bluuebunny/crossref_metadata_2025_split huggingface dataset:
12475 Revisiting Myxedema Coma
Authors: Hamad Islam Muhammad , Jimenez Corado Daniel Ricardo , Siddiqui Shiza , Aquino Camey Maria Fernanda , Yeasmin Shamima 
Published: October 2024

Abstract
Disclosure: M.H. Islam: None. D.R. Jimenez Corado: None. S. Siddiqui: None. M.F. Aquino Camey: None. S. Yeasmin: None.
Background: Myxedema coma is a rare and life-threatening complication of hypothyroidism.Although it is rare in the era of better diagnostics and treatment modalities, its life-threatening nature mandates its timely recognition and better understanding. Case:81-year-old female with a history of hypothyroidism (unclear medication compliance) and alcohol use disorder was admitted due to alcohol withdrawal and treated with benzodiazepines. A few days prior to the presentation, she was found to have worsening confusion, unsteady gait, and multiple falls. On presentation, she was hemodynamically stable, tremulous, anxious, and oriented to person only. Blood work was remarkable for mild transaminitis. CT scan of the head revealed sequelae of microvascular disease. The day after admission, she was noted to be lethargic, and benzodiazepines were held. Later, she became hypothermic, hypotensive, bradycardic, and hyponatremic. Further investigation was pursued, revealing a TSH of 55 (normal 0.27 to 4.2 mlU/L), free T4 of &lt;0.10 ng/dL (normal 0.8-1.7 ng/dL), free T3 of &lt;1.0 pg/mL (normal 2.2-4 pg/mL), and cortisol of 10.7 ug/dL. Due to concerns of myxedema coma, she was started on stress dose steroids and IV levothyroxine. She was transferred to the ICU as her mental status continued to deteriorate; she underwent endotracheal intubation and received additional doses of IV levothyroxine and liothyronine. After a few days, her clinical condition and her cortisol, free T4, and free T3 levels improved; she was extubated and later discharged with an adjusted levothyroxine dose. Conclusion: It is of absolute importance to keep myxedema coma as a differential diagnosis when evaluating encephalopathic elderly patients, especially those with a history of thyroid disorders.There is a paucity of evidence to suggest a clear benefit of combining levothyroxine-liothyronine over levothyroxine alone. Treating initially with intravenous levothyroxine over oral is beneficial, as GI absorption and bioavailability are likely variable and unpredictable. In this case, oral liothyronine was used with IV levothyroxine to speed up clinical and biochemical recovery.Adrenal insufficiency often coexists with hypothyroidism, with considerable overlap in clinical features like hypotension, hypoglycemia, and hyponatremia. Administration of levothyroxine before steroids can lead to a rapid increase in metabolic rate and subsequent depletion of the existing reserves. Considering this, it can be said with fair confidence that patients need prior or concomitant stress doses of corticosteroids on an emergent basis. Later, biochemical testing can be done to evaluate the functioning of the hypothalamic-pituitary-adrenal axis and then adjust steroid doses accordingly.
Presentation: 6/1/2024
5103 Synthroid Absorption Conundrum: A Case Deciphered
Authors: Nadeem Hana , Alzohaili Opada 
Published: October 2024

Abstract
Disclosure: H. Nadeem: None. O. Alzohaili: None.
Hypothyroidism is a disorder requiring lifelong Synthroid therapy. Untreated patients have high morbidity rate and suffer from weight gain, cold intolerance, fatigue and constipation. Inadequate therapeutic outcomes may result in the case of malabsorption, like GI tract conditions, medication interactions and dietary ingredients. Here, we describe the case of a 50-year-old woman who despite compliance to therapy, had refractory hypothyroidism. Complexity of unexplained Synthroid malabsorption is highlighted, emphasizing the importance of managing and optimizing thyroid hormone replacement therapy. A 50-year-old woman with a history of papillary carcinoma s/p thyroidectomy and radioactive iodine therapy came in with fatigue, weight gain and constipation. Despite taking Synthroid 150 mcg, thyroid function tests (TFTs) remained high with TSH 150 uIU/mL and fT4 0.25 ng/dL. Her dose was gradually increased until it reached 1800 mcg yet repeat TFTs showed refractory hypothyroidism with TSH 179 uIU/mL, fT4 0.8 ng/dL. Compliance was addressed to which she demonstrated strict adherence, while avoiding concurrent intake of food, supplements or medications interfering with the absorption. Autoimmune conditions were ruled out and no dietary patterns affecting absorption were identified. A thyroid absorption test was then performed, during which 2100 mcg of Synthroid were given orally in the AM, and thyroid hormones were measured for 8 hours. She was found to have a TSH in 200s uIU/mL and fT4 &lt;0.10 ng/dL, deeming her to have refractory hypothyroidism. She was seen by GI and had an EGD/ colonoscopy, revealing no abnormalities. In a follow up visit, she was still complaining of the same symptoms, periorbital edema, and mild confusion. Her TSH was still elevated at 225 uIU/mL. She was then started on IV 500 mcg of weekly Synthroid infusions and after several weeks, she reported symptoms improvement. Subsequent TFTs showed a progress in TSH, now 26.6 uIU/mL, with fT4 1 ng/dL, indicating successful management of Synthroid malabsorption. During this process, she had a nutritional assessment and was consistently having hyperlipidemia with LDL 243 mg/dL. She was compliant with Praluent and max dose of atorvastatin 80 mg, but LDL only decreased to 134 mg/dL after adjusting her thyroid hormone levels. With nonadherence being the top cause of medication non responsiveness, ruling out causes of malabsorption is vital. In this case, compliance, nutritional assessment, medication interactions, GI abnormalities, autoimmune conditions were all addressed and no interfering factors were identified. IV treatment with unexplained thyroid hormone malabsorption was the effective treatment, ultimately improving outcomes. With the hope to transition her to oral medication, the possibility of it happening is still not clear. More research is necessary to discover the underlying causes in such an exceptional case.
Presentation: 6/2/2024
8078 TERT Positive Thyroid Nodule in the Setting of Metastatic Melanoma
Authors: Langnas Emily , Chao Shing , Gomes Kellyann M , Bhan Arti 
Published: October 2024

Abstract
Disclosure: E. Langnas: None. S. Chao: None. K.M. Gomes: None. A. Bhan: None.
Metastatic disease to the thyroid gland is uncommon with a reported incidence of up to 4% in post-surgical specimens. Lung cancer is the most common primary tumor site in autopsy series. Clinically, renal cell carcinoma is the most common primary tumor site. Metastatic melanoma to the thyroid gland is clinically rare, however, in autopsy series, it has been reported with incidence of up to 39%. A 61-year-old man presented to the endocrinology clinic for an incidentally detected thyroid nodule. He had recently presented with a chronic cough, prompting a chest x-ray that revealed pulmonary nodules. Subsequent computed tomography (CT) showed numerous bilateral lung nodules measuring up to 2.5 cm and an incidental thyroid nodule. Ultrasound of the thyroid identified a 2.7 cm mixed cystic-solid right thyroid nodule. No risk factors for thyroid cancer were identified. His TSH was 3.51uIU (0.45 - 5.33 uIU/mL). The thyroid nodule was biopsied, and pathology revealed atypical spindle cells with irregular nuclear membranes and scattered histiocytes. A further review with cytopathology suggested non-thyroidal origin of the cells. Molecular testing with AFIRMA reported a telomerase reverse transcriptase (TERT) promoter mutation at C228T. The sequencing was negative for TERT C250T, BRAF, RET, PETC1, PTC3 and MTC. Due to concerns about metastatic disease, a positron-emission tomography (PET)-CT was conducted, revealing hypermetabolic lesions in numerous bilateral lung nodules, right thyroid nodule, porta hepatis lymph node, and a soft tissue nodule within the greater curvature of the gastric body. Subsequent biopsies of the right lung and gastric body confirmed the diagnosis of metastatic melanoma. On further questioning, it was found that the patient had a history of a skin lesion on his back that was excised several years ago with pathology reporting tumoral melanosis. Malignant melanoma has a poor prognosis due to high recurrence and metastatic rates. In melanoma, TERT promoter mutations are the most common mutations in noncoding regulatory regions. TERT C228T mutations and C250T mutations are seen in malignant melanoma and studies have shown that TERT promoter mutations are associated with aggressive clinical behavior. These TERT promoter mutations can also be seen in various other cancers including primary thyroid cancers with a similar association with more aggressive thyroid tumor characteristics. Our case describes a patient with a thyroid nodule and molecular testing noting a TERT promoter mutation. Both primary thyroid cancer and metastatic disease to the thyroid should be considered in these cases. This case also highlights the importance of obtaining a thorough history of prior malignancy in patients with thyroid nodules to assess the risk of metastatic disease.
Presentation: 6/1/2024
8490 The mRNA for the Nonsyndromic Deafness Gene Atp2b2 Is Reduced Following Developmental Hypothyroidism
Authors: Gregersen Emily A , Patrick Peeters Robin , Forrest Douglas , Sharlin David S 
Published: October 2024

Abstract
Disclosure: E.A. Gregersen: None. R.P. Peeters: None. D. Forrest: None. D.S. Sharlin: None.
Thyroid hormone (TH) is essential for auditory system development. In rodent models, low levels of TH during the early postnatal period delay cochlear tissue remodeling and alter ion channel function required for normal auditory function. TH receptors are ligand-dependent transcription factors that regulate gene expression. Considering this, auditory deficits observed in hypothyroidism are thought to be largely the result of altered expression of specific TH target genes. However, few TH-regulated genes in the developing cochlea have been reported. TH is reported to impact calcium signaling in several tissues, but whether regulators of calcium signaling are altered following developmental hypothyroidism in the cochlea is largely unexplored. In this report, we investigated the spatial and temporal expression of the ATPase, Ca++ transporting, plasma membrane 2 (Atp2b2) gene in a mouse model of developmental hypothyroidism. Timed-pregnant dams were treated with thyroid gland inhibitors to induce developmental TH insufficiency from embryonic day 12.5 (E12.5) through post-natal day 15 (P15). Untreated timed-pregnant dams served as euthyroid controls. Control and experimental cochleae were collected over a developmental period ranging from embryonic day 18.5 (E18.5) through P15. Cochleae were then processed to detect Atp2b2 mRNA by in situ hybridization or quantitative real-time PCR. In situ hybridization showed that Atp2b2 localizes to inner and outer hair cells as expected, but Atp2b2 was also observed at lower levels in the greater epithelial ridge and spiral ganglion. Quantification of Atp2b2 mRNA revealed an effect of postnatal day and treatment on Atp2b2. In euthyroid animals, Atp2b2 expression gradually increased until P10, then decreased slightly by P15. In hypothyroid animals, Atp2b2 mRNA was consistently decreased (2-2.5 fold). Hypothyroidism similarly impacted expression regardless of sex. The reduction in Atp2b2 mRNA expression in the hypothyroid animals suggests that Atp2b2 is developmentally regulated in part by thyroid hormone signaling. This study characterizes the relationship between TH and Atp2b2 expression during early cochlear development while providing insight into abnormal cochlear development due to hypothyroidism.
Presentation: 6/3/2024
7650 Thionamide Induced Pancreatitis and Agranulocytosis, a Rare Case of Concurrence
Authors: Lin Jack , Shariff Julia 
Published: October 2024

Abstract
Disclosure: J. Lin: None. J. Shariff: None.
Introduction: Thionamides are considered first line in the treatment of Graves’ Disease due to their efficacy and safety. We present a case of Graves’ in which methimazole resulted in not only agranulocytosis but also pancreatitis. Case Report: A 29yo female was diagnosed with Graves’ 5 months postpartum by her PCP. Her labs at diagnosis revealed a TSH &lt;0.01 uIU/mL, free T4 of 6.4 ng/dL, and positive TRAb. She was started on methimazole 10mg and propranolol 20mg three times a day by her PCP. One month after starting treatment, she presented to the ED due to throat pain/fevers and was diagnosed with tonsilitis. She was given a 10mg dose of dexamethasone and sent home with antibiotics. No labs were drawn that visit. She went to her PCP 3 days later due to persistent symptoms and nausea/vomiting. A CBC revealed she had a WBC of 0.7 K/uL and an absolute neutrophil count (ANC) of 0.1 K/uL. Her last dose of methimazole had been the day prior to seeing her PCP. It was recommended she be seen in the ED due to concern for agranulocytosis where she was started on antibiotics and a CT abdomen pelvis with contrast revealed she had acute pancreatitis. She was admitted and started on filgrastim 5mcg/kg daily for thionamide-induced agranulocytosis. Her pancreatitis improved with conservative measures. Her propranolol was resumed at 30mg three times a day with symptom improvement. On her fifth hospitalization day, her ANC had recovered to 2.22 K/uL, WBC was 6 K/uL. Her free T4 was 1.65 ng/dL, free T3 4.1 pg/mL, TSI &gt;40 IU/L. This change was suspected to be from propranolol, steroids, iodine load from her CT, and prior methimazole use. It was strongly recommended she pursue surgery that hospitalization given inability to treat her Graves’ medically. The patient refused, stating she wished to consider her options further outpatient. She would be seen one week later in a satellite ED. Her free T4 was 5.9 uIU/mL, T3 &gt;30 pg/mL, TSH &lt;0.010 uIU/mL. She left against medical advice. She subsequently declined further endocrine follow-up. Clinical Lessons: Thionamide-induced agranulocytosis is a rare but known complication of use, with some studies showing a prevalence as low as 0.2-0.5% [1]. Pancreatitis is a lesser-known complication of thionamides. There are several case reports of its occurrence, with the European Medicines Agency even listing it in the potential adverse reaction. Absolute risk of occurrence remains low, some studies showing &lt;0.4% [1]. This case shows a rare concurrence of two uncommon complications from thionamide use and brings awareness to both pancreatitis and agranulocytosis as potential adverse events. References: [1]: Lee SY, Pearce EN. Hyperthyroidism: A Review. JAMA. 2023 Oct 17;330(15): 1472-1483. doi: 10.1001/jama.2023.19052. PMID: 37847271.
Presentation: 6/2/2024
8409 Thyroid Nodules A to V: A Discussion on Thyroid Nodules and a Case Report of a Rare Thyroid Arteriovenous Malformation
Authors: Townsend Mary , Brennan Michael , Kazmierczak Chris , Czako Peter 
Published: October 2024

Abstract
Disclosure: M. Townsend: None. M. Brennan: None. C. Kazmierczak: None. P. Czako: None.
Introduction: Thyroid nodules are an increasingly common finding on imaging, and the differential is broad. Arteriovenous malformations (AVMs) are a very rare cause of thyroid lesions, with only 6 reported cases to date. Given their scarcity, there is a lack of information regarding these lesions and how they are diagnosed and managed. Our case aims to address these gaps in information. Case: A 58-yo female with a history of hypertension was found by her PCP to have an enlarged left thyroid lobe with a new left sided bruit and palpable thrill. She had undergone prior thyroid ultrasonography for the enlarged left thyroid lobe which noted dilated and tortuous vascular structures at the posterior aspect of the left thyroid consistent with varices. These were being monitored clinically. Thyroid function tests were all normal. Due to concern for atherosclerotic disease, carotid ultrasound was obtained and showed patent carotid arteries with a large left sided thyroid mass. CTA of the neck revealed the mass to be a large (6.0 x 3.0 x 2.4 cm) AVM centered at the left thyroid gland. She underwent diagnostic angiography that confirmed the size of the mass and showed predominant arterial supply from the left superior thyroidal artery as well as bilateral inferior thyroidal arteries. Since the patient was asymptomatic with no reported neck pain, dysphagia or dyspnea, non-operative management with angioembolization was pursued given the risk of significant blood loss with surgical intervention. Following angioembolization, the results and adequacy of treatment are to be followed with repeat imaging given the high risk of reoccurrence. Discussion: AVMs of the thyroid are a very rare but clinically significant cause of thyroid lesions. Left untreated, they can grow in size and lead to compression of the esophagus or trachea, serious bleeding and high output heart failure. Their presentation is often non-specific and on routine thyroid imaging they can be difficult to differentiate from malignant tumors or varices, as in the case of our patient. Management prioritizes embolization, either alone or in conjunction with surgery, depending on the clinical scenario. Regardless of the treatment modality, reoccurrence rates remain high. Conclusion: Our case aims to add to the available information about thyroid AVMs and discuss the clinical presentation, challenges in diagnosis, imaging findings and treatment modalities available to manage these lesions.
Presentation: 6/2/2024
7618 Thyroid Nodules, Normal Thyroid Levels, and Chronic Anxiety: A Case for Sub-Clinical Toxic Multinodular Goiter
Authors: Barrera Carlos M 
Published: October 2024

Abstract
Disclosure: C.M. Barrera: None.
Introduction: Chronic anxiety and panic disorders, as described in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), are the most common psychiatric conditions. Hyperthyroidism is a known cause of both chronic anxiety and panic disorder. Case 1: A 36-year-old overweight Latin female is referred for evaluation of multiple thyroid nodules. The thyroid ultrasound was heterogeneous, with multiple bilateral nodules. In her history, the patient has chronic anxiety with panic attacks resulting in frequent emergency room visits. The TSH and T4 levels were TSH 0.59 mIU/L (0.40-4.5) and T4 10.7 mcg/dL (5.1-11.9). An I[1]23- Thyroid Scan showed a hot nodule with mild suppression and an uptake of 31.8% (The top limit is 35%). The patient started methimazole 2.5 mg daily, and after two months, her chronic anxiety and panic attacks resolved. Post-methimazole TSH rose to 1.18 mIU/L, and T4 10.0 mcg/dL and she has weaned off anxiety medications. Case 2: A 49-year-old overweight Latin female is referred for increased thyroid nodules. She complained of six months of tachycardia and anxiety. The TSH and T4 levels were TSH of 0.828 mIU/L (0.40-4.5) and T4 of 7.9 mcg/dl (4.5-12.0). An I[1]23-Thyroid Scan showed no dominant hot or cold nodules, with an uptake of 36.4% (The top limit is 35%, within normal error limits). She started methimazole 5 mg daily, resolving her tachycardia and anxiety within five weeks. Post-methimazole TSH was 1.64 mIU/L (0.45-4.5), and T4 6.7 mcg/dL (4.5-12.0). Case 3: A 60-year-old overweight Latin female is referred for evaluation of multiple thyroid nodules of ten years. She complained of chronic anxiety and panic attacks for two years. The TSH and T4 were normal at TSH 0.36 mIU/L (0.35- 5.50) and T4 9.7 mcg/dL (4.5-10.9). The thyroid ultrasound showed multiple bilateral nodules. An I[1]23-Thyroid Scan showed a suspected hot nodule without appreciable suppression and an uptake of 33% (The top limit is 35%). The patient started methimazole 5 mg daily. After eight weeks, she reported the resolution of most of her chronic anxiety with post-methimazole TSH 2.39 mIU/L and T4 7.1 mcg/dL (4.5-12.0). Discussion: The normal range of TSH, typically from 0.4-4.5 mIU/L, is calculated by measuring the TSH levels among a normal population. The group range then determines the laboratory reference range. This contrasts with individual values, which have a narrower range, suggesting that each person has a unique thyroid level. This suggests that TSH levels at the extremum, associated with hyperfunctioning nodules contributing to a rise in uptake, may not be normal for that patient and may explain the anxiety and other symptoms. Learning Points: Evolving multiple autonomous thyroid nodules lowers TSH levels while raising thyroid uptake. Symptoms of chronic anxiety and panic attacks can predate abnormal thyroid levels and resolve with low-dose methimazole.
Presentation: 6/1/2024
7699 Unanticipated Harmony: PD-L1 Inhibitor Treatment for Urothelial Cancer Resolving Graves' Disease in a Patient - A Case of Immune Modulation Surprises
Authors: Tiwari Kripa , Resta Christine A 
Published: October 2024

Abstract
Disclosure: K. Tiwari: None. C.A. Resta: None.
Introduction: Programmed death ligand 1(PD-L1) inhibitors constitute a class of immune checkpoint inhibitors (ICI) employed in treating various cancers. Thyroid-related immune-related adverse events (irAEs), such as hypothyroidism, are found to be in 3.9% of patients with PD L1 treatments. This case explores a unique scenario where a patient with pre-existing Graves' disease, undergoing PD-L1 inhibitor therapy for cancer, experienced an unexpected sequence of events leading to the default treatment of Graves' disease and subsequent progression to hypothyroidism. Case Presentation: A 59-year-old male, who had been effectively managed on methimazole for Graves' disease over two years and had chosen not to pursue definitive therapy for the condition, presented with tremors and a bilaterally enlarged thyroid gland during treatment for urothelial carcinoma. Laboratory findings included a TSH of 0.03 mIU/L (nl 0.40-4.50 mIU/L), fT4 of 3.4 ng/dL (nl 0.8-1.8 ng/dl), and tT3 of 284ng/dl (nl 76-181 ng/dl). The patient had recently started treatment with Avelumab, a PD-L1 inhibitor, as maintenance therapy following 4 cycles of gemcitabine/cisplatin cycles. Concerned about worsening Graves' disease, the methimazole dose was increased, and follow-up labs were performed after three weeks. These results showed low-normal fT4 of 0.8 ng/dL, TSH of 1.01 mIU/L(N), and low T3 of 58 ng/dL. TSI was mildly elevated at 168%. Due to rapidly changing thyroid function tests and suspicion of thyroiditis, methimazole was stopped. A PET scan a week later indicated diffuse thyroid uptake consistent with thyroiditis. Repeat labs 10 days later revealed a TSH of 67.36 mIU/L(H) and fT4 of 0.4 ng/dL(L), indicative of overt primary hypothyroidism. The patient exhibited symptoms including fatigue, constipation, and cold intolerance. The patient was initiated on levothyroxine therapy to address overt primary hypothyroidism, likely secondary to destructive thyroiditis from ICI. Discussion: Thyroid irAEs are typically incidentally discovered during routine monitoring of ICI treatment. It includes thyrotoxicosis, subclinical hypothyroidism, and overt hypothyroidism. These events commonly occur in patients lacking pre-existing thyroid conditions. In contrast, our patient, with a history of Graves' disease, experienced resolution of Graves' disease following treatment with PD-L1 inhibitor use with subsequent progression to hypothyroidism. Conclusion: This case emphasizes the importance of recognizing atypical presentations of thyroid irAEs in individuals with pre-existing thyroid disorders undergoing ICI treatment.
Presentation: 6/3/2024