bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-115 Inappropriate Ordering of Parathyroid Scintigraphy in an Academic Medical Center
Authors: Kimura Brad , Nagelberg Jodi , Koo Sonya , McCowen Karen Clare 
Published: May 2020

Abstract
Introduction: The diagnosis of primary hyperparathyroidism is a biochemical, not radiologic one. Unfortunately, many practitioners even in academic centers order parathyroid scintigraphy to “confirm a diagnosis of adenoma” or distinguish primary from secondary hyperparathyroidism. Knowing the location of single or multiple parathyroid adenomas is unnecessary unless parathyroidectomy is planned. The financial burden of nuclear imaging is substantial. The goals of this study were to determine the proportion of inappropriately ordered parathyroid scans and the cost to the health care system.
Methods: We generated a database of patients who had consulted with at least one physician at our institution and underwent parathyroid scan between December 2012 and December 2017. We focused on the subset that did not undergo parathyroidectomy. “Slicer dicer” software in our EMR was used to generate the database. Chart review extracted data on diagnoses and reasons for parathyroid scintigraphy.
Results: Over 5 years, a total of 325 parathyroid scans were performed. 171 of these did not have parathyroidectomy in our system. However, 18 underwent surgery elsewhere leaving 153 that received parathyroid scans but no surgery (47% of the total). Of the 91 cases so far analyzed of the 153 in our database, average age is 64, with 28 males and 63 females. 61 of the 91 scans (67%) were performed to confirm the diagnosis of parathyroid adenoma; 3 performed because of possible parathyroid adenoma seen on other imaging; and 24 (26%) were done supposedly to localize the adenoma for surgery. Ordering physicians were from primary care (41%), endocrinology (26%), nephrology (18%), and surgery (10%). Final diagnoses for these 91 patients were true primary hyperparathyroidism in 37 (41%), secondary hyperparathyroidism in 38 (42%), unclear in 10 and FHH in 4. In the primary hyperparathyroidism group, 19/37 met criteria for consideration of parathyroidectomy, but only 5/19 received surgical consultation. These 5 patients either refused surgery or surgeon decided against, usually because of high surgical risk.
Conclusion: 47% of parathyroid scans at an academic institution were performed in patients who did not undergo parathyroidectomy. Many parathyroid scans were ordered inappropriately to “confirm” a diagnosis of primary hyperparathyroidism, leading to unnecessary charges and resource waste. Physician charges for sestamibi scans range from $237-$1942, depending on whether planar imaging, SPECT, or SPECT-CT is used; hospital charges are $1165-$3211. We propose to change the ordering system for parathyroid imaging to clarify that this is not a method to diagnose parathyroid adenoma, rather a tool to optimize surgical planning when the diagnosis is secure.
MON-040 11-Oxygenated C19 Steroids in Polycystic Ovarian Syndrome
Authors: Mody Armaiti , Lodish Maya Beth , Auchus Richard Joseph , Huddleston Heather Gibson 
Published: May 2020

Abstract
BACKGROUND: Polycystic ovarian syndrome (PCOS), an endocrine and reproductive disorder consisting of hyperandrogenism, menstrual dysfunction and ovarian changes, affects 6–20% of reproductive aged women worldwide. While hyperandrogenemia is traditionally determined by evidence of elevated testosterone (T), this hormone can be difficult to accurately measure in women with relatively lower circulating levels compared to men. Recent studies have suggested that four adrenal androgens known as 11-oxygenated C19 steroids (11OxyAs), specifically 11-ketotestosterone (11KT), may be good alternative markers for hyperandrogenism in PCOS. Using a multiethnic population seeking evaluation for PCOS symptomatology, we sought (1) to investigate the utility of 11OxyAs to differentiate women with and without NIH PCOS relative to classical androgens such as T, androstenedione (A4) and DHEAS levels, and (2) to evaluate the relationship of 11OxyAs to clinical findings of androgen excess.
Methods: Using the University of California, San Francisco PCOS Tissue Bank, serum samples from 131 women seen for a PCOS evaluation were selected sequentially and identified as PCOS or non-PCOS (controls) based on meeting NIH criteria at the time of evaluation. In addition to obtaining gonadotropin and metabolic profiles, classical androgens and 11OxyAs were measured using mass spectrometry. The relationship of these androgens to modified Ferriman-Gallwey (mFG) scores and ovarian morphology were also assessed.
Results: Out of 131 women selected, 83 met NIH PCOS criteria at the time of evaluation and 48 did not (controls). Age and BMI did not differ among the two groups. As expected, total T, A4 and LH were all significantly higher in NIH PCOS. A trend towards higher HOMA-IR levels was also seen in NIH PCOS, but this did not reach statistical significance (3±3.9 mg/dL vs. 1.9±1.7 mg/dL, p = 0.12). No difference was seen in all four 11OxyAs between NIH PCOS and controls. Unlike previous studies, we also did not find mean 11KT levels to exceed that of T in both controls (T 393±143 pg/mL vs. 11KT 389±206 pg/mL) and PCOS (T 530±245 pg/mL vs. 11KT 388±201 pg/mL). In addition, no relationship was seen between HOMA-IR and 11β-hydroxyandrostenedione (11OHA4) or 11-ketoandrostenedione (11KA4) levels. Within PCOS, DHEAS and A4 were noted to have a weak but inverse relationship to BMI (r2 0.05 p = 0.05; r2 0.08 p = 0.007), whereas no correlation was seen between any of the four 11OxyAs or T and BMI. Lastly, 11OxyAs, T, and A4 levels did not predict mFG scores or polycystic ovarian morphology.
Conclusions: 11OxyAs levels were not statistically higher among women with NIH PCOS compared to at risk women who did not meet NIH criteria. There was no significant relationship between these androgens and mFG scores or ovarian morphology. Further studies are necessary to show the utility of 11OxyAs levels as a marker for hyperandrogenism or metabolic risk.
MON-613 The Expression of TBC1 Domain Family, Member 4 (TBC1D4) in Skeletal Muscles of Insulin-Resistant Mice in Response to Sulforaphane
Authors: Rizk Nasser M , Saleh Amina , ElGamal Abdelrahman , Elsayegh Dina , Cakir Isin , Ghamari-Langroudi Masoud 
Published: May 2020

Abstract
The Expression of TBC1 Domain Family, member 4 (TBC1D4) in Skeletal Muscles of Insulin-Resistant Mice in Response to Sulforaphane.
Background: Obesity is commonly accompanied by impaired glucose homeostasis. Decreased glucose transport to the peripheral tissues, mainly skeletal muscle, leads to reduced total glucose disposal and hyperglycemia. TBC1D4 gene is involved in the trafficking of GLUT4 to the outer cell membrane in skeletal muscle. Sulforaphane (SFN) has been suggested as a new potential anti-diabetic compound acting by reducing blood glucose levels through mechanisms not fully understood (1). The aim of this study is to investigate the effects SFN on TBC1D4 and GLUT4 gene expression in skeletal muscles of DIO mice, in order to elucidate the mechanism(s) through which SFN improves glucose homeostasis.
Methodology: C57BL/6 mice (n=20) were fed with a high fat diet (60%) for 16 weeks to generate diet induced obese (DIO) mice with body weights between 45–50 gm. Thereafter, DIO mice received either SFN (5mg/kg BW) (n=10) or vehicle (n=10) as controls daily by intraperitoneal injections for four weeks. Glucose tolerance test (1g/kg BW, IP) and insulin sensitivity test (ITT) were conducted (1 IU insulin/ g BW, IP route) at the beginning and end of the third week of the injection.
At the end of 4 weeks of the injection, samples of blood and skeletal muscles of both hindlimbs were collected. The expression levels of GLUT4 and TBC1D4 genes were analyzed by qRT-PCR. Blood was also used for glucose, adiponectin and insulin measurements.
Results: SFN-treated DIO mice had significantly lower non-fasting blood glucose levels than vehicle-treated mice (194.16 ± 14.12 vs. 147.44 ± 20.31 mg/dL, vehicle vs. SFN, p value=0.0003). Furthermore, GTT results indicate that the blood glucose levels at 120 minutes after glucose infusion in was (199.83±34.53 mg/dl vs. 138.55±221.78 mg/dl) for vehicle vs. SFN with p=0.0011 respectively. ITT showed that SFN treatment did not enhance insulin sensitivity in DIO mice. Additionally, SFN treatment did not significantly change the expression of TBC1D4, and GLUT4 genes in skeletal muscles compared to vehicle treatment (p values &gt;0.05).
Furthermore, SFN treatment did not significantly affect the systemic insulin (1.84±0.74 vs 1.54±0.55 ng/ml, p=0.436), or adiponectin (11.96 ±2.29 vs 14.4±3.33 ug/ml, p=0.551) levels in SFN vs. vehicle-treated DIO mice, respectively.
Conclusion: SFN treatment improves glucose disposal in DIO mice, which is not linked to the gene expression of GLUT4 and TBC1D4 and its mechanism of glucose disposal in skeletal muscles. Furthermore, SFN treatment did not improve insulin level, and the insulin sensitizer hormone adiponectin as potential players for enhancing insulin sensitivity.
1.
Axelsson AS, Tubbs E, Mecham B, Chacko S, Nenonen HA, Tang Y, et al. Sci Transl Med. 2017;9(394).
SUN-908 Mediastinal Paraganglioma: A Rare Presentation of a Rare Tumor
Authors: Deepika Fnu , Andre Karla Bermudez Saint , Kansara Abhishek 
Published: May 2020

Abstract
BACKGROUND
Paragangliomas (PPGL’s) are extra-adrenal chromaffin-cell originating tumors that arise from the para-aortic ganglia and are exceptionally rare making up only 1% of the mediastinal tumors. They are slowly growing and highly vascular tumors associated with high morbidity and mortality due to proximity and invasion into the heart, great vessels. The majority of them are asymptomatic and hence discovered incidentally. Surgical resection remains the standard of care with good long term survival. We describe a case of a young male with middle mediastinal PPGL who remained asymptomatic despite large functional tumor.
CLINICAL CASE
A 38-year old Arab male with no previous smoking history was referred to our hospital for evaluation of mediastinal mass that was incidentally noted on an echocardiogram done 1 year ago in his home country when he presented with intermittent exertional shortness of breath for 10 years. The workup done there with CT chest revealed a large mediastinal mass measuring 10.4×8.8×8.6 cm extending into ascending aorta, right pulmonary artery, right superior pulmonary vein, right and left atria as well as the main bronchi bilaterally invading the superior vena cava. However, he had no further treatment until he was seen 1 year later in the US at another institution where biochemical testing showed elevated plasma norepinephrine of 2697 (70-750 pg/ml, supine), dopamine 7667 (&lt;30 pg/ml). 24hr-urine studies showed elevated normetanephrine of 3418 (111-419 mcg/24hr), metanephrine 3488 (200-614 mcg/24hr), and Homovanillic acid (HVA) 51.5 (&lt;0.8 mg/24hr). He underwent endobronchial ultrasound with mediastinal tissue biopsy of the mass that revealed pheochromocytoma. The patient was subsequently referred for cardiovascular intervention at our hospital and endocrinology was consulted for pre-operative preparation. One week before surgery, he was started on doxazosin 2mg daily followed 3 days later by propranolol 10 mg twice daily and recommend high salt and fluid intake. The patient underwent surgical resection of the mass and pathology showed mediastinal PPGL. The postoperative course was complicated by bradycardia with the placement of a permanent pacemaker. He recovered well after surgery with the resolution of symptoms and a significant decline in catecholamines to urine normetanephrine of 385 mcg/24hr and metanephrine 497 mcg/24hrs. There was no evidence of metastatic or residual disease on follow-up CT chest 5 months later.
CONCLUSION
There are limited case reports of PPGL in the middle mediastinum. This case highlights that mediastinal PPGL’s can remain clinically silent for many years prior to the presentation which can lead to delayed diagnosis, yet a strong collaborative team approach between oncology, cardiovascular surgery and endocrinology can confer favorable clinical outcome.
SUN-489 MetastaticThyroidCancer
Authors: Vásquez Romyna La Rosa 
Published: May 2020

Abstract
Background In many cases, thyroid cancer leads to metastasis; however, isolated metastasis to the liver from thyroid cancer is a rare event. When this occurs, patients have a very poor prognosis. Case Study A clinical case of a 33-year-old woman, born in Piura and coming from Lima, with no major history, diagnosed with a 4-month-old cervical tumor is presented. An ultrasound scan and a further biopsy were performed before an eventual diagnosis of papillary thyroid carcinoma. Operation was performed, and a classical papillary carcinoma of 0.90 inches was detected, along with macro-metastasis in a parathyroid ganglion. Post-surgical thyroglobulin was 1071 ng/ml (n&lt; 50 ng/ml). The tomography in her lung showed three nodules in the middle lobe. A further dose of 150 millicuries of radioactive iodine (I-131) was given, with whole-body scanning, post positive in both lung fields and right lank pain. The tomography in the abdomen revealed a hepatic pedicle injury, compatible with teratoma. A liver resection surgery was scheduled, and metastatic papillary carcinoma was identified. A V600 mutation in BRAF gene was present in thyroid gland and not detectable in the liver. Conclusions This case shows an example of thyroid cancer with uncommon metastasis in the liver, which occurs in 0.5% of all thyroid metastases. It is even rarer that positive iodine was found. Liver metastasis represents a poor prognosis, however it has been reported that resective surgery offers patients a better chance of survival. Multiple factors influence its pathogenesis, including BRAF mutations. In this case, mutation was detected in thyroid gland, but not in liver metastasis, which could represent diverse BRAF mutations.
SAT-471 A Rare Case of Pretibial Myxedema Preceding Graves’ Hyperthyroidism
Authors: Bao Ginny W , Kirkeby Kjersti Meyer , Kwan Christina 
Published: May 2020

Abstract
Introduction:
Pretibial myxedema, also known as thyroid dermopathy, is typically seen as a manifestation of long-standing Graves’ disease. We report a rare case of pretibial myxedema as the initial presentation of Graves’ disease in a patient without ocular or overt hyperthyroid symptoms.
Case:
The patient is a 68 year old male with a past medical history of type 2 diabetes and hypertrophic cardiomyopathy, presenting with a one year history of a mildly pruritic, violaceous plaque of his left shin. He was referred to Dermatology Clinic, and biopsy came back as pretibial myxedema. Of note, his thyroid function studies were normal 6 months prior, and he had no symptoms of active thyroid disease at presentation. Additionally, he did not have any ocular abnormalities on exam. Upon repeat laboratory studies, he had low but detectable TSH, normal free T4, mildly elevated free T3, and elevated TSI/TRAb, overall consistent with early Graves’ hyperthyroidism. His pretibial myxedema was treated with high-dose topical steroids with improvement of his dermopathy. For his hyperthyroidism, he was started on low dose methimazole and never developed Graves’ ophthalmopathy.
Discussion:
Although the exact pathophysiology of pretibial myxedema is unknown, it is thought to be mediated by TSH receptor expression on fibroblasts, similar to Graves’ ophthalmopathy. It is usually seen in patients with active or longstanding Graves’ disease, often with high levels of thyroid receptor antibodies and concomitant Graves’ ophthalmopathy. However, there are a few cases of pretibial myxedema occurring in euthyroid patients with or without ocular symptoms, usually in the setting of elevated TSI, TRAb, or TPO antibodies. Our patient is a rare case of pretibial myxedema preceding active thyroid disease without ophthalmologic manifestations. Patients with hyper-pigmented, non-pitting plaques or nodules on pretibial regions should prompt providers to consider pretibial myxedema and test for thyroid studies, even in those without symptoms of hyperthyroidism or Graves’ ophthalmopathy.
SAT-049 Testosterone Therapy Reduces Inflammatory Activation of Human Monocytes in Hypogonadal Type-2 Diabetic Men as a Potential Mechanism to Improve Atherosclerosis
Authors: Bateman Lauren , Rao Preethi , Jones Thomas Hugh , Kelly Daniel Marcus 
Published: May 2020

Abstract
Testosterone deficiency is prevalent in men with type 2 diabetes (T2D) and is associated with greatly elevated risk of cardiovascular mortality. Testosterone replacement has beneficial effects on surrogate markers and risk factors of atherosclerosis including inflammation, cholesterol and insulin resistance improving survival in men with T2D. The underlying mechanisms of this action remain poorly understood. Inflammation is a central feature to both T2D and atherosclerosis and is driven by monocyte/macrophages, placing these immune cells at the crossroads of disease pathology. The recruitment of immune cells to atherosclerosis-prone areas of the vasculature is influenced by many factors including the inflammatory status of the circulating monocytes. The present study investigates the influence of testosterone replacement on monocyte inflammatory markers in a randomised double blinded placebo controlled clinical trial. 65 men with poorly controlled diabetes (HbA1c between 53 and 80 mmol/mol) and confirmed hypogonadism via early morning [0800−1200h] total testosterone ≤12 nmol/L or calculated free testosterone ≤255 pmol/L on two occasions ≥1 week apart, with at least two symptoms of hypogonadism were included in the study. Patients were randomly assigned to either placebo or treatment (depot testosterone undecanoate, 6 weekly followed by 3 monthly intramuscular injections) for 6 months. Monocytes were isolated from whole blood collected at baseline, 3 and 6 month visits followed by gene expression of key inflammatory targets IL-1β, IL-6, IL-10, TNFα, ICAM1, TLR2, TLR4, SCARB1 and MCP1 assessed via qPCR. Pro-inflammatory targets TNFα and MCP1 were significantly reduced over time in monocytes from patients treated with testosterone between 3 and 6 months (1.39±0.39 Vs 0.68±0.09, P&lt;0.01; 15.36±7.79 Vs 1.88±0.93, P&lt;0.01 respectively) and TNFα at 6 months compared to the start of the study (1.00±0.00 Vs 0.68±0.09, P&lt;0.001) when normalised to baseline. TNFα expression was also significantly reduced compared to placebo treated patient monocytes at 6 months (0.68±0.09 Vs 3.45±1.50, P&lt;0.01). Other targets were not significantly altered over time or between treatment groups. These findings importantly indicate for the first time that testosterone influences monocyte inflammatory activation in type 2 diabetic men by altering expression of the most potent atherogenic chemokine MCP1 and potent pro-inflammatory cytokine TNFα, as a potential mechanism to protect against atherosclerotic plaque development in hypogonadism.
MON-727 The Chromatin Landscape of Glucocorticoid Regulated Genes in Mouse Embryonic Neural Stem / Progenitor Cells
Authors: Berry Kimberly , Chandran Uma , Mu Fangping , DeFranco Donald 
Published: May 2020

Abstract
Stem/Progenitor Cells
Antenatal administration of Dexamethasone (Dex), a synthetic glucocorticoid (GC), is a common clinical intervention for women at risk for preterm birth or in preterm labor that effectively reduces fetal risk of mortality and bronchopulmonary-related comorbidities. Despite the therapeutic potential of Dex, excess GC act adversely in the developing central nervous system to reprogram distinct neural circuits in the brain by acting through the glucocorticoid receptor (GR). For example, prenatal exposure to excess GCs can impact neural stem and progenitor cell (NSPC) proliferation leading to long-term alterations in prefrontal cortical neuronal complexity, which could contribute to behavioral and cognitive impairments later in life. The GR is a member of the nuclear receptor superfamily that, when bound by a ligand, translocates from the cytoplasm to the nucleus and associates indirectly or directly with DNA elements (e.g. glucocorticoid responsive elements or GREs) resulting in the activation and/or repression of target genes. While GR-regulated transcriptomes have been identified in many NSPC models, the mechanisms responsible for programming these cells for GC-responsiveness remain largely unknown. We therefore used transposase accessible chromatin followed by genome-wide sequencing (Omni ATAC-seq) to characterize the chromatin landscape of primary embryonic mouse NSPCs in response to an acute in vitro treatment with Dex. We identified a small, yet distinct fraction (0.002%, p&lt;0.05) of open chromatin sites that were Dex-inducible. 95% of these Dex-induced changes in chromatin accessibility occur within intronic or intergenic regions, suggesting the presence of long-range enhancer-promoter contacts that mediate NSPC transcriptional responses to Dex. Motif enrichment analysis revealed putative GRE sites located in Dex-inducible open chromatin within -5kb/+2kb of a Dex-induced gene, providing possible DNA targets of GR for further validation. A number of other transcription factors implicated in neurodevelopmental processes were found to underlie both Dex-inducible and constitutively open chromatin regions. Characterization of the precise epigenetic and transcriptional response to excess GC in-utero, and its influence on acute and chronic neurological outcomes, will encourage the development of alternative GC treatment regimens that could protect the developing brain from insult while providing optimal health outcomes in neonates.