormal thyroid function tests and ultrasound. She reported feeling anxious with associated palpitations, she denied weight loss. Physical examination was remarkable for regular rate and rhythm, no goiter, no palpable nodules, no proptosis, and deep tendon reflexes +1. Laboratory testing revealed a suppressed TSH of 0.224 uIU/mL, normal free T4 at 1.17 ng/dL, normal total T3 at 142.5 ng/dL, and positive thyroid stimulating immunoglobulins at 345%. Thyroid ultrasound showed a normal size gland with multiple complex nodules. In the right lobe there was a mixed cystic and solid nodule, measuring 1.48x1.21x1.71cm, wider than tall, with internal vascularity and punctate calcifications. In the left lobe there was an isoechoic and solid nodule measuring 0.7x0.5x0.7cm, wider than tall, without calcifications. Thyroid uptake scan with SPECT-CT demonstrated a focus of increased tracer uptake on the upper pole of the right thyroid lobe that corresponds to the one found on CT scan and a diminished and nonuniform uptake of the tracer in the reminders of the thyroid gland. The 24-hour radioactive iodine uptake was 17.5%. Diagnosis of MLS was made, and the patient was started on methimazole 5mg daily, which she has been tolerating well. Follow up laboratories show a biochemically euthyroid state. Marine-Lenhart syndrome is a rare entity of Graves’ disease which is currently defined as GD and accompanying functioning nodule(s). To establish the diagnosis, it is important the evaluation with scintigraphy and autoimmune testing. Multiple treatment options are available and patients with GD should be evaluated for the presence of thyroid nodules and their functional status to achieve optimal therapy. Patients with GD have a chance of remission when treated with antithyroid drugs. Due to the pathophysiology of AFTN, patients with MLS (concurrent GD and AFTN) have lower remission rates with antithyroid drugs and may require definitive management therapy with radioactive iodine or surgery. Presentation: Friday, June 16, 2023

SAT538 Thyrotoxicosis in the Setting of Metastatic Poorly Differentiated Thyroid Carcinoma, a Marker of Disease Progression?

Abstract Disclosure: B.L. Chang: None. M.A. Fernandez: None. K.M. Shikuma Lee: None. Background: Thyrotoxicosis is a rare manifestation of thyroid cancer, and poorly differentiated thyroid carcinoma (PDTC) causing thyrotoxicosis has even more rarely been reported. Here, we report a case of PDTC with thyrotoxicosis developing in a previously euthyroid individual with longstanding untreated follicular neoplasm. Clinical Case: A 79-year-old veteran presented to routine endocrine follow up with new symptoms of thyrotoxicosis. Although previously euthyroid, the evaluation revealed new findings of low serum thyrotropin (TSH) (<0.01 uIU/mL, n=0.34 – 5.60 uIU/mL), elevated free thyroxine (FT4) (2.6 ng/dL, n=0.58 – 1.64 ng/dL), and high total T3 (TT3) levels (223 ng/dL, n=76 – 181 ng/dL). Thyroid stimulating immunoglobulin antibodies (TSI) were positive (214, n<140). Patient has a nine-year history of a fine needle aspiration (FNA) of a large right-sided thyroid nodule with cytology suspicious for follicular neoplasm but declined surgical removal. Thyroid uptake and scan showed heterogeneous uptake throughout the right lobe with a relative photopenic region centrally and spots of more increased activity in areas within the right lobe. The left thyroid lobe showed uniformly low uptake. PET-CT evaluation confirmed spotty FDG-avid areas within the right thyroid mass but did not show other areas of hyperactivity. Methimazole was started with clinical and biochemical improvement. Patient underwent total thyroidectomy, and histopathologic examination showed PDTC with extensive angioinvasion involving the majority of the right thyroid lobe with the left lobe containing a mix of benign thyroid tissue and PDTC fragments. Areas of hyperintensity on the uptake scan correlated to pathological PDTC locations within the right lobe. Within three weeks of thyroidectomy, patient developed recurrent hyperthyroidism. Laboratory studies showed low TSH (0.04 uIU/mL) and elevated FT4 (2 ng/dL). In contrast to pre-operative studies, repeat TSI was below the reference range. Levothyroxine (LT4) was held in anticipation of radioactive iodine therapy, but four weeks later the TSH remained suppressed. 131I was administered which showed accumulation within small thyroid remnants and a single left level three 131I-avid lymph node without other metastases. Following 131I treatment, patient returned to a euthyroid state on standard LT4. Conclusion: Hyperthyroidism has rarely been associated with PDTC, although previous reports have linked more aggressive, multifocal, and locally invasive thyroid cancers to concurrent Graves’ disease or productive bulky metastatic disease. Even without bulky metastatic disease, clinicians should be aware that hyperproductivity may indicate development of autoimmune thyrotoxicosis within PDTC. Presentation Date: Saturday, June 17, 2023

SAT495 Persistent Euthyroid State in a Patient with Biochemical and Imaging Evidence of Graves' Disease

Abstract Disclosure: M. Antony: None. S. Gundlapally: None. M. Joglekar: None. B. Fritz: None. S. Patel: None. V. Verma: None. R. Kant: None. INTRODUCTION: Elevated TSI antibody and/or diffuse uptake on radioactive Iodine-123 scan is diagnostic of Graves’ disease. Thyromegaly with increased blood flow on color doppler seen on thyroid USG can also aid in the diagnosis. Rare presence of positive TSI antibody without hyperthyroidism has been reported1. Rare co-existence of both Graves’ disease and Hashimoto’s thyroiditis in a patient causing a challenging clinical course has been reported2. Presence of a neutralizing or blocking antibody against the TSH receptor1 or a false positive TSI have been implicated in such rare cases. CLINICAL CASE: A 37-year-old Caucasian Female was seen at our endocrinology clinic for further evaluation of thyroid disorder. Patient initially experienced goiter during 1st pregnancy at age 18, followed by hypothyroidism during last pregnancy needing levothyroxine treatment. Due to goiter history, patient underwent work-up by her primary physician in 2021. Thyroid ultrasound (usg) showed bilateral hyperemia, heterogeneous echotexture, and 0.2 cm cystic nodule in the right upper lobe. Labs showed normal TSH 1.33 uIU/ml (0.3-4.0 uIU/ml), normal Free T4 0.99 ng/dl (0.8-1.8 ng/dl), normal total T3 140 ng/dl (71-180 ng/dl). Patient underwent further work-up by endocrinology in 2022. Thyroid ultrasound again revealed bilateral hyperemia with other similar findings. Labs showed normal TSH 2.02uUI/ml, normal free T4 0.93 ng/dl, normal total T3 138 ng/dl. Interestingly, TSI antibody and TPO antibody were significantly elevated at 66.70 IU/L (0.0-0.55 IU/L) and 517 IU/ml (0-34 IU/ml), respectively. Repeat labs in April 2022, again showed normal TSH 1.77 uIU/ml, normal free T4 0.90 ng/dl and normal free T3 2.94 (2.0-4.40 pg/ml). Thyroid uptake scan was not performed due to persistently normal TSH values. Patient denied the use of biotin supplementation. Patient continues to remain clinically and biochemically euthyroid without treatment. CONCLUSION: Our case supports the rare presence of TSI antibody without hyperthyroidism. Close monitoring is warranted due to possibility of future progression to overt hyperthyroidism. REFERENCE: 1. Alvin Mathew A, Papaly R, Maliakal A, et al.(November 10, 2021)Elevated Graves’ Disease-Specific Thyroid-Stimulating Immunoglobulin and Thyroid Stimulating Hormone Receptor Antibody in a Patient With Subacute Thyroiditis. Cureus 13(11): e19448. doi:10.7759/cureus.194482. Vipin Verma, MD, Mc Anto Antony, MD, PSAT346 Persistent Fluctuation Between Hypothyroidism and Hyperthyroidism in a Patient with Both Hashimoto's Thyroiditis and Graves’ Disease: Challenges in Diagnosis and Treatment Approach, Journal of the Endocrine Society, Volume 6, Issue Supplement_1, November-December 2022, Page A833, https://doi.org/10.1210/jendso/bvac150.1723 Presentation Date: Saturday, June 17, 2023

A-052 The Importance of Thyroid-stimulating Immunoglobulin (TSI) in the Diagnosis and Follow-up of Marine-Lenhart Syndrome

Abstract Introduction Marine-Lenhart syndrome is a rare cause of hyperthyroidism, occurring in 0.8%–2.7% of patients with Graves’ disease (GD). In this syndrome, GD, which is an autoimmune disease, coexists with one or more hyperfunctioning nodules—Toxic nodular goiter (TNG), or toxic multinodular goiter (TMNG)—which are usually thyroid adenomas. Both induce clinical hyperthyroidism, with suppressed thyroid-stimulating hormone (TSH) and elevated thyroid hormones (TH). Radioactive iodine uptake and thyroid scintigraphy are indicated when there is a nodule on ultrasonography (US) with suppressed TSH, for the differential diagnosis between GD and toxic nodules. However, in this syndrome, scintigraphy does not always define the diagnosis, as the aspects observed do not show the usual pattern. In these cases, it is necessary that a reliable autoimmune thyroid disease marker be performed in order to prove the concomitant autoimmunity. Objectives The aim of this study was to demonstrate the usefulness of thyroid-stimulating immunoglobulin (TSI) for diagnosing hyperthyroidism due to Marine-Lenhart syndrome. Methods The authors prospectively followed 19 patients with suspected Marine-Lenhart syndrome between 2018 and 2020. TSH and TH were measured by Electrochemiluminescence, Roche Diagnostics, and TSI was measured by Chemiluminescence, Siemens Diagnostics. Results All patients had TSH ≤ 0.01 mIU/L, free thyroxine (FT4) was 3.1 ± 0.9 ng/dL, and triiodothyronine (TT3) 312 ± 42.1 ng/dL. All of them had increased radioactive iodine uptake, but the scintigraphy showed nodules sometimes with increased, normo, or low uptake in relation to the adjacent tissue, a finding that is explained by the fact that, both, the nodule and the rest of the thyroid tissue, uptake the radioidine in excess and the pattern varies according to the activity of the DG and nodules in the period in which the test was performed. TSI was 3.98 ± 0.9 IU/L (Negative if <0.55). All patients had positive TSI, confirming concomitant GD with TNG/TMNG. During treatment monitoring, in 14 cases the hyperfunctioning nodules were treated by local sclerosis procedure, with percutaneous injection of ethanol. Despite complete nodular sclerosis, with normal TH but still suppressed TSH, the TSI still remained elevated. This demonstrated that, despite the successful treatment of the nodule, the underlying GD was still active, requiring complementary treatment with antithyroid drugs until TSI was negative, after 18 ± 4 months of treatment. Conclusion In atypical cases of hyperthyroidism, the TSI measurement is decisive for the diagnosis, as in the rare Marine-Lenhart syndrome. This contributes in a relevant way to the definition of the treatment, which can be different between the two causes that occur concomitantly. Likewise, during treatment follow-up, the TSI was essential in defining the need to maintain clinical treatment, even if the nodule had been already adequately treated.

Preoperative Risk Factors for Proptosis Recurrence After Rehabilitative Orbital Decompression in Graves’ Orbitopathy Patients

PurposeRehabilitative orbital decompression treats disfiguring exophthalmos in Graves’ orbitopathy (GO) patients. This study aimed to identify risk factors associated with the postoperative recurrence of proptosis after orbital decompression. DesignRetrospective case-control study MethodsThis retrospective review included patients with GO who underwent rehabilitative orbital decompression for disfiguring proptosis in an inactive state with a low clinical activity score (0-2) between Jan 2017 and Dec 2020 by a single surgeon. Exophthalmos was measured using a Hertel exophthalmometer, and recurrence was defined as an increase of 2 mm or more after decompression during the follow-up period. The association between preoperative variables and proptosis recurrence was analyzed using multivariable logistic regression. ResultsOf the total 217 patients, eleven (5.1%) developed recurrence of proptosis during the follow-up period (range 3-30, mean 15.6 months). Univariate logistic regression analysis identified thyroid-stimulating hormone receptor antibody (TRAb) and thyroid-stimulating immunoglobulin (TSI) as significant factors for recurrence with age, sex, smoking, disease duration, orbital radiotherapy, and total thyroidectomy history being non-significant. TRAb remained significant in a multivariate logistic regression analysis (OR 1.06; p=0.014). Receiver operating characteristic (ROC) curve analysis revealed an area under curve 0.86 with a sensitivity 90.9% and specificity 82.0% at TRAb level 7.96 IU/L. ConclusionPreoperative TRAb and TSI are valuable markers to predict proptosis recurrence after orbital decompression. These results may help surgeons to decide the optimal timing for orbital decompression to lessen the risk of postoperative recurrence of proptosis.

Code Pseudo Stroke - A Case of Hypokalaemic Periodic Paralysis Mimicking Stroke.

Hypokalaemic periodic paralysis is an acute flaccid paralysis secondary to hypokalaemia, triggered by hyperthyroidism, environmental elements such as a high carbohydrate intake or rest after intense exercise, and an underlying genetic component with mutations in the muscle ion channels.The pursuit of code stroke protocol in the in-patient setting must bear in mind reversible but potentially fatal and disabling alternative diagnoses such as stroke mimics including hypokalaemic periodic paralysis.Stroke mimics defined as acute onset neurological deficits that are not related to vascular cause are a true challenge, multiple scales have been created to distinguish them from an actual stroke, such as the Recognition of Stroke in the Emergency Room (ROSIER) scale.

Echographic characterization of extraocular muscles in pediatric patients with thyroid dysfunction

ABSTRACT Purpose To characterize the size of extraocular muscles (EOMs) in a pediatric population with thyroid dysfunction using orbital echography. Methods Patients under age 18 with thyroid dysfunction who presented to an academic ophthalmology department from 2009 to 2020 and received orbital echography were included in this IRB-approved retrospective study. Data collected included age, clinical activity score (CAS), thyroid stimulating immunoglobulin (TSI), and extraocular recti muscle thickness on echography. Patients were organized into three age cohorts, after which statistical analysis compared recti measurements to previously reported normal ranges. Results Twenty patients with thyroid dysfunction were included. When comparing average recti muscle thicknesses of study patients to those of previously published normal children in similar age ranges, the levator-superior rectus complex was significantly increased in all age groups of children with thyroid dysfunction (p-values = <.004), and the levator-superior rectus complex was most frequently enlarged compared to published normal values (78% of eyes). CAS was not correlated with EOM size in the youngest group (5–10 years old, p-values >.315) but was significantly correlated in older groups (11–17 years old, p-values <.027). TSI was not correlated with EOM size in any group (p-values >.206). Conclusions Echographic reference ranges for EOMs in children with thyroid dysfunction were established. There are increased rates of levator-superior rectus complex enlargement in children with TED compared to adults with TED, and EOM size is correlated with CAS in children older than 10 years. Though limited, these findings may serve as an additional tool for ophthalmologists to ascertain disease activity in pediatric patients with thyroid dysfunction.