Free T4 Levels Research Articles

THU657 Racing Hearts: A Closer Look At The Connection Between Hyperthyroidism And Coronary Vasospasm

Abstract Disclosure: A. Elahi: None. R.I. Mateo: None. The cardiovascular system is a major target of thyroid hormone action in which subtle changes in thyroid function can lead to cardiac complications such as coronary vasospasm. There are many proposed mechanisms in how this occurs, but further studies are needed to understand the specific pathophysiology. This case illustrates the clinical relevance of encountering a hyperthyroid patient complaining of chest pain and how to address it in real work practice. A 62 year old African American male with history of Graves hyperthyroidism, type 2 diabetes, hypertension, peripheral artery disease, and stroke with residual aphasia presented with acute onset chest pain, shortness of breath, and palpitations. He was noncompliant with his methimazole (MMI) and subsequent labs were significant for free T4 of 2.5 ng/dL, undetectable TSH, and free T3 of 11.53 pg/mL. His high sensitivity troponins were elevated at 29,569 ng/dL. EKG showed sinus tachycardia with T-wave inversions in leads II, III, and AVF with a bedside echo showing inferior lateral wall motion abnormality. He was started on MMI 20mg daily and admitted to the intensive care unit for non-ST elevation myocardial infarction management. Left heart catheterization (LHC) was done after 1 dose of MMI with findings suggestive of vasospasm; specifically, decreased blood flow of the right coronary artery which improved when the catheter was withdrawn and significant dampening of the arterial wave form of the left main coronary artery. Given the unclear differentiation between true coronary artery disease and vasospasm he needed a repeat LHC once his hyperthyroidism was more controlled. His free T3 levels were monitored every 1-2 days with administration of escalating doses of MMI up to 40mg daily. By day 7 of admission, his free T3 level was 4.54 pg/mL, free T4 was 2 ng/dL and repeat LHC was performed showing open vessel lumens with multiple occlusions requiring 2 stents in the right coronary artery and 1 stent in the left circumflex artery. Given that thyroid hormone receptors are present in the myocardium and vascular tissue, alterations in thyroid hormone concentration can affect cardiovascular function. The documentation of coronary spasm, however, is rare and to date, there are only a few limited cases describing the underlying pathophysiology. This case illustrates via cardiac catheterization images and corresponding labs, the positive correlation of coronary vasospasm with thyroid hormone levels in hyperthyroidism. Presentation: Thursday, June 15, 2023

THU025 Acromegaly And Central Hyperthyroidism

Abstract Disclosure: A. Akhtar: None. M.A. Mahmood: None. Introduction: Pituitary adenomas are usually benign neoplasms that are the third most common type of central nervous system tumors. Although TSH releasing tumor accounts for 1% of pituitary adenomas, about one-third of the time it co-secretes Growth Hormone. Co-secretion of TSH and GH can further promote the prognosis of the tumor, therefore, must be immediately treated medically or surgically. Case Report: The case is of a 42 years old male patient who presented to his orthodontist with the complaint of loosening teeth and was referred to a primary care physician. According to the patient, he has observed an increase in his ring size up to 3 times his usual size, one and a half increase in his shoe size, some degree of joint pain, occasional visual blurriness, no weight loss, and snoring. He has no history of headaches, breast tenderness, or discharge. He works at a farm and has no family history of pituitary tumors. His laboratory findings in May 2021 show IGF-1 1028 ng/mL (normal less than 278 ng/mL), ACTH 72.2 pg/mL (normal <60pg/mL), Prolactin, TSH, LH and FSH levels were normal. These findings suggested an IGF-producing pituitary adenoma. During further workup, he had high levels of free T4 and free T3, 2.7 ng/dL and 8.2pg/mL (Normal 2.3 - 4.2pg/mL), respectively, along with elevated TSH levels, which were 8.1mIU/L (normal 0.27-4.2mIU/L). Magnetic resonance imaging showed a pituitary mass of 1.8cm x 2.0cm x 1.6cm in the suprasellar region, abutting the optic chiasm, and showed heterogeneous enhancement. There were no signs of hemorrhage. His visual field examinations were normal. He was prescribed to take 50mg of octreotide every 8 hours. In six weeks, the patient had improved levels of serum TSH which was lowered to 0.785mIU/L, and free T4 and free T3, which were 1.62pmol/L and 3.45pmol/L, respectively. He had transsphenoidal pituitary surgery. Pathology showed a 2.6 x 2.0 x 0.3 cm tumor of somatotropic type. Post-surgery MRI showed no tumor residues. Discussion: We report a middle-aged man with a rare case of the pituitary tumor with acromegaly and central hyperthyroidism. Thyrotropinomas, also known as TSHomas, are benign pituitary adenoma that produces thyroid stimulating hormones. Although rare, they are macroadenomas 80% of the times and 20-25% of the time co-secrete other pituitary hormones. These tumors may show elevated fT3, fT4, and TSH, and increased alpha-subunit. There is not enough evidence to proof the exact origin of the pathology, however, immunohistologically, the tumor cells arise from PIT1-lineage adenohypophyseal cells and could be associated with MEN 1 mutation on chromosome 11q13. Surgical removal of the tumor is a preferred approach to TSHomas, but recent studies have shown a significant improvement with medial therapy of somatostatin analogs by interacting with somatostatin receptors. Octreotide, a somatostatin analog has been clinically shown to bring the thyroid hormones to a normal level in 80% if cases and shrinkage of tumor size in pituitary adenoma in 60% of cases. It can be used as a pre-operative therapy to reduce the levels of free thyrotropin. It also reduces GH and serum IGF-1 levels. Co-secretion of TSH and GH promotes the prognosis of tumors which may be prevented with early diagnosis and treatment. Presentation: Thursday, June 15, 2023

FRI511 Bexarotene: A Deceptive Cause Of Iatrogenic Hypothyroidism

Abstract Disclosure: S. Ghaith: None. A. Ramachandran: None. C. Alcorn: None. F. Amer: None. A. Thompson: None. A. Ramachandran: None. Background: Bexarotene, an antineoplastic agent used for the treatment of cutaneous T cell lymphoma, is associated with a rapid and profound suppression of thyrotropin, which may lead to central hypothyroidism. Case: A Seventy-four-year-old female with a recent diagnosis of Cutaneous T cell lymphoma presented with a 1-week history of progressive fatigue, lightheadedness, and night sweats. She was found to have hypotension and hypothermia. She was started on oral Bexarotene chemotherapy 225 mg daily five days prior to admission. The physical exam was unremarkable except for sinus bradycardia and hypothermia. Labs were significant for TSH 0.48 [0.4-4.2 uIU/mL] dropped from 3.3 uIU/mL one week prior, FT4 0.5 [0.8-1.7 ng/dL] and Total T3 111 ng/dL [87- 187 ng/dL] consistent with central hypothyroidism. Bexarotene was held during her hospitalization per hematology recommendations. The patient was started on Levothyroxine 50 mcg, which was later advanced to 75 mcg daily based on free T4 levels. At one month follow up, free T4 level normalized while on Levothyroxine and Bexarotene was restarted again by her hematologist. Discussion: Bexarotene, an antineoplastic agent approved for treating cutaneous T cell lymphoma, can rapidly suppress TSH levels by directly inhibiting its secretion and affect thyroid hormone metabolism, leading to central hypothyroidism. The degree of suppression of TSH increases with higher doses of Bexarotene while reduction in free T4 and TSH are reversible. Patients already receiving thyroid hormone therapy may require increased thyroid hormone doses to achieve therapeutic levels. If bexarotene is permanently discontinued, levothyroxine can either be stopped or can be resumed to doses used prior to bexarotene therapy. Recovery of thyroid function usually occurs within weeks of Bexarotene discontinuation. Conclusion: Oral Bexarotene can cause central hypothyroidism therefore, thyroid function tests should be measured at baseline and treatment. Thyroid hormone replacement should be considered if central hypothyroidism is suspected. Presentation: Friday, June 16, 2023

FRI539 Vitamin D and Endocrine Immune-Related Adverse Events in Patients Treated with Immune Checkpoint Inhibitors

Abstract Disclosure: Z. He: None. A. Leiter: None. E. Carroll: None. G. Santiago Pichardo: None. I. Khanna: None. E. Gutowski: None. E.J. Gallagher: Research Investigator; Self; Novartis Pharmaceuticals, Flare Therapeutics, Seagen. Background: Low vitamin D levels have been previously associated with the development of thyroid dysfunction in non-cancer populations. Thyroid dysfunction is one of the most common immune-related adverse events (irAEs) induced by immune checkpoint inhibitors (ICIs). Currently, the effect of vitamin D deficiency or vitamin D supplementation on the development of ICI-induced thyroid dysfunction is unknown. This study was design to examine the association between baseline vitamin D levels and vitamin D supplementation, and the development of ICI-induced thyroid dysfunction. Methods: In this IRB-approved, retrospective cohort study, we collected demographic and clinical characteristics in addition to TSH, free T4, and vitamin D levels from patients with melanoma, multiple myeloma (MM), and transitional cell carcinoma (TCC) treated with ICIs between 2011 and 2020, in a large urban hospital system. The primary outcome was the occurrence of thyroid dysfunction defined by abnormal TSH or free T4 level after ICI initiation. Vitamin D deficiency / insufficiency was defined as serum 25-hydroxy-vitamin D level <30ng/mL. Patients were followed until the first occurrence of the primary outcome or the date of the most recent normal TSH level. Descriptive data are presented as n(%) and median±SD. Univariate and multivariate analysis were performed to examine the association between the primary outcome and vitamin D deficiency/ insufficiency or supplementation. Results: 288 patients with melanoma (n=111), MM (n=86) or TCC (n=91) were identified, with a median age of 65±13 years, and 64% were male. 110 (38%) patients experienced thyroid dysfunction. Among the TCC subgroup, the mean baseline TSH levels for patients who experienced the outcome was significantly higher than that for patients who did not (p = 0.0066). No statistical significance was found for the melanoma (p=0.42) or MM subgroups (p=0.30). Amongst patients with baseline vitamin D levels measured, we found no statistically significant association between thyroid dysfunction and baseline vitamin D deficiency (OR = 0.62, p = 0.34). In the entire cohort, the 1-year outcome-free rates for patients taking and not taking vitamin D supplementation were 68% and 61%, respectively (p=0.07). Vitamin D supplementation was found to reduce the risk of ICI-induced thyroid abnormality by approximately 40% (RR = 0.606, p=0.03) in the multivariate analysis. No difference in mortality was found between those who developed thyroid dysfunction and those who did not. Conclusions: In individuals with melanoma, MM and TCC, vitamin D supplementation may have a protective effect against ICI-induced thyroid dysfunction. Whether vitamin D supplementation impacts cancer response to ICIs is unknown at this time. Presentation: Friday, June 16, 2023

FRI481 Clinical Characteristics Of Neutropenic Patients Under Anti-thyroid Drug: A Retrospective Cohort Study In Taiwan

Abstract Disclosure: C. Tseng: None. C. Tseng: None. H. Chen: None. P. Chen: None. C. Huang: None. Background: Thionamide-induced agranulocytosis (TiA), is a rare adverse event with a reported incidence of around 0.1-1.75%. To reduce mortality, prompt recognition is critical but the differential diagnosis of TiA cases from non-TiA neutropenia can be challenging as other causes of neutropenia, such as concomitant chemotherapy, liver dysfunction or infection, may simultaneously exist. The present study aimed at investigating the possible factors associated with the development of TiA. Method: This is a retrospective cohort study of patients treated with anti-thyroid drugs (ATDs) in Taipei Veterans General Hospital from 2006-2018. Patients who developed a neutropenic event under treatment of ATDs were identified from the medical records. TiA was defined as (1) development of neutropenia under treatment or within 7 days of previous exposure to the same ATDs; (2) total recovery of neutropenia within one month after discontinuation of the culprit drug with absolute neutrophil count > 1500/μL; (3) exclusion of other causes for neutropenia. The incidence and risk factors for developing TiA were analyzed and compared to those with non-TiA neutropenia. Results: Among 6644 patients treated with ATDs, 66 (mean age, 53±15 years; 16.2% men) developed a neutropenic event and 20 were diagnosed with TiA (incidence: 0.3%). In univariate analysis, TiA was associated with shorter treatment duration, lesser cumulative ATD dosage, higher ATDs dosage, higher absolute neutrophil count and higher free T4 level at the time of the neutropenic event, compared to non-TiA neutropenia. After accounting for age, gender and time to neutropenia, ATDs dosage at the time of neutropenic event [odds ratio (OR) and 95% confident intervals (CIs): 635.47, 1.88-214562.36], free T4 level (OR and 95% CIs: 17.23, 1.02-290.58), and absolute neutrophil count (OR and 95% CIs: 1.00, 1.00-1.01) were still independently associated with TiA in multivariable logistic regression. Conclusions: TiA patients were more likely to have higher free T4 level, higher absolute neutrophil count at the time of neutropenic event and had received higher dosage of ATDs, compared to non-TiA cases. Presentation: Friday, June 16, 2023

FRI512 Thyrotoxic Periodic Paralysis With Extreme Hypokalemia Precipitated By Acute Alcohol Intoxication In A Patient With Graves’ Disease

Abstract Disclosure: J. Batra: None. A.R. Ankireddypalli: None. J. Kaur: None. Introduction: Thyrotoxic periodic paralysis (TPP) is a muscle and electrolyte disorder, mostly seen in the setting of hyperthyroidism. It is characterized by reversible painless muscle weakness and hypokalemia. Prevalence is highest in East Asian populations, approximately 2%, and 0.1-0.2% in other populations. Males are much more likely to be affected. Common provoking factors include exercise, fasting, and changes in diet. Clinical case: A 29-year-old male of East Asian ethnicity presented to the hospital with the complaint of multiple bouts of inability to lift his extremities for 1 day. He also complained of generalized weakness. He did not have any changes in his mental status and was fully oriented at the time of the presentation. No breathing difficulty was reported. He had been drinking the night before with his friends and drank 1 L of vodka. His past medical history was significant for hyperthyroidism secondary to Graves’ disease, which was diagnosed a year ago. He had been prescribed methimazole but had not been adherent to the medication. The basic metabolic panel revealed undetectable serum potassium of <1.5 (3.4 to 5.3 mmol/L). The rest of the electrolytes and renal function were unremarkable. TSH was suppressed at <0.01 (0.3 to 4.20 uIU/L) and free T4 levels were significantly elevated at 7.77 (0.9 to 1.70 ng/dL). The thyrotropin receptor antibody was 33 (0.00 to 1.75 IU/L). EKG showed sinus tachycardia with nonspecific T-wave abnormalities. Thyroid ultrasound showed diffusely heterogenous parenchyma with diffusely increased blood flow throughout the thyroid on doppler. Echocardiogram showed a normal ejection fraction of 55-60% with mild concentric left ventricular wall thickening consistent with left ventricular hypertrophy. He was initially treated with intravenous potassium replacement and high doses of propylthiouracil, hydrocortisone, and propranolol, leading to the resolution of his symptoms. He was discharged on methimazole and propranolol therapies. Learning points: • Patients with Graves’ disease are routinely counseled against tobacco use to avoid worsening of orbitopathy. Hyperthyroid patients should also be counseled regarding avoidance or moderation of alcohol intake to avoid this rare but potentially life-threatening complication of thyrotoxic periodic paralysis. • The incidence of TPP is significantly higher in the East Asian populations, especially among males (8.7-13%). Counseling regarding provoking factors, the importance of adherence to medications, and the maintenance of euthyroidism to avoid TPP is essential. Presentation: Friday, June 16, 2023

SAT479 A Case of Thyroiditis Cause by Cabozantinib

Abstract Disclosure: S. Bulchandani: None. N. Janicic-Kahric: None. Introduction: Thyroiditis is an inflammatory disease of the thyroid; the cause can be autoimmune, infectious or drug induced. Patients can have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release of preformed thyroid hormone from damaged thyroid cells. This can be followed by hypothyroidism, when the thyroid stores are depleted, and then eventual restoration of normal thyroid function. Some patients may develop permanent hypothyroidism.1 We report a case of thyroiditis caused by cabozantinib. CASE REPORT: 39-year-old female presented with abdominal pain, vomiting and palpitations. Past medical history was significant for metastatic clear cell renal carcinoma. Eight weeks before the presentation, she had started on cabozantinib 60 mg daily as part of therapy for her renal carcinoma. On presentation, the patient’s temperature was 36.6 Celsius, heart rate was 118 beats/minute, blood pressure was 114/84 mm Hg and oxygen saturation was 100% on room air. Laboratory evaluation was notable for white blood cell count of 12.3 k/uL, Hemoglobin of 16.5g/dl, Platelet count of 573 k/uL bicarbonate level of 13 mmol/L, anion gap 24 mmol/L, Total bilirubin of 0.6 mg/dl, Aspartate aminotransferase of 36 units/L, Alanine aminotransferase of 30 units/L, Alkaline phosphatase of 121 units/L. Thyroid function tests revealed thyroid stimulating hormone (TSH) which was low at 0.045 uIU/ml and free thyroxine level (Free T4) which was elevated at 4.29 ng/dl. Thyroid function tests performed eight weeks prior to presentation showed TSH of 6.9 uIU/ml, attributed to immunotherapy that the patient received 1 month prior. She was admitted and received intravenous fluids. Prednisone at 40 mg orally daily was initiated. Labs demonstrated a decrease in Free T4 level. She was discharged on a tapering course of prednisone. Free T4 one week later was normal at 1.35ng/dl. Repeat laboratory evaluation three weeks later revealed that the patient had developed hypothyroidism with TSH level of 8.7 uIU/ml and she was started on 50 micrograms of levothyroxine. Cabozantinib was discontinued. Discussion: Tyrosine Kinase inhibitor therapy can result in clinically significant thyroid dysfunction. Cabozantinib treatment can result in thyroid dysfunction varying from subclinical hypothyroidism to symptomatic thyrotoxicosis. Early detection and close follow-up are essential to provide adequate management2 Presentation Date: Saturday, June 17, 2023

FRI480 Uncovering The Mystery Of Macro TSH

Abstract Disclosure: F. Anwar: None. Z.I. Saeed: None. Introduction: An isolated elevation in TSH level, while uncommon, may result in incorrect diagnosis and improper treatment. We present a case of suspected hypothyroidism that was later found to be caused by macroTSH in the blood. Clinical Case: A 21-year-old asymptomatic female was diagnosed with hypothyroidism and started on levothyroxine at age 16 when routine lab work revealed TSH of 34.2 MCU (0.550-4.780 MCU) and free T4 of 1.1 ng/dl (0.89-1.76 ng/dl). She denied any personal or family history of thyroid disorders in the past. Patient later reported symptoms including palpitations and weight loss leading to discontinuation of levothyroxine. Repeat lab work showed TSH of 0.112 MCU and free T4 of 1.71 ng/dl. After discontinuing levothyroxine, TSH levels were found in range of 89.26 MCU to 106 MCU (0.550-4.780 MCU). Free T4 levels remained normal, even when tested using dialysis method. Total T3 level also remained normal at 87 ng/dl (80-200 ng/dl). TPO antibodies were slightly elevated at 9.3 IU/mL (0.0-9.0 IU/ml), TSI and TSH receptor antibodies were negative. Patient's high TSH level, lack of symptoms, and normal free T4 levels prompted the use of different assays to test TSH. We contacted Mayo Clinic Lab for further testing. One assay (Roche Elecsys) showed TSH level of 90.8 mIU/L, but this result was not significantly changed when sample was incubated with a commercial heterophile antibody blocking reagent. Another assay (Beckman Coulter Access TSH) produced a significantly different but still elevated result of 43.1 mIU/L. For research purposes, the sample was further tested for macroTSH using polyethylene glycol (PEG) precipitation, which resulted in TSH level of 5.8 mIU/L which was reduced from 90.8 mIU/L (94% reduction). These results were higher than the mean +/- 2 standard deviations of the control group (range 0% to 65% reduction in TSH with PEG in controls). This suggested presence of macroTSH, although the assay's performance characteristics and reference ranges had not been established at the time of testing for this patient. Patient's TSH levels remain high and she was advised not to begin the medication unless circulating thyroid hormone levels are abnormal. Conclusion: Macro TSH is a combination of monomeric TSH and anti-TSH antibodies, similar to macro-prolactin. It is considered inactive and has an estimated prevalence of 0.6-1.6%. In a review of over 150 patients, more than 50% of documented thyroid interferences, including macro TSH, led to incorrect diagnosis and improper treatment. This case demonstrates the significance of identifying macro TSH to avoid misdiagnosis and inappropriate management of euthyroid patients with isolated TSH elevation. Presentation: Friday, June 16, 2023

FRI535 Quality Of Life And Symptomatology In Patients With Autoimmune Thyroiditis

Abstract Disclosure: L.M. Pereira: None. C. Neves: None. J. Neves: None. L. Delgado: None. D. Carvalho: None. Introduction: Autoimmune thyroiditis (AIT) may be associated with physical, psychological and behavioral symptoms even in patients achieving normal TSH and free T4 levels with levothyroxine treatment. Objective: Our aim was to evaluate the associations the resistance to thyroid hormone, assessed by the Parametric Thyroid Feedback Quantile-Based Index (PTFQI), and laboratorial parameters with Quality of life (QoL) in AIT. Methods: We evaluated 145 patients with AIT treated with levothyroxine followed in outpatient clinic. We assessed lipid profile, high-sensitivity C-reactive protein, B12 vitamin, folic acid, thyroid antibodies, thyroid function tests and calculated the index PTFQI of resistance to thyroid hormones. The following questionnaires were applied to participants: the Thyroid Dependent Quality of Life questionnaire (ThyDQoL), the Thyroid Symptom Rating Questionnaire (ThyTSQ), the Thyroid Treatment Satisfaction Questionnaire (ThyTSQ) and the Brief Symptom Inventory (BSI). Statistical analysis was performed with the One-way ANOVA test and Pearson’s correlation test. P values ≤ 0.05 were considered as statistically significant. Results: In this sample, the age was 54.4 ± 15.3 years, 89.7 % were female, BMI was 28.4 ± 5.2 Kg/m2, TSH was 2.69 ± 8.48 µUl/mL and FT4 was 1.15 ± 0.40 ng/dL. Patients reported a mean QoL value of -2.11 points (range from -9 to 1). In regard to the ThySRQ, 46.2 % of patients reported at least moderately memory problems, 50.4% of patients reported at least being moderately tired and 62.7 % showed some type of depressive feelings. Regarding ThyTSQ, 83.5 % demonstrated being satisfied with treatment and 82 % believe that treatment is working well. We found that PTFQI correlates positively with thyroid peroxidase antibodies (r = 0.19; p = 0.03) and negatively with triglycerides (r = -0.26; p = 0.002) and BMI (r = -0.21; p = 0.01). In relation with symptomatology, we observed negative correlations among PTFQI and constipation (r = -0.18; p = 0.02), skin problems (r = -0.27; p = 0.01), nail problems (r = -0.19; p = 0.01) and dizziness symptoms (r = -0.18; p = 0.03). Conclusions: In this study, we observed a high prevalence of memory problems, tiredness and depressive feelings in patients with AIT treated with levothyroxine. We also found that PTFQI is associated with physical and psychological symptoms. Further studies are needed to analyze the role of autoimmunity and PTFQI for the worsening of the QoL in patients with AIT. Presentation: Friday, June 16, 2023

SAT550 Warthin-like Variant of Papillary Thyroid Carcinoma: An Even Rarer Presentation

Abstract Disclosure: J. Kunadia: None. S. Chablani: None. Introduction: We present a rare case of Warthin-like variant of papillary thyroid carcinoma (WLPTC) with later development of a second primary malignancy. Clinical Case: A 56 year old female with hypertension, hyperlipidemia, ulcerative colitis, asthma, and a strong family history of cancer presented in 2017 for evaluation of an enlarged thyroid gland noted by her primary care provider. Patient was asymptomatic and denied prior thyroid disease and head or neck radiation. Labs demonstrated normal TSH and free T4 levels. TPO antibodies were elevated to 1,155 IU/mL (reference range 0.0 – 5.5 IU/mL). Thyroid US was notable for a diffusely enlarged thyroid gland containing a 1.4 x 0.6 x 1.0 cm solid, hypoechoic nodule without calcifications in the upper pole of the right lobe. Shared decision-making resulted in a plan for continued surveillance. Repeat thyroid US in 2018 demonstrated that this nodule had increased in volume by 56.25%, now measuring 1.4 x 0.75 x 1.25 cm. Fine needle aspiration (FNA) biopsy was performed and positive for papillary thyroid carcinoma (PTC). Patient underwent total thyroidectomy; pathology revealed a 1.2 x 1 x 0.9 cm WLPTC and 0.2 cm papillary thyroid microcarcinoma. There was no evidence of extrathyroidal extension, angioinvasion, or lymph node involvement. Follow-up neck US in 2020 demonstrated a 0.4 cm hypoechoic ovoid structure in the left thyroid bed and an enlarged but morphologically normal-appearing right level II lymph node. Repeat neck US in 2021 showed the appearance of a new 2.8 cm right level II lymph node; FNA was positive for malignancy with negative thyroid transcription factor-1 staining and undetectable thyroglobulin. Patient underwent an excision biopsy of the lymph node, and pathology was consistent with metastatic adenoid cystic carcinoma (ACC). A right submandibular gland lesion detected on subsequent MRI head and neck was resected and confirmed to be the primary source of ACC. Patient was treated with adjuvant radiation therapy with adequate response to therapy. Conclusion: WLPTC is a rare subtype of PTC that accounts for 0.2-1.9% of cases and carries a strong association with Hashimoto’s thyroiditis. It is histologically characterized by papillary architecture, oncocytic changes, nuclear features of PTC, and dense lymphoplasmacytic infiltration of the papillary cores. WLPTC is considered to have a favorable prognosis given its low frequency of lymphovascular invasion and low recurrence risk. This case also highlights the importance of keeping a broad differential when evaluating new findings on neck US in patients with a history of thyroid cancer. Metastases to cervical lymph nodes most commonly occur from head and neck tumors. However, to date, only one other case of PTC with second primary malignancy of salivary ACC has been reported. Presentation Date: Saturday, June 17, 2023

FRI473 Central Hypothyroidism Following Neonatal Graves Presentation

Abstract Disclosure: E. Metzinger: None. K. Halpin: None. Background: Neonatal Graves’ disease is a rare disorder of neonatal autoimmune hyperthyroidism secondary to the transplacental passage of thyroid-stimulating hormone receptor antibodies. Although neonatal Graves’ disease is transient, it is associated with cardiac dysfunction, intrauterine growth restriction, prematurity, craniosynostosis, and developmental delay and can be life-threatening. Additionally, infants with neonatal Graves’ disease can rarely present with primary or central hypothyroidism later in infancy or childhood. This is suspected to be due to the disruption in the hypothalamic-pituitary-thyroid axis or development of the thyroid gland. Clinical Case: Here we describe a case of neonatal Graves’ disease that has been complicated by persistent central hypothyroidism requiring levothyroxine treatment. This was a preterm infant with tachycardia, biventricular heart failure, and hepatomegaly who was transferred to a higher level of care NICU for cardiac and respiratory failure. Pregnancy was complicated by history of maternal Graves’ disease status post radioiodine ablation. Maternal TRAB and thyroid levels were unavailable. Initial thyroid studies on DOL 1 were notable for suppressed TSH of <0.02mcIU/mL, elevated free T4 6.9ng/dL, and elevated total T4 >24.9mcg/dL. Total T3 was normal at 161ng/dL (50-452ng/dL) on DOL 2, and TSI was elevated at 4.8 (TSI Index, normal </= 1.3) on DOL 3. For neonatal thyrotoxicosis, the infant was treated with methimazole, potassium iodide (KI), propranolol, and hydrocortisone. Hydrocortisone was discontinued as the infant clinically improved, and KI was discontinued after 1 week. TFTs were closely followed during admission and methimazole dosing was adjusted as needed. He was discharged from the NICU on DOL 19 on methimazole and propranolol with close outpatient lab monitoring and follow-up. Propranolol was discontinued by 1.5 months of life, and methimazole was discontinued by 2 months of life as TFTs normalized. TSI was negative by four months of life. TSH remained low with decreasing free T4 levels. Ultimately, he was started on levothyroxine at 8.5mcg/kg/day at 2.5 months of age for central hypothyroidism. At that time, TSH was 0.06mcICU/mL and FT4 was 0.7ng/dL. TSH remained low through the first 14 months of treatment with normal free T4 levels on levothyroxine. He has been continued on levothyroxine (average 20mcg/day). Conclusion: This case highlights the severity of neonatal Graves’ disease and the possibility of the subsequent development and persistence of central hypothyroidism following neonatal Graves’ diagnosis despite the resolution of hyperthyroidism and normalization of TSI antibody. Due to the risk of the development of hypothyroidism, it may be worthwhile to continue to trend TSH and FT4 to ensure that the infant has not developed hypothyroidism. Presentation: Friday, June 16, 2023

SAT477 Consumptive Hypothyroidism In A Patient With Plasma Cell Neoplasm

Abstract Disclosure: G. Sidhu: None. I. Madahar: None. A. Haider: None. J. Giordano: None. Introduction: Thyroxine (T4) is converted into metabolically active form triiodothyronine (T3) by deiodinase enzyme 1 & 2 (D1 & D2). Deiodinase 3 converts T4 and T3 into metabolically inactive form reverse T3 (rT3)& di-iodothyronine (T2) . Consumptive hypothyroidism syndrome (CHS) is a very rare form of hypothyroidism seen in patients with neoplasms, which express high levels of D3 enzyme. Case: 68-year-old female withhistory of Multiple Myeloma (MM), POEMS, hyperlipidemia and hypothyroidism was admitted with acute kidney injury, cirrhosis of unclear etiology, large volume ascites and anasarca. She weighed 92 kg on admission. She was complaint with her 50 mcg of levothyroxine and on admission her TSH was 7.14 (N: 0.43-3.55 uIU/ml), Free T4 (FT4): <0.42 (N: 0.7-1.25 ng/dl), total T4 (TT4): 2.6 (N: 4.8-11.7 ug/dl), total T3 (TT3): <20 (N: 80-200 ng/dl). Oral LT4 was switched to IV form due to underlying concerns of malabsorption from anasarca. rT3 was noted to be 40 (N: 8-25 ng/dl). Despite escalated intravenous levothyroxine doses for seven days her FT4, FT3 continued to remain undetectable So her LT4 dose was increased to 75 mcg IV daily initially and eventually to 100 mcg IV daily and 125 mcg daily. On 10th day of hospitalization, after her IV LT4 dose was increased to 200 mcg daily, (almost 2.5 mcg/kg/day) her FT4 levels became detectable, 0.50, rT3: 68 and TT3: <20 and TT4: 3.1. Since her rT3 levels were noted to rise after increasing the dose of LT4, liothyronine (LT3) 5 mcg BID was added to her regimen. PET scan showed small sclerotic bone lesions suspicious for active malignancy. Chromogranin A was elevated 313 (N: <311 ng/ml). IR guided biopsy of scapular sclerotic lesion was done and specimen was sent University of Chicago to measure DI-3 activity in the specimen Pathology results were suggestive of plasma cell neoplasm but unfortunately deiodinase activity could not be quantified. Patient developed hepato-renal syndrome during hospitalization and her family decided to pursue hospice care. Discussion: Critical care illness thyroid disease is also associated with increased DI-3 activity and increases rT3, however T4 and TSH are also low in the setting of critical care illness, and most patient do not require supraphysiologic T4 replacements. The presence of D3 in normal tissues such as the brain & placenta has been hypothesized to protect tissues from the effects of excessive thyroid hormone. However, aberrant expression of the enzyme can lead to severe hypothyroidism from inactivation of both endogenously produced and exogenously administered thyroid hormone. Previously this rare syndrome was described in association with massive hemangiomas in children and in a single case of a hemangioendothelioma in an adult. However case reports in adults have been described in nonvascular tumors who required supraphysiologic doses of levothyroxine prior to the resection of a large malignant solitary fibrous tumor. Presentation Date: Saturday, June 17, 2023

SAT486 A Case of Superior Vena Cava Syndrome Caused by Untreated Multinodular Goiter

Abstract Disclosure: K. Blanchard: None. C. Musurakis: None. A. Ojha: None. C.P. Barsano: None. A. Havrylyan: None. A 92-year-old female with heart failure, COPD, obstructive sleep apnea, longstanding exertional dyspnea, and a 15-year history of a toxic multinodular thyroid on methimazole presented to our emergency department with one week of right arm swelling. Physical exam showed a 4 cm midline goiter with right-sided jugular venous distention and right upper extremity pitting edema. On admission, TSH, free T4 and free T3 levels were within normal limits on methimazole 5 mg daily. PTT, PT and INR were normal. Thyroglobulin antibodies and TSI measured two years prior were normal. Right arm venous duplex was negative for acute deep venous thrombosis (DVT) but showed heterogenous structures in the right neck with collateral vessels, likely related to a large multinodular thyroid gland with substernal extension. Left arm venous duplex showed chronic sequela of DVT in the left central subclavian vein. Chest x-ray revealed right-sided tracheal deviation due to goiter. A CT chest performed 6 months prior revealed a massive multinodular goiter with mass effect on the trachea, narrowing the tracheal opening to only 7 mm (ref 10-21 mm in females) and significant mass effect upon adjacent venous structures with resultant collateralized flow. Of note, the patient has a 15-year documented history of this goiter and repeatedly declined aggressive surgical intervention. We recommended ENT consultation for minimally invasive treatment options. ENT recommended thoracic surgery evaluation at a tertiary center and suggested tracheal stenting as a possible solution. Regarding the chronic left subclavian vein thrombosis, the patient opted to forego anticoagulation therapy after discussion of risk versus benefit. She again declined surgical evaluation and was discharged home with primary care and Endocrinology outpatient follow-up. Superior vena cava (SVC) syndrome is the result of either a partial or complete obstruction of the SVC, resulting in symptoms such as upper extremity swelling, dyspnea, cough, face or neck swelling, and dilated venous collaterals in the chest. Compression of the SVC by a mediastinal malignancy is the most common cause of SVC syndrome. However, retrosternal goiter as a cause is extremely rare, with only a few cases previously reported in the literature. Interestingly, the incidence of malignancy in retrosternal goiters is reported to be as high as 35 percent. Large intrathoracic goiters are primarily seen in long periods of neglected disease, as in our patient. The presence of a substernal goiter, regardless of symptoms, is an indication for thyroidectomy, as this is the only way to prevent mediastinal enlargement of the goiter. Non-surgical treatment options documented in the literature include temporary tracheal stent placement followed by radiofrequency thyroid ablation and ultrasound-guided needle aspiration of a dominant thyroid cyst. Presentation Date: Saturday, June 17, 2023

FRI591 Association Of TSH Levels And NAFLD Severity In Children And Adolescents

Abstract Disclosure: M. Untalan: None. N.A. Crimmins: None. A. Mencin: None. K. Yates: None. X. Stavra: None. V. Thaker: None. Background: Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic lipid accumulation and is now the most common form of chronic liver disease in children and adolescents. Recent studies have indicated an association between subclinical hypothyroidism (SH) and NAFLD. An underactive thyroid gland produces insufficient T3 and T4 involved in hepatic fat metabolism that could contribute to NAFLD. While increased TSH has been documented in individuals with NAFLD, its independent role with NAFLD disease severity is yet to be clarified. Objective: To study the relationship of TSH levels and the severity of NAFLD/NASH, as well as determine whether changes in TSH levels are associated with changes in NAFLD/NASH among children. Methods: This retrospective study used data from two cohorts within the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN). TSH, free and total T4, total T3, TPO antibodies and thyroglobulin (TBG) levels were assessed in samples obtained first at baseline and then at 52-96 weeks. Individuals with overt hypothyroidism, abnormal TPO antibody levels, and those receiving thyroid treatment were excluded from analysis. SH was defined as TSH > 4.4 mIU/L. Linear and multinomial regression models were used to identify the association between TSH, SH and NAFLD severity measured by NAFLD activity score (NAS), fibrosis stage, steatosis level, lobular and portal inflammation and ballooning while adjusting for potential confounders (sex, age, race, BMI-z, HOMA-IR and non-HDL levels). Longitudinal analysis was conducted by mixed-effects model. Analyses were performed with SAS and R statistical software. Results: 218 individuals and 421 observations were included in the cross-sectional and longitudinal analyses, respectively. Children with more severe grades of steatosis were more likely to be younger (p = 0.03) and male (p = 0.02). At baseline, TSH was not significantly associated with any NAFLD histological measures. Longitudinal analyses revealed a positive association of change in TSH and steatosis level after adjusting for covariates, and follow-up time (p = 0.03). Change in SH was associated with change in fibrosis stage (p = 0.01). Adding HOMA-IR and non-HDL levels to the models did not change this relationship. The positive relationship of total T3 and T4 with NAS was explained by TBG. Conclusion: In a large cohort of pediatric patients with biopsy-confirmed NAFLD, high TSH levels correlated with increasing steatosis grade and NAS, and SH with increased liver fibrosis. Markers of impaired thyroid function may help predict disease severity in pediatric patients with NAFLD. Presentation: Friday, June 16, 2023

THU265 A U-Shaped Relationship Between Undiagnosed Diabetes And Thyroid Function

Abstract Disclosure: Z.Z. Alvi: None. R. Karnchanasorn: None. H. Ou: None. L. Chuang: None. A.G. Gianoukakis: None. K.C. Chiu: None. Thyroid dysfunction is present in about 20 million people in the United States, with about 60% percent unaware of their condition. Thyroid hormone is one of the key hormone regulators of energy metabolism, while diabetes mellitus (DM) is a disorder of dysregulated fuel metabolism. Thus, thyroid hormone can affect glucose metabolism. Unfortunately, this area has received little attention over the past few decades. This study investigates the rate of undiagnosed DM in relation to thyroid function. A representative and noninstitutionalized US adult (aged 20 years or older with BMI available) population from the National Health and Nutrition Examination Survey 2007-2012 was used for this study. Subjects with known thyroid diseases and/or diabetes were excluded. This study only included subjects with available TSH, free T4 (FT4), and free T3 (FT3) levels and the defined status of glucose tolerance by HbA1c, fasting, and/or 2-hour post-challenge plasma glucose concentrations (n=6,843). The rates of previously undiagnosed DM were determined for each quintile of TSH, FT4, and FT3 with sample-weighted analysis. The adjusted odds ratio (AOD) with a 95% confidence interval (95%CI) for DM was calculated with the lowest quintile as a reference after consideration of age, gender, BMI, and racial/ethnic groups. Amongst 6,834 subjects in this study, DM was found in 488 subjects. The rates of DM from quintile 1 to quintile 5 were 3.37%, 3.95%, 3.84%, 6.42%, and 7.26 % for TSH quintiles (P<0.0001 by ANOVA); 5.69%, 4.27%, 5.05%, 4.74%, and 6.46% for FT4 quintiles (P<0.0001 by ANOVA); and 4.82%, 4.63%, 5.33%, 5.33%, and 4.93% for FT3 quintiles (P<0.0001 by ANOVA). Although the correlations were imperfect among TSH, FT4, and FT3 quintiles, the U-shaped relationship of DM with thyroid function was confirmed by the lowest AOD of 0.80 (95%CI: 0.80 - 0.80, P<0.0001) for the 3rd quintile of TSH (TSH: 1.321 - 1.771 mIU/L). The association of DM with low thyroid function was confirmed by the AOD of 1.31 (95%CI: 1.30 - 1.32, P<0.0001) for the 5th quintile of TSH (TSH: 2.519 - 80.968 mIU/L). The association of DM with high thyroid function was confirmed by AOD of 2.45 (95%CI: 2.44 - 2.46, P<0.0001) for the 5th quintile of FT3 (FT3: 3.51 - 28.82 pg/mL). FT4 confirmed the U-shaped relationship with the highest AOD of 1.07 (95%CI: 1.07 - 1.08, P<0.0001) for the 5th quintile of FT4 (FT4: 0.91 - 4.80 ng/mL) and the lowest AOD of 0.82 (95%CI: 0.82 - 0.82, P<0.001) for the 2nd quintile of FT4 (FT4: 0.91 - 4.80 ng/mL). Our study revealed a U-shaped relationship between the rates of undiagnosed DM with thyroid function in a representative and noninstitutionalized US adult population without a prior diagnosis of thyroid dysfunction and diabetes. Different underlying mechanisms may be responsible for the association of DM with high and low thyroid function. Further studies are required to elucidate the underlying mechanisms. Presentation: Thursday, June 15, 2023

FRI502 Myxedema Coma With An Unusual Pattern Of Thyroid Function Tests Due To Amiodarone-induced Hypothyroidism

Abstract Disclosure: S. Nguyen: None. B. Force: None. R. Schneider Aguirre: None. Introduction: Myxedema coma is an endocrine emergency characterized by severe hypothyroidism resulting in altered mental status or coma, hypothermia, cardiovascular compromise, pulmonary edema or pleural effusions, and/or gastrointestinal hypomotility, classically in the context of an elevated TSH and low thyroxine levels. Amiodarone use is associated with alteration of thyroid function tests and could cloud the laboratory presentation of myxedema coma. Here we present a case of myxedema coma in a patient with amiodarone-induced hypothyroidism with an elevated free T4 (FT4) and low total T3 (TT3). Clinical Case: A 64-year-old female with a history of chronic systolic heart failure, persistent atrial flutter treated with amiodarone, cerebrovascular accident, hypertension, chronic kidney disease stage 4, but not hypothyroidism, presented with constipation, confusion and lethargy worsening over 3 days. On initial evaluation, she was minimally responsive, hypothermic to 95.6 °F and bradycardic to low 50s. She was intubated for airway protection and vasopressors were started due to concern for cardiogenic shock. Exam was notable for coarse facial features, edema and cold extremities. A bedside echocardiogram showed reduced cardiac function from baseline. Her TSH was 40.65 uIU/mL (RR, 0.45-5.33 uIU/mL), FT4 1.79 ng/dL (RR 0.64-1.42 ng/dL), total T4 14.30 mcg/dL (RR 6.09-12.23 mcg/dL), TT3 70 ng/dL (RR 87-178 70 ng/dL). Sodium was 135 mmol/L (RR 136-145 mmol/L), serum glucose was 42 mg/dL, (RR 70-110 mg/dL), and eGFR was 18 mL/min/1.73 m2 (baseline eGFR 28 mL/min/1.73 m2). Evaluations for myocardial infarction and infectious etiology were initiated and ultimately negative. While elevated FT4 is not characteristic of myxedema coma, the overall constellation of stupor, constipation, bradycardia, hyponatremia, hypoglycemia, decreased eGFR and decreased cardiac function, in the setting of an elevated TSH and low TT3, made the diagnosis of myxedema coma extremely likely. The patient was started on levothyroxine 200 mcg IV daily and hydrocortisone 100 mg IV every 8 hours. After 16-20 hours on this regimen, the patient was weaned off sedation and vasopressors, extubated, and recovered baseline mental status. Hydrocortisone was stopped and on day 3 of hospitalization, she was transitioned to oral levothyroxine 88 mcg daily. Due to premature ventricular contractions her dose was decreased to 50 mcg orally daily five days after her initial presentation to the hospital. During this time, the TSH decreased to 3.59 uIU/mL and the FT4 rose to 2.83 ng/dL. Conclusion: We conclude that in patients treated with amiodarone, myxedema coma can still occur even if T4 levels are normal or elevated, likely due to decreased T4 to T3 conversion. In these cases, elevated TSH and a clinical picture consistent with severe hypothyroidism are more reliable indicators if the (free) T4 levels are unexpectedly elevated. Presentation: Friday, June 16, 2023

FRI475 The Impact Of Suppression Of Androgen Signaling On Thyroid Hormone Homeostasis In Prostate Cancer Patients

Abstract Disclosure: K. David: None. G. Devos: None. W. Devlies: None. N. Narinx: None. L. Antonio: None. L. Deboel: None. D. Schollaert: None. D.M. Vanderschueren: None. F.A. Claessens: None. S. Joniau: None. B. Decallonne: None. Next to the classical androgen deprivation therapy (ADT) with GnRH-(ant)agonists, androgen receptor signaling inhibitors (ARSIs) such as apalutamide (APA) have become available for the treatment of prostate cancer (PC) patients in the last years. Hypothyroidism was more frequent in APA-treated patients compared to placebo in the SPARTAN trial (NCT01946204) (8.1% vs 2%). We collected serum of PC patients included in a RCT (ARNEO; NCT03080116) before and after 12 weeks of neo-adjuvant ADT (GnRH-antagonist degarelix (DGX) with APA or placebo). We aimed to explore changes in thyroid homeostasis under deep androgen suppression with combined GnRH-antagonist and ARSI. Of the 88 patients ending the trial, 1 was excluded because of history of hypothyroidism for which he received levothyroxine. 43 and 44 patients were included in the DGX+placebo and DGX+APA group, respectively. Mean age was 66.3y. Sex steroid levels measured by LC-MS/MS decreased significantly to castrate range with median testosterone 10.5 ng/dL and estradiol 3.6 ng/L. TSH levels increased in both treatment groups, but more pronounced in the DGX+APA group (DGX+placebo before: 1.18 mIU/L and after: 1.33 mIU/L, p 0.0351 vs. DGX+APA before: 1.07 mIU/L and after: 1.87 mIU/L, p <0.0001; difference between groups after treatment: p <0.0001). Free T4 and total T4 levels decreased in the DGX+APA group, but remained unaltered in the DGX+placebo group (free T4 after: 16.53 vs 13.87 pmol/L, p<0.0001 and total T4 after: 8.77 vs. 7.78 µg/dL, p 0.0055). Total T3 and free T3 increased in the DGX+APA group, and again did not differ after treatment in the DGX+placebo group. (free T3 after: 5.03 vs 5.41 pmol/L, p 0.0066 and total T3 after: 132.30 vs 149.50 ng/dL, p 0.0003). As a result, the total and free T3/T4 ratio increased in the DGX+APA group with 32% and 35%, respectively. Reverse T3 decreased in both treatment arms, but greater in the DGX+APA group (19.55 vs 14.20 ng/dL, p 0.0157). Thyroxine binding globulin (TBG) increased in both treatment arms, with 6.9% and 8.4%, respectively. In conclusion, interference with androgen signaling alters thyroid homeostasis in PC patients, and is most pronounced under deep androgen suppression with combined GnRH-antagonist and ARSI therapy. The increase in T3 and decrease in rT3 may indicate additional effects of ARSI on deiodinase activity. Longer follow-up trials are needed to confirm these findings and assess the clinical implications of these changes in thyroid homeostasis. Presentation: Friday, June 16, 2023

THU654 The Use Of Plasmapheresis In A Severe Case Of Amiodarone Induced Thyrotoxicosis

Abstract Disclosure: T. Moazezi: None. C. Koh: None. Thyroid storm is an endocrine emergency that results in a hypermetabolic state due to excess levels of circulating thyroid hormone and carries a high mortality rate. Therapeutic plasma exchange (TPE) can be used in cases of thyrotoxicosis refractory to medical management to achieve hemodynamic and clinical stability. We present a case of a 74-year-old male with severe amiodarone-induced thyrotoxicosis who presented with altered mentation and ultimately required intubation and intensive care for management of thyroid storm. Standard medical therapy for treatment was initiated immediately with antithyroid drugs, beta blockers, glucocorticoids, potassium iodide solution, and cholestyramine. However, the patient remained unresponsive and intubated with worsening biochemical parameters with increased total T3 levels and sustained elevated levels of free T4 even after five days of maximal medical therapy. Due to the lack of a clinical and biochemical response to conventional medical therapy, the patient was started on plasmapheresis and underwent a total of seven cycles of plasmapheresis over a period of ten days. He significantly improved with TPE and was successfully bridged to a total thyroidectomy, which was completed without complications. Our case demonstrated a decrease in total T3 concentration of roughly 45% after one session of plasmapheresis and roughly 76% with seven sessions of plasmapheresis by the time of thyroidectomy. Free T4 levels remained elevated above reference range until the day after the fifth session of plasmapheresis. This case is important because the literature surrounding the use of TPE in thyroid storm is sparse, and there have only been case reports and retrospective studies published on the subject. Ultimately, while TPE is not conventionally used as part of routine treatment for thyroid storm, endocrinologists should keep this tool at the forefront of their management strategies to deliver quicker treatment to critically ill patients and prevent complications of thyroid storm. Nonetheless, more research is needed to delineate concrete guidelines and specific protocols for use of TPE in thyroid storm. Presentation: Thursday, June 15, 2023

FRI496 A Rare Case Of Thyroid Hormone Resistance Beta

Abstract Disclosure: H.K. Rai: None. R.M. Pradhan: None. A. Chaudhuri: None. Background: Genetic mutation in the thyroid hormone receptor leads to the reduced affinity of hormone binding; thus, causing thyroid hormone resistance. It is characterized by a wide range of phenotypic variations and subsequent diagnostic and treatment challenges. Here, we present a case of resistance to the thyroid hormone Beta, with a rare genetic abnormality, that was misdiagnosed as hyperthyroidism. Case: A 46-year-old woman diagnosed with hyperthyroidism s/p RAIA resulting in hypothyroidism on levothyroxine therapy (112mcg daily, weight: 55kg), presented with ten pounds of weight gain, constipation, and cold intolerance for the past six months. TFTs were as follows: TSH: 6.493 mcUnits/ml (normal: 0.400-5.00 mcUnits/ml), and free T4: 1.83 ng/dL (normal: 0.80-1.80 ng/dL). The patient was clinically hypothyroid despite having an elevated FT4 and TSH level. She was also on metoprolol succinate 25 mg daily for sinus tachycardia for the past 1 year. Upon inquiring about further details, the patient informed that at the age of 22, she had significant weight loss, palpitations, and anxiety, but also reported dry skin. The patient was seen by multiple endocrinologists and was provided with contradictory diagnoses. She had RAI scan which was significant for increased uptake and subsequently underwent RAIA. The patient was seen by multiple physicians in the past, levothyroxine dose was adjusted on various occasions but her TFTs never normalized. Post-ablation, she continued to require a higher than the weight-based dose of levothyroxine. Upon review of family history, the patient reported that her father, sister, and daughter had a similar pattern of TFTs with elevated FT4 and TSH values. All of them had palpitations and anxiety that were not severe enough to seek medical care. Family history was also significant for ADHD and hyperlipidemia present in the daughter and father. All affected family members have short stature. The levothyroxine dose was slowly titrated based on the clinical presentation. She was euthyroid with 150 mcg daily of levothyroxine with TSH of 4.869 mcUnits/ml and free T4: 1.85 ng/dl. Given her presentation and suspicion of thyroid hormone resistance, we decided to proceed with genetic testing. The result was positive for the THRB (Resistance to thyroid hormone beta) variant c.904A>G.p.(IIe302Val), which is classified as a variant of uncertain significance, as there is currently insufficient evidence to support its disease-causing role. However, there is a strong association between the gene and the patient's phenotype. Conclusion: The distinctive feature of RTH beta is high levels of free T4 while TSH concentration is normal or elevated, with a combination of hypothyroid and hyperthyroid symptoms. Such patients are often misdiagnosed. We herein describe a novel pathogenic RTH beta gene variant causing thyroid hormone resistance that needs to be further explored. Presentation: Friday, June 16, 2023

THU230 Consumptive Hypothyroidism Secondary To Hemangioma

Abstract Disclosure: R. Thirunagari: None. D. Taha: None. Background: Peripheral Hypothyroidism also known as consumptive hypothyroidism has been rarely described in association with vascular tumors such as hemangiomas. It is due to excessive production of type 3 iodothyronine deiodinase (D3) enzyme by the hemangioma leading to increased rate of deiodination of T4 and T3 to inactive forms. Clinical case: We report a 4-year-old girl who was diagnosed with consumptive hypothyroidism at the age of 2 months. She was born at full term via scheduled C-section. Mother has hypothyroidism. She was admitted to NICU for respiratory distress and needed oxygen supplementation. She had a large hemangioma covering most of her back on exam. An ultrasound of the head/neck soft tissue showed an ill-defined lobular heterogeneous mass measuring 3.4 x 1.2 x 4.5 cm, markedly hypervascular with both arterial and venous flow likely consistent with hemangioma. At follow up plastic surgery clinic she had respiratory distress which necessitated readmission to the NICU for further workup and possible initiation of Propranolol. An abdominal ultrasound showed enlargement of the right adrenal and on further dedicated ultrasound a right suprarenal lobulated mass as well as intrathoracic soft tissue mass were found. MRI of the abdomen and thorax, revealed multiple large bilateral paraspinal masses throughout the thoracic and lower cervical spine(largest measuring 3.3 x 7 x 15 cm AP) invading the neural foramen at multiple levels, and causing mass effect on the spinal cord which is displaced to the left. There was mass effect on adjacent vascular structures without significant vascular compromise. Biopsy was consistent with hemangioma. Thyroid Newborn screening result was normal. Thyroid evaluation done at 3 months age revealed, free T4 level of 1.04 ng/dL and TSH level of 11.3 µIU/mL. She was started on Levothyroxine 50 mcg daily. Reverse T3 was elevated at 139.2 ng/dl (reference range 13-107 ng/dl) 2 weeks after treatment initiation. She was initiated on propranolol and was followed up by plastic surgery and oncology. She had a very good response to Propranolol. Follow up MRI at 4 years shows almost complete resolution of the mass. She continues to be on Levothyroxine but is requiring smaller dose. Conclusion: Infantile hemangiomas can express high levels of type 3 iodothyronine deiodinase (D3), an enzyme that catalyzes the inner-ring deiodination of T4 to reverse T3 (rT3) and of T3 to 3,3'-diiiodothyronine (T2), both of which are biologically inactive. The hypothyroidism is a result of degeneration of thyroid hormones at rates that exceed the synthetic capacity of the infant's thyroid gland. Our case illustrates the importance of closely monitoring thyroid function tests in infants with large hemangiomas even if newborn thyroid screening result is normal. Some infants may require higher Levothyroxine doses than usual. Hypothyroidism usually resolves after resolution of the mass. Presentation: Thursday, June 15, 2023