bluuebunny/crossref_metadata_2025_split huggingface dataset:
7527 Subacute Thyroiditis in First Trimester of Pregnancy: Rare Cause of Thyrotoxicosis
Authors: Wilcher K , Gupta A 
Published: October 2024

Abstract
Disclosure: K. Wilcher: None. A. Gupta: None.
Background: Subacute thyroiditis (SAT) is extremely rare in pregnancy with only 8 prior cases reported in the literature. SAT can result in maternal and fetal complications. In this case report, we describe a case of subacute thyroiditis presenting in the first trimester of pregnancy. Case Presentation: A 38-year-old female with past medical history of stillbirth presented with thyrotoxicosis in gestational week 10 of her pregnancy. The patient has a history of stillbirth in gestational week 38 of her first pregnancy requiring cesarean section one year prior to presentation. She was in the process of getting in vitro fertilization (IVF) and had an egg retrieval. During the process, she started on thyroxine 50 mcg daily for blood thyroid-stimulating hormone (TSH) 3.77 mcIU/mL. She became pregnant without the help of IVF and stopped thyroxine. One month later, labs showed low TSH 0.022 mcIU/mL (reference range: 0.4-4.5 mcIU/mL) and high blood free thyroxine (FT4) 1.87 ng/dL (reference range: 0.7-1.8 ng/dL). Repeat labs two weeks later showed low blood TSH 0.012 mcIU/mL, high FT4 2.08 ng/dL, and high blood free triiodothyronine (FT3) 5.2 pg/mL (reference range: 2.3-4.2 pg/mL). She was referred to endocrinology for evaluation. She reported mild intermittent right sided neck pain since diagnosis of pregnancy. She denied any history of viral infection, cough, or fever. She reported symptoms of severe nausea, mild constipation, and mild anxiety. She denied diarrhea, tremors, changes in voice, palpitations, or weight loss. Her family history is significant for hypothyroidism in her father. Physical exam demonstrated a non-tender, symmetric thyroid without enlargement or nodules. Ultrasound showed heterogenous thyroid with an ill-defined heterogenous area in the right lobe appearing pseudo-nodule, and increased vascularity. At this time, the patient was diagnosed with mild gestational hyperthyroidism with a plan to monitor thyroid hormone levels. Repeat labs two weeks later showed low blood TSH 0.005 mcIU/mL, high FT4 2.35 ng/dL, and high FT3 6.4 pg/mL. TSH-receptor antibodies, thyroid stimulating immunoglobulin, and thyroid peroxidase antibodies were normal on testing. In gestational week 16, labs showed normal TSH 2.76 mcIU/mL, low FT4 0.56 ng/dL, and low FT3 2.1 pg/mL. At that time, she started on levothyroxine 75 mcg daily and was diagnosed with subacute thyroiditis. Follow up labs in gestational weeks 18, 20, and 24 showed improvement in TSH and FT4 on thyroid hormone supplementation. Conclusion: This case report discusses the findings of SAT in first trimester pregnancy. Currently, she is in gestational week 28 and still requiring thyroid hormone supplementation. SAT in pregnancy is very rare. This case report significantly contributes to the literature and current knowledge of the prevalence, presentation, and disease process of subacute thyroiditis in first trimester pregnancy.
Presentation: 6/2/2024
6423 The Storm in a Healthy 26-year-old Hispanic Female
Authors: Reyes-Torres Paola M , Hernandez-Hernandez Marimar 
Published: October 2024

Abstract
Disclosure: P.M. Reyes-Torres: None. M. Hernandez-Hernandez: None.
Uncontrolled hyperthyroidism can cause thyrotoxicosis and lead to end-organ dysfunction known as thyroid storm. The incidence is .20 and .76 per 100,000 persons per year, with an incidence of 4.8–5.6 per 100,000 hospitalized patients. Of those hospitalized with thyrotoxicosis in the U.S., thyroid storm is diagnosed in 16%. Most commonly affects females, middle-aged patients, and Caucasians. Can be precipitated by acute illnesses, surgery, or non-compliance with medications. Symptoms are characterized by fever, cardiac and gastrointestinal dysfunction, and altered mentation along with impaired thyroid function tests.A 26-year-old Hispanic female presented to our ER complaining of palpitations, general malaise, dysphagia, and fevers after attending a social event 3 days before. Physical examination revealed a fever of 101F, restless patient with pressured speech, and diffusely enlarged non-tender thyroid without discrete nodules. Labs were remarkable for WBC: 12 000, urinalysis, b-HCG, and CXR were all negative. Burch-Wartofsky Point Scale: 55 and biochemical tests (TSH: 0.005 ml/UL, free T4 &gt;5 ng/dL, Total T3: 8.5 ng/mL, Total T4: 28.87 uG/DL, Thyroglobulin 34.81 ng/mL) for which diagnosis of thyroid storm was made. She was transferred to the ICU and treatment was initiated with fluids, Propranolol 60 mg PO q4hrs, PTU 250 mg PO q4hrs, and Hydrocortisone 300 mg IV as loading dose then 100mg IV q8hrs. TSI and TRAb were ordered. Thyroid US remarkable for bulky thyroid gland with heterogeneous, increased vascularity, no obvious cystic/solid lesions seen. Repeated tests showed a decreasing trend of free T4: 4.71 ng/dL and Total T3: 2.42ng/dL for which PTU was discontinued and Methimazole 15 mg PO BID was started. Five days after treatment started, the patient continued symptom-free and was discharged with Propranolol 60 mg PO q6hrs and Methimazole 15 mg PO BID. TSI and TRAb samples were obtained but results were pending before discharge. Follow-up was scheduled in 2 weeks with routine labs but the patient was lost to follow-up.This case highlights the importance of early recognition and treatment of thyroid storm in Hispanics, undiagnosed patients given the presenting nonspecific, life-threatening symptoms. We conclude that our patient's cause of thyrotoxicosis was an undiagnosed case of Graves Disease and the storm was most likely triggered by an upper viral respiratory tract infection. This case could potentially help physicians identify hyperthyroidism in an earlier phase, reducing incidence, mortality, and hospitalizations of thyroid storm since a variety of mimics make the diagnosis challenging. Furthermore, we could contribute to updated statistical knowledge regarding the risk of patients with thyrotoxicosis developing thyroid storm which despite advancements in technology, are currently lacking.
Presentation: 6/1/2024
7046 Thyroid Storm After Thyroidectomy Without Underlying Hyperthyroidism
Authors: White-Cotsmire A J , Kodali B , McHenry C , Rahhal M N 
Published: October 2024

Abstract
Disclosure: A.J. White-Cotsmire: None. B. Kodali: None. C. McHenry: None. M. Rahhal: None.
Background: Thyroid storm is a feared complication of total thyroidectomy; however, this is a rare phenomenon seen primarily in patients with undiagnosed or poorly controlled thyrotoxicosis from Graves’ disease. Preoperative treatment of patients with hyperthyroidism with beta-adrenergic blockers and anti-thyroid medication to ensure that patients are euthyroid prior to thyroidectomy have largely eliminated this risk of thyroid storm. (1) We report a case of thyroid storm caused by release of preformed thyroid hormone, following extensive manipulation and resection of a large retrosternal nontoxic multinodular goiter. To our knowledge, this has not yet been previously described. Clinical Case: A 57yo female underwent a total thyroidectomy with resection of a large benign multinodular goiter with retrosternal extension, which was causing compressive symptoms. She had a nodular goiter for 7 years that was increasing in size. Fine needle aspiration 2 years prior to surgery demonstrated colloid and adenomatoid nodules with Hurthle cell changes. She had no history of hypo- or hyperthyroidism. TSH prior to surgery was 0.576µIU/ml (normal = 0.450-5.330µIU/ml). Extensive manipulation was required to deliver the goiter from beneath the manubrium. Pathology from her thyroid revealed a multinodular goiter without evidence of malignancy. Post-operative course was uncomplicated, and after an overnight stay, the patient was discharged home with 150mcg (1.5mcg/kg) levothyroxine daily. She presented to the emergency department 4 days later and was admitted to the intensive care unit with diffuse abdominal pain, nausea, vomiting, and myalgias, and she was diagnosed with atrial fibrillation with rapid ventricular response. TSH on admission was 0.020 µIU/ml, thyroglobulin levels were &gt;2,250.0ng/mL (n=0.8 – 48.0 ng/mL), thyroglobulin antibodies were negative. Her levothyroxine was stopped, her heart rate was controlled with metoprolol, and she was started on oral anticoagulation with rivaroxaban. She was discharged after a 7-day hospital stay. At 3 weeks follow-up her TSH was 35.67µIU/ml and her thyroglobulin levels were 23.9ng/mL. Her symptoms had resolved, and levothyroxine was resumed at a lower dose of 137mcg daily. Six weeks later her TSH level was 7.785µIU/ml, and her thyroglobulin was 1.8ng/mL. Conclusion: To our knowledge, this is the first case of thyroid storm reported following thyroidectomy in a patient with nontoxic multinodular goiter in a clinically and biochemically euthyroid patient. Massive increase in thyroglobulin postoperatively and rapid resolution of symptoms suggest that the release of preformed thyroid hormone related to vigorous thyroid manipulation was likely the cause. Reference: (1) Christou N, Mathonnet M. Complications after total thyroidectomy. Journal of Visceral Surgery. 2013;150(4):249-256. doi:10.1016/j.jviscsurg.2013.04.003
Presentation: 6/1/2024
8238 Thyroidectomy for Thyroid Storm Complicated by Drug-Induced Hepatotoxicity and Thyrotoxic Cardiopulmonary Disease
Authors: John Tara A , Suarez Audry C , Genkil Jessica , Patil Shivaraj , Anastasopoulou Catherine 
Published: October 2024

Abstract
Disclosure: T.A. John: None. A.C. Suarez: None. J. Genkil: None. S. Patil: None. C. Anastasopoulou: None.
Case Presentation: A 59-year-old female with hypertension and type 2 diabetes presented with palpitations, and several months of hyperthyroid symptoms, lower extremity swelling, and dyspnea on exertion. On presentation, patient was diaphoretic, tachycardic, volume overloaded and had symmetric swelling of the thyroid gland. Lab results revealed FT4 3.28 ng/dL, total T3 384.59 ng/dL, TSH &lt; 0.01 µIU/mland elevated TSI. Electrocardiogram showed sinus tachycardia. Chest radiography showed pulmonary edema. Echocardiography showed a reduced ejection fraction of 35%, dilation of right ventricle, severe mitral and tricuspid regurgitation, and severely elevated pulmonary artery systolic pressure (55-60 mm Hg). Thyroid ultrasound revealed enlarged, heterogeneous thyroid gland with normal vascularity. The diagnosis of thyroid storm due to Graves' disease was made with a score of 50 on the Burch-Wartofsky Point Scale. Patient was started on propylthiouracil (PTU), metoprolol tartrate and furosemide. Corticosteroid therapy was not utilized due to the risk of worsening heart failure from sodium retention. After two days of PTU, patient developed drug induced liver injury (DILI). Patient was then transitioned to methimazole which was also discontinued thereafter due to progression of DILI. She was started on potassium iodide to suppress thyroid hormone production, and N-Acetyl cysteine (NAC) for DILI. Due to persistent thyrotoxicosis, the patient underwent a total thyroidectomy on hospital day 13 and was started on levothyroxine for post-surgical hypothyroidism. Liver function returned to normal on day 16. A surveillance echocardiogram obtained 3 months later showed recovered biventricular function (ejection fraction 55-60%), mild mitral and tricuspid regurgitation and normal pulmonary pressures. Educational value: Thyroid storm is an uncommon, life-threatening emergency. Thioamides remain the cornerstone of treatment, but rarely, they can result in adverse events such as hepatotoxicity. When thioamides are contraindicated, other agents (e.g., iodine, lithium, potassium perchlorate, cholestyramine, glucocorticoids) can be utilized; however, refractory cases might require total thyroidectomy as definitive treatments. Our patient had marked recovery of cardiac function and resolution of pulmonary hypertension and DILI after timely surgical intervention. Multidisciplinary care is pivotal for the successful management of thyroid storm.
Presentation: 6/3/2024
12598 Tides of the Thyroid: Myxedema Ascites Unveiled
Authors: O’Neal Eric , Duong Diana , Caplan Michael , Bird Kimberly 
Published: October 2024

Abstract
Disclosure: E. O'Neal: None. D. Duong: None. M. Caplan: None. K. Bird: None.
Background: Primary hypothyroidism is a common clinical condition, complicated by ascites in less than 4% of cases. Myxedema ascites, caused by hypothyroidism, is also a rare cause of ascites in less than 1% of new onsets. Clinical Case: We present a 78-year-old female who initially presented to the hospital for abdominal swelling. CT of the abdomen/pelvis revealed a large amount of ascites in the abdomen and pelvis, along with bilateral pleural effusions. Labs were remarkable for a TSH level of 149 uIU/mL and a free T4 level of 0.41 ng/dL. A review of the patient’s chart showed a period of hyperthyroidism in 2022, and the patient had been placed on methimazole 10 mg by mouth daily. After several months, the patient transitioned to hypothyroidism. Methimazole was discontinued and levothyroxine was initiated. Improper medication reconciliation later occurred when she was admitted into a nursing home, causing the patient to be on methimazole and levothyroxine concomitantly in the outpatient setting. During the patient’s hospitalization, three liters of ascitic fluid were removed via ultrasound-guided paracentesis. The etiology of hypothyroidism-induced ascites includes multiple theories. This unique phenomenon can be explained by the following: increasing capillary permeability due to low levels of circulating thyroid hormone, formation of hyaluronic acid-albumin complexes, low nitric oxide, increased Vascular Endothelial Growth Factor, and diminished free water clearance due to excess Antidiuretic Hormone. When capillary permeability is elevated, this allows for protein extravasation. Lymphatic homeostasis becomes compromised, and this leads to the development of ascites. Investigations for this condition include an abdominal paracentesis and ascitic fluid analysis, which demonstrates an elevated protein count and lymphocyte count, with variability in leukocyte count and serum-ascites albumin gradient. Treatment for this reversible condition requires adequate thyroid replacement therapy. Our patient’s levothyroxine was increased to 100 mcg by mouth daily, and the patient demonstrated an appropriate response with monitoring of TSH. Discussion: Although ascites is typically thought to be of hepatic or cardiac origin, it is important to remember to rule out other potential causes such as thyroid disease. Reference: [1] Khalid, S., Asad-Ur-Rahman F., Abbass, A., Gordon, D., Abusaada, K. Myxedema Ascites: A Rare Presentation of Uncontrolled Hypothyroidism. Cureus 2016 Dec;8(12); e912.
Presentation: 6/2/2024
7962 Transformation of Poorly Differentiated Papillary Thyroid Carcinoma to Anaplastic Thyroid Carcinoma, an Atypical Course!
Authors: Altaweel Tamara , Makadsi Sarah , Hussein Marwah , Samantray Julie 
Published: October 2024

Abstract
Disclosure: T. Altaweel: None. S. Makadsi: None. M. Hussein: None. J. Samantray: None.
Introduction: Anaplastic thyroid cancers are undifferentiated, rare and aggressive. The transformation of papillary thyroid cancer to anaplastic thyroid cancer is documented in literature, however, rare. In this report, we present a case of Anaplastic thyroid carcinoma likely arising from a co-existing poorly differentiated Papillary carcinoma. Case Presentation: A 74-year-old male with past medical history of tobacco smoking who presented with the onset of voice hoarseness for 6 months. He has also noticed a left neck mass that is in the mid supraclavicular region. A Neck CT neck was performed at the time of presentation and was significant for a 4.6x3.4x5.9 cm left thyroid mass with displacement of the trachea. FNA biopsy showed papillary carcinoma with focal features of Tall Cell Variant. Poorly differentiated components with fragments of stroma and muscle were seen and suggested invasion. These findings raised the possibility of anaplastic thyroid carcinoma in the setting of papillary carcinoma and poorly differentiated carcinoma. BRAF V600E pathogenic variant mutation along with TERT mutation were found. Patient underwent direct laryngoscopy, bronchoscopy with biopsies, and tracheostomy with surgical pathology confirming papillary thyroid cancer with muscles invasion. Combination dabrafenib and trametinib were started. No surgical resection of thyroid tissue was planned. A follow up CT showed a significant decrease in the low-density soft tissue involving the medial thyroid gland bilaterally, consistent with interim positive response to therapy. Three months later, CT neck showed near complete resolution of low-density soft tissue involving the medial thyroid and parathyroid glands and subglottic trachea consistent with further interim positive response to therapy. Six months post initiation of therapy, CT Neck showed focal low density in the mid and inferior right thyroid gland which may represent residual and/or recurrent thyroid carcinoma. That density was further demonstrated on a repeat CT neck as a 1.8 cm hypodense nodule in the inferior right thyroid gland and concerning for recurrent thyroid tumor with possible infiltration of the trachea. Conclusion: ATC prognosis is affected by many factors such as metastasis, age, treatment strategies, socioeconomic status and the presence of BRAF V600E and TERT mutations. Diagnosis can be challenging. Our patient presented months after his symptoms started and this is an atypical course of Anaplastic Thyroid Carcinoma as it usually progresses aggressively and rapidly. Given the pathology reports and the more slow presentation of this patient’s carcinoma, it can be suggested that this is a case of papillary carcinoma with a later transformation to ATC. In these cases, surgical resection
Presentation: 6/2/2024
7617 Two Cases of Severe Beta-hCG-Mediated Hyperthyroidism with Gestational Trophoblastic Disease
Authors: Morvant A , Mashayekhi M 
Published: October 2024

Abstract
Disclosure: A. Morvant: None. M. Mashayekhi: None.
Introduction: Hyperthyroidism is most commonly caused by Graves’ disease and toxic nodules and affects 2.5% of the world’s population. Hyperthyroidism due to elevations in beta-hCG (b-hCG), which has thyroid-stimulating activity due to homology with TSH, is a rare process that requires high clinical suspicion. We present two cases of hyperthyroidism caused by severely elevated b-hCG due to gestational trophoblastic disease (GTD), with rapid resolution of hyperthyroidism after treatment of the underlying conditions. Clinical Cases Case 1: A 35-year-old at 28-weeks gestation presented with dyspnea, palpitations, and 6-pound weight loss over the prior month. Labs revealed b-hCG 5.2 million (0-5 mIU/mL), TSH &lt;0.015 (0.35-3.6 mcU/mL), and free T4 2.42 (0.7-1.37 ng/dL). Imaging revealed extensive pulmonary lesions concerning for metastatic disease and a 2.4 cm ovarian mass. Due to worsening respiratory distress and the need to start chemotherapy urgently, she underwent Cesarean section to deliver the viable infant and take out the ovarian mass. Pathology confirmed choriocarcinoma. Methimazole was started post-operatively, and she started chemotherapy. Labs after cycle one of chemotherapy showed b-hCG 1.3 million, TSH &lt;0.015, and free T4 1.46. The methimazole dose was decreased and ultimately stopped as free T4 levels decreased with subsequent chemotherapy cycles. After three cycles, labs showed b-hCG 4,652, TSH 1.55, and free T4 0.68. She was discharged without thyroid-targeting therapy. Case 2: A 33-year-old woman at 12-weeks gestation presented with nausea, vomiting, and 10-pound weight loss over 1 month. Labs showed TSH &lt;0.015, free T4 2.39, and total T3 351 (58-160 ng/dL), which were thought to be due to hyperemesis gravidarum. Two months later she presented with vaginal bleeding and imaging showed an enlarged placenta with a moth-eaten appearance and theca lutein cysts concerning for partial molar pregnancy. Beta-hCG level was 3.3 million, TSH &lt;0.015, free T4 1.76, and total T3 289. She underwent dilation and evacuation and pathology confirmed partial hydatidiform mole. Beta-hCG level decreased to 1.8 million and free T4 normalized after surgery, with b-hCG 3,300, normal TSH, and normal total T3 one month later. Conclusion: These cases highlight the importance of considering possible GTD when evaluating a patient with hyperthyroidism, particularly in women of childbearing age and cases of early pregnancy when the degree of hyperthyroidism seems out of proportion to that expected. Clinicians should consider checking a b-hCG level in consultation with an obstetrician when indicated. Treatment is aimed at the GTD and can yield rapid resolution of hyperthyroidism. References: Pereira JV, Lim T. Hyperthyroidism in gestational trophoblastic disease - a literature review. Thyroid Res. 2021 Jan 14;14(1):1. doi: 10.1186/s13044-021-00092-3. PMID: 33446242; PMCID: PMC7807451.
Presentation: 6/2/2024
8062 Uncommon Presentation Of Multiple Myeloma As A Rapidly Growing Thyroid Goiter Initially Thought To Be Hashimoto's Thyroiditis
Authors: Singh Shah Mahabir , Humayon Salman , Paul Sanu Kevin , Peñaherrera Carlos 
Published: October 2024

Abstract
Disclosure: M.S. Shah: None. S. Humayon: None. K.P. Sanu: None. C. Peñaherrera: None.
We present a unique case of an 85-year-old female with rapidly growing anterior neck swelling and subclinical hyperthyroidism, initially suggestive of Hashimoto's thyroiditis. The goiter initially responded well to steroids but rebounded back in size despite two courses of prednisone. This prompted further diagnostic workup which revealed unexpected findings, ultimately leading to the diagnosis of multiple myeloma involving the thyroid parenchyma and lymph nodes. The patient had no history of thyroid disorders or recent upper respiratory tract infections. She exhibited sudden neck swelling, mild subclinical hyperthyroidism, and positive TPO antibodies. Initial fine needle aspiration suggested lymphoid tissue with Hurthle cell differentiation, raising suspicion of Hashimoto's thyroiditis. Flow cytometry supported this diagnosis, but the potential for a Hurthle cell neoplasm persisted. Prednisone temporarily reduced thyroid size, but disease recurrence necessitated surgical excisional and incisional biopsies. Subsequent biopsies revealed plasma cell neoplasms consistent with multiple myeloma. The pathologic report confirmed MYC rearrangement, indicative of multiple myeloma involvement in lymph nodes and thyroid tissue. Protein electrophoresis revealed two restricted bands migrating in the gamma globin region. The patient experienced subclinical hyperthyroidism that evolved into euthyroidism over a month. Incidental findings included non-invasive, low grade papillary urothelial carcinoma. Disease progression was evident in a follow-up PET/CT, prompting oncology consultation. The patient initiated Revlimid with chemotherapy. Levothyroxine was prescribed for postoperative hypothyroidism, with adjustments based on thyroid panel results. This case report illustrates the intricate diagnostic challenges posed by multiple myeloma masquerading as a thyroid disorder. The unexpected evolution of the disease, marked by MYC rearrangement and metastatic spread, emphasizes the need for heightened vigilance in managing such cases. Clinicians should consider alternative diagnoses when treatment efforts fail to provide adequate response. This will ensure timely and appropriate management in clinical practice. This report contributes valuable insights into the diagnostic complexities and multidisciplinary considerations for addressing similar presentations in endocrine and oncology settings.
Presentation: 6/1/2024