bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-596 A Rare Presentation of Early Onset Wernicke Encephalopathy Following Sleeve Gastrectomy
Authors: Gilreath Nathan , Kant Ravi , Antony Mc Anto , Verma Vipin 
Published: May 2020

Abstract
Background: Wernicke encephalopathy (WE) has been reported after malabsorptive bariatric surgeries but is an uncommon complication of sleeve gastrectomy. Since 2011, the number of patients receiving a sleeve gastrectomy has tripled, with almost 60% of patients undergoing bariatric surgery receiving a sleeve gastrectomy in 2017 (1). We present a case of WE in a young woman as a rare and early complication of sleeve gastrectomy.
Clinical Case: A 32-year old female with a past medical history significant for hypertension, pseudotumor cerebri, and morbid obesity status post sleeve gastrectomy two months prior presented to the emergency department with complaints of blurry vision and lower extremity numbness. Physical examination showed sluggish light reflex and decreased extraocular movements. Given history of pseudotumor cerebri, patient underwent a therapeutic lumbar puncture with removal of 13 ml of CSF. Opening pressure was 20 cm of water and patient experienced no relief of her symptoms. Ophthalmology consult did not offer an explanation for the blurry vision. MRI-brain with and without contrast showed findings highly suggestive of WE. It showed faint linear symmetric hyperintensities along the bilateral mesial thalamus, dorsal midbrain and periaqueductal gray matter, which were determined to be acute in nature in comparison with a MRI performed three weeks prior. Upon further investigation, thiamine level was low at 43.6 nmol/L [66.5 – 200] confirming the diagnosis of WE. Thiamine supplementation was started immediately and patient reported improvement of her vision the next day with return to baseline in 3 days.
Conclusion: There have been a handful of cases of WE reported in literature as a complication of sleeve gastrectomy. Zheng, L also reported a case of WE 7 weeks after sleeve gastrectomy (2). Although sleeve gastrectomy does not directly affect the primary absorptive pathway of thiamine in the gastrointestinal tract, it is imperative to consider WE in patients presenting with suspicious neurologic symptoms after a recent sleeve gastrectomy. WE was suspected in our case due to typical MRI findings and neurological presentation after bariatric surgery, which was later confirmed by low serum thiamine level. Early detection and thiamine supplementation resulted in complete reversal of symptoms in our patient. WE is a rare but severe and preventable consequence of bariatric surgery that warrants attention given its rapid onset and detrimental course.
Reference: (1) Estimate of Bariatric Surgery Numbers, 2011-2017. (2018, June 26). Retrieved from https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers. (2) Zheng, L. (2016).
Wernicke Encephalopathy and Sleeve Gastrectomy. American Journal of Therapeutics, 23(6).
SAT-192 Eletriptan (RelpaxaTm) Causing False Positive Elevations in Urinary Metanephrine
Authors: Bloomer Zachary , Priti Nath , Hoang Thanh Duc , Shakir Mohamed K M 
Published: May 2020

Abstract
Background:
The diagnosis of pheochromocytoma depends crucially on the demonstration of excessive production of catecholamines. This step, however, is fraught with several difficulties, in particular with false-positive test results. Drugs such as phenoxybenzamine and tricyclic antidepressants are the most frequently associated causes for false-positive results. Other medications are also known to cause a false positive elevation of urinary metanephrines. We are reporting a patient with markedly elevated urine metanephrines associated with the use of Eletriptan hydrobromide (RelpaxaTM), a drug commonly used for treating migraine.
Clinical Case:
A 29-year-old man with a history of migraine managed on ibuprofen and recently started Eletriptan presented to the emergency room complaining of a 24-hour history of progressively worsening headaches. At the time of initial evaluation his blood pressure was in the 220s/160s with a creatinine of 1.9 mg/dL with unknown baseline. He was managed on an IV nicardipine drip. Due to his young age he underwent an evaluation for secondary causes of his hypertension. Laboratory: normal aldosterone/renin level (ratio was 0.4), normal midnight salivary cortisol and normal thyroid function studies. Urine screening for drug abuse was also negative. A 24-hour urine metanephrine level, while the patient was taking Eletriptan, was markedly elevated (normetanephrine 1341mcg (ref 82–500) and metanephrine level of 2494 mcg (ref 45–290). In contrast, the plasma metanephrines were only mildly elevated (metanephrines level 27 pg/ml (ref 0–62) and normetanephrine level of 255 pg/ml (ref 0–145)). Adrenal CT did not reveal any evidence of adrenal nodules. Additionally a Gallium-68 PET/CT scan did not reveal any evidence of pheochromocytoma or paraganglioma. Eletriptan was discontinued and his blood pressure was controlled on oral medications. Within one week of stopping Eletriptan his urine metanephrines (metanephrine 76 mcg/ 24 hrs, normetanephrine 277 mcg/dL) and plasma metanephrines (metanephrine 39 pg/mL, normetanephrine 148 pg/mL) normalized.
Conclusion: The discrepancy between plasma and urine metanephrines in our patient suggests the possibility of a false positive test. Eletriptan, a second generation triptan drug, is a selective 5-hydroxytryptamine 1B/1D receptor agonist and has been shown to reduce carotid arterial blood flow, with only a small increase in arterial blood pressure at high doses. However, Eletriptan has no significant affinity or pharmacological activity at adrenergic α1, α2, or β; dopaminergic D1 or D2; muscarinic; or opioid receptors. It is also interesting to note that Eletriptan use is contraindicated in uncontrolled hypertension. It is possible Eletriptan may affect the assay of urine metanephrines. However, the exact mechanism of Eletriptan causing elevated urine metanephrines in our patient is not clear.
SUN-210 Differentially Expressed Mirnas in Zona Reticularis (ZR) Cells of the Human Adrenal Cortex
Authors: Garcia Francisco , Colman Diego , Zoff Luciana , Saraco Nora Isabel , Belgorosky Alicia , Baquedano Maria Sonia 
Published: May 2020

Abstract
The human adrenal cortex, involved in adaptive responses to stress, fluid homeostasis, and secondary sexual characteristics, arises from a tightly regulated development of a zone and cell type-specific secretory pattern. However, the molecular mechanisms governing adrenal zonation, particularly postnatal ZR development, which produces adrenal androgens in a life-time-specific manner, remain poorly understood. The hallmark of ZR is the low expression of type 2 3β-hydroxysteroid dehydrogenase (HSD3B2). However, the mechanisms underlying HSD3B2 downregulation in the ZR remain unknown. MiRNAs are seen as regulators of cell phenotypes. The objective of the study was to compare miRNA expression profiles in human adrenal ZR and zona fasciculata (ZF). ZF and ZR were microdissected from human adrenals tissues (n=5, from boys aged 16, 17 and 19 yr and girls aged 12 and 16 yr) by laser capture microdissection (LCM). Total RNA was extracted from 5 ZF/ZR pairs and next-generation sequencing (NGS) was used to perform the microRNA expression profiling. 281 mature microRNAs were identified in human adrenal cortex. Among them, 7 microRNAs were significantly differentially expressed between ZF and ZR. The expression of miR-375-3p, miR-483-3p and miR-7-5p was higher in ZR compared with its paired ZF by 2-fold or greater. Multiple available bioinformatic algorithms (TargetScan, miRanda, DianaLab and PicTar) were employed to search for its target genes. Among predicted target genes, several genes (GATA-6, GATA-4, SF1, NR4A2, and IGF-1) are known to be involved in HSD3B2 regulation. In summary, LCM combined with NGS provided a robust approach to explore the adrenal zone-specific micro-RNA profiling. Our data gave first hints that miRNAs might be novel regulatory modules associated with human adrenal ZR cell-specific transcript regulation underlying developmental androgen production.
SUN-543 Real World Evidence of Successful Weight Management for the Obese Population: Complete Reversal of Obesity Related Metabolic Co-Morbidities and Weight Loss in Patients Attending a Multidisciplinary Weight Management Clinic in Australia
Authors: Rock Zoe , Chen Juliana , Jaques Joanna , Champion Bernard L , Lord Reginald V , Preda Veronica Angela 
Published: May 2020

Abstract
Over 2.5 billion people worldwide are overweight or obese. Multidisciplinary weight management interventions have evolved to address the complexity of weight loss for those with one or more chronic diseases, and the trend of weight regain. The aim of these interventions is to encourage sustainable lifestyle changes, resulting in weight loss and weight maintenance and improvements in comorbidities. While some prospective clinical trials have demonstrated efficacy, results are often not reported by real life practices.
The aim of this study was to evaluate the effectiveness of a Sydney based multidisciplinary weight management clinic with endocrinology, dietetics, exercise physiology, psychology, and bariatric surgical domains. All patients who attended the clinic for weight loss purposes between March 2017 and April 2019 were included (n=220). A retrospective chart review was conducted. Patient data on weight, BMI, waist circumference, body composition measurements, and selected blood test results and co-morbidities were analysed. All patient therapy included endocrinological input for co-morbidity identification and management, lifestyle intervention (dietetic and exercise physiology input) with optional adjunct pharmacotherapy or psychological counselling. Of the 220 cohort, 20 of the patients had sleeve gastrectomy.
Patient retention in the clinic after the first consultation was 85% (n=186), a high rate within the weight management community. 59% of patients achieved a minimum of 5% total body weight loss, including 18% who achieved greater than 10% total body weight loss. Additionally, 31% of patients lost enough weight to decrease their BMI class by up to 2 or more classes. Of the gastric sleeve cohort average excess body weight loss was 32kg (21-56kg) enhanced by multidisciplinary care in the lead up to surgery. Across the cohort some patients completely reversed co-morbidities; including dyslipidaemia (n=1), hypertension (n=3), NAFLD (n=1), pre-diabetes (n=8) and type 2 diabetes (n=3), OSA (n=1). These results demonstrate that obesity is a chronic condition that can be successfully managed. We have demonstrated significant durable weight loss and improvement in metabolic co-morbidities with holistic coordinated care. Future directions include translating this model of care into standard practice in Australia and other countries where obesity to date not received the same coordinated approach as other chronic conditions.
SAT-125 A Tough NUT (Midline Carcinoma) to Crack
Authors: Lavelle Kristen , Kirkeby Kjersti 
Published: May 2020

Abstract
Introduction
NUT midline carcinoma (NMC) is a rare, highly aggressive cancer with poor prognosis. To date, there is no established therapeutic strategy; further studies are necessary to compare treatment modalities as well as investigate novel immunotherapeutic agents.
Case presentation
A 39-year-old female presented with a rapidly enlarging right neck mass and a recent 40-lb weight loss and was found to have a 5 cm poorly defined infiltrative hypoattenuating mass on CT scan concerning initially for anaplastic thyroid malignancy. Endocrinology and ENT were consulted and the patient underwent thyroid biopsy, which was positive for NMC. PET scan demonstrated hypermetabolic lymphadenopathy in the bilateral neck and mediastinum, but no distant metastases were identified. She then underwent total thyroidectomy with extensive dissection of the bilateral neck; pathology revealed one positive lymph node. On endobronchial biopsy, the mediastinal lymph nodes were benign. Immunohistochemistry revealed PD-L1 expression and gene assay showed an NSD3-NUTM1 fusion of the NUT gene. Oncology advised systemic treatment with carboplatin/taxol and considered Pembrolizimab, an anti-PD-L1 immunotherapy agent.
Discussion
The prognosis of NMC is less than 1 year and only 20-30 cases are reported per year in the USA. NMC is a poorly differentiated subtype of squamous carcinoma characterized by a chromosomal rearrangement of the NUT gene, involving molecular translocation with the BRD4 gene in 70% of cases. It remains challenging to treat NMC, as metastasis is present on diagnosis in most cases and there is currently no established approach. In a report of 40 patients from the NUT Midline Carcinoma Registry, surgical resection correlated with significantly improved survival in contrast to initial radiation or chemotherapy. Recently, BET domain inhibitors have emerged as a promising class of targeted agents for tumors with BRD4-NUT fusions. Their efficacy is unknown for other NUTM1 fusions. Both BET domain and histone deacetylase inhibitors are in clinical trials, and next-generation BET and CDK9 inhibitors have shown preclinical activity. Our patient likely benefited from early intervention with surgical therapy. Her PET scan findings suggest that re-sampling her mediastinal tissue would be prudent. Given her lack of BDR4-NUTM1 fusion, it is unknown if she would benefit from BET inhibitor.
Conclusion
NMC is an underrepresented cancer that warrants further investigation into treatment modalities and novel immunotherapies.
References
Bauer, DE et al (2012). Clinicopathologic features and long-term outcomes of NUT midline carcinoma. Clinical cancer research,18(20),5773–5779.
Liu S, et al (2018). NUT carcinoma: a rare and devastating neoplasm. Case Reports.
Napolitano, M et al (2019). NUT midline carcinoma of the head and neck: current perspectives. OncoTargets and therapy,12,3235–3244.
SUN-506 Hyperthyroidism Induced Hepatic Apoptosis
Authors: Ahmed Sabreen , David Julia , Melendez-Ramirez Lydia Yvonne 
Published: May 2020

Abstract
Background:
Graves’ disease is commonly associated with abnormal liver function tests, most frequently ALP, but the exact mechanism is not fully understood. In vitro and in vivo animal studies have shown elevated T3 activity can induce hepatocyte apoptosis via a mitochondrial-mediated pathway. This case demonstrates a patient with elevated aminotransferases and hepatic apoptosis most likely secondary to severe hyperthyroidism.
Clinical Case:
50 year old female with a past medical history of migraines was seen by primary care for fatigue and 15 lb weight loss in one month. She was found to be hyperthyroid with TSH &lt; 0.1 uIU/L (n=0.34-5.6), free T4 3.48 ng/dL (n=0.58-1.64) and mildly elevated aminotransferases of AST 77 IU/L (n=15-41), ALT 144 IU/L (n=12-63), which increased within a week to 159 IU/L and 309 IU/L respectively. ALP and bilirubin were within normal range. She was started on methimazole 20 mg twice daily by her PCP. The patient developed vomiting and stopped taking methimazole after 3-4 days. Upon initial presentation to endocrine clinic, found to be clinically hyperthyroid and as LFTs were improved but still elevated, she was re-challenged with methimazole at a lower dose as well as started on a beta blocker and cholestyramine. TT3 checked was elevated at 2.10 ng/mL (n 0.87-1.78). Graves’ disease was confirmed with elevated TSI as well as RAI uptake and scan showing increased homogenous uptake.
She had extensive workup for another etiology by hepatology including autoimmune, which were negative. Her fibrosis score was stage F1-F2 (n=F0) and necroinflammatory activity grade A3 indicating severe activity (n=grade A0). Core needle biopsy of the liver showed focal lytic necrosis/apoptosis and abundant pigment-laden Kupffer cells signifying recent hepatocellular injury. Her AST and ALT down trended and normalized with repeat fibrosis score of F1 and necroinflammatory activity grade A0. She eventually had definitive therapy with RAI treatment.
Conclusion: In most cases of hyperthyroid induced liver dysfunction, liver histology showed fatty infiltration, cytoplasmic vacuolization, nuclear irregularity and hyperchromatism.
This case, without any other known causes that could explain her hepatic injury, indicates the possible role of hyperthyroidism in hepatic apoptosis.
MON-263 Renal Cell Cancer Metastasis to the Pituitary Masquerading as a Non-Functioning Adenoma
Authors: Vedere Tarunya , Vance Mary Lee 
Published: May 2020

Abstract
A 47 yr. old male with history of RCC and hypertension was seen in pituitary clinic for management of a pituitary mass. He initially presented to an outside hospital with persistent headaches, unintentional weight loss, severe fatigue, dizziness, cold intolerance, low libido and difficulty with erections. CT head showed a pituitary mass. Lab work revealed pan-hypopituitarism with adrenal insufficiency [random cortisol 0.7 ug/dL (4- 19 ug/dL); ACTH 13 pg/mL (7-63 pg/mL)], hypothyroidism [T4 0.52 ng/dL (0.7-1.5 ng/dL); TSH 0.1 mIU/L (0.45-4.5 mIU/L)] and hypogonadism [total testosterone 15 ng/dL (200-1000 ng/dL); LH of 0.6 mIU/mL (1.5-9.3 mIU/mL); FSH of 3.5 mIU/mL (1.6- 8.0 mIU/mL)]. Prolactin was slightly elevated at 34 ng/mL (2- 18 ng/mL) from stalk compression. IGF-1 was 78 ng/mL (Z score -1.2).
When we saw him, he was already on hormone replacement with significant improvement in symptoms. He had no visual field defects or symptoms of diabetes insipidus (DI). As for his history of RCC, he underwent a partial left nephrectomy in 2015, followed by a completion nephrectomy shortly after. Pathology was consistent with clear cell RCC. He did not receive any adjuvant therapy; Follow up imaging studies were reportedly negative for recurrence. Pituitary MRI showed a 1.6 X 1.4 X 1.5 cm enhancing sellar and suprasellar mass without compression of optic chiasm. He was thought to have a presumed non-functioning adenoma, and chose to proceed with trans-spenoidal surgery (TSS). Intra operatively, a very vascular tumor was encountered, which could only be debulked safely. Pathology was consistent with metastatic clear cell RCC. A follow up CT showed innumerable lung nodules and a 3.2 cm right adrenal nodule consistent with metastases. He completed stereotactic radiation to the sella and is currently on Ipilimumab and Nivolumab for immunotherapy.
MP is uncommon, and seen in 1-4% of patients with cancer in autopsy studies. Breast (40%) and Lung cancer (25%) are the most common tumors causing MP in women and men respectively, with very few case reports of RCC MP (2.6%). DI is the most common symptom of MP, which is thought to be due to direct vascular supply from hypophyseal arteries to the posterior pituitary. Interestingly in RCC MP, anterior pituitary dysfunction is more prevalent (90%) compared to DI (24%). There is also a tendency for suprasellar extension, causing vision loss. Radiologic features that could help distinguish MP from an adenoma include a rapidly enhancing sellar mass, erosion of sellar floor or posterior clinoid process, infundibular thickening, and the presence of intra-tumoral vascular flow voids. There reportedly is no benefit to using FDG- PET to diagnose MP from RCC. There are no standardized treatment guidelines and the choice of treatment is also influenced by the extent of systemic disease.
SUN-486 Unusual Presentation of Metastatic Follicular Thyroid Cancer
Authors: Proudan Nikoletta , Andre Kersthine 
Published: May 2020

Abstract
Distant metastasis of follicular thyroid cancer to the bone has been well documented. However, spinal cord compression as the initial presentation of metastatic follicular thyroid cancer without any thyroid symptoms is relatively rare. Here we discuss such a case. A 78-year-old female with history of HTN and melanoma presented to the ED with a 1-month history of middle back pain that progressed to lower extremity weakness, numbness, and inability to ambulate. MRI showed a T7 vertebral mass with cord compression and edema. Metastatic work up was unremarkable except for incidental bilateral thyroid nodules, the largest on the right lobe, at 1.6 cm, with peripheral calcifications. The patient underwent T6-T7 laminectomy with vertebral decompression, partial colpectomy, and T4-T10 fusion. Pathology of the thoracic vertebral mass was positive for CAM 5.2, cytokeran 7, TTF-1, and PAX8 consistent with either metastatic pulmonary adenocarcinoma or thyroid carcinoma. The patient denied shortness of breath, dysphagia, hoarseness, or neck tenderness. She had no personal history of hyperthyroidism or hypothyroidism, or radiation exposure. She also did not have any family history of thyroid cancer. Laboratory work up was significant for TSH of 3.71 mcU/mL (0.4-4.0 mcU/mL), Free T4 1.56 ng/dL (0.7-1.9 ng/dL), thyroglobulin (Tg) 6940 ng/mL (1.6-55.0 ng/mL), and thyroglobulin antibody (Tg Ab) 20 IU/mL (0-115 IU/mL). FNA of the right thyroid nodule showed follicular neoplasm with very similar morphological features to the epidural pathology, favoring a follicular carcinoma. She underwent total thyroidectomy. Pathology showed a 1.6 x 1.1 cm follicular carcinoma with capsular and angiolymphatic invasion, but with uninvolved margins of resection. TNM staging was pT1b, pNx, pM1. She was ablated with 109 mCi of I-131 after withdrawal therapy. Whole body scan after treatment revealed radioiodine avid metastatic disease at T7 and activity in the thyroid bed compatible with residual thyroid tissue. Patient completed 10 fractions of external beam radiotherapy to the spine for a total of 30 Gy. Three months follow up lab work showed Tg 580 ng/mL and negative Tg Ab with a suppressed TSH. Thyroid bed ultrasound did not show any residual tissue or abnormal lymph nodes. Ten-year survival rates in patients with bony metastatic differentiated thyroid cancer range from 13-21% (1). Metastatic thyroid carcinoma should be considered in the differential diagnosis of every patient with new onset bony metastasis and thyroglobulin should be considered as a tumor marker in the initial work up. Research shows increased survival with I-131 avidity and complete bone metastasis resection (1). 1. Ramadan, Sami et al. “Spinal metastasis in thyroid cancer.” Head & neck oncology vol. 4 39. 25 Jun. 2012, doi:10.1186/1758-3284-4-39