Thyroid Autoantibodies Research Articles

12233 Weight Gain Following Thyroidectomy For Benign Conditions

Abstract Disclosure: A. Krueger: None. A. Chiu: None. S. Pabich: None. S. Syed: None. A. Poloju: None. S. Holoubek: None. Background: Weight gain is a common complaint of patients with hypothyroidism irrespective of etiology that causes dissatisfaction and decreased quality. Patients often report thyroidectomy as the precipitating event leading to subsequent weight gain and resistance to weight loss. Reported data on body weight changes following surgery are conflicting and there is limited literature on patients with benign pathologies. The average weight gain in the general population has been reported as 0.5/year. The primary outcome of this study was to determine if patients undergoing thyroidectomy for benign conditions experienced greater than expected weight gain compared to the general population when TSH values were controlled. Secondary outcomes assessed were whether pre-operative disease pathology or antibody status affected weight changes. Methods: A retrospective review was performed on 325 patients undergoing total thyroidectomy for benign conditions from January 2015 to December 2020 using the University of Wisconsin Thyroid Surgery Database. The weight change was determined from the time of surgery to the following intervals: 1-2 years, 2-5 years, and >5 years. Study groups were then compared by pathology and presence of antibodies. Exclusion criteria included age <18 years, thyroid cancer, pregnancy within one-year post-surgery, incomplete weight or TSH data, post-operative gastric-bypass surgery, and patients who were not euthyroid pre- and post-op. Results: Our patient population (n=219) gained a mean of 1.58 kg at the 1-2 year interval. There was no significant difference in weight gain based on pathology or antibody status. At the 2-5 year interval, the average weight gain was 2.05 kg and those with antibodies had significantly higher weight gain. Patients with TPO antibodies (n=34) gained a mean weight of 4.58 kg, and those with TRAB and or TSI antibodies (n=17) gained a mean weight of 4.67 kg. Those with both types of antibodies (n=10) did not have any significant weight gain. Conclusion: Conservatively, the expected weight gain of the general population over 2-5 years is 2.5 kg. Using a logistic regression model, patients with autoimmune thyroid disease had twice the odds of gaining more weight than expected by 2-5 years. The presence of auto-immune thyroid antibodies may serve as a target population for intensive weight management programs following surgery. Presentation: 6/1/2024

12511 Rhabdomyolysis Related Acute Kidney Injury Presenting as First Manifestation of Autoimmune Hypothyroidism: A Case Report

Abstract Disclosure: A. Tiwari: None. S. Mantravadi: None. N. Doshi: None. A. Dabaja: None. C. Saad: None. Introduction: Autoimmune thyroiditis is the predominant cause of primary hypothyroidism, with an incidence of estimated 0.3-1.5 cases per 1000 people, with female to male predominance of 7-10[1]. Hypothyroid myopathy affects 79 % of the affected population. Its common presentation is fatigue and cramp but in rare instances rhabdomyolysis can occur with trivial triggers like alcohol, exercise2, Case Presentation: A 32-year-old male with no significant medical history, presented with generalized weakness, myalgia, and facial puffiness for last three months. The patient engaged in regular-intensity workouts and reported consuming 12 beers several times a week for past 5 years. Physical examination revealed facial puffiness and proximal muscle weakness. Initial Laboratory findings showed elevated creatinine (1.68 mg/dL, baseline 1.0 mg/dL in April 2020), CK (8113 U/L), AST (260 U/L), ALT (129 U/L). Urinalysis revealed hematuria and mild proteinuria. Serum electrolytes were unremarkable. Abdominal ultrasound showed diffuse hepatic steatosis with normal kidney appearance. This could not explain the reason for the Acute Kidney Injury and further workup showed TSH (>150 mIU/L) and TPO antibodies (197.9 U/mL). Autoimmune panel was unremarkable. Thyroid ultrasound done subsequently revealed a markedly heterogeneous gland. Treatment included parenteral crystalloids, low-dose prednisone which was empirically added for suspected autoimmune myositis and was later discontinued once the autoimmune panel was negative, and Levothyroxine at the recommended dose. At the time of discharge, his creatinine was reduced to 1.33 mg/dL and CK to 2,298 U/L. Discussion: Severe rhabdomyolysis is a rare but significant complication of autoimmune thyroiditis, potentially leading to acute kidney injury (AKI) if not promptly diagnosed and treated. Resident physicians often attribute symptoms like myalgia and generalized weakness in males to clear evident rhabdomyolysis if they find a cause like alcohol consumption and exercise, potentially overlooking the actual etiology. We recommend thyroid workup in such patients to promptly detect and manage underlying etiology predisposing to muscle damage and subsequent kidney injury. Our patient never had any Physician encounter as his prior medical history was unremarkable, however we suggest thorough family history and thyroid profile should be a part of outpatient workup as well for patients who show other risk factors for rhabdomyolysis like daily alcohol consumption, vigorous workout, consume medications like HMG CoA inhibitors, antipsychotics etc. Presentation: 6/3/2024

8705 Autoimmune Polyglandular Syndrome Type 2 Presenting As Recurrent Cardiac Tamponade

Abstract Disclosure: E.M. Niedzialkowska: None. D. Shelden: None. Introduction: Autoimmune polyglandular syndrome type 2 (APS2) is a rare endocrinopathy with co-occurrence of autoimmune adrenal insufficiency, autoimmune thyroiditis and/or type 1 diabetes. In rare cases, APS2 can predispose patients to recurrent pericardial effusion and tamponade. Case presentation: 32 y.o male with medical history of hypothyroidism on replacement therapy diagnosed 2 weeks prior to admission presented with progressive dyspnea and hypotension. The patient was found to have pericardial effusion with tamponade requiring pressor support. Initial lab tests showed TSH 148.7 uIU/ml (N 0.4-4.5), free t4 0.7 ng/dl(N 0.7-1.5 ), free t3 2 pg/ml (N 1.7-3.5), Hb a1c 4.7% (N <5.6%), thyroglobulin antibody 851 IU/ml (N <20), TPO antibody >1 000 IU/ml (N<=35), TSI 0.1 IU/l (<0.1), sodium 127 mmol/l (N 135-145), and a negative adrenal antibody panel. The patient was started on IV levothyroxine (400 mcg daily) and stress dose steroids in the setting of shock requiring 4 pressors. Shock resolved after pericardiocentesis and the patient was weaned off pressor support. Pericardial fluid showed neutrophil predominance and was negative for an infectious process, lab tests showed negative ANA, ANCA and GBM. The day following admission lab tests showed TSH of 23.86 uIU/ml, ft4 1.3 ng/dl, the patient was transitioned to oral levothyroxine 125 mcg and the steroid regimen was tapered and discontinued. Follow up tests showed normal TSH and resolution of pericardial effusion. Four weeks after initial admission the patient was readmitted due to hypotension. Laboratory tests showed random cortisol <1.0 ug/dl (N 2.9-19.4), ACTH 17 pg/ml (N 6-48), adrenal antibody titers 1:20 (N < 1:10), cosyntropin stimulation test was positive for adrenal insufficiency and the patient was started on steroid regimen with symptomatic improvement. He was diagnosed with APS type 2 based on his constellation of endocrinopathies. Repeat echocardiogram was negative for pericardial effusion. Two months later, the patient presented with chest pain. Imaging was positive for recurrent pericardial effusion requiring pressor support and pericardiocentesis. The patient was subsequently started on colchicine. Infectious and rheumatologic workup continued to be negative. The patient did not exhibit symptoms of connective tissue disease. Seven months after the initial presentation the patient was readmitted with COVID-19 infection complicated by hypotension and a small pericardial effusion. Symptoms improved after initiation of stress dose steroids. Conclusion: Cardiac tamponade is a rare presentation of APS2 with 9 cases reported in the literature up to date. Increased incidence of pericardial effusion is presumed to be a result of autoimmune inflammation leading to fluid accumulation. The patients are prone to tamponade due to intravascular volume depletion, decreased vascular tone and impaired stress response. Presentation: 6/3/2024

6781 A Rare Case of Diffuse Large B Cell Lymphoma of the Thyroid

Abstract Disclosure: D. Deyar: None. M. Herrera: None. M. Ahmad: None. P. Ucciferro: None. Introduction: Primary thyroid lymphoma (PTL) is rare, comprising less than 5% of thyroid cancers. It is frequently seen in middle-aged women and 1.5% of patients with Hashimoto’s thyroiditis. PTL may present with rapidly growing mass, dysphagia, stridor, or hoarseness. We describe a case of a female patient presenting with a neck mass and new onset hypothyroidism who was found to have DLBCL of the thyroid. We aim to raise clinical awareness regarding PTL and elucidate its association with Hashimoto’s disease and discuss treatment strategies. Case presentation: The patient was a 62-year-old female with a past medical history of type 2 diabetes, hypertension, and hyperlipidemia, presenting for worsening neck swelling for the past four weeks. She reported tenderness around the mass along with voice hoarseness and difficulty swallowing. She also reported increased shortness of breath associated with the mass while lying flat and denied any heat intolerance, cold intolerance, weight changes or bowel habit changes. The patient’s vitals were as follows: blood pressure: 146/104 mmHg, heart rate: 58 beats per minute, temperature: 36.3 C, respiratory rate: 20 breaths per minute. Initial blood work demonstrated the following: sodium: 137 mmol/L, potassium: 4.2 mmol/L, 9.4 mg/dL, white blood cell count: 12.1 × 109/L, hemoglobin: 14.5 g/dL, platelets: 330 × 109/L, thyroid stimulating hormone: 17.1 uIU/mL, free T4: 0.4 ng/dL, and TPO antibodies: 300 IU/mL. A CT scan of her neck demonstrated a left sided mass measuring 6.6 cm, by 5.6 cm, by 11 cm. The patient was started on 50 mcg of levothyroxine and was assessed by otorhinolaryngology and underwent fine needle aspiration biopsy. The patient’s biopsy demonstrated diffuse large B cell lymphoma of the thyroid gland. The patient was started on R-CHOP chemotherapy for her lymphoma as an outpatient and had a significant decrease in the size of her neck mass and improvement in her compressive symptoms. She is scheduled for six cycles of R-CHOP therapy and continues to follow with oncology. Discussion: Diffuse Large B Cell Lymphoma (DLBCL) of the thyroid is rare and necessitates distinct therapeutic considerations. Patients with Hashimoto's thyroiditis have been found to be 60-fold times more likely to develop primary thyroid lymphoma as compared to those without thyroiditis. The pathophysiology regarding this association remains unclear, however some suggest it may be due to chronic lymphocytic inflammation of the thyroid gland leading to monoclonal lymphocyte growth. Treatment of DLBCL of the thyroid requires immunotherapy, most commonly with the R-CHOP therapy which distinguishes it from the conventional management of thyroid carcinomas. Physicians should be vigilant in considering these treatment differences and to consider PTL as an etiology of growing thyroid mass in patients with Hashimoto’s thyroiditis. Presentation: 6/2/2024

6441 Hyperthyroidism in a patient with Lyme disease

Abstract Disclosure: J. Epstein: None. C. Berman: None. Background: Lyme disease is known to cause inflammation in many organs. There are few case reports in the literature that discuss the association between Lyme disease and thyroiditis. This case underscores the need to further research the association between Lyme disease and thyroid physiology. Clinical Case: A 15-year-old female with a history of polycystic kidney disease is referred to a pediatric endocrinologist for primary amenorrhea and hyperthyroidism. Initial thyroid function tests demonstrated suppressed TSH of 0.03 mIU/L with an elevated free T4 level of 4.0 ng/dL and total T3 of 437 ng/dL. The patient was asymptomatic with normal vital signs, and physical exam was normal without goiter, tremor, tongue fasciculations, or exophthalmos. Thyroid ultrasound demonstrated a mildly heterogenous appearance without nodules. Incidentally, Lyme disease was concurrently diagnosed based on a positive screen confirmed with immunoblot. There was no known tick exposure or rash, but the patient had recently spent time outdoors in upstate New York. Doxycycline was started for the treatment of Lyme disease and repeat thyroid tests one week later showed a decrease in free T4 and total T3 levels, although still elevated. Thyroid antibodies including thyroid peroxidase (TPO), thyroglobulin and thyroid-stimulating immunoglobulin (TSI) were negative. After finishing doxycycline treatment, she developed a hypothyroid state with a TSH of 6.39 mIU/L, free T4 of 0.6 ng/dL, and a normal total T3 of 148 ng/dL. Free T4 has since normalized however TSH remains elevated. The patient continues to be monitored closely without pharmacologic treatment. The evolution of this patient’s thyroid function is consistent with thyroiditis and appears similar to the course of Hashitoxicosis, however antibodies remain negative. There is literature that suggests molecular mimicry between Borrelia proteins and thyroid autoantigens due to amino acid sequence homology. Some Borrelial proteins are found to share antigenic properties with multiple thyroid related proteins, specifically the TSH receptor, TPO, thyroglobulin and sodium iodine symporter, potentially leading to thyroiditis. Three case reports describe adults with hyperthyroidism in the setting of Lyme disease, however in these cases thyroid antibodies (TPO +/- thyroglobulin) were positive. Two of these patients were asymptomatic, similar to our patient. This phenomenon has never been described in a pediatric patient and illustrates the need to consider Lyme disease as a potential cause of destructive, transient, thyroiditis. Presentation: 6/1/2024

8471 A Rare Case of Graves' Disease in a Three-Year-Old

Abstract Disclosure: A. Rajesh: None. A. Ravari: None. L.E. Kimball-Ravari: None. H. Roan: None. Graves’ Disease (GD) is an autoimmune disease that causes hyperfunctioning of the thyroid gland which may be triggered by environmental factors such as infection or stress. Though the leading cause of hyperthyroidism in both adult and pediatric populations is GD, it is extremely rare in children under the age of four years old. Some studies show the incidence to be 1 per 1,000,000 cases[1],2. Detecting GD in children early is very important as untreated GD poses a risk for failure to thrive. There have also been cases of young children suffering from psychomotor delays, craniosynostosis, and language delays because their suspected diagnosis of GD had not been detected for one to two years. In this article, we report the case of a previously healthy three-year-old Caucasian female who presented to the pediatric endocrinologist after collapsing from an episode of hypoglycemia; plasma glucose 47 mg/dL (71-180) . The patient was diagnosed with Graves’ Disease due to her significantly elevated free T3 and T4, decreased TSH, positive thyroid peroxidase (TPO) antibodies, and elevated TSIg. She was started on methimazole treatment; however, she did not respond after six months of ATD and underwent total thyroidectomy. Her hypoglycemia was attributed to abnormal proinsulin processing and glucose metabolism, which has been associated with hyperthyroidism; thyroid hormones can produce increased GLUT2 transporters3. This case report demonstrates the importance of recognizing the signs and symptoms of GD early, as well as discuss the importance of increasing the recognition of autoimmune diseases in the pediatric population.

6575 From Tonsils to the Thyroid: A Rare Case of Acute Suppurative Thyroiditis in an Immunocompetent Adult

Abstract Disclosure: F. Sajid: None. A. Mubashir: None. F. Mohsin: None. M. Sattar: None. Introduction: Acute suppurative thyroiditis (AST) is a rare infection of the thyroid gland due to its high vascularity, protective encapsulation, and high iodine content. Most AST cases occur in children with anatomical aberrations or in immunosuppressed adults. Here, we describe a case of AST in an immunocompetent woman. Case: A 54-year-old woman with no medical history presented to the emergency department due to dyspnea, dysphagia, and odynophagia for two days. She reported a four-day history of sore throat, fever, and chills. She was saturating well on room air but was sitting in a tripod position. She had erythema, swelling, tenderness to palpation in the anterior neck with a hoarse voice, and moderate trismus. Nasopharyngoscopy revealed no mass, but the scope could not pass beyond the velum due to edema. The patient’s condition quickly deteriorated, necessitating emergent intubation for acute hypoxic respiratory failure. After intubation, the patient had cardiac arrest with asystole requiring resuscitation and successful ROSC. The initial CT scan showed extensive soft tissue abnormalities in the nasopharynx and parapharyngeal tissues, extending to the thyroid gland and mediastinum with the possibility of developing abscesses. A thyroid ultrasound showed a heterogeneous thyroid gland without nodules or increased vascularity. Treatment commenced with ampicillin-sulbactam. Laboratory results showed Free T4 of 4.74 ng/dL (0.58-1.64), TSH 0.03 MCIU/mL (0.39-4.08), Total T3 1.56 ng/dL (0.72-1.35), WBC 19.3 K/UL (4.8-10.8), and elevated ESR and CRP levels. Thyroid-stimulating Immunoglobulin (TSI), Thyroid Peroxidase (TPO) Antibody, and Thyrotropin Binding Inhibitory Immunoglobulin (TBII) were negative, making AST the top differential. Methimazole was initiated due to concerns of thyroid storm, but it was quickly tapered due to a significant decrease in Free T4 levels and suspicion of AST. A repeat CT scan revealed more defined abscesses along the bilateral pharyngeal walls extending to the thyroid bed. The patient underwent bilateral tonsillectomy and drainage of the abscesses. She was extubated the following day. Cultures from the abscesses grew rare Klebsiella pneumoniae, susceptible to Ampicillin-sulbactam. A barium swallow on day 14 showed no evidence of a pyriform sinus fistula. She was discharged on day 15 with Augmentin for 7 days. On discharge, free T4 decreased to half (2.39 ng/dL), and Total T3 normalized (1.08ng/dL). Conclusion: This case presents a rare instance of AST in an immunocompetent patient without anatomical anomalies, stemming from the spread of peritonsillar and parapharyngeal abscesses into the thyroid bed. AST should be considered in cases of deep neck infections, as it is a potentially life-threatening disease. It is crucial to identify and treat AST early to prevent complications. The primary treatment involves antibiotics, incision, and drainage. Presentation: 6/1/2024

12393 Myxedema Presenting With Impending Cardiac Tamponade : A Case Report

Abstract Disclosure: A. Hoskote: None. V. Gupta: None. J. Seidenberg: None. The widespread availability of thyroid stimulating hormone (TSH) assays, routine screening and affordable replacement therapy has resulted in decreased prevalence of complications of untreated hypothyroidism. “Myxedema heart” is a rare syndrome that results in bradycardia, cardiomyopathy and pericardial effusion. We present a rare case of cardiac tamponade due to myxedema in a patient with unidentified hypothyroidism. A 49-year-old male was brought to the ER by his family for several weeks of cognitive slowing, weakness and inappropriate behavior involving defecating on himself eating old food and barricading in his room. The patient denied past medical or psychiatric history, medication use or recent physician evaluation. On exam he had macroglossia, was disheveled, forgetful but alert with slow speech, ataxia and muscle wasting. He was afebrile and hemodynamically stable. EKG showed sinus bradycardia. Labs were notable for sodium 133, hemoglobin 8.8g/dL and TSH was incidentally >100U. Levothyroxine was begun. The next day, he was noted to have increased lethargy, bradycardia and hypoglycemia and was transferred to the intensive care unit with concern for myxedema coma. Free T4 was <0.3 ng/dL (0.6-1.6) and free T3 was 1.6pg/mL (2.5-3.9). An echocardiogram revealed a large circumferential pericardial effusion with right atrial and ventricular collapse with tamponade. Treatment with 5 mcg liothyronine, intravenous levothyroxine and stress dose hydrocortisone was begun. A pericardial drain was placed, draining 980mL of sanguineous fluid. After clamping trials, the drain was removed 48 hours later. Labs revealed thyroglobulin <0.1ng/mL (1.6-50), thyroid peroxidase (TPO) antibody 574 IU/mL (<9), thyroglobulin antibody >2500 (<4) and thyroid ultrasound showed a normal sized thyroid gland with heterogenous echogenicity confirming a diagnosis of Hashimoto’s thyroiditis. Serial echocardiograms during the admission and a follow-up two months later showed a stable posterior effusion with no recurrence of the anterior pericardial effusion. Gradually mentation, hemodynamics and electrolyte derangements improved, and he was discharged on oral levothyroxine. TSH values showed sequential improvement to 48U in 15 days and to 11U in 2 months. Myxedema is a manifestation of severe hypothyroidism. The pericardium, a collagen-rich structure, is susceptible to myxedematous infiltration, leading to pericardial effusion. While small pericardial effusions are common with chronic hypothyroidism, a large pericardial effusion with tamponade is a rare life-threatening complication that requires prompt recognition and management. Clinicians must promptly identify myxedema and replace thyroid hormone to prevent progression of pericardial effusion to tamponade, maintaining especially high suspicion in those at risk of poor access to healthcare or inadequate health literacy. Presentation: 6/3/2024

6601 A Case of Recurrent Painless Thyroiditis and Discussion of Management

Abstract Disclosure: M.C. Slack: None. S. Grock: None. Introduction: Painless (silent) thyroiditis is characterized as a subacute and generally self-limited disease process in which patients develop transient thyrotoxicosis, which is often followed by a hypothyroid phase before entering the recovery euthyroid phase. Given high frequency of positive thyroid antibodies, it may be autoimmune-mediated; recurrence is rare. Here we present a case of recurrent painless thyroiditis and discuss management options. Clinical Case: A Korean woman was followed by endocrinology from age 38 to 60 and experienced at least seven episodes of painless thyroiditis over this time. The episodes occurred without an identifiable trigger and were not preceded by viral illness. During episodes she developed palpitations, hair loss, and dyspnea on exertion and biochemical evidence of thyrotoxicosis with TSH suppressed to <0.2 mIU/mL (normal 0.3-4.7) and elevated free T4 levels as high as 5.4 ng/dL (normal 0.8-1.7). TSI, TPO, and TSH receptor antibodies were checked during multiple episodes and resulted negative, though thyroglobulin antibody was significantly elevated. A radioactive iodine uptake scan was obtained during an active episode of thyroiditis and revealed diffusely low uptake. The patient’s episodes lasted approximately two to three months before normalization of her TSH and FT4. She had at least one instance of transient hypothyroidism after thyrotoxicosis with a TSH of 13.2 and FT4 of 0.6 which subsequently normalized 6 weeks later. The patient did not have known cardiovascular disease and DXA scans revealed mild osteopenia with the lowest T-score -1.3. RAI was considered for the patient based on the total number and increasing frequency of her episodes. She ultimately declined treatment with RAI and continues to follow with endocrinology. Clinical Lessons: While the deleterious effects of prolonged hyperthyroidism (e.g. osteoporosis, arrhythmia, cardiovascular disease) are well known, it is unclear what risk recurrent painless thyroiditis episodes pose. As there are no guidelines regarding treatment, clinical gestalt incorporating frequency and duration of episodes, as well as symptoms, is often used to determine if definitive management is indicated. There are case reports in the literature of treatment of recurrent thyroiditis with RAI ablation performed during a euthyroid state, which eliminated recurrence of episodes but did lead to permanent hypothyroidism necessitating hormone replacement. Surgical thyroidectomy may also be considered in select patients. This case highlights the challenges in treating rare cases of recurrent painless thyroiditis given the lack of research or established guidelines. It is reasonable to consider the frequency, severity, and total number of episodes, as well as patient risk factors, symptoms, and preferences when making recommendations regarding management. Presentation: 6/1/2024

12616 Pembrolizumab-induced Autoimmune Adrenal Insufficiency: A Case Report And Literature Review

Abstract Disclosure: A. Calderon: None. E. Calderon-Martinez: None. J. Shakil, MD: None. A. Kansara: None. Immunechekpoint inhibitors (ICI)-related Primary Adrenal Insufficiency (PAI) is an uncommon entity. Compared to other endocrine-related adverse effects (irAES), antibody detection is less consistent. TPO and GAD65 antibodies are usually present in about 40-80% of the cases with hypothyroidism, hyperthyroidism, and diabetes. On the contrary, case reports and series for PAI seldom report the presence or absence of 21OH antibodies. We present a case and perform a literature review of PAI, in a patient who received pembrolizumab and developed PAI with 21 hydroxylase antibodies. A 62-year-old man with history HIV on ART (last CD4 count 590 cells/mm3) and locally advanced urothelial cancer on Pembrolizumab, presented with nausea, vomiting, abdominal pain, and decreased urine output. He was noted to be confused, and in hypoactive delirium. On admission, his chemistry panel he was noticed to have normal sodium and potassium levels. The CT scan of the abdomen revealed regional enteritis and was started on IV fluid therapy. His adrenal glands were described as normal on imaging. On the 16th day of hospitalization, the patient became unresponsive and hypotensive. He was transferred to the ICU. His sodium level was 132 mEq/L and potassium level was 6.1 mEq/L, bicarbonate level was 18 mEq/L, calcium of 10.3 mg/dl, and eosinophils of 15%. Random cortisol levels measured before administration of steroids were undetectable twice, 9 hours apart, with an ACTH level of 94. He underwent an ACTH stimulation test with cosyntropin 250 mcg IV with resulting undetectable cortisol levels after 30 and 60 minutes. CT and MRI of the brain showed no signs of hypophysitis. He was started on high-dose hydrocortisone with improvements in his mental status, hypotension, and gastrointestinal symptoms. He was discharged on hydrocortisone. His 21-Hydroxylase antibody was later found out to be positive. After combination immunotherapy regimens, CTLA-4 inhibitors are the most common to cause any irAE, however endocrine irAE particularly are mostly associated with PD-1 inhibitors. Among these, thyroid and pituitary disorders are the most common ones. Reports show that about 10% of patients receiving immunotherapy will develop endocrinopathy. ICI-induced PAI has been reported to occur in 7.6% of patients receiving combination therapy, and 2% of patients receiving Pembrolizumab. It has been reported that only 15% of patients will recover adrenal function. A meta-analysis that gathered 15 cases of ICI-induced PAI, found that only 2 cases had positive 21-hydroxylase antibodies. In our presented case, we have robust biochemical confirmation of PAI, with positive 21 hydroxylase antibody, after being on pembrolizumab for 9 months. Further information is needed to establish the pathophysiology, presentation, and prognosis of ICI-related PAI when anti adrenal antibodies are positive. Presentation: 6/1/2024

7443 Severe Hypothyroidism and Adrenal Insufficiency in a 27-Year-Old Male with Klippel-Feil Syndrome: A Case Report

Abstract Disclosure: S. Almardini: None. F. Haddadin: None. L. Aoun: None. F. Saliba: None. J. Zaidan: None. Background: Klippel-Feil syndrome (KFS) is a rare congenital disorder characterized by improper segmentation of the cervical vertebrae. The classical clinical triad consists of short neck, low posterior hairline, and limited neck mobility. It is uncommonly associated with endocrine abnormalities. We present a rare case of KFS with severe primary hypothyroidism. Case Presentation: A 27-year-old male with KFS presented for evaluation of profound fatigue and lack of energy. His vital signs revealed a heart rate of 50 and a borderline low blood pressure. On physical exam patient was noted to be lethargic and icteric, thyroid exam was limited due to patient short neck. Labs were consistent with severe hypothyroidism TSH of 825 mIU/L, total T4 <0.4 mcg/dL, low 8 AM cortisol of 4.3 mcg/dL, elevated LDL at 333 mg/dL, elevated liver enzymes AST 491 U/L, ALT 294 U/L, neutropenia with WBC 2.69 x10^3/uL 20% neutrophils and anemia Hb 12 g/dL. TPO and thyroglobulin antibodies were positive at 149.0 and 109.0 IU/mL respectively, 21 hydroxylase antibodies were negative. Thyroid Ultrasound showed small and diffusely heterogenous thyroid. Patient was started on Levothyroxine 125 mcg daily and hydrocortisone with improvement in his symptoms as well as normalization of his lipid panel, liver enzymes and neutropenia. The patient was continued on levothyroxine 125 mcg, hydrocortisone was tapered and repeat cortisol levels were normal. Discussion: This case demonstrates an unusual association between KFS and hypothyroidism secondary to Hashimoto thyroiditis, likely representing an incidental finding rather than a causative relationship. The cervical spinal abnormalities and short neck characteristic of KFS could potentially lead to compression of neurological and vascular structures in the neck. However, this is unlikely to fully explain our patient's hypothyroidism. There are few published case reports of KFS with endocrine disorders in the literature that describe incidental findings like autoimmune thyroiditis and hypoparathyroidism, but there is no known biological mechanism linking KFS and endocrine dysfunction. Moreover, there is no evidence in either our patient's case or in existing literature to suggest a higher occurrence of autoimmune disorders like Hashimoto in such individuals. Conclusion: we present a novel case of KFS found incidentally with primary hypothyroidism. While these endocrine disorders could compound the growth delay and developmental issues typically seen in KFS, they do not appear to be causally related. This case highlights the need to monitor endocrine function in KFS patients and serves as a reminder that common conditions may co-occur simply by chance. Presentation: 6/3/2024

5039 Chronic Painful Hashimoto's Thyroiditis

Abstract Disclosure: S. Ahmed: None. M. Vahidi Rad: None. S.A. Westphal: None. M.D. Whitaker: None. Introduction: Painful Hashimoto thyroiditis is a rare variant of Hashimoto thyroiditis that mostly affects women. Most cases are empirically treated as subacute thyroiditis with corticosteroids, levothyroxine, or nonsteroidal anti-inflammatory drugs. However, no medical treatment may provide sustained pain resolution, so optimal treatment remains unclear. We describe the case of a 40-year-old female with longstanding throbbing anterior neck discomfort that failed medical therapy and her symptoms completely resolved with total thyroidectomy. Case Report: A 40-year-old lady with anterior neck pain centered over the thyroid for more than 16 years, shortly after she delivered her last child. The pain is described as intense, it tends to wax and wane but there is a constant throbbing with occasional radiation to the angle of the jaw. Over the years the pain has gradually worsened and during its flares, the thyroid itself is very tender to the point where she experiences difficulty in swallowing and hoarseness of voice. Complicating the issue is her underlying diagnosis of fibromyalgia, as she tends to experience discomfort in many other areas of her body. However, the neck pain appears to be of a different character. No symptoms of hyper or hypothyroidism. The anterior neck pain has been difficult to alleviate, she has used chronic opioids for it which seems to have helped to some extent, in the past she was on prednisone for 1 month however this made no difference to it. On examination, the thyroid is tender and somewhat firm without lymphadenopathy. Thyroid levels have been consistently normal and the most recent of which was a TSH: 1.48, FT4: 1.4, FT3: 3.5 with negative TPO and thyroid stimulating antibodies. ESR and CRP were unremarkable. Thyroid ultrasound showed mildly heterogeneous parenchyma with no solid nodules or lymphadenopathy. Interestingly she had an elevated thyroid uptake in her scan dated April 1st 2022, 4 hour and 24-hour uptakes were abnormal at 23% and 49% respectively which can be seen with Hashimoto's. She underwent total thyroidectomy and her surgical pathology showed benign thyroid tissue with multiple foci of chronic lymphocytic thyroiditis and hyperplastic nodules. Her pain completely resolved after total thyroidectomy. Discussion: Painful Hashimoto thyroiditis is a rare diagnosis and optimal treatment remains unclear. The painful variant of Hashimoto's thyroiditis should be considered in the differential diagnosis of pain and tenderness of the thyroid which can be managed successfully by surgical treatment. Thyroidectomy not only can lead to alleviation of symptoms but also provides the definitive diagnosis. The risks of surgical intervention must be taken into consideration, especially because painful Hashimoto thyroiditis can be associated with a small fibrous gland; hence, the importance of access to highly skilled, experienced surgeons cannot be overemphasized. Presentation: 6/1/2024

8176 An Unusual Case of Thyroid Eye Disease (TED) Occurring in Autoimmune Hypothyroidism

Abstract Disclosure: K. Prasongdee: None. C.M. Tessier: None. Background: It is unusual for TED to present in patients with autoimmune thyroid disease who are euthyroid or hypothyroid. Clinician recognition of this rare presentation is important in ensuring proper treatment and improving patient outcomes. Clinical Case:Our patient is a 57-year-old female with a past medical history of COPD, hypothyroidism presenting with several months of blurry vision. She reports double vision when looking down, and eye pain at rest and with eye movement. She was diagnosed with hypothyroidism one year prior to presentation, and her TSH subsequently normalized after titration to levothyroxine of 112 mcg daily. She reported no history of head or neck radiation. No family history of thyroid disease. She smoked for 30 pack years but stopped 2 years prior. Physical exam showed eye lid swelling and redness, pain and diplopia on end-lateral gaze, no chemosis, no conjunctival injection, or inflammation of the caruncle, lids closed completely, proptosis with Hertel ophthalmometer measured 23 mm on the right eye and 22 mm in the left eye (normal range < 18 to 20 mm for Caucasians), thyroid not enlarged with no palpable nodules, no thyroid bruits. The initial Clinical Activity Score (CAS) was 4, which indicated active TED. A thyroid ultrasound showed Inhomogeneous echogenicity with increased vascularity consistent with autoimmune thyroiditis. An MRI of the orbits revealed diffuse extraocular muscle enhancement and enlargement with tendinous insertion sparing, increased T2 hyperintensity findings which favored thyroid eye disease. Further laboratory testing confirmed the presence of multiple thyroid autoantibodies: Thyrotropin binding inhibitory immunoglobulin 2.76 IU/L (normal range < 1.75 IU/L), Thyroid peroxidase antibody 1135 IU/mL (normal range <9 IU/mL), Thyroglobulin antibodies 157 IU/mL (normal range < 116 IU/mL), thyroid-stimulating immunoglobulin 447% (normal range <140 % Baseline). She was referred to ophthalmology for management of TED and was started on teprotumumab. Her CAS improved to 0 and her diplopia resolved. Her proptosis remained stable. This case illustrates an unusual clinical course in a patient who initially presented with autoimmune hypothyroidism, later developed Thyroid Eye Disease. A study by Kahaly GJ et al showed that in Hashimoto’s thyroiditis (HT), thyroid-stimulating autoantibodies are highly correlated with thyroid eye disease (TED) with positive thyroid-stimulating autoantibodies detected in 5.5% of the patients with HT and 68.2% in the patients with HT and TED. Even though it is less common, up to 6% of patients with HT may be affected by TED. Rare presentations such as this case emphasizes the need to be vigilant when evaluating eye symptoms in patients with autoimmune thyroid disease. Teprotumumab that showed improvement in patients with Grave’s and thyroid eye disease, was also successful in treating our patient symptoms. Presentation: 6/3/2024

6812 A Rare Case of Polyglandular Autoimmune Syndrome Type 3B Presenting with Unsteady Gait Due to Subacute Combined Degeneration of the Spinal Cord Associated with Pernicious Anemia

Abstract Disclosure: F. Mohammadrezaei: None. F. Sajid: None. C.A. Resta: None. J.G. Karam: None. A Rare Case of Polyglandular Autoimmune Syndrome Type 3B Presenting with Unsteady Gait due to Subacute Combined Degeneration of the Spinal Cord associated with Pernicious Anemia Background: The coexistence of Hashimoto's thyroiditis and pernicious anemia is well established and is recognized as Polyglandular Autoimmune Syndrome (PAS) Type 3B [1]. We describe a rare case of a patient presenting with subacute combined degeneration of the spinal cord leading to the diagnosis of PAS Type 3B. Case Presentation: A 37-year-old man with no known medical history presented to the Emergency Department after a fall in the subway station. On history, he complained of progressive bilateral lower extremity weakness of 10 months duration, necessitating assistance with ambulation, and significant weight gain, described as an increase in his pants size from 40 to 56. His physical examination was relevant for weight of 145kg, BMI of 46.5, normal motor strength and sensation of the upper extremities, decreased strength at 4 out of 5 of bilateral hip flexion and extension, and decreased vibration sensation of bilateral lower extremities. He could not fully stand or walk due to imbalance and weakness. Blood testing revealed a hemoglobin level of 11.4 gm/dl (14-18), MCV of 108.8 FL (80-94), a significantly low vitamin B12 at 89 pg/ml, and normal folate level. His TSH level was 9.26 MCIU/ML (0.39-4.08), with a free T4 of 0.74 ng/dl (0.8-1.8) and significantly elevated Thyroid Peroxidase Antibody titer at 4320 IU/ml (< 34.9). Intrinsic factor antibody and parietal cell antibody tests both came back elevated at 13.4 AU/mL (0.0-1.1) and 1.8 (<1.2), respectively. A head CT scan showed no acute pathology, but MRI spine with contrast revealed abnormal T2 hyperintensity, primarily affecting the lateral columns throughout the cervical and thoracic cord, likely indicative of subacute combined degeneration. The patient was diagnosed with autoimmune Hashimoto's thyroiditis, pernicious anemia, and subacute combined degeneration of the spinal cord due to vitamin B12 deficiency. He was treated with daily vitamin B12 1000mcg muscular injections, levothyroxine 75mcg orally daily (after ruling out adrenal insufficiency), and physical therapy. Conclusion: This case highlights the complexity of polyglandular autoimmune syndromes and the importance of recognizing atypical presentations early in the history of disease. Comprehensive evaluation and timely intervention are essential to mitigate the progression of these conditions and improve patients' quality of life. Reference: (1) Betterle C, Furmaniak J, Sabbadin C, Scaroni C, Presotto F. Type 3 autoimmune polyglandular syndrome (APS-3) or type 3 multiple autoimmune syndrome (MAS-3): an expanding galaxy. J Endocrinol Invest. 2023 Apr;46(4):643-665. Presentation: 6/1/2024

8105 Radiation-Induced Hyperthyroidism in the Context of Palliative Radiation Therapy

Abstract Disclosure: A. Randhawa: None. G. Palaguachi: None. J.G. Karam: None. Introduction: Palliative radiotherapy, designed to alleviate focal symptoms in advanced, incurable cancer, aims to enhance quality of life with minimal treatment burden. The thyroid gland's susceptibility to neck radiation is known, primarily leading to hypothyroidism. However, hyperthyroidism is a much less frequently reported adverse effect that is poorly understood. This case report highlights an unusual instance of radiation-induced hyperthyroidism. Case Presentation:The patient is a 53 years-old woman with history of Ewing’s sarcoma of the sacrum diagnosed in August 2022, treated initially with chemotherapy (cyclophosphamide, vincristine, etoposide and ifosfamide), but diagnosed with leptomeningeal metastasis and T12/L1 mass in October 2023 when she presented with lower extremities weakness and urinary incontinence. She underwent T12-L1 laminectomy, resection of tumor and fusion, and was started on palliative intent radiation therapy for the brain and C-spine. A month later, she was admitted for altered mental status and was found to be persistently tachycardic at 140 bpm. Thyroid function testing was sent and revealed hyperthyroidism with TSH of 0.07 mIU/L (0.39-4.08), Free T4 of 1.74 ng/dl (0.58-1.64), T4 of 10.7ug/ml (4.4-9.5), T3 of 0.54 ng/ml (0.72-1.35), with undetectable Thyroid Peroxidase Antibodies and Thyroid Stimulating Immunoglobulin level. Thyroid Ultrasound showed a small and homogenous thyroid gland with no discrete nodules. Radioactive Iodine uptake and scan was not obtained because of exposure to iodized contrast during hospital stay. The patient had no available baseline thyroid function tests. She had no recent fever or viral illness. Unfortunately, her clinical condition deteriorated rapidly, and she passed away on the seventh day of admission. Conclusion: While hypothyroidism is a well-established consequence of high-dose irradiation, the mechanisms behind the rarer radiation-induced hyperthyroidism remain unclear. Speculation includes the release of autoantigens from damaged thyroid glands, triggering an immune response and potentially leading to Graves' hyperthyroidism. However, our case more likely represents a hyperthyroid phase in the triphasic sequence of destructive subacute thyroiditis, given the absence of elevated thyroid antibodies, thyroid nodules, and other causes of thyroiditis. Increasing awareness of radiation-induced hyperthyroidism, unraveling its mechanisms, and refining diagnostic strategies such as obtaining baseline and monitoring thyroid function testing are crucial, particularly in the context of palliative therapy, where striking the delicate balance between efficacy and minimizing toxicity is paramount. Presentation: 6/3/2024

6641 Observation in Lieu of Surgical Management in Hurthle Cell Neoplasm: Role of Thyroseq V3 Molecular Testing

Abstract Disclosure: R. Kaur: None. L. Kaur: None. T. Chaudhary: None. M. Shrivastava: None. N. Patel: None. The diagnostic utility of fine needle aspiration biopsy with cytology is often confounded in thyroid nodules with predominance of hurthle cells, often interpreted as an oncocytic/hurthle cell lesion with intermediate risk of malignancy, bethesda category (BC) III or IV. With the advent of molecular testing like thyroseq V3, it is helpful in ruling out substantial risk of cancer and considering observation in lieu of surgical management in such difficult cases. We present a case of a 75 year old woman with past medical history significant for type 2 diabetes mellitus and hypothyroidism who was found to have a left lobe complex nodule within a non-toxic multinodular goiter In 2022. Ultrasound of the neck showed a 1.6 x 1.8 x 2 cm intermediate nodule, followed by a fine needle aspiration biopsy which was non-diagnostic and reported as benign, showing only cystic contents and insignificant follicular cells, Bethesda class II. Follow up for the nodule was recommended in one year. Repeat Imaging one year later revealed left nodule without significant changes and repeat fine needle aspiration cytology was advised. The biopsy result was reported as an oncocytic/ Hurthle cell neoplasm, Bethesda class IV. The specimen was also submitted for thyroseq molecular testing and results were awaited. The patient was euthyroid with negative anti thyroid antibodies. There was no family history of thyroid cancer or radiation exposure. The patient denied any active symptoms like shortness of breath, neck pain or pressure, recent voice changes, dysphasia, loss of appetite or weight .On examination the patient was found to have a left thyroid nodule with no signs of tracheal deviation. CT scan of the neck demonstrated a left thyroid nodule with no compression. The patient was followed by both endocrinology and oncology and surgical options were discussed depending upon the biopsy results while awaiting molecular testing report. Molecular testing with thyrosec V3 revealed an absence of gene mutations and reported a low probability of cancer. Depending upon the results observation was considered in lieu of surgical management. Hence It was decided to keep the patient under observation considering the molecular test results in conjunction with all relevant imaging, clinical findings, symptoms, patients family history as well as patients preference. This case report demonstrates the crucial role of molecular Diagnostics specifically thyroseq V3 in the often difficult clinical management of hurthle cell thyroid nodules for ruling out surgical management. Thyroseq V3 shows reliable performance in Hurthle cell cancers with sensitivity of 93% and specificity of 69%. In times of patient guided decision making and ability to narrow down the need of surgery based on pre-operative fine needle aspiration cytology, molecular profiling of thyroid nodules has become increasingly utilized. Presentation: 6/1/2024

6581 Case of Conversion from Hashimoto’s Thyroiditis to Graves’ Disease: An Unusual Sequence

Abstract Disclosure: A. Atri: None. C. Anastasopoulou: None. Introduction: The two most common autoimmune thyroid diseases are Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). HT is a destructive thyroiditis, via autoantibodies most commonly against the thyroid peroxidase enzyme (anti-TPO), while GD results in hyperthyroidism, due to TSH-receptor stimulating antibodies (TSAb) and Thyroid Stimulating Immunoglobulin (TSI). Case Report: A 23-year-old male presented to the clinic with complaints of weight gain, dry skin and excessive hair loss. His physical examination was non-contributory and laboratory evaluation revealed a TSH of 130 uIU/ml (ref: 0.45-4.5), free T4 (fT4) 0.4 ng/dl (ref: 0.82-1.77), and positive anti-TPO antibodies, for which he was started on levothyroxine (LT4) supplementation for newly diagnosed HT. Over the first five months on treatment, his TSH and T4 progressively improved to 31.8 uIU/ml and 1.48 ng/dl, respectively. Six months later, his TSH rapidly decreased to 0.01 uIU/ml, with an fT4 elevation to 2.45 ng/dl, alongside developing hyperthyroid symptoms like weight loss, insomnia and palpitations. Due to persistently positive anti-TPO antibody titers, his hyperthyroidism was considered iatrogenic, and LT4 dose was gradually reduced, but eventually required to be discontinued. A thyroid ultrasound depicted generalized increase in vascularity, consistent with active thyroiditis. He continued to have a significantly suppressed TSH <0.005 uIU/ml and elevated fT4, off all medications, and was also found to have multiple positive antibody titers [TSI of 1.02 IU/L (ref: < 0.55), thyroglobulin antibody of 351 IU/ml (< 0.9) and anti-TPO Ab >600 IU/ml (ref< 34)]. He was then diagnosed with new GD, and thyroid suppression therapy with 10mg/day of methimazole was initiated, to which he rapidly responded, with a TSH of 0.059 uIU/ml and reduced fT4 of 1.37 ng/dl. His diagnosis of GD was confirmed via an I-123 thyroid uptake scan which revealed a homogenous increased tracer uptake of 57% at 24 hours (ref 15-35%), following which he received definitive therapy for GD, with radio-active iodine (RAI) ablation with 20.6 mCi of I-131. Discussion: As HT and GD have a common autoimmunity-based pathophysiology, conversions between the two clinical states have been described, though HT to GD, as seen in our patient is much less common than the reverse conversion. Some described mechanisms include an antibody switch from thyrotropin receptor blocking to stimulating action, HT-induced thyrotroph destruction resulting in GD antibody formation, and treatment with LT4. Simultaneously elevated levels of both TSI and anti-TPO can occur, and therefore treatment and diagnosis should be based on thyroid function tests and clinical presentation. Patients with autoimmune thyroid disease require close monitoring, due to the potential risk of conversion from one clinical end of the spectrum to the other, and early recognition is important. Presentation: 6/1/2024

8806 A Case of Autoimmune Thyroid Switching

Abstract Disclosure: J. Case: None. R.V. Chemitiganti: None. D. Suravajjala: None. Autoimmune thyroid disease comprises both hyper- and hypothyroid states including Graves' disease and Hashimoto's thyroiditis, respectively. The predominant antibody activity, demonstrable by thyrotropin receptor antibody, predicts the clinical presentation and treatment; thyrotropin receptor antibodies may act as a stimulatory or inhibitory stimulus upon the thyroid gland recognized as thyroid stimulating antibody(TSAb) and thyroid blocking antibody(TBAb). Rarely patients may transition from a hyperthyroid to a hypothyroid state and vice versa if the predominant antibody activity shifts which may occur due to a variety of mechanisms and characteristics related to each individual patient and treatment course. A 29 year old female presented to establish care for autoimmune thyroiditis. She was diagnosed with Graves' disease at age 19 when pregnant and treated with propylthiouracil; she switched to methimazole for the next six years when her thyroid function normalized and therapy discontinued. Two years later she became concerned with weight gain and her thyroid function was reevaluated demonstrating hypothyroidism and she was treated with levothyroxine 25mcg daily until presentation. Further labwork revealed undetectable TSI, and TPO antibody elevated at 177 u/mL. She became clinically and biochemically euthyroid on levothyroxine 50mcg daily. Switching between hyper- and hypothyroid states is a rare occurrence among patients with may attributable factors. Both antithyroid drugs including methimazole as well as replacement therapy with levothyroxine may alter the antibody milieu and so the predominant ratio and activity among TSAb and TBAb thereby leading to a shift in clinical presentation and thyroid state. Pregnancy may lead to hemodilution contributing to lessening of autoimmune activity which may return following delivery leading typically to a shift from TSAb to TBAb. Uncontrolled hyper- and hypothyroidism may affect dendritic activity leading to altered presentation and increased immune reactivity. The unlikely occurrence of switching from a hyperthyroid to a hypothyroid state based upon autoimmunity as in this patient was likely affected these factors. Recognition of this potential transition and associated factors would lead to beneficial monitoring and possibly development of assays more attuned to this phenomenon with better capability in maintaining a euthyroid state and potentially predicting a transition. Presentation: 6/3/2024

7668 Rhabdomyolysis Associated with Severe Hypothyroidism

Abstract Disclosure: H. Soe: None. P. Mikkilineni: None. Background: Over 70% of the patients with newly diagnosed hypothyroidism can present with muscle complaints such as weakness, fatigability, cramps, myalgia. However, rhabdomyolysis, which is the rapid breakdown of skeletal muscle cells, is the rare presentation. Clinical Case: A 70-year old male patient with history of rheumatoid arthritis, hyperlipidemia, prior CVA (left hemispheric subcortical stroke) 6 months ago without residual deficit presented to the hospital with poor oral intake and generalized muscle weakness for 3 weeks. He was unable to get out of bed without assistance and also needed adult diapers. Found to have new-onset severe hypothyroidism with TSH 228 uIU/ml (Ref: 0.350-4.940) and FT4 <0.40 ng/dL (Ref: 0.70-1.50), positive TPO antibody 197 IU/ml (Ref: 0-34). No prior thyroid labs were available and no known history of thyroid disorder was recorded. He has never been on Amiodarone or Lithium before. On physical exam, he was alert and oriented. There was no goiter or palpable thyroid nodule. There was no focal neurological deficit and no peripheral edema. There were no other signs and symptoms pertinent to hypothyroidism except mild bradycardia (HR 56-60) and borderline low blood pressure. AM cortisol was 10.1 ug/dL (Ref: 3.7-19.4). EKG showed low-voltage sinus bradycardia. Echocardiogram was normal. Urinalysis was positive for large blood but only 3 RBCs were present which raised the suspicion of rhabdomyolysis. Creatinine kinase (CK) was 15,584 IU/L (Ref: 30-200). Other laboratory studies were significant for acute renal failure with mild hyperkalemia and mild hypocalcemia, also transaminitis; BUN 130 mg/dl (Ref: 8-26), Creatinine 9.51 mg/dl (Ref: 0.72-1.25), eGFR 5 ml/min/1.73 m2 (Ref: >59), AST 435 IU/L (Ref: 5-34), ALT 269 IU/L (Ref: <55), ALP 171 IU/L (Ref: 40-150). On medication review, he was started on Atorvastatin 80 mg daily during prior admission for CVA 6 months ago. He received IV fluids, s/p 1 dose of Hydrocortisone 100 mg IV, Levothyroxine IV 200 mcg, followed by Levothyroxine IV 50 mcg daily x 3 days and switched to Levothyroxine PO 100 mcg daily (weight-based dose). Atorvastatin was on hold. He became anuric during the hospital course and received 2-3 sessions of hemodialysis. 3-4 days later, CK was trending down to 3000 IU/L, FT4 improved to 0.54 ng/dl and there was also significant improvement in kidney and liver functions. The patient was diagnosed with acute renal failure secondary to rhabdomyolysis associated with severe hypothyroidism caused by Hashimoto's thyroiditis, in the setting of high dose statin use. Conclusion: Clinicians should raise the suspicion of rhabdomyolysis in a patient with severe hypothyroidism, especially in patients with recent high dose statin use as rhabdomyolysis can be a rare and fatal complication of severe hypothyroidism, in the presence of precipitating factors. Presentation: 6/2/2024

8791 A Case of Hyperfunctioning Thyroid Nodules Evaluated for Thyroid Metastasis in the Setting of Oropharyngeal Squamous Cell Carcinoma

Abstract Disclosure: M. Alashoor: None. J. Gogineni: None. A. Bakar: None. Introduction: Identifying and evaluating hyperfunctioning thyroid nodules in the setting of metastatic head and neck cancers represents a diagnostic challenge that may result in inaccurate identification of perithyroidal lymph node metastasis as malignant or metastatic thyroid nodules with standard workup. Case presentation: A 72-year-old male with a history of stage IV metastatic oropharyngeal squamous cell carcinoma, metastasized to the lymph nodes, lungs, mediastinum, and bilateral iliac bones. He was diagnosed two years ago and received chemotherapy, maintenance immunotherapy with pembrolizumab, and targeted palliative radiation therapy, with good clinical response. Restaging PET-CT two years later revealed local progression. During his workup, he was noted to have persistently abnormal thyroid function test with low TSH (0.03​​µIU/mL, n 0.3-5.33), normal free T4 (0.97ng/dL, n 0.60 - 1.40), mildly elevated free T3 (3.91pg/mL, n 2.5-3.9), negative thyrotropin receptor antibodies levels, negative TSI, negative TPO antibody, noted evidence of subclinical hyperthyroidism consistent over the past year. Radioactive iodine uptake demonstrated multinodular gland, mildly elevated 24-hour uptake of 28% consistent with hyperthyroidism, with decreased activity in the left lobe. Thyroid ultrasound revealed multiple probable malignant thyroid nodules, a 1.8 cm TI-RADS 5 lesion of the deep margin of the lower pole of the right lobe, and a 1.6 cm TI-RADS 5 lesion of the upper pole on the right lobe. He was treated with methimazole 5 mg. Further workup with fine needle aspiration demonstrated the right upper lobe nodule sample was positive for squamous cell carcinoma, findings suspicious for metastasis. He subsequently proceeded with radical tonsillectomy, right neck dissection, and right hemithyroidectomy. Surgical pathology results noted, right neck metastatic HPV-associated squamous cell carcinoma involving the lymph nodes with extranodal extension, right oropharyngeal HPV-mediated squamous cell carcinoma. The thyroid gland biopsy was significant for incidental papillary microcarcinoma 2mm, thyroid follicular nodular disease, without evidence of squamous cell carcinoma or metastatic infiltration. Post-hemithyroidectomy, his thyroid function normalized, and methimazole was discontinued. Conclusion: Thyroid metastasis from head and neck cancers represent a rare entity. In patients with a history of malignancy, evaluation of new thyroid masses remains crucial. While FNA is a sensitive method for detecting thyroid metastases, inaccuracies may occur, impacting the identification of thyroid nodules in the presence of local metastatic lymphadenopathy. Identifying squamous cell carcinoma in the thyroid can significantly influence the treatment plan of patients with metastatic carcinomas, therefore careful consideration must be undertaken on evaluation. Presentation: 6/1/2024