bluuebunny/crossref_metadata_2025_split huggingface dataset:
ODP484 Hyperthyroidism During Prostaglandin I2 Treatment in Pulmonary Hypertension and Its Molecular Mechanism
Authors: Ishida Emi , Yoshikawa Masashi , Hiraga Haruna , Nishikido Ayaka , Toki Akiko , Horiguchi Kazuhiko , Matsumoto Shunichi , Yoshino Satoshi , Ozawa Atsushi , Yamada Masanobu 
Published: November 2022

Abstract
Continuous intravenous infusion of prostaglandin I2 (PGI2) analog, epoprostenol, has improved the survival rate for severe pulmonary hypertension, but longer treatment with PGI2 sometimes occurs hyperthyroidism. For the hyperthyroidism during PGI2 treatment, two molecular mechanisms are speculated; the direct effect of PGI2 on thyroid follicular cells via PGI2 receptor which is coupled with G-protein alpha subunit like TSH receptor, and the indirect effect of PGI2 on activated T helper 17 cells which are associated with autoimmune disease (1). Here, we experienced three different cases of hyperthyroidism during PGI2 treatment in pulmonary hypertension. In case 1, epoprostenol had been administered intravenously for about ten months before the onset of hyperthyroidism. TSAb became positive (591%) and technetium uptake was elevated (4.7%), which were similar to the typical observations in Grave's disease. Total thyroidectomy was needed to control the thyroid function in case 1. In case 2, no thyroid antibody was detected and technetium uptake was almost vanished, as in the destructive thyroiditis. The thyroid function eventually normalized without any intervention. In case 3, hyperthyroidism occurred during oral PGI2 analog selexipag administration, but no evidence of Grave's disease or destructive thyroiditis was observed. Hyperthyroidism was declined when the dose of selexipag was reduced. To investigate the molecular mechanism underlying each case, we added the drugs which were used in each case on a thyroid follicular cell line, FRTL5. The thyroid tissue which was resected in case 1 and FRTL5 cells expressed PGI2 receptors in immunohistochemistry and immunofluorescence study. Human thyrotropin alpha (TSH) and epoprostenol elevated the intracellular cyclic AMP (cAMP) in FRTL5 (1.33 fold and 1.20 fold each, P&lt;0. 05, n=3), but the other PGI2 analogs and the other drugs for pulmonary hypertension didn't change the cAMP in FRTL5. The gene expression level of Na/I symporter was up-regulated only by TSH (2.39 fold, P=0. 02, n=3), but not by PGI2 analogs in qPCR study. It is suggested that PGI2 increases the intracellular cAMP in thyroid follicular cells, but does not cause the same genetic changes as TSH. In conclusion, PGI2 analog may not directly affect the thyroid hormone synthesis in follicular cells, but further analysis is needed to elucidate the molecular mechanism underlying hyperthyroidism during PGI2 analog treatment. Reference: (1) Satoh et al.,Endocrine Journal 2017,64(12),1173-1180
Presentation: No date and time listed
ODP507 PREVALENCE OF CARDIOVASCULAR DISEASE IN PATIENTS WITH SUBCLINICAL HYPOTHYROISIM
Authors: Park Kyeeun , Konindala Navya , Konindala Navya , Aung Pyi Phyo , Enriquez Leidy Plaza 
Published: November 2022

Abstract

Introduction
Thyroid hormones play an essential role in maintaining cardiovascular homeostasis. Experimental studies have revealed that subtle changes in thyroid hormone levels, as observed in subclinical hypothyroidism, have adverse effects on the cardiovascular system due to predisposition to endothelial dysfunction, dyslipidemia and direct effects of thyroid hormones on the myocardium. We conducted a retrospective cohort study to elicit the role of subclinical hypothyroidism as an independent risk factor for cardiovascular diseases.

Methods
We conducted a retrospective analysis of 3 years of the National Inpatient Sample (NIS) database, 2016 to 2018. Study populations were selected using ICD-10 diagnosis code. Discharge-level weight analysis was used to produce a national estimate. We conducted multivariate regression analysis to calculate odds ratio with STATA 17.

Results
During the study period, 106,970,745 study population met the inclusion criteria and 37,215 of subclinical hypothyroidism (SCH) patients were discharged. SCH patients tended to be more female (63.48% v 56.40%), older (mean age 58.22± 0.25 v 49.48 ± 0. 01), diabetic (24.84% v 21.47%) and obese (18.63% v 13.54%). Prevalence of hyperlipidemia and hypertension were similar in both SCH and non-SCH groups (3.75% v 3.24% and 29. 09% v 29.35% each). Caucasian patients were predominant in both groups with similar ethnicity distribution (62.26% v 64.96%). 3.56% of SCH patient had acute coronary artery syndromes (ACS), whereas 2.78% of non-SCH patients developed the ACS. For the patients without history of heart failure (HF), 2.54% of SCH patients developed new onset of HF, whereas 1.11% of non-SCH patients developed HF. After adjusting for age, sex, race and comorbid burden, SCH is not associated with ACS (p = 0.375) or Afib (p= 0.74) but associated with elevated risk for new onset of HF (OR 1.88, 1.62–2.18, p &lt; 0. 0001).

Conclusion
Our study shows that subclinical hypothyroidism is not associated with higher rates of ACS or Atrial fibrillation, however it is associated with statistically significant higher risk of new onset HF. Further research needs to be done to determine subclinical hyperthyroidism as a potential risk factor for HF and assess the benefit of lower threshold for treating subclinical hypothyroidism in preventing or delaying the onset of HF in patients with associated cardiac risk factors.
Presentation: No date and time listed
ODP510 Pseudolymphoma of the Thyroid Gland in Association with Hashimoto's Thyroiditis: A Benign Lesion in Whitish Thyroid Gland
Authors: Chatchomchuan Waralee , Thewjitcharoen Yotsapon , Krittiyawong Sirinate , Nakasatien Soontaree , Veerasomboonsin Veekij , Kanchanapituk Auchai , Junyangdikul Pairoj , Himathongkam Thep 
Published: November 2022

Abstract

Background
Pseudolymphoma or reactive lymphoid hyperplasia is a benign localized tumor-forming lymphoid hyperplasia found in various organs. Its occurrence in the thyroid gland is rare and could mimic malignant lesion. Here, we present a case of pseudolymphoma of the thyroid in a patient with Hashimoto's Thyroiditis.

Case description
A 24-year-old woman without underlying disease presented with incidentally found thyroid nodule. Ultrasound revealed mild thyroid enlargement with diffuse heterogeneous parenchymal echotexture. A 5×7×8.5-mm hypoechoic solid nodule with irregular margin was found in the left upper pole. No microcalcification was detected. Multiple subcentimeter lymph nodes at bilateral cervical group VI and left cervical group IV were also detected, measuring up to 5 mm in short axis. Fine-needle aspiration was performed and suggested malignancy (Bethesda class V). Laboratory testing showed euthyroid state with positive anti-thyroglobulin antibodies and anti-thyroid peroxidase antibodies. The blood test and ultrasound findings suggested the underlying of Hashimoto's thyroiditis. The patient underwent total thyroidectomy and lymph node dissection without postoperative complication. Gross examination of the thyroid showed multiple well-demarcated whitish nodular lesions, ranging from 2-10 mm, in the upper pole of both thyroid lobe and a well-circumscribed area of a 7-mm greyish nodule in left thyroid lobe. Microscopically, the whitish lesion in both lobe composed of hyperplastic lymphoid tissues with many follicular centers on the background of lymphocytic thyroiditis. The immunohistochemistry study revealed a polyclonal nature of the plasma cell infiltrates. No abnormal staining with AE1/AE3 or cyclin D1 was found. Pseudolymphoma was diagnosed based on these findings. Papillary thyroid microcarcinoma (6 mm) without capsular invasion was also diagnosed in the lesion of left mid lobe. The cervical lymph nodes showed metastatic papillary thyroid carcinoma (1.5 mm) in level III cervical lymph nodes. No perinodal extension was found. Postoperative course was unremarkable and the patient was in stable condition at 18 months after the operation.

Conclusion
Although primary thyroid lymphoma is often considered in patients with Hashimoto's thyroiditis. The possibility of pseudolymphoma characterized by the presence of well-demarcated pearly white nodules and polyclonal cell populations should also be considered.
Presentation: No date and time listed
ODP513 Rhabdomyolysis: A Rare Presentation Of Central hypothyroidism
Authors: Humphries Derrek , Haddad Joseph , Mahase Anesia , Quaries Jake , Aleem Abdul 
Published: November 2022

Abstract

Background
Hypothyroidism is one of the most common endocrine disorders affecting approximately 5 percent of Americans aged 12 and older. The most common cause of hypothyroidism globally is iodine deficiency whereas in the United States, Hashimoto's thyroiditis is the most prevalent. Less frequently, hypothyroidism can be caused by central hypothyroidism. In uncontrolled states, this entity can lead to an array of complications with rhabdomyolysis being among the latest manifestations. We present a case when the patient was admitted to the hospital for significant rhabdomyolysis, and after workup, was found to be related to new onset central hypothyroidism.

Clinical Case
A 34-year-old African American male presented to our facility with proximal muscle weakness and pain in the bilateral hips and right shoulder for three days. During the interview, the patient was acutely debilitated demonstrating slow body movements and grimaces on passive and active range of motion. Motor strength and sensation was preserved in bilateral extremities. The patient denied any recent injury, compression, extensive exercise, seizure, or durg use. The patient, however, reported a family history of rheumatological and endocrine conditions. Labs were obtained and revealed a creatinine kinase level of 10,5000 U/L; creatinine kinase- MB 53.5 ng/mL; creatinine 1. 0 mg/dL; AST 146 U/L; ALT 72 U/L; CRP 8.6 mg/L. The patient was stabilized with appropriate fluid and steroid therapy. On further investigation, TSH and T4 levels were 0.30 µlU/mL and 0.55 ng/dL, respectively. MRI with and without contrast did not show any intracranial pituitary abnormality or mass. The patient was started on levothyroxine and instructed to remain on the drug as an outpatient to prevent future occurrences. He was subsequently discharged after CK levels normalized and proximal muscle weakness improved. The patient was instructed to have a repeat thyroid function test and T4 levels in 6 weeks with appropriate follow up.

Conclusion
Idiopathic central hypothyroidism is a rare cause of hypothyroidism estimated to occur in 1: 20,000-80,000 in the general public. The lack of a pituitary mass lesion on MRI added to the rarity of this presentation. Hypothyroid myopathy causing rhabdomyolysis is a known but rare consequence of untreated hypothyroidism, which may present with muscle weakness, pain, and elevated serum muscle enzyme. Prompt workup to rule out a multitude of other causes is required, and the patient should be closely monitored for electrolyte and kidney function changes. Levothyroxine remains the treatment of choice for correction of central hypothyroidism with dose adjustments based on patient symptoms and serum free T4 values.
Presentation: No date and time listed
ODP515 Severe thyrotoxicosis caused by subacute thyroiditis
Authors: Guo Rong R , Panday Deepika 
Published: November 2022

Abstract

Background
Subacute thyroiditis, also named giant cell thyroiditis, painful thyroiditis, and de Quervain's thyroiditis, usually presents with neck pain or discomfort, a tender diffuse goiter and mild or moderate elevation of serum free T4 and T3 levels. Here we report a case of subacute thyroiditis patient presenting with severe thyrotoxicosis. Clinical case: A 27-year-old woman with no significant past medical history presents to the emergency room with palpitations and abnormal EKG with heart rate at 160 beats per minute. She developed a sore throat 3 days prior to the presentation, but she did not have neck pain or fever. She reports a 3-month history of hair loss, headaches and weight gain. Labs showed significantly elevated free T4 greater than 7.7 ng/dl (0.8-1.7) and free T3 level at 20.7 pg/ml (2. 0-4.8), and suppressed TSH less than 0. 01 uIU/ml (0.45-4.5) and normal ESR at 15 mm/hour. Her TPO antibody was greater than 1300 u/ml. Thyroid stimulating immunoglobulin (TSI) and TSH receptor antibody (TRab) were obtained but results were pending when she was discharged from the hospital. She has no typical clinical features of subacute thyroiditis with normal ESR and her free T3 and free T4 levels were significantly elevated. She was discharged on Methimazole and Propranolol and to do neck ultrasound as outpatient and follow-up TSI and TRab results and repeat free T4 and T3 in 1 week. Her neck ultrasound revealed mild hypervascularity but no Graves’ features. Her TSI and TRab were negative and free T4 level had no improvement even on significant dose of Methimazole. All the findings argue against Graves’ disease, but support subacute thyroiditis. Then Methimazole was discontinued and Prednisone was started at 20 mg daily and quickly taper to 5 mg daily in 2 weeks then stopped. After on Prednisone for 3 weeks, her free T4 was close to normal at 2. 0 ng/dl, T3 normal at 120 ng/dl, although TSH is suppressed. After stopped Prednisone for 2 weeks, her free T4, T3 and TSH were all back to normal. She is currently euthyroid without any medication at 5 months after her initial presentation.

Conclusion
Treatment of patients with subacute thyroiditis is pain relief with NSAID or Prednisone when NSAID is not effective. Anti-thyroid medications are rarely effective even in subacute thyroiditis patient with thyroid storm. Our case illustrated the role of corticosteroids in the treatment of subacute thyroiditis patient with severe thyrotoxicosis. Neck ultrasound and thyroid antibodies including TSI and TRab are critical to make a correct diagnosis in subacute thyroiditis patient with severe thyrotoxicosis.
Presentation: No date and time listed
ODP519 Thyroid Cyst Grows E. coli
Authors: Hayes Clarissa , Stezzi Mark , Skutnik Emily , Scheckelhoff Trevor , Lam Henry , Wright Jeffrey , Egeler David , Perilli Gretchen 
Published: November 2022

Abstract

Background
Thyroid abscesses are extremely rare, representing less than 1% of all thyroiddiseases. The thyroid gland is very robust against infections due to its vastlymphatic drainage, dual blood supply, encapsulation, and iodine concentration. Immunocompromised patients are at greater risk of developing thyroid abscesses. 1 Case: A 51-year-old female presented to her primary care provider with acute onset ofpainful right neck mass with associated cough, hoarseness, fever, and fatigue. She was seen by an Otolaryngologist who aspirated 6 cc of brown purulentmaterial from a suspected thyroid mass. The thyroid fluid was sent for culture,and she was empirically started on Augmentin. CT neck demonstrated a cysticlesion of the right thyroid gland, retropharyngeal edema, and mass effect withleftward deviation of the larynx and trachea without airway obstruction. Due tothese findings, the patient was admitted to the hospital where initial two setsof blood cultures were negative but repeat blood cultures revealed 2 of 2positive for E. coli. Thyroid cyst fluid also grew E. coli. Urine culture hadno growth. She was found to have a suppressed TSH of 0.24 uIU/mL, elevated free T4 of 1.80 ng/dL, and suppressed total T3 of 0.52 ng/mL. Previous TSH was within normal limits, 0.82 uIU/mL. The suppressed TSH and suppressed T3 were thought to be secondary to euthyroid sick syndrome. She was maintained onCeftriaxone while admitted and discharged on Ciprofloxacin. Pathology from theright thyroid cyst revealed acute inflammatory cells only consistent with anabscess, negative for malignancy. The patient elected to undergo a righthemithyroidectomy with isthmusectomy.

Discussion
Thyroiditis is defined as inflammation of the thyroid gland and has a variety ofetiologies. Suppurative thyroiditis, which includes thyroid abscess as in thiscase we have described, is an infrequent cause of thyroiditis. It is usuallycaused by hematogenous spread or direct inoculation of a pathogen. Treatmentincludes systemic antibiotics targeting the causative organism; although thegold standard remains surgical drainage. Surgical management is the mainstay ofmanaging patients with thyroid abscesses. 2 References: 1 Sharma, R., McManus, C., Kuo, J. (2020). MON-485 Thyroid Abscess in a Healthy 22 Year Old Female. Journal of the Endocrine Society, 4(1), A792-A793. https://academic.oup.com/jes/article/4/Supplement_1/MON-485/5832886 2 Singh, G., Jaiswal R., Gulati, N.,Granieri, E. (2019). A case of idiopathic thyroid abscess caused by Escherichia coli. Journal of Community Hospital Internal Medicine Perspectives. 9(2): 159-161. https://europepmc.org/article/MED/31044048
Presentation: No date and time listed
OR04-2 WNT2B Deficiency Results in Hyperreninemic Hypoaldosteronism in Humans and Mice
Authors: Azova Svetlana , Basham Kaitlin , Breault David , Hammer Gary , LaPensee Christopher , O’Connell Amy , Ribeiro Claudio , Silva Borges Kleiton , Turcu Adina , Little III Donald 
Published: November 2022

Abstract
Proper development and zonation of the adrenal cortex is intimately connected with its lifelong capacity to produce steroid hormones. Both adrenocortical development and homeostasis are mediated in part by paracrine WNT/β-catenin signaling, an essential pathway for zonal maintenance and aldosterone production. Patients harboring homozygous or compound heterozygous loss-of-function (LOF) mutations in the WNT ligand WNT2B present with congenital diarrhea and require parenteral nutrition. Despite evidence for euvolemia, WNT2B-null patients exhibit markedly elevated plasma renin levels with no corresponding increase in aldosterone, suggesting a primary adrenal defect in aldosterone synthesis. To test this hypothesis, we generated both global and conditional Wnt2b knockout mouse models. In the mouse adrenal, Wnt2b is expressed exclusively in the capsule, the outer compartment of mesenchymal cells that overlay and signal to the subcapsular zona glomerulosa (zG), the adrenocortical zone that harbors aldosterone-producing cells and critical long-term progenitor cells. Global loss of Wnt2b from early mouse development results in a near-complete absence of the histological zG. Moreover, Wnt2b-null mice exhibit significantly increased plasma renin but normal aldosterone levels compared to wild-type controls. These data suggest that WNT2B-null patients indeed have an adrenocortical phenotype caused by apparent zG hypofunction. To further define the mechanism(s) by which Wnt2b LOF leads to zG hypofunction, we temporally deleted Wnt2b in the adrenal capsule of adult mice. Wnt2b conditional knockout (cKO) adrenals exhibit a zG-restricted decrease in Wnt/β-catenin signaling as determined by decreased β-catenin activity and target gene expression. Moreover, Wnt2b cKO mice demonstrated a disorganized zG and disrupted adrenocortical zonation. To determine the contribution of WNT2B to aldosterone production, we administered a sodium-deficient diet to control and Wnt2b cKO mice to activate the renin-angiotensin-aldosterone system. Indeed, while control mice exhibited the expected increase in both plasma renin and aldosterone, Wnt2b cKO mice showed marked elevation of renin despite normal aldosterone compared to controls, consistent with hyperreninemic hypoaldosteronism. Together, our work supports a WNT2B-dependent mechanism for adrenal zG development and maintenance in mice and humans and provides relevant models to study the consequences of WNT2B deficiency within the zG.
Presentation: Saturday, June 11, 2022 11:45 a.m. - 12:00 p.m.
PSAT294 Black Thyroid – Is It a Benign or a Malignant Finding?: A Case Report and Review of the Literature
Authors: Cordero-Garate Juana , Naranjo Eddy P Lincango , Dominguez Carla M , Godoy Richard , Jacome Carolina Polanco , Pérez Carla Rocha , Solis-Pazmino Paola , Soto Jacome Cristian , Cevallos Belen , García-Bautista Andrea , Dy Benzon , Kawkgi Omar E , Garcia Cristhian 
Published: November 2022

Abstract

Background
Black thyroid is a rare condition with fewer than 70 cases reported around the globe. Black thyroid is seen almost exclusively in patients upon minocycline ingestion, and the process has previously been thought to be generally benign. Despite the favorable impact of this drug on thyroid function, several studies have reported an association between black thyroid and thyroid cancer. Herein, we report a black thyroid associated with papillary thyroid cancer.

Clinical Case
A 30-year-old woman with no significant medical history and no risk factors for thyroid cancer, but with a history of acne treated with minocycline for 2 months 10 years ago, came to the office for a thyroid nodule found during a routine healthcare visit. The patient was asymptomatic and euthyroid. Physical examination was unremarkable. The thyroid ultrasonography showed a 1.4 × 1.0 cm hypoechogenic solid nodule with irregular borders and microcalcifications located in the right lobe. No cervical lymph nodules were found. Fine-needle aspiration of the nodule displayed a Bethesda VI category. Total thyroidectomy was performed. No lymph node dissection was implemented. During surgery, the thyroid parenchyma was diffusely black in color, increased in size, and multinodular. The patient was uneventfully discharged on postoperative day 1. Histopathology revealed a diffuse black discoloration of the specimen with a well-defined 1.2×0.8×0.6 cm nodule in the right upper lobe with features of classic papillary thyroid carcinoma. Recently the patient was seen at his 3-month follow-up, and there were no signs or symptoms of recurrence or metastasis.
Clinical lessons: Although several studies describe a higher incidence of malignancy (being papillary thyroid carcinoma the most frequently associated) in black thyroid compared to non-black thyroid glands, a causal relationship has never been proven. Perhaps in this case the thyroid ultrasonography screening triggered the overdiagnosis and subsequently the overtreatment. Finally, having a "black organ" can be distressing for patients. Therefore, we should be meticulous in explaining "this disturbing fact".
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.