Severe Hyperthyroidism Research Articles

Efficacy of tablet glucocorticoids depending on their starting dose in patients with type 2 amiodarone-induced thyrotoxicosis: a prospective randomized study

Background: Glucocorticoids are the first-line pharmacotherapy for amiodarone-induced destructive thyroiditis. Despite the availability of clinical guidelines, there is no unified approach to patient management (indications for prescription, starting dose, duration of therapy and withdrawal algorithm). The issues of dose-dependent effect of glucocorticoids, verification of factor of delayed treatment response, prediction of severity and duration of thyrotoxicosis remain unresolved. Aim: To evaluate the efficacy of various regimens of tablet glucocorticoids in patients with type 2 amiodarone-induced thyrotoxicosis. Methods: This was a prospective randomized open-label comparative controlled trial of the efficacy of two starting doses of prednisolone 30 mg (n = 22) and 60 (n = 22) mg daily. The study groups were comparable for gender (men to women ratio 2:1), age, anthropometric and main clinical and laboratory characteristics. After euthyroidism has been achieved, thyroid function was assessed twice at 1 and 2 months during the dose reduction and at 1, 3, 6, 9, and 12 months after prednisolone withdrawal. The follow up was 15 to 24 months. The efficacy of therapy was evaluated by the time to euthyroidism, thyrotoxicosis duration, rate of recurrent waves of destruction and relapses. We looked for predictors of delayed treatment response and severe and prolonged thyrotoxicosis. Results: There were no significant differences in the time to euthyroidism (Mantel-Cox log rank test 0.859), duration of thyrotoxicosis (Mantel-Cox log rank test 0.813), rate of recurrent waves of destruction (0.721) and relapses (0.464). Within 30 days of therapy, remission was obtained in 11/22 (50.0%) patients in active control group (prednisolone 30 mg) and in 12/22 (54.5%) patients in the 60 mg group. Delayed response ( 60 days) was defined by recurrent waves of destruction (RR = 34.7, 95% CI: 3.7–321.8; R² = 0.430; p = 0.002). High risk of severe thyrotoxicosis was predicted by the age ≤ 54 years (AUC 0.749 ± 0.095, 95% CI: 0.562–0.936; p = 0.038; sensitivity 71.4%, specificity 62.2%). The duration of thyrotoxicosis was associated with body mass index (B = -7.4, R = 0.481, R² = 0.0231; p = 0.024) and cumulative amiodarone dose (B = 0.4, R = 0.472, R² = 0.223; p = 0.026). A combination of adverse events (hyperglycemia, infection, proximal myopathy, change in appearance, hematomas) and their severity were more frequent in the patients who had received the 60 mg prednisolone starting dose (p = 0.014). Conclusion: Compared to lower doses, the use of high doses of glucocorticoids is associated with a greater severity of side effects and does not ensure any significant acceleration of thyrotoxicosis remission. The potential factors of unfavorable clinical course of type 2 amiodarone-induced thyrotoxicosis are age, body mass index, and cumulative dose of amiodarone.

5125 Severe Gestational Thyrotoxicosis Leading to Unwarranted Treatment

Abstract Disclosure: C. Bell: None. L.A. Barbour: None. Introduction: Gestational transient thyrotoxicosis (GTT) is the most common cause of thyrotoxicosis in pregnancy yet is often confused with Graves’. Although usually mild, we present a severe case leading to the unsupported use of anti-thyroid drugs (ATDs), which could have resulted in fetal hypothyroidism if continued. Case: A 30-year-old female G1P0 at 10 wks with a single gestation presented with 4 wks of vomiting, palpitations, and weight loss. She had no history of thyroid disease. She was diaphoretic and ill-appearing and had a non-tender, smooth normal-sized thyroid, a stare without exophthalmos, and a fine tremor. TSH was < 0.01, FT4 5.57 ng/dL (0.89-1.76), and TT3 201 ng/dL (60-181). TPO Ab 51 (< 60). TRAb, TSI Ab, and TgAb were negative. β-hCG level was 334,106 mIU/mL. She was diagnosed with GTT and briefly hospitalized for dehydration but was re-hospitalized 2 wks later with worsening symptoms and 25 lb weight loss. Unexpectedly, her FT4 and TT3 rose to 6.24 ng/dL and 339, respectively. A thyroid ultrasound showed mildly increased vascularity. PTU was started for seronegative Graves’ at 50 mg tid with metoprolol. After 3 days, her FT4 improved to 3.59 ng/dL and TT3 was 176. Further consultation recommended stopping PTU. She was sent home with metoprolol. Her symptoms and FT4 levels improved. FT4 was normal and hCG levels dropped to 54,821 by 18 wks. Discussion: GTT is caused by a transient elevation in T4 due to direct hCG stimulation of the TSH receptor. It is more common with multiple or molar gestations and hyperemesis gravidarum, also mediated by hCG. It typically results in mild thyrotoxicosis, highlighting the uniqueness of this case. Only a couple of case reports exist where GTT presented as severe thyrotoxicosis or thyroid storm and persisted this long. It is critical to distinguish GTT from Graves’ given their different outcomes and treatment. GTT is commonly misdiagnosed as Graves’ as both result in thyrotoxic labs and symptoms and can present in 1st trimester. GTT typically presents at 8-10 wks and lasts until 14-16 wks when hCG levels fall, but Graves’ may also improve by 2nd trimester due to the immune suppression of pregnancy. It is also possible for both to co-exist. hCG levels >100,000 are associated with GTT but due to the variable sialylation of hCG, which changes its affinity to the TSH receptor and half-life, they are unreliable diagnostically. Key clues supporting GTT include no goiter, exophthalmos, or symptoms pre-pregnancy, negative TRAb and TSI, and, notably, a lower T3/T4 ratio compared to Graves’, as seen in this case. To conclude, GTT is often mistaken for Graves’ but inappropriate use of ATDs can result in fetal hypothyroidism and does not improve outcomes. Although the severity of our case is unusual, accurate distinction from Graves’ by endocrinologists is crucial to ensure optimal maternal-fetal outcomes. Presentation: 6/1/2024

8113 Thyroid Storm in a Patient with Thyroid Nodule on Anticoagulation

Abstract Disclosure: R. Kulkarni: None. S.S. Krishnasamy: None. N. Mon: None. R. Downs: None. Background: There are very few case reports related to hyperthyroidism due to anticoagulation use. We describe a case, of a less common cause of hyperthyroidism due to hemorrhagic thyroiditis in a patient on anticoagulation and history of metastatic colon cancer. Clinical case: A 67-year-old white male with PMH significant for colon cancer with liver metastasis s/p exploratory laparotomy with sigmoid colectomy, end-colostomy with Hartman's pouch creation, pre-diabetes, recent left IJ & axillary vein thrombus on Eliquis, and thyroid nodule; presented with complaints of shortness of breath, difficulty swallowing and dizziness. Other symptoms included weight loss, complaints of heart racing and generalized body aches. The patient had a recent admission for similar complaints and was newly diagnosed with left IJ/axillary vein thrombus and expanding hemorrhagic thyroid nodule on imaging. He was discharged on anticoagulation for the DVT with 2 week follow up for elective thyroidectomy for goiter. The patient was admitted to the ICU for worsened respiratory status needing ventilatory support and pressor support. Physical findings on admission included jaundice, sinus tachycardia, lethargy with agitation. Initial labs showed TSH 0.02 uIU/mL, FT4 4.85 ng/dL and FT3 6.8 pg/mL, LFTs >500 U/L. Burch-Wartofsky Point Scale score was >60 suggestive of thyroid storm. Imaging with PET CT was concerning for thyroid enlargement with multiple nodules with increased uptake. Thyroid US was consistent with heterogenous gland with hemorrhagic nodules. Based on clinical history, physical findings, diagnostic labs, and imaging the patient was diagnosed with severe hyperthyroidism with thyroid storm secondary to hemorrhagic thyroid nodules in the setting of anticoagulation. The patient underwent thyroid artery angiogram with particle embolization of left inferior and right superior thyroid arteries. Endocrinology started the patient on methylprednisolone, cholestyramine and propranolol. Thionamide was held since the patient had abnormal liver function tests in the setting of shock liver. The patient’s thyroid function slowly improved on current regimen to TSH 0.05 uIU/mL, FT4 1.7 ng/Dl and FT3 4.1 pg/mL on day 3. At the family interdisciplinary meeting, due to guarded prognosis, family opted for comfort care, and the patient finally succumbed to multiple co-morbidities. Conclusion: The case presented discusses diagnosis and management of less common causes of hyperthyroidism and management of thyroid storm in liver dysfunction. The patient would have needed a thyroid biopsy at a later date to rule out colonic metastasis as a cause of hemorrhage if he had survived the thyroid storm and comorbid illnesses. Presentation: 6/3/2024

8557 Osteitis Fibrosa Cystica as the Initial Manifestation of Severe Primary Hyperparathyroidism: A Case Report

Abstract Disclosure: L.A. Robles Gomez: None. G. Gill: None. A. Vincent, DO: None. A. Mahmoud, MD: None. Introduction: Osteitis fibrosa cystica (OFC) is a pathognomonic yet uncommon finding of hyperparathyroidism seen in less than 2% of patients with primary hyperparathyroidism in Western countries. We present a case of infrequent finding of late-stage severe hyperthyroidism with asymptomatic hypercalcemia and incidental findings of osteolytic bone lesions. Clinical Case: A 28-year-old female with a history of PCOS, fatigue, and chronic abdominal pain presents to the clinic after recent work-up during an ED visit demonstrated incidental findings of osteolytic bone lesions in the setting of mild hypercalcemia. Physical examination was relatively unremarkable except for mild tenderness to palpation on the right lower quadrant. Laboratory significant calcium 10.7 mg/dl (8.6-10.2 mg/dL), albumin 3.6 g/dL, Creatinine 0.56 mg/dL, GFR 127 mL/min, Alkaline phosphatase 187 IU/L (37-127 IU/L), AST 24 IU/L, ALT 45 IU/L, Intact PTH and calcium: PTH 413 pg/mL (15-65 pg/mL), Calcium 11.5 (8.7-10.4 mg/dL), Bone Specific Alkaline Phosphatase: 54.5 mcg/L (4.7-17.8 mcg/L), Phosphorus 2.1 mg/dL (2.4-4.8 mg/dL), Magnesium 1.7 mg/dL (1.5-2.5 mg/dL), Vitamin D 25 10 mg/mL (20-100 ng/mL), TSH 2.12 uIU/mL (0.46-5.05 uIU/mL). CT abdomen pelvis w/o contrast with multiple predominantly lytic expansile bone lesions, mainly in the pelvis, with the most extensive 6.2 cm lesion in the superior, posterior right ilium, the anterior acetabulum, and the posterior right ischium. A prior CT done in 2018 showed a similar distribution of lytic lesions. The patient denied any previous personal or family history of hypercalcemia or parathyroid abnormalities despite a review of prior outside records revealed abnormal labs dating back to 2018 with intact PTH 406 pg/mL, calcium 10.3 mg/dL, Ionized calcium 10.7 mg/dl (3.30-6.0 mg/dL), albumin 3.3g/dL, alkaline phosphatase 288 IU/L. The patient denied prior symptomatology of hypercalcemia, including renal stones, or prior treatment for hypercalcemia. Further work-up was ordered, and the patient was referred to endocrine surgery for management. Conclusion: Osteitis fibrosa cystica (OFC) has become a rare manifestation of primary hyperparathyroidism (PHPT) due to early diagnosis of hypercalcemia by routine lab monitoring. Skeletal findings typically seen on PHPT can vary from bone reabsorption-acroosteolysis, subchondral bone resorption, brown tumors, salt-and-pepper skull, and osteopenia. Subchondral reabsorption around specific joints commonly affects pubic symphysis and sacroiliac joints, as seen in our patient. The mechanism is due to PTH-mediated osteoclastic absorption of bone and surrounding cartilage. Due to the rare presentation of PHPT with associated osteitis fibrosa cystica, diagnosis requires a high degree of clinical suspicion, as delayed diagnosis can lead to avoided manifestation, as described by our report. Presentation: 6/3/2024

Patients with graves' disease have more severe biochemical thyrotoxicosis and develop higher rates of post radioiodine hypothyroidism than those with nodular disease

Patients with graves' disease have more severe biochemical thyrotoxicosis and develop higher rates of post radioiodine hypothyroidism than those with nodular disease

Therapeutic plasma exchange as a bridge to radioactive iodine treatment in a patient with severe thyrotoxicosis and serious adverse effects to antithyroid drugs: a case report

Therapeutic plasma exchange as a bridge to radioactive iodine treatment in a patient with severe thyrotoxicosis and serious adverse effects to antithyroid drugs: a case report

A Comprehensive Overview of a Rare Case of Type 2 Autoimmune Polyglandular Syndrome

Introduction: Polyglandular deficiency syndromes reflects a wide spectrum of disorders. Autoimmune polyglandular syndrome (APS) is a rare condition generally divided into two categories APS -1 and APS -2.  Case Report: We report a case of APS-2 in a 28 years old male with marfanoid habitus, presented with significant weight loss, fever and hemoptysis. upon examination, he had exophthalmos, pallor, marfanoid habitus with systolic murmur in all cardiac areas and coarse crepitation in left hemithorax. Laboratory evaluation revealed left upper lobe pneumonia secondary to Acinetobacter. Further evaluation revealed severe hyperthyroidism, anti TPO, TRAB antibody was elevated, megaloblastic anemia with atrophic gastritis and positive 21 alpha hydroxylase.  Diagnosis: The above findings were consistent with the diagnosis of APS type 2 (Graves’ Disease, Adrenal Insufficiency, Pernicious Anaemia, Vitiligo). The presence of two or more endocrine deficiencies defines APS-2 which may include graves’ disease, type 1 Dm, primary adrenal insufficiency, hypogonadism and features like pernicious anaemia, vitiligo and alopecia.  Conclusion: Circulating antibodies may precede development of clinical disease by many years but would allow clinician to follow the patient and identify the disease onset at the earliest.

Amiodarone-induced thyrotoxicosis type 2: the role of differential diagnosis in patient management

The antiarrhythmic drug amiodarone can affect the function of the thyroid gland, contributing to the development of thyrotoxicosis or hypothyroidism. The development of thyrotoxicosis exacerbates the cardiovascular pathology present in patients: it leads to the progression of left ventricular dysfunction, recurrence of rhythm disturbances, increasing the risk of adverse outcomes. Timely diagnosis of thyrotoxicosis in the treatment of amiodarone is of fundamental importance in choosing the right therapeutic tactics, which is determined by the type of amiodarone-induced thyrotoxicosis (AmIT), the state of the cardiovascular system, and the risk of recurrent arrhythmias. In type 1 AMIT, the main method of controlling the relief of thyrotoxicosis is thyroostatic therapy with the possibility of subsequent radical treatment (radioiodine therapy, thyroidectomy). Type 2 AmIT is a self-limiting process, however, for the treatment of patients with moderate to severe amiodarone-induced thyrotoxicosis type 2, glucocorticoids are the first-line drugs. With a mixed version of AmIT, a combination of antithyroid drugs and glucocorticoids is recommended. This review presents a clinical case of a patient with type 2 AmIT who was treated with thyrostatic drugs for a long time without achieving an effect.

Adrenal decompensation precipitated by severe graves' thyrotoxicosis

Adrenal decompensation precipitated by severe graves' thyrotoxicosis

Multidisciplinary medical management of severe thyrotoxicosis with multiorgan dysfunction in pregnancy: A case report

Multidisciplinary medical management of severe thyrotoxicosis with multiorgan dysfunction in pregnancy: A case report

STEMI and Thyroid Storm: A Case Report of Thyrotoxicosis-Induced Cardiomyopathy

Thyrotoxicosis-induced cardiomyopathy is a rare but potentially fatal form of non-ischemic cardiomyopathy that warrants immediate medical intervention. A 51-year-old female with no known disease sought consultation because of severe chest pain accompanied by easy fatigability and palpitation. Upon arrival at the ED, there was persistence of chest pain accompanied by vomiting, tachycardia and hypotension. ECG showed STEMI in the lead aVR, and she eventually underwent coronary angiogram, which revealed normal coronary arteries. Ancillaries showed severe hyperthyroidism with a Burch – Wartofsky score of 50. There was an elevated NT-proBNP level, and echocardiogram showed a reduced EF of 28.7% with dilated LV and global hypokinesia. She was hooked to a norepinephrine and dobutamine drip and immediately initiated a hyperthyroid regimen, specifically methimazole, propranolol, and steroids. She was admitted to the critical care unit where initiation of SGLT-2 inhibitor and spironolactone were administered as part of the heart failure regimen. When she was out of thyroid storm, a sestamibi myocardial perfusion scan was requested, which showed normal results with improved EF. The goals of management in thyrotoxicosis-induced cardiomyopathy are early initiation of heart failure regimen, medication to prevent further ventricular remodeling, and treatment of thyroid storm. Early recognition and prompt administration of hyperthyroid treatment leads to a decreased burden of the patient’s disease and a good overall prognosis.

Emotional Stress-Induced Thyroid Storm

AbstractThyroid storm is an endocrine emergency with high mortality due to severe uncontrolled thyrotoxicosis, often associated with precipitating factors. The chance of survival will increase with early suspicion, prompt diagnosis, and immediate treatment. In this case report, we are presenting a 49-year-old female who came to the emergency department with acute pulmonary edema, agitation, severe tachycardia, high-grade fever with uncontrolled thyrotoxicosis. A diagnosis of thyroid storm was made. The patient presentation was following severe emotional stress after the passing of her mother-in-law. In the literature review, only a few cases reported as emotional stress induced thyroid storm, and we would like to present this life-threatening endocrine emergency.

Pulmonary and Systemic Hemodynamics in Patients with Hyperthyroidism

BackgroundThere is an association between hyperthyroidism and pulmonary hypertension. However, the prevalence of pulmonary hypertension in hyperthyroidism and the underlying mechanisms are incompletely defined. MethodsConsecutive patients with severe hyperthyroidism, mostly due to Graves disease, were included in this single-center study. Echocardiographic assessment of pulmonary hemodynamics was performed at the time of hyperthyroidism diagnosis (baseline) and after normalization of thyroid hormones (follow-up; median 11 months). In a subset of patients, right heart catheterization and noninvasive assessment of central hemodynamics was performed. ResultsAmong all 99 patients, 31% had pulmonary hypertension at baseline. The estimated systolic pulmonary artery pressure correlated significantly with the estimated left ventricular filling pressure (E/e′). The invasively measured systolic pulmonary artery pressure correlated well with the estimated systolic pulmonary artery pressure. Cardiac output, E/e′, left and right ventricular dimensions were significantly reduced from baseline to follow-up, whereas the estimated pulmonary vascular resistance did not differ. Diastolic blood pressure was significantly higher at follow-up, with no change in systolic blood pressure. The central systolic blood pressure, however, exhibited a trend for a reduction at follow-up, while the pulse wave velocity was significantly lower at follow-up. ConclusionsApproximately one-third of patients with hyperthyroidism have evidence of pulmonary hypertension. Our data suggest that an increased cardiac output and left ventricular filling pressure are the main mechanisms underlying the elevated systolic pulmonary artery pressure in hyperthyroidism, whereas there is no evidence of significant pulmonary vascular disease.

A Rare Case of Painless Destructive Thyroiditis Resulting in Thyroid Storm.

Thyroid storm is a life-threatening clinical condition that is usually triggered by untreated or interrupted treatment of Graves' disease, leading to the sudden onset of severe thyrotoxicosis, which requires an immediate diagnosis and treatment based on diagnostic criteria. Cases of thyroid storm caused by painless/painless subacute thyroiditis are very rare. We herein report an 85-year-old man with features of severe thyrotoxicosis caused by painless/painless subacute thyroiditis who had no uptake of 99mTcO4 and was negative for thyroid-stimulating hormone receptor antibodies. In thyroid storm patients in whom the findings are inconsistent with Graves' disease, careful follow-up and management are necessary, assuming the possibility of painless or painless subacute thyroiditis.

Abstract 17328: A Case of Reversible Severe Systolic Cardiomyopathy; Thinking Outside the Box

Introduction: Non-ischemic systolic cardiomyopathy is associated with significant morbidity and mortality. Prompt evaluation and timely removal of the potential insult may lead to reverse remodeling and recovery of the left ventricular (LV) systolic function. Case: A 39-year-old female with BMI 40 presented with dyspnea and bilateral lower extremity edema. Vital signs significant for mild tachycardia and hypertension. ECG showed sinus tachycardia. Physical exam revealed bibasilar crackles and 3+ pitting edema of the lower extremities. Laboratory significant for NTpro BNP 563 pg/dL and TSH <0.005 IU/mL with a free T4 of 2.73 ng/dL. Chest x-ray showed pulmonary vascular congestion. Echocardiogram showed severely reduced LV systolic function with ejection fraction (EF) of 27%, global LV hypokinesis and diastolic LV diameter of 6.85 cm. No significant atrial or ventricular arrhythmias noted on Telemetry. A CT angiography of the coronary arteries showed no evidence of calcification or obstructive coronary disease. Additional labs revealed severely elevated TSH receptor antibody and thyroid stimulating immunoglobulin. Diffuse thyroid enlargement noted on ultrasound. Patient was diagnosed with Grave’s disease (GD) with Burch-Wartofsky score of 30 indicating an impending thyroid storm. She was treated with Metoprolol and Methimazole. She underwent intravenous diuresis and was started on guideline-directed medical therapy for systolic cardiomyopathy. In follow-up after 6 months, her TSH had normalized. On repeat imaging, her LVEF improved to > 50% with diastolic LV diameter of 5.6 cm. Discussion: This patient was diagnosed with non-ischemic dilated systolic cardiomyopathy due to severe hyperthyroidism from GD. Thyrotoxicosis-induced systolic cardiomyopathy occurs in about 1% of patients with GD and is associated with increased morbidity and mortality. Excess thyroid hormones in thyrotoxicosis can affect multiple regulatory and structural genes of cardiac myocytes resulting in abnormal intracellular calcium regulation and impaired LV systolic and diastolic function. Our experience is consistent with literature demonstrating the importance of timely diagnosis and treatment of this reversible cause of systolic cardiomyopathy.

Massive Cerebral Venous Sinus Thrombosis as an Unexpected Complication of Severe Hyperthyroidism

Cerebral venous sinus thrombosis (CVST) is a rare but potentially fatal neurological condition frequently associated with prothrombotic states. Identifying the underlying cause of CVST is crucial but can be challenging, especially when it is reported as uncommon. Here, we present a case of a previously healthy 31-year-old Malay man who presented with massive CVST complicated with status epilepticus and arrhythmia in the setting of undiagnosed severe hyperthyroidism. The patient subsequently improved with intensive care therapy, thyroid storm protocol treatment, and antiplatelet medications. This case highlights the need to rule in hyperthyroidism in patients with atypical neurological symptoms, particularly CVST, even in the absence of associated risk factors.

FRI570 Repatha Induced Thyroid Storm

Abstract Disclosure: L.R. Sepulveda-Garcia: None. L.N. Madera Marin: None. L. El Musa Penna: None. W. Medina-Torres: None. M.A. Ortiz-Rivera: None. A. Rosado-Burgos: None. M. Alvarado: None. M. Ramirez: None. L.A. Gonzalez-Rodriguez: None. Introduction: Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors are an effective medical therapy for lowering plasma LDL-cholesterol and enhancing the LDL-cholesterol ability of statins. In 2020, a case of transient hyperthyroidism secondary to evolocumab was reported. We present a case of impending thyroid storm after a patient received evolocumab. Patient description: 60 y/o female patient with medical history remarkable for hyperlipidemia, anti-TPO positive non-toxic multinodular goiter, hypertension, fibromyalgia, and coronary artery disease who presented with heat intolerance, palpitations, tremors, and insomnia after second dose of evolocumab. At physical exam found with tachycardia, hypertension, anxious mood, tremors, leg pitting edema +1 bilateral, and deep tendon reflexes +3 in lower extremities, although no palpable or painful goiter. Laboratories compatible with hyperthyroidism [TSH < 0.008 uIU/mL (0.3 – 3.0 uIU/mL), Free T4 4.29 ng/dL (0.89 – 1.76 ng/dL), Total T4 20.03 ug/dL (4.5-12 ug/dL)] and clinically with severe thyrotoxicosis. Patient was sent to ED for further evaluation and management. Case outcomes: Upon admission patient presented with a tonic-clonic seizure with short post ictal state. Burch-Wartofsky scale Point Scale 35, consistent with impending thyroid storm. Thyrotoxicosis management given requiring high doses of PTU, hydrocortisone and propranolol, including the need to add cholestyramine to the regime. By day 9 of therapy, patient was transitioned to methimazole 30mg daily with discontinuation of hydrocortisone and cholestyramine. Upon discharge, 2 weeks later, thyroid function tests had normalized to a FT4 of 1.39 ng/dL and a Total T4 of 9.6 ug/dL. Case discussion: A case of transient hyperthyroidism with PCSK9 inhibitor was previously reported requiring only symptomatic treatment. In this case a patient presented with severe thyrotoxicosis after she received her second dose of evolocumab. PCSK9 inhibitor therapy immunological influence on thyroid remains unknown. This case shows the importance of thyroid function test follow up in patients on PCSK9 inhibitor therapy and the possibility of immunological influence on the thyroid. Presentation: Friday, June 16, 2023

SAT488 Wolff-Chaikoff’s Revenge: There-and-Back Again Graves Thyrotoxicosis

Abstract Disclosure: A. Akofu: None. S.A. Brietzke: None. N. Sheung: None. A. Uddin: None. N. Akabogu: None. S. Dejhansathit: None. F. marium: None. Grave’s disease is due to autoantibodies activating TSH receptors, driving downstream effects of iodine organification, iodotyrosine coupling, and release of T4 and T3 from intracellular stores. Severe thyrotoxicosis is traditionally treated with high dose thionamides to block thyroid hormone synthesis, iodides to slow iodine transport and block thyroid hormone release (collectively known as the Wolff-Chaikoff effect), and beta-blockers to slow heart rate and relieve tremulousness. We report the case of a health-conscious patient who had taken OTC iodide for years, and whose thyrotoxic condition abruptly worsened with discontinuation of his iodide supplement. A 67-year-old man was found in a delirious state wandering in the woods and was taken to the hospital ED. He had afib with RVR and evidence of high-output CHF. Diffuse goiter twice normal size was obvious on exam, and he was tremulous and diaphoretic. Serum TSH was <0.005 mcU/ml, with FT4 > 7.77 ng/dl and FT3 7.8 pg/ml. Initial treatment was metoprolol 25 mg TID, propylthiouracil (PTU) 300 mg TID, cholestyramine 4g BID and Lugol’s iodine 10 drops TID. Encephalopathy resolved after 2 days and FT4 decreased to 3.72 ng/dl after 8 days. Cholestyramine and Lugol’s iodine were thus discontinued. 2 days later, FT4 further declined to 2.75 ng/dl and he was switched from PTU to methimazole 30 mg twice daily. After 3 days, FT4 had increased to 5.17 ng/dl, and in response methimazole was increased to 40 mg TID. 3 days later FT4 increased further to 6.43 ng/dl, prompting a switch from methimazole back to PTU 300 mg TID. Because of further increase in FT4 and FT3, cholestyramine and Lugol's iodine were resumed. 3 days later, FT4 had declined from > 7.7 to 5.4 ng/dl, and he was discharged with plan to perform thyroidectomy once FT4 and FT3 reached nearly normal levels. Near the end of his hospitalization, he divulged that he had taken iodide drops for “thyroid health” for many years independent of medical advice, but hadn’t taken it for several days during the period of being lost in the woods prior to admission. Possible explanations for resistance of thyrotoxicosis to aggressive prescribed treatment include medication non-adherence, drug malabsorption, hyperaccelerated drug metabolism, anti-drug antibodies and antagonism of thionamide action by excessive intrathyroidal iodine. In this case, we hypothesize that his use of iodide serendipitously attenuated severity of Graves disease, by giving him a prolonged Wolf-Chaikoff effect. Discontinuation of iodide over a matter of days allowed reversal of this phenomenon and prevented control of his hyperthyroid condition until the deliberate restoration of the Wolf-Chaikoff effect with therapeutically prescribed Lugol’s solution. Whenever response to usual hyperthyroidism treatment is ineffective or paradoxical, as in this case patients should be specifically queried regarding use of OTC iodine preparations. Presentation Date: Saturday, June 17, 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

THU662 Poor Response To Medical Treatment In A Patient With Amiodarone-induced Hyperthyroidism: A Therapeutic Dilemma

Abstract Disclosure: A.A. Asiri: None. R. Sulimani: None. W. Alkhidady: None. Introduction: Hyperthyroidism is a well-known complication of amiodarone therapy. An incidence of 3% is reported in North America1, and even higher percentages in amiodarone deplete areas of about 10%.2 Treatment of amiodarone-induced hyperthyroidism (AIH) is challenging, it depends on various factors including the type of AIH, dependence of the patient’s cardiac condition on amiodarone therapy, other complications or comorbidities of the patient such as hepatic injury or dysfunction and the response of the patient to antithyroid therapy. Clinical Case: We present a case of a 32-year-old lady with a therapeutic dilemma in treating type I AIH, resistant to medical therapy. Our patient first had acquired COVID-19-induced myocarditis in 2020 and subsequently developed sustained ventricular tachycardia and was treated with amiodarone and placed on an implantable cardioverter-defibrillators (ICD) device. Two years later in 2022, the patient developed type I amiodarone-induced hyperthyroidism, with a free T4 reaching 100 pmol/L (Reference range 15-22 pmol/L) and complicated with transaminitis. She was unresponsive to medical therapy including: anti-thyroid medications, IV high-dose hydrocortisone, potassium iodide drops, and cholestyramine. She also developed adverse events with two of the antithyroid medications, Carbimazole and PTU; where she had elevated liver enzymes more than five time upper limit of normal and a generalized skin rash with PTU. Plasmapheresis was not an option as some of her cardiac medications drug levels could be affected. She underwent an emergent total thyroidectomy with dual beta blockade (Propranolol and Sotalol) successfully without any post op events. Her T4 level normalized within 8 days of her operation and her liver enzymes normalized within 2 weeks. Conclusion: We report the success and safety of surgical management in a patient with a cardiac arrhythmia and uncontrolled severe amiodarone-induced hyperthyroidism in the setting of adequate beta blockade.