bluuebunny/crossref_metadata_2025_split huggingface dataset:
7679 The Role of Thyrotoxicosis in Determining Clinical Outcomes for Hospitalized Patients with Dilated Cardiomyopathy: A Propensity Match National Cohort
Authors: Mukhtar R , Younas H , Taha A , Virlan D , Ceban A , Racovita A , Patel J 
Published: October 2024

Abstract
Disclosure: R. Mukhtar: None. H. Younas: None. A. Taha: None. D. Virlan: None. A. Ceban: None. A. Racovita: None. J. Patel: None.
Background: Thyrotoxicosis, a condition associated with high morbidity and mortality, has been notably linked to adverse clinical outcomes in patients with cardiovascular diseases. This study aims to comprehensively analyze the clinical impact of thyrotoxicosis on in-hospital outcomes in patients hospitalized with DCM. Methods: Based on 2020 National In-patient Sample Database, DCM patients were categorized into two groups depending on whether thyrotoxicosis was present or absent at the time of admission. To evaluate the impact of thyrotoxicosis on clinical outcomes, comparative analyses were conducted using propensity score matching and multivariable regression analysis. All statistical analyses were performed using STAT v 17. Results: Among 545,390 hospitalizations for DCM, 2,900 (0.5%) patients were presented with thyrotoxicosis. Propensity score matching revealed that DCM patients with thyrotoxicosis had higher heart failure rates (7.87% vs. 5.62%, aOR: 1.39, 95% CI: 1.04-1.86, p-value: 0.03). There was no statistically significant difference in in-patient mortality (2.60% vs. 3.65%, aOR: 0.81, 95% CI 0.58-1.13, p-value: 0.21), conduction disorders (3.26% vs. 2.70%, aOR: 1.38, 95% CI: 0.89-2.13, p-value: 0.15), acute coronary artery syndrome (0.62% vs. 0.86%, aOR: 0.94, 95% CI: 0.54-1.64, p-value: 0.82), acute kidney injury (18.57% vs. 18.59%, aOR 0.99, 95% CI: 0.77-1.17, p-value: 0.62), and acute stroke (0.29% vs. 0.30%, aOR: 0.60, 95% CI: 0.15-2.44, p-value: 0.48) between DCM patients with and without thyrotoxicosis. Thyrotoxicosis was associated with increased length of stay [5 days (IQR: 6) vs. 4 days (IQR: 7)] and total charge [$54,256 (IQR: 82,126) vs. $47,942 (IQR: 75,003)] in patients admitted with DCM. Conclusion: This research indicates that DCM patients co-presenting with thyrotoxicosis have an increased risk of heart failure and resource utilization during hospitalization. There were no significant effects observed in conduction disorders, in-patient mortality, acute coronary, kidney, or stroke outcomes among DCM patients hospitalized with or without thyrotoxicosis. Future prospective studies are warranted to enhance our understanding of clinical outcomes associated with thyrotoxicosis in patients hospitalized with DCM.
Presentation: 6/3/2024
7865 Thyroid Acropachy: A Clinical Response to Teprotumumab
Authors: Lira J , Zaidi M , Kim S M 
Published: October 2024

Abstract
Disclosure: J. Lira: None. M. Zaidi: None. S. Kim: None.
Background: Thyroid acropachy is a rare extrathyroidal manifestation of Graves disease (1). Due to its rarity, generally benign clinical course and the limited understanding of its pathophysiology, there is currently no specific treatment for thyroid acropathy. Clinical Case: A 25-year-old Asian male with a history of Graves disease, for which he had undergone total thyroidectomy 2 years prior, presented with worsening double vision. The patient also complained of swelling in the legs, and pain and stiffness in his hands and feet. On exam, he displayed bilateral asymmetric proptosis, conjunctival injection, and lid lags. Nodular and plaque-like lesions with non-pitting edema were observed on both pretibial skin. The fusiform swelling of fingers and prominent clubbing of finger- and toe-nails was noted. Upon further questioning, he admitted to smoking at least a pack of cigarettes a day. His laboratory findings were as follows: TSH 0.40 uIU/ml (0.4 - 4.2) with levothyroxine supplement, thyrotropin receptor Ab (TRAB) 81.1 IU/L (0.0 - 1.75), which was significantly elevated compared with 34.6 IU/L right after thyroidectomy. A skin biopsy was performed, revealing well-differentiated myxomatous lesion involving dermis and subcutaneous fat, with a splaying of the collagen by abundant mucin representing hyaluronic acid, confirming thyroid dermopathy. Bilateral hand X-rays showed soft tissue swelling and extensive bilateral periostitis and subperiosteal bone formation in metacarpals and phalanges, consistent with thyroid acropachy. After showing non-response to a trial of Prednisone, Teprotumumab was initiated for Graves ophthalmopathy. The patient was advised to quit smoking. Following five infusions, significant improvement was observed in proptosis and orbital inflammation. The pretibial myxedematous lesion also improved. Furthermore, there was a marked decrease in swelling in bilateral metacarpals and phalanges with regaining full range of motion. All extrathyroidal manifestations further improved after the completion of a total of eight infusions of Teprotumumab, with TRAB levels down to 14.3 IU/L. Conclusion: Our case is the first example demonstrating clinical improvement in patients with thyroid acropathy following Teprotumumab treatment. This observation implies that the pathophysiology of thyroid acropathy encompasses the interplay between TSH receptor and IGF-1 receptor signaling, akin to Grave ophthalmopathy, and suggests that the direct skeletal effect of TSH may be caused by the interaction with IGF-1 pathway, as shown in pre-clinical study (2). Reference: (1) Fatourechi V et al, J Clin Endocrinol Metab. 2002 (2) Boutin A et al, Front Endocrinol (Lausanne). 2020
Presentation: 6/1/2024
7553 Thyroid Paraganglioma: A Complex Tale of the Familiar Thyroid Nodule
Authors: Moorthy Vivek , Kondapally Apoorva , Kimball-Ravari Laura Elizabeth 
Published: October 2024

Abstract
Disclosure: V. Moorthy: None. A. Kondapally: None. L.E. Kimball-Ravari: None.
Background: Thyroid paragangliomas are rare and often misdiagnosed on fine-needle aspiration (FNA). Clinical Case & Discussion: A 58-year-old female presented with an asymptomatic “cold” thyroid nodule. Ultrasound demonstrated a 2 cm hypoechoic nodule in the isthmus. FNA yielded a follicular lesion of undetermined significance, and genomic sequencing estimated a 50% risk of malignancy prompting the patient to opt for total thyroidectomy. Histopathology and immunohistochemistry (IHC) confirmed the diagnosis of benign paraganglioma (PGL). SDH-B (succinate dehydrogenase subunit B) was notably absent on IHC. Past medical history is significant for hysterectomy for uterine fibroids and obesity, along with a confirmed family history of Hereditary Leiomyomatosis with Renal Cell Cancer (HLRCC). The patient and several family members tested positive for a pathogenic variant of fumarate hydratase (FH) gene implicated in HLRCC and undergo annual MRIs for cancer surveillance. The loss of SDH-B suggests underlying mutation. Germline SDH mutations occur in 20% of patients with pheochromocytoma and PGLs, predisposing to hereditary syndromes. PGLs are catecholamine-secreting neuroendocrine tumors with carotid body and jugular PGLs accounting for 80% of head and neck PGLs (HNPGLs). Thyroid PGLs originate from the inferior laryngeal paraganglia. They are very rare, often non-secretory, and commonly present as asymptomatic solitary nodules. For these reasons, FNA, while contraindicated, is frequently performed. If FNA is considered, pre-procedural alpha-adrenergic blockade is recommended, although catecholamine secretion triggered by FNA is uncommon. Thyroid PGLs are misdiagnosed on FNA as other thyroid neoplasms. Awareness of the more unique cytopathology of thyroid PGLs and a comprehensive IHC can aid in accurate diagnosis. Interestingly, SDH (complex 2) and FH are closely linked enzymes in the Krebs cycle. Emerging evidence correlates germline FH mutations and hereditary pheochromocytoma-paraganglioma. PGLs are less commonly associated with MEN 2A and 2B, NF type 1, VHL, and Carney-Stratakis syndrome and Carney triad. Therefore, additional testing for SDH, RET, VHL and MAX genes was recommended in this case. Total thyroidectomy or lobectomy with or without elective lymph node dissection remains the treatment of choice. Annual 24-hour urine and plasma metanephrine testing will help screen for potential recurrence. Use of GLP1 agonists for weight loss in this patient warrants further genetic and safety evaluation. Clinical Lesson/Conclusion: Often misdiagnosed on FNA, thyroid paragangliomas are rare, with multiple genetic predispositions. FNA is contraindicated and if considered, must be performed after alpha-blockade. Germline SDH mutations are implicated in PGLs and increasing evidence links FH mutations to hereditary PGLs.
Presentation: 6/3/2024
8113 Thyroid Storm in a Patient with Thyroid Nodule on Anticoagulation
Authors: Kulkarni Rohit , Krishnasamy Sathya S , Mon Nandar , Downs Richard 
Published: October 2024

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 &gt;500 U/L. Burch-Wartofsky Point Scale score was &gt;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
9355 Thyroid Storm: In the Aftermath of Thyrotropin Stimulated Scan
Authors: Bhandari S , Jamshed I , Bag A , Rastogi N , Ramsetty A 
Published: October 2024

Abstract
Disclosure: S. Bhandari: None. I. Jamshed: None. A. Bag: None. N. Rastogi: None. A. Ramsetty: None.
Introduction: Cases of thyroid storm have been reported in metastatic follicular thyroid cancer following surgery and radioactive iodine treatment [1]. Our patient developed thyroid storm after receiving thyrotropin followed by radioactive iodine scan (RAIU), a phenomenon not described in any formal reports to date. Clinical Case:74-year-old woman with history of metastatic follicular thyroid cancer, presented with altered mental status. CT head was negative. CT C/A/P showed heterogeneous thyroid gland with substernal extension, lucent 2 cm lesion involving T10 vertebrae. She had received 0.9 mg of recombinant human thyrotropin (rhTSH) 2 days before presentation and had thyrotropin-stimulated whole-body scan, and RAIU scan showing enlarged multinodular goiter. RhTSH is used to augment the thyroid radioiodine uptake (RAIU) in the surveillance of thyroid cancer without rendering the patient hypothyroid. TSH was 0.008 ng/ml (n 0.270-4.200 UIU/ml) a month back. Labs now revealed TSH 6.58 UIU/ml (reflecting residual rhTSH activity), total T4 19.8 ng/dl (n 4.9-11.7 ng/dl), free T4 3.0 ng/dl (n 0.7-1.5 ng/dl), total T3 2.52 ng/ml (n 0.35-1.93 ng/ml) and thyroglobulin 2525 ng/ml (n 2.8-40.9 ng/ml) concerning for thyroid storm. Treatment with IV hydrocortisone, methimazole, and beta blockers was initiated which led to normalization of thyroid levels (TSH 3.75 UIU/ml, Total T4 10.6 ng/dl, Free T4 1.4 ng/dl, Total T3 0.47 ng/ml), and clinical improvement.Our patient had a co-occurrence of follicular thyroid cancer with multinodular goiter. Administration of thyrogen could have activated the multinodular goiter leading to precipitation of thyroid storm. Thyroid storm in patients with thyroid cancer following treatment is usually due to destruction of thyroid tissues and activation of metastatic thyroid glands from the primary tumor[2]. Thyroidectomy or radioactive ablation of thyroid is the definitive treatment. Patients should however be bridged to euthyroid state prior to this. Our case highlights a unique presentation in terms of pathophysiology for patients with thyroid cancer in the setting of thyrogen use. Conclusion: Although rare, if patients with known thyroid cancer receive thyrotropin subsequently develop symptoms concerning for thyroid storm, clinicians should evaluate with a thyroid panel for prompt diagnosis and treatment. References: 1.Raef H, Dahhan T, Ahmed M, et alRecurrent thyroid storm induced by heretofore unrecognised causes in a patient with thyroid cancer Case Reports 2009;2009:bcr0720080442. 2.Folkestad L, Brandt F, Brix T, Vogsen M, Bastholt L, Grupe P, Krogh Petersen J, Hegedüs L. Total Thyroidectomy for Thyroid Cancer Followed by Thyroid Storm due to Thyrotropin Receptor Antibody Stimulation of Metastatic Thyroid Tissue. Eur Thyroid J. 2017 Sep;6(5):276-280. doi: 10.1159/000479061. Epub 2017 Aug 3. PMID: 29071241; PMCID: PMC5649237.
Presentation: 6/1/2024
7342 Thyrotoxic Periodic Paralysis
Authors: Arora Gunjan 
Published: October 2024

Abstract
Disclosure: G. Arora: None.
Case presentation: A 40 year old male with no significant past medical history presented to the emergency department with diffuse body weakness for one day. On the night prior to admission, his thighs started getting sore which in a matter of a few hours, progressed to weakness involving his entire body. He was unable to flex his hips, shoulders, and neck. He was unable to get up or move without assistance. He was found to have an irregular heartbeat two weeks prior to admission and had undergone a thyroid ultrasound which showed inflammation of the thyroid gland. He was not started on any new medications. He endorsed fatigue, palpitations, neck swelling, and 45 lbs unintentional weight loss over 6 months. No fever, chills, vision changes, congestion, chest pain, shortness of breath, cough, tingling, numbness or weakness. He denied alcohol or drug use. Physical examination was notable for blood pressure 151/80 mm Hg, heart rate 120 bpm, enlarged thyroid gland tender to palpation, and muscle weakness (motor strength 3/5 in flexors and extensors of hips and knees). Labs were notable for K 2.3 (3.5 - 5.1 mmol/L), ALP 218 (32 - 91 U/L), TSH &lt;0.010 (0.400 - 4.300 mcIU/mL), Free T4 3.5 (0.6 - 1.6 ng/dL), CK 608 (49 - 397 U/L). Urine toxicology was negative. MRI spine did not show any acute abnormality except for thyromegaly. He received potassium supplementation which led to symptomatic improvement and was admitted to medical floor. Further tests revealed: TSI 39.50 (&lt;=0.54 IU/L), TSH receptor antibody 26 (&lt;=1.75 IU/L), thyroid microsomal antibody 773.3 (0.0 - 9.0 IU/mL), anti-thyroglobulin antibody 4 (&lt;4 IU/mL). Thyroid ultrasound showed an enlarged, heterogenous, hypervascular thyroid without any nodules. He was started on Propranolol and Propylthiouracil, which led to symptom resolution and he was discharged. Discussion: Thyrotoxic periodic paralysis (TPP) is a rare muscle disorder, belonging to the family of diseases called channelopathies. Thyroid hormone increases tissue responsiveness to beta-adrenergic stimulation, which increases Na-K ATPase activity on the skeletal muscle membrane driving potassium into cells. This leads to hyperpolarization of the muscle membrane and relative inexcitability of the muscle fibers, especially in the presence of a trigger such as provocation with exercise, fasting state or a high carbohydrate meal (insulin stimulates Na-K ATPase pump). Furthermore, more than 95% of TPP cases occur in males. This predominance is due to androgen-induced Na-K ATPase sensitization, more pronounced hyperinsulinemia, comparatively higher sympathetic and catecholamine-induced Na-K ATPase activity and higher muscle mass in males. Given the life-threatening association of severe hypokalemia, TPP should be considered in all patients presenting with acute painless muscle weakness.
Presentation: 6/3/2024
7683 Tipping the Balance: Development of Graves’ Disease in a Patient with Longstanding Hashimoto’s Thyroiditis
Authors: Hazen K S , Gigliotti B J 
Published: October 2024

Abstract
Disclosure: K.S. Hazen: None. B.J. Gigliotti: None.
Background: Development of persistent Graves’ hyperthyroidism in patients with hypothyroidism from Hashimoto’s thyroiditis is a rare phenomenon that is presumed to be due to a shift in the shift in the balance of inhibitory, neutral, and stimulatory thyroid stimulating hormone (TSH) receptor autoantibodies. Clinical Case: A 70-year-old female with a history of obstructive sleep apnea, hypertension, hyperlipidemia, osteopenia, positive antinuclear antibody, positive antinuclear ribonucleoprotein antibody, and hypothyroidism on relatively stable dose of levothyroxine 75 mcg 6 days weekly for about 20 years was slowly weaned off levothyroxine over 3 years by her primary care physician due to persistently low TSH levels. Symptoms included increased thirst, cold intolerance, dry skin, increased appetite, and fatigue. Exam showed no thyromegaly. Despite levothyroxine discontinuation, her TSH remained suppressed at 0.21 uIU/mL (0.27-4.20 uIU/mL) with normal free T4 1.0 ng/dL (0.9-1.7 ng/dL) and total T3 122 ng/dL (80-200 ng/dL). The patient had been taking biotin, but thyroid function testing remained unchanged after discontinuation. Additional testing revealed a thyroid stimulating immunoglobulin (TSI) 29.30 IU/L (&lt;= 0.54 IU/L), TSH receptor antibody 33.40 IU/L (&lt;= 1.75 IU/L), thyroglobulin Ab &gt;2,500.0 IU/ml (0.0-3.9 IU/mL), and thyroid peroxidase Ab 2,792.8 IU/mL (0.0-8.9 IU/mL). After remaining off the levothyroxine for several months, her TSH rose to 11.20 uIU/ml (0.27-4.20 uIU/mL) and she was restarted on low dose levothyroxine with a subsequent decrease in TSH to 0.11 uIU/ml (0.27-4.20 uIU/mL) after 5 weeks. Conclusion: This case demonstrated a rare situation in which a patient with hypothyroidism from Hashimoto’s thyroiditis subsequently developed hyperthyroidism from Graves’ disease. Given she was not on a weight-based levothyroxine replacement dose, it is suspected she still had underlying active thyroid tissue that was able to respond to stimulatory antibodies. Elevation of the TSH receptor antibody and TSI suggest that the patient also had underlying Graves’ disease with either new onset, or a possible shift of antibodies from inhibitory or neutral to stimulatory, resulting in decreased levothyroxine requirement and subsequent endogenous hyperthyroidism. This demonstrates the importance of considering non-iatrogenic causes of dramatic changes in levothyroxine dose requirements and close monitoring required for such patients.
Presentation: 6/2/2024
8208 Unexpected And Significant Rise In TSH In The Setting Of Relugolix Use
Authors: Groysman A Y , Poloju A , Majety P , Abraham T 
Published: October 2024

Abstract
Disclosure: A.Y. Groysman: None. A. Poloju: None. P. Majety: None. T. Abraham: None.
Background: Relugolix is a gonadotropin-releasing hormone antagonist used as androgen deprivation therapy for metastatic and nonmetastatic castration-resistant prostate cancer that was FDA-approved in December 2020. Common side effects include hot flashes, increased glucose and triglycerides, and decreased hemoglobin. We report a case of Relugolix interference with the absorption of levothyroxine, which has not been reported in the literature. Case: A 79-year-old white man with high-risk, Gleason 9 prostate cancer and Hashimoto’s hypothyroidism presented for evaluation of elevated thyroid stimulating hormone (TSH) level- 52.87 mIU/L (0.28-4.10 mIU/L). He did not have cold intolerance, constipation, fatigue, or weight gain. He was diagnosed with hypothyroidism in 1998 and was on a stable dose of levothyroxine 88mcg daily from 2016 until the time of this presentation. He is adherent and reports following a routine of having breakfast with coffee soon after taking levothyroxine for many years. In June 2022, his TSH was 4.48 mIU/L. In July 2022, he started taking Relugolix along with levothyroxine. Following this, his TSH levels increased to 30.08 mIU/L (FT4: 0.67 ng/dL), 35.43 mIU/L (FT4: 0.57 ng/dL), 52.87 mIU/L (FT4: 0.48 ng/dL) on 2/24/23, 3/3/23, and 3/14/23, respectively. No new medications were reported. His other medications were atorvastatin, tamsulosin, and vitamin D, which he took at night. He did not take calcium or biotin supplements. He had gradual weight gain (8 lbs) over the last 9 months. Levothyroxine dose was increased from 88 to 125 mcg daily and he was instructed to separate Relugolix from levothyroxine so he started taking Relugolix at bedtime. Repeat TSH was low at 0.12 mIU/L. The levothyroxine dose was eventually titrated back to 88 mcg daily and TSH was 5.2 (appropriate for age). Conclusion: Several medications are known to interfere with the absorption of levothyroxine. Our case suggests that Relugolix may be one of them. The significant rise in TSH and levothyroxine requirements months after starting Relugolix and the ability to return to the previous dose of levothyroxine only by separating Relugolix from levothyroxine strongly suggests that there is an interference between these medications that has not been reported.
Presentation: 6/2/2024