bluuebunny/crossref_metadata_2025_split huggingface dataset:
FRI542 Long-term Metabolic Outcomes In Graves’ Disease: Is There A Difference Between Oral Anti-thyroid Medications And Radioactive Iodine Treatment?
Authors: Shemesh Elad , Kolitz Tamara , Nathan Alexandra , Michele Tordjman Karen , Greenman Yona , Izkhakov Elena 
Published: October 2023

Abstract
Disclosure: E. Shemesh: None. T. Kolitz: None. A. Nathan: None. K.M. Tordjman: None. Y. Greenman: None. E. Izkhakov: None.
Introduction: The treatment of hyperthyroidism in patients with Graves’ disease (GD) is associated with various metabolic comorbidities, including weight gain and an increased risk of cardiovascular and cerebrovascular diseases. Few studies have assessed the potential differences in metabolic outcomes between radioactive iodine (RAI) and oral anti-thyroid drug (ATD) therapies. Aim: We sought to investigate the long-term (&gt;10 years) metabolic effects of RAI versus ATD therapy in GD. We also compared the occurrence rates following long-term use to those with short-term (&lt;5 years) use in order to explore a potential "legacy effect". Hypothesis: RAI and oral ATD treatment will differ in their associated risk of metabolic sequelae, including the occurrence of hypertension, dyslipidemia, obesity, and diabetes. Methods: Patients attending the Institute of Endocrinology at the Tel Aviv Sourasky Medical Center filled in a questionnaire on post-RAI or post-ATD treatment for GD. Results: In total, 143 participants had been followed-up for 5 years, and 87 of them (age range 31-88 years, 65 females [74.7%]) had completed &gt;10 years of follow-up (mean follow-up period 14±1 years). During the initial 5-year follow-up period, RAI treatment was associated with a significantly increased rate of obesity and dyslipidemia in the short-term, but no comparable differences persisted into the &gt;10-year follow-up period. However, mean fasting glucose concentrations were higher among RAI recipients compared to ATD recipients (106 and 91 mg/dL, respectively, p=0.037) even after 10 years, and the mean triglyceride concentration was also higher in the former (127 and 88 mg/dL, respectively, p=0.02). There were no significant group differences in the rates of diabetes mellitus or dyslipidemia in the &gt;10-year follow-up period. Conclusions: RAI therapy is associated with long-term higher glucose and triglyceride levels compered to ATD therapy in patients with GD. Clinical metabolic diagnosis are comparable. The significant group differences in the occurrence of metabolic morbidities that had been observed after the first 5 years of follow-up persisted to a greater or lesser extent into the extended &gt;10-year follow-up period, as evidenced by fasting glucose and triglycerides concentrations
Presentation: Friday, June 16, 2023
FRI194 Pheochromocytoma Presenting As Catecholamine-Induced Cardiomyopathy: A Case Report
Authors: Vafea Maria Tsikala , Lee Donna 
Published: October 2023

Abstract
Disclosure: M. Tsikala Vafea: None. D. Lee: None.
Introduction: Pheochromocytoma (PCC) is a rare catecholamine-secreting neuroendocrine tumor presenting with the classic triad of episodic headache, sweating and tachycardia. Catecholamine-induced cardiomyopathy (CICMP) can occur as a complication of PCC in 7-11% of patients. It presents more commonly as dilated cardiomyopathy and inverted Takotsubo cardiomyopathy but also as hypertrophic or unspecified cardiomyopathy. Following appropriate pharmacologic treatment and resection of PCC, these cardiac complications usually resolve. Case report: 36 year old man with history of hypertension presented to the hospital with worsening orthopnea and cough. Following antibiotic treatment failure for suspected pneumonia, he was re-admitted with hemoptysis, tachycardia, hypoxia, and hypertensive emergency. Troponin and brain natriuretic peptide were found to be elevated. CT chest and abdomen showed pulmonary nodules and a large left adrenal mass measuring 9.6x9.3x9.4 cm, concerning for metastatic PCC. He was subsequently started on doxazosin. Transthoracic echo showed bi-atrial enlargement, diffuse severe left ventricle hypokinesis, reduced ejection fraction 25% and diastolic dysfunction. Stress cardiac MRI showed non-ischemic cardiomyopathy, corroborating the diagnosis of CICMP. After achieving adequate alpha-adrenergic blockade, he was started on goal-direct medical therapy consisting of valsartan, metoprolol and empagliflozin. His pulmonary nodular opacities improved on repeat imaging, congruent with pulmonary edema rather than metastases. Plasma and 24-hour urine metanephrines (2,964 pg/mL and 23,310 mcg/24 hr, respectively) and normetanephrines (9,266 pg/mL and 33,927 mcg/24 hr, respectively), as well as dopamine (493 pg/mL), epinephrine (3,205 pg/mL) and norepinephrine (above reportable range of 4,800 pg/mL) eventually came back significantly elevated, confirming his diagnosis of PCC. A month after presentation, he underwent left adrenalectomy, which revealed an 11 cm composite PCC ganglioneuroma. One-month postoperatively, urine metanephrines and normetanephrines were normal but his ejection fraction remained unchanged. Discussion: CICMP should be considered in patients presenting with acute heart failure and an incidental adrenal mass to avoid delays in treatment. Acute pulmonary edema may resemble pulmonary nodules on CT, so interpretation of these findings should correlate with the clinical presentation. Timely initiation of alpha-adrenergic blockade upon suspicion of PCC is crucial as it can significantly improve hemodynamics, and biochemical markers take time to result. 96% of CICMP cases improve after resection of PCC within a variable time frame ranging from one week to several months. Our patient’s CICMP had not improved one month after his adrenalectomy, but it remains to be seen whether he eventually recovers his cardiac function.
Presentation: Friday, June 16, 2023
FRI552 Orbitopathy As The Sole Manifestation Of Hashimoto’s Thyroiditis In A Euthyroid Patient: A Case Report
Authors: Labib Christine , Saeed Zainab , Trabulsi Maja , Ramharrack Frank 
Published: October 2023

Abstract
Disclosure: C. Labib: None. Z. Saeed: None. M. Trabulsi: None. F. Ramharrack: None.
INTRODUCTION: Thyroid associated ophthalmopathy (TAO) is caused by an autoimmune process involving the orbital tissue, however, its etiopathogenesis is still largely unclear. It is common in hyperthyroid patients with Graves’ disease and has also been reported in euthyroid and hypothyroid Graves’ patients with positive thyroid receptor antibodies (TRAb). However, only 5% of patient with Hashimoto’s thyroiditis (HT) develop orbitopathy. Here we report an unusual case of a male patient, clinically and biochemically euthyroid, who had severe bilateral exophthalmos due to underlying Hashimoto’s thyroiditis. CASE PRESENTATION: A 68-year-old male patient was evaluated for worsening bilateral eye protrusion associated with redness and grittiness for many years. The patient was otherwise asymptomatic; denied fatigue, any change in weight, constipation, joint/muscle pain or any other symptoms. On physical examination he was noted to have bilateral moderate periorbital edema, conjunctival injection along with mildly enlarged thyroid. Initial labs showed normal TSH 4.10 mIU/L (0.4-5.0mIU/L) and free T4 0.8 ng/dL (0.8-1.8 ng/dL). Further labs were notable for normal antithyrotropin antibody (TRAb) 1.09 IU/l and normal TSI less than 89%. Anti-thyroid peroxidase antibody (anti-TPO) level was as high as 12 IU/mL (less than 9 IU/mL). Thyroid US showed multinodular goiter with bilateral nodules. A Subsequent FNA was benign. The degree of exophthalmos on the Hertel ophthalmometer was 30 mm bilaterally. Orbital magnetic resonance imaging (MRI) showed proptosis of the left and right globes as well as prominence of intraorbital fat. Extraocular musculature was symmetric bilaterally and only minimally prominent but diffuse. Treatment with teprotumumab infusion was started with improvement in the patient’s symptoms. CASE DISCUSSION: Usually mild eye symptoms are seen in Hashimoto’s thyroiditis such as dryness, blurred vision, upper eyelid retraction and loss of lateral third of eyebrows. In rare cases it can cause orbitopathy similar to that seen in Graves’ disease. Like Graves’ orbitopathy, in addition to reversing the underlying thyroid abnormalities, moderate-to-severe orbitopathy is treated with corticosteroids or teprotumumab. This case sheds the light on exophthalmos being an atypical presentation of Hashimoto’s thyroiditis in a clinically and biochemically euthyroid patient. Physicians should be cognizant of this rare manifestation for prompt recognition and early treatment which can prevent corneal involvement and blindness due to optic nerve compression.
Presentation: Friday, June 16, 2023
FRI198 Acute Pancreatitis And Diabetic Ketoacidosis As A Presentation Of Subclinical Cushing Syndrome
Authors: Alkhidady Wijdan Hasan , Almefgaie Noura B , Ekhzaimy Aysha 
Published: October 2023

Abstract
Disclosure: W.H. Alkhidady: None. N. Almefgaie: None. A. Ekhzaimy: None.
Case Report: A 43-year-old Saudi woman, presented to the emergency department with two days history of right upper quadrant pain, radiating to the back. Associated with nausea and vomiting with no history of diarrhea, constipation, or constitutional symptoms. She has a 4-year history of hypertension on 5 mg amlodipine with no history of endocrine or malignant tumors. On Examination she was alert, severely dehydrated with temperature of 37 °C, pulse of 124 per minute, blood pressure of 147/61 mmHg. The abdomen was tender in the right upper quadrant area. A laboratory examination showed lipemic sample with high triglycerides level 11mmol/L (0.4-1.48), high amylase 763nu/l (25-115), lipase 5773 u/l (73-393), low potassium level 2.6 mmol/l (3.50-5.10) and low calcium level 1.25 mmol/l (2.10-2.55). The urine analysis showed 4+ glucosuria and ketonuria. Her venous blood gas showed pH of 7.18 and bicarbonate of 10 mmol/L, random blood glucose was 16 mmol/L and anion gap could not be calculated at that time. A diagnosis of DKA secondary to acute pancreatitis secondary to high triglycerides level was made and management was started along with plasmapheresis. A CT pancreatitis protocol was done which showing a 4.2 x 3.5 cm well-circumscribed left adrenal lesion. An MRCP showed 4.3 cm well defined collision tumor in left adrenal gland, its peripheral part is suggestive of adenoma. further work up showed negative 24-hours urine metanephrins, normal Aldosterone Renin ratio, High 24-hour urine cortisol level 644 nmol/l, low ACTH 0.6 pmol/l and morning cortisol level post 1 mg DST was not suppressed on two different occasions. Since the patient had no phenotypical presentation of Cushing’s a diagnosis of SCS was made. She underwent left robotic assisted adrenalectomy, with pathological diagnosis of adrenocortical adenoma. 2 days later, AM cortisol level reduced to 230 nmol/L. while blood pressure and serum potassium remained normal with no signs of adrenal insufficiency. Her Diabetes mellitus and Hypertriglyceridemia resolved after left adrenalectomy. Conclusion: This case report demonstrates the uncommon association of subclinical Cushing syndrome and acute pancreatitis as a first presentation therefore it highlights the significant role of endocrine evaluation of any young patient with unexplained acute metabolic presentations.
Presentation: Friday, June 16, 2023
SAT476 A Case of Thyroid Hemiagenesis
Authors: Kachhadia Palak , Khan Shaza , Ukponmwan Esosa U , Aldasouqi Saleh , Limon Ahmad Abu 
Published: October 2023

Abstract
Disclosure: P. Kachhadia: None. S. Khan: None. S. Aldasouqi: None. A. Abu Limon: None.
Introduction: Thyroid hemiagenesis is congenitally rare, in which one side of the thyroid does not develop. Hemiagenesis is more common with an absent left thyroid lobe, at a 4:1 ratio. Though prevalence is sited at 0.05%, actual incidence of hemiagenesis amongst the population is unknown as most patients are euthyroid and asymptomatic. We present a case of a patient who was referred to our clinic for unilateral thyroid enlargement on physical exam. Thyroid Ultrasound (US) was done which showed an absent left thyroid lobe along with enlarged right thyroid lobe and hypervascularity. There was also an incidental thyroid nodule noted on US. Case Presentation: Patient is a 38 year old female who presented to the clinic 4 years prior for enlarged thyroid nodule noted on ultrasound. With symptoms of dysphagia and a visibly enlarged gland, an US with labs was prompted by her primary physician. US showed absent left thyroid lobe and right lobe enlargement with hypervascularity and incidental subcentimeter nodule. Clinically and biochemically, the patient was euthyroid. Singular right lobe was verified on clinic real time ultrasound and on NM uptake scan. The 24 hour uptake was at 30.5%, with the upper limit of normal being 30%. With increased uptake and hypervascularity, thyroid stimulating immunoglobulin and thyrotropin receptor antibodies were checked and were not detected. It was thought that the right thyroid gland enlargement and hypervascularity were compensatory due to the left hemiagenesis. The thyroid nodule was monitored, and within 3 years of original imaging, it enlarged to 0.98 x 0.59 x 0.39 cm, with TI-RADS 5 assessment per ACR criteria. Patient chose to undergo thyroid biopsy which showed Bethesda III, Follicular Lesion of Undetermined Significance (FLUS). Microscopy showed follicular cells arranged in microfollicles and crowded groups with round, enlarged, irregular nuclei and overlapping nucleoli. Intranuclear chromatin clearing and intranuclear grooves are present. Background is hemorrhagic with minimal colloid. Molecular Thyroseq testing was at 5-10% chance of malignancy or noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP). Genetic markers were only positive for copy number alterations. Discussion: Thyroid Hemiagenesis, though rare, has been associated with other thyroid pathologies such as hypothyroidism, hyperthyroidism and thyroid malignancies. Genetic studies have not found a common background within cases reported. As these patients are more likely to incur additional thyroid pathologies, questions still remain as to the clinical management and outcome of such patients. Due to concerning cytological features for PTC, the patient was offered right thyroidectomy and will be looking to make a decision in the near future.
Presentation Date: Saturday, June 17, 2023
SAT482 A Case of Falsely Elevated Free T4 and Free T3 Levels Caused by Human Anti Mouse Antibodies.
Authors: Romao Isabela J , Shanik Michael Howard 
Published: October 2023

Abstract
Disclosure: I.J. Romao: None. M.H. Shanik: None.
Introduction: When there are clinical and biochemical discrepancies with thyroid function tests immunoassay interference should be considered (1). Human anti mouse antibodies (HAMA) are antibodies found in humans that react with immunoglobulins in mice and are used as diagnostic reagents for laboratory measurements. The presence of HAMA most commonly causes a false elevation of thyroid stimulating hormone but can also increase Free T4 and Free T3 levels. Case presentation: A 31 year old woman presented for evaluation of elevated Free T4 and Free T3 levels. For several weeks she complained of feeling neck soreness and palpitations. She had a recent infection and low-grade fever. She also felt pressure behind her eyes. She had a history of anxiety and took Xanax as needed, multivitamin and probiotic. Cousin had thyroid disease. On exam her blood pressure was 138/86, heart rate 80, respiratory rate 12, weight 149 lbs., height 5’5”. Her thyroid was firm and not tender. She had a thyroid ultrasound that showed a homogenous gland with no discrete nodules. TSH was 1.3 uIU/mL (0.27-4.2), Total T4 10.4 ug/dL (4.5 – 12), Free T4 4.6 ng/dL (0.9-1.7), Total T3 1.6 ng/mL (0.8-2.0), Free T3 10.1 pg/mL (2.0-4.4). C reactive protein, erythrocyte sedimentation and interleukin 6 levels were in the normal range. Thyroid peroxidase antibodies and thyroglobulin antibodies were elevated. The differential diagnosis included thyroiditis, pituitary tumor producing thyroid stimulating hormone and thyroid hormone resistance. She did not have a thyroid uptake and scan because she had small children at home. To rule out a pituitary adenoma she had a pituitary MRI that showed a normal small pituitary gland. The test for resistance to thyroid hormone mutation analysis was negative. Over a few months she had some clinical improvement, and her thyroid function tests remained the same which would not be consistent with thyroiditis. HAMA level was checked to evaluate for immunoassay interference with thyroid function tests. The HAMA level was elevated at greater than 600 ng/mL (0-188). Free T4 by equilibrium dialysis was normal at 1.6 ng/dL (1.1 – 2.4). Conclusion: HAMA can cause falsely elevated Free T4 and Free T3 levels. It is important to suspect immunoassay interference when there are inconsistencies in the clinical presentation and thyroid function tests. Identifying the presence of elevated HAMA can prevent misdiagnosis and inappropriate patient management. 1. Favresse J, Burlacu MC, Maiter D, Gruson D. Interferences with thyroid immunoassays: Clinical implications and detection algorithm. Endocrine Reviews. 2018. Pages 830-850.
Presentation Date: Saturday, June 17, 2023
SAT498 A Challenging Case of Hypothyroidism Requiring Frequent Primary Care Visits to Achieve Euthyroidism
Authors: Kaul Sabrina , Gupta Ankur 
Published: October 2023

Abstract
Disclosure: S. Kaul: None. A. Gupta: None.
Introduction: We report a patient with persistent primary hypothyroidism despite multiple adjustments in thyroid medication. Clinical Case: A 67-year-old white man with multinodular goiter underwent total thyroidectomy in 2016 for abnormal thyroid nodule biopsy. Surgical pathology revealed papillary thyroid cancer with lymph node metastasis. He subsequently received radioactive iodine ablation treatment. His plasma thyroid stimulating hormone (TSH) level was noted to be 0.275 uIU/mL (normal range 0.35-4.00 uIU/mL) in January 2017 on levothyroxine 224 micrograms daily. Subsequently, his plasma TSH level continued to remain elevated with variable levels despite multiple titrations of his levothyroxine dosage, counseling, and multiple follow-up visits. Plasma TSH level went up as high as 108.140 uIU/mL (normal range changed to 0.55-4.78 uIU/mL). In January 2022, plasma TSH level normalized to 3.125 uIU/mL with high plasma free thyroxine level of 2.45 ng/dL (normal range 0.89-1.76 ng/dL), but plasma TSH level increased again to 5.190 uIU/mL in April 2022. Home care nurse was involved in monitoring of the patient taking thyroid medication daily and correctly but was unsuccessful. The patient and his son reported taking thyroid medicine daily and correctly. There was no concern for malabsorption or interference with any of his medications. The patient was subsequently asked to come to primary care clinic every week for six weeks with all his medications. He was unable to come to endocrinology clinic due to travel time being more than one hour. His repeat plasma TSH normalized to 1.010 uIU/mL. The etiology of previously high plasma TSH level was suspected due to non-compliance with taking his thyroid medication. Non-compliance was discussed in detail with the patient and his son, including life-threatening consequences of hypothyroidism. The patient verbalized understanding and was willing to comply with the recommendations. The patient was then asked to stop coming weekly to primary care clinic. Repeat plasma TSH level in October 2022 was again noted to be high at 80.723 uIU/mL. He again claimed compliance, but weekly visits to primary care clinic were resumed. In December 2022, he was noted to have low plasma TSH level of 0.232 uIU/mL. Conclusion: Once weekly visits seem impractical but might be required in a certain group of patients with persistent abnormal thyroid hormone levels where no etiology can be found.
Presentation Date: Saturday, June 17, 2023
SAT503 Acute Psychosis and Paranoia as an Initial Manifestation of Myxedema Madness
Authors: Atam Sarin , Ahmad Mobeen , McGrath Glenn Alan 
Published: October 2023

Abstract
Disclosure: S. Atam: None. M. Ahmad: None. G.A. McGrath: None.
Introduction: Hypothyroidism is a common disease affecting approximately 1 in 300 Americans, with autoimmunity being the most common cause in the United States. Hypothyroidism is known to present with numerous psychiatric manifestations, including depression, cognitive deficits, and rarely psychosis. We present a case of profound hypothyroidism found in a patient who presented with visual hallucinations and paranoia. Case description: The patient was a 64-year-old man with past medical history of follicular Non-Hodgkin's Lymphoma, Type 2 diabetes, hypertension, and sinus bradycardia who presented to the emergency department with three-week history of increasing agitation, insomnia and cold intolerance. He had auditory and visual hallucinations with paranoid ideations, which started a few days prior. His initial vitals were temperature: 98.2°, heart rate: 81 beats per minute, respiratory rate: 20 breaths per minute, and blood pressure: 135/88 mmHg. The patient’s initial lab work was significant for: sodium: 143 mmol/L, potassium: 3.6 mmol/L, creatinine: 1.55 mg/dL (baseline of 1.2 mg/dL), AST: 240 IU/L, ALT: 252 IU/L, INR: 1.1, ammonia: 20 mcmol/L, TSH: 51.7 uIu/ml, free t4: &lt;0.1 ng/dL, free t3: &lt;0.4 ng/dL, and urine drug screen positive for cannabinoids. MRI imaging of the patient’s brain was negative for any acute intracranial process. Although the absence of hypothermia made myxedema coma unlikely, both the acuity and the severity of his psychiatric symptoms in the context of profound hypothyroidism, with no other identifiable cause, collectively suggested “myxedema madness”. The patient was started on intravenous levothyroxine therapy along with quetiapine and haloperidol for agitation. Further lab work demonstrated an anti-tpo antibody of 9.0 IU/mL (&lt; 9) along with a benign lumbar puncture (glucose: 89 mg/dL, protein: 54 mg/dL, WBC: 9/uL, RBC: 1/uL). A review of his recent medical history revealed that last summer, as part of a chemotherapy regimen for relapsed lymphoma, he had been started on Lenalidomide, which is reported to cause primary hypothyroidism in 7% of patients. His overall neurologic function improved over a two-week course, and he was subsequently discharged. Discussion: Hypothyroidism can present with a spectrum of different psychiatric manifestations. However, cases of hypothyroidism-induced psychosis are infrequent. It is reported that only 5-15% of myxedematous patients develop some form of psychosis. Treatment of this altered mental state is centered on thyroid hormone supplementation along with the administration of antipsychotic medications. Improvement in psychotic symptoms is typically seen within weeks to months after initiation of treatment. Through this case, we hope to highlight this rare presentation of hypothyroidism and current proposed treatment strategies.
Presentation Date: Saturday, June 17, 2023