bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-512 Graves’ Disease Induced Renal Tubular Acidosis
Authors: Aljaberi Asma Khaled , Shamsi Shamma Al 
Published: May 2020

Abstract
Thyroid gland can affect kidney function in different ways. Thyroxine as a master hormone of metabolism and growth works in many cellular levels include the renal tubules.
We present a 34-year-old Emirati gentleman who presented with multiple episodes of hypokalemic periodic paralysis. Blood test revealed thyrotoxic state, with highly positive serology for thyroid peroxidase, anti-thyroglobulin and thyrotropin receptor antibodies. Thyroid uptake scan confirmed homogenous diffuse uptake consistent with toxic diffuse goitre [Graves’ disease]. In view of recent fracture, bone profile and DXA scan were done. Investigations revealed vitamin D deficiency and below expected for age bone mass density.
The patient was started on symptomatic treatment with propranolol, IV and oral potassium along with IVF hydration. Routine blood work during admission showed a persistent normal anion Gap metabolic acidosis, serum bicarb 15 mmol/l. 24 hours urine electrolytes revealed normal potassium, sodium, high magnesium, low calcium and PH levels. Biochemical lab results suggested type 1 renal tubular acidosis. As the patient had hypokalaemia, high urine magnesium and low urine calcium and limbs weakness, Gitleman Syndrome was considered in the differential diagnosis. Whole Exome Sequencing (CentoXome GOLD®) was sent which came back negative. The following gene panels were studied: Renal tubular acidosis panel: ATP6V0A4, ATP6V1B1, CA2, EHHADH, HNF4A, SLC34A1, SLC4A1, SLC4A4. Bartter Syndrome panel: ATP6V1B1, BSND, CA2, CASR, CLCNKA, CLCNKB, CLDN16, CLDN19, FXYD2, HSD11B2,KCNJ1, KCNJ10, KLHL3, NR3C2, SCNN1A, SCNN1B, SCNN1G, SLC12A1, SLC12A2, SLC12A3, SLC4A1, SLC4A4, WNK1. Gene related to Gitelman syndrome: SLC12A3
Renal tubular acidosis was treated with KCL 600mg PO TID, Na bicarb 1200mg PO BID and spironolactone 25 mg PO OD. The patient received radioactive iodine (RAI) as the ultimate treatment for Graves’ disease. He developed hypothyroidism post RAI ablation and commenced on levothyroxine. Improvement of the metabolic acidosis was noticed in line with improvement of thyroid function. Na bicarb and spironolactone tablets were stopped eventually as the patient was euthyroid clinically and biochemically.
Overt hyperthyroidism is associated with accelerated bone remodelling, leading to hypercalciuria, which can predispose to nephrocalcinosis and renal tubular damage, and therefore causes type 1 renal tubular acidosis. Once the patient becomes euthyroid, bone remodelling and urine calcium return to normal levels and that would correct the renal acidosis.
This case report serves to highlight the effect of Graves’ disease on renal tubules which may result in type 1 renal tubular acidosis. This effect could be reversible with normalization of thyroid function.
MON-133 Hyponatremia in Hospital Care
Authors: Durkan Maeve Catherine , O’ Murchu Oisin 
Published: May 2020

Abstract
Hyponatremia (serum sodium &lt;136 mmol/L) is associated with significant morbidity and mortality. International guidelines suggest a clear algorithm for investigation, inclusive of measurements of paired urine sodium and osmolality, TFTs and a morning cortisol. The aim of this study was to prospectively investigate the assessment, management and clinical outcomes associated with hyponataemia in hospital admissions. Methods:This prospective study was conducted from Sept 9, 2018-Oct 3,2018. All admissions through the MAU were included excepting surgery & oncology and admissions in the prior 3 months. Follow-up data was collected in the six months post admission. Information on all hyponatremic admissions was through combined review of patient charts and hospital laboratory database. Results: 418 patients in total were admitted, of whom 75 (18%, 35 male, 40 female) had measurable hyponatremia. Mean age was 74 (SD=14). 63 patients (84%) had mild hyponatremia (130-135mmol/L), 9 (12%) had moderate hyponatremia (125-129mmol/L) and 3 (4%) had severe (&lt;125 mmol/L) hyponatraemia on admission. 4 (5%) patients only had measurements of paired serum and urine osmolality & sodium, 19 (25%) had TFTs measured, and 1 (1%) had an early morning cortisol. Only 9 (12%) were assessed by a consultant endocrinologist. 47 (63%) were taking a culprit medication (known to cause hyponatremia) on admission, and 15 patients/47 (32%) had the presumed causal medication discontinued. This resulted in an average rise in serum sodium of 4.7mmol/L by discharge. Mean length of hospital stay was 7 days for mild, 9 days for moderate and 16 days for severe hyponatremia cases, and 2 patients died in-hospital. Of the 73 surviving patients, 23 (31%) did not have a sodium remeasured at discharge and 27 (37%) were discharged with persistent hyponatraemia. 20 patients (27%) were re-admitted in the following 6 months. Over the same time period, 12/73 (16%) of hyponatraemic patient admissions died, compared to 13 /332 (4%) of normo-natraemic admissions,which was statistically significant χ²(1, N = 405) = 16.2, p &lt; 0.01. Conclusions:Hyponatraemia was a highly prevalent condition on admission accounting for 18% of all admissions, which was under investigated and underestimated. Endocrine evaluation was underutilised. Hyponatraemia was associated with a longer length of stay, and a four-fold excess in mortality in the six months post-discharge. These findings emphasise the need for formal assessment and treatment along a dedicated protocol for all patients and we have proposed a ‘hospital alert’ system be installed for automatic consultation.
SAT-460 Myxedema Coma Mimicking Cardiogenic Shock Treated with Levothyroxine
Authors: Chaker Bayan , Chaker Mahmoud , Alim Hussam , El-Zein Louna S 
Published: May 2020

Abstract
Myxedema coma is a medical emergency with a mortality rate of 30–50%. It is a commonly missed diagnosis and can lead to multiple cardiovascular complications which are reversible with levothyroxine treatment. IV levothyroxine should be initiated based on clinical suspicion without waiting for laboratory results.
We report a case of a 71-year-old female with a history of CABG 10 years ago, who presented to the emergency department with a syncopal episode. The patient denied aura, vomiting, jerky movements, rolling eye movements, bowel/bladder incontinence, and palpitations. She reported having exertional chest pain for a couple of months. Her home medications included metoprolol succinate 50 mg daily, hydralazine 50 mg twice daily, Imdur 30 mg daily, and levothyroxine 300 mcg daily which the patient reported taking rarely. On admission, the temperature was 36°C, HR 43, BP 75/49 which dropped to 60/40, RR 9, and SpO2 of 93% on 2LPM. Physical exam showed euvolemia with brisk reflexes and delayed relaxation. Blood work revealed Na of 133 mM/L (L), Cr 6.4 mg/dL (H) from a baseline of 2.4 mg/dL, and a troponin of 0.26 ng/mL (H). EKG showed first degree AV block with new T-wave flattening not seen on previous EKGs. A fluid challenge for hypotension elicited no response and the patient was started on a dopamine drip for cardiogenic shock, a heparin drip for ACS, and was transferred to the CCU. BP improved to 140s/70s with a HR remained in the 50s. On the 2nd day of admission, blood work revealed a TSH of &gt;150 (H), free T4 of 0.6, total T3 of 34 (L) and a random cortisol of 15.5 microgram/dL. On the 3rd day of admission, the patient was given 200 mcg of IV levothyroxine. At that time, the patient was on a dopamine drip with a BP of 144/94 with a HR of 64. Twelve hours later, the patient’s BP went up to 197/105 with a heart rate of 65 prompting discontinuation of the dopamine drip and administration of hydralazine and amlodipine. On the morning of the fourth day of admission, BP went up to 236/116 with a HR of 75 and the patient was started on a nicardipine drip. Blood work 3 days after starting levothyroxine revealed a TSH of &gt;150, free T4 of 0.9, and a total T3 of 70. The patient was discharged on levothyroxine 150 mcg daily, amlodipine 10 mg, hydralazine 50 mg q6hrs, and Imdur 30 mg daily.
The patient’s myxedema score was 75 on admission. However, thyroid function tests were not checked with initial labs despite the presence of avert clinical features. As a result, the patient was started on a dopamine drip which could have been avoided. This underlines the importance of early recognition and management of myxedema coma. Having a low total T3 with a low normal FT4 could be explained by recent intake of high dose levothyroxine at home after a significant period of non-compliance. Fortunately, levothyroxine administration to this patient has reversed cardiovascular abnormalities including bradycardia and hypotension within hours when it was given promptly.
MON-356 Atypical Femur Fracture with Denosumab
Authors: Mirza Faryal S , Nallu Ravali 
Published: May 2020

Abstract
Background: Osteoporosis (OP) is a systemic disease that is associated with increased risk for fractures. Anti-resorptive medications (ARM) are an effective modality for treatment and prevention of fractures in OP. Long-term use of ARM like bisphosphonates (BP) is associated with increased risk of atypical femoral fractures (AFF). Denosumab (DM) is monoclonal antibody that targets receptor activator of nuclear factor KB ligand (RANKL). A few cases of AFF with DM have been reported in patients who have previously been on long term BP therapy. We present a case where the patient had only received two zoledronic acid (ZA) infusions, last one three years prior to being initiated on DM and experienced AFF.
Case: 73-year-old postmenopausal woman presented to the emergency room with sudden onset pain in the right thigh. Patient was standing and reaching into her closet when she felt a snap in right thigh followed by inability to move the right leg or bear weight on it. X-ray of the right femur showed a displaced femoral shaft fracture with a short transverse fracture line and a spike, without comminution.
History was significant for OP for which she received raloxifene for a couple of years followed by ZA in 2013 and 2015 by her primary care. Fracture history was significant for a wrist fracture in 2015, and T12 and L1 fractures in 2017 from coughing while on Medrol dospak for an acute episode of bronchitis. In 2017, bone density showed L1-L4 T score of -2.0, the left total hip T score was -1.8 and left femoral neck T score was -2.5 consistent with OP. Work up for secondary causes of OP was unremarkable. Due to recent T12 and L1 compression fractures, she was recommended DM. She received DM in June 2018 as she was undergoing a dental implant followed by December 2018 and June 2019 and presented with the right femoral fracture in November 2019.
Past history was significant for idiopathic pulmonary fibrosis which had been relatively stable without need for long-term steroid therapy. History was negative for diabetes or kidney disease. Menarche was at age 14, menopause at 52 and she did not take any hormone replacement therapy.
She underwent surgical fixation with intramedullary rod. Due to concern about ARM associated sub-trochanteric fracture in the right femur, left femur was imaged. She had cortical beaking in the distal third of the left femur, and underwent prophylactic medullary nailing of the left femur as well.
Conclusion: AFF are an uncommon complication of ARM used for OP. Not many cases of AFF have been reported with the use of DM and most of the reported cases are associated with prolonged BP therapy. Our case is unusual in that AFF occurred in the absence of prolonged BP therapy and raises concern that a couple of ZA infusions in the past can also increase the risk of AFF. Clinicians need to have a high index of suspicion and may consider doing femur x-rays in patients who have previously been on BP prior to starting DM.
MON-346 Secondary Hyperparathyroidism and Other Complications in a Post-Roux-En-Y Patient: A Case Report
Authors: Chan Jessica Michelle , Havins Bradley S 
Published: May 2020

Abstract
Roux-en-y Gastric Bypass is a very common surgical procedure in managing morbid obesity. Approximately 303,890 roux-en-y surgeries were performed in the United States in between the years of 2012 to 2017, and the number is steadily increasing as more Americans are diagnosed with obesity.i
This featured case report describes a 52-year-old female presenting with complications seven years following Roux-en-y gastric bypass. Four years post-operatively, she presented to the ER with a pelvis fracture. It was incidentally found that she had osteoporosis with a t-score of -2.9. It was also found that her bone mineral density (BMD) for women for her age was low with a z-score of -3.5 and her 10-year probability of getting fractures was high with a Fracture Risk Assessment Tool (FRAX) score of 6.2%. Seven years following Roux-en-y gastric bypass, she presented to our primary care office with Vitamin B12 deficiency and secondary hyperparathyroidism due to Vitamin D deficiency. We attempted to correct the deficiencies with high dose of Vitamin D, Vitamin B12, and calcium citrate. Eight months later, the B12 levels was normalized, but the secondary hyperparathyroidism and Vitamin D deficiency were not corrected. This case illustrates the complications that can occur following a Roux-en-y Gastric Bypass, importance of supplement compliance, and proper follow-up with Roux-en-y patients.
Endnotes
i American Society for Metabolic and Bariatric Surgery. (2018). Estimate of Bariatric Surgery Numbers, 2011-2017 | American Society for Metabolic and Bariatric Surgery. [online] Available at: https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers [Accessed 31 Oct. 2019].
SUN-261 Deletion of Hepatic Kisspeptin Results in Abnormal Glucose Metabolism in Female Mice
Authors: Aloqaily Bahaa , Kwon Hyokjoon , Negron Ariel L , Wondisford Fredric E , Radovick Sally 
Published: May 2020

Abstract
Kisspeptin is a hypothalamic protein critical for neuroendocrine control of pubertal development and fertility and is modulated by nutritional signals. Kisspeptin has been localized to specific neurons located in the arcuate and anteroventral periventricular (AVPV) nuclei of the hypothalamus and is secreted to control GnRH mediated pubertal maturation and reproduction. Kisspeptin has also been localized to peripheral tissues including the liver, fat, gonads, intestine and placenta, although its role in these tissues is unclear. The objective of current study is to define the role of hepatic kisspeptin as a metabolic sensor. A floxed Kiss1 mouse has been developed, and ablation of liver-specific Kiss1 was achieved in two to three month old Kiss1f/f male and female mice given a single tail vein injection of thyroid hormone-binding globulin (TBG) promoter-driven Cre recombinase adeno-associated virus (AAV-CRE). A control group of Kiss1f/f male and female mice received an injection of AAV-GFP, expressing green fluorescent protein. Two weeks after injection, a glucose tolerance test (GTT) was performed followed by an insulin tolerance test. To determine whether changes had occurred in the reproductive axis, estrous cyclicity was assessed by daily vaginal smears and estrous cycle phases determined by vaginal cytology. Mice were euthanized four weeks post-injection and tissues were collected for RNA extraction and gene expression analysis via qRT-PCR. As expected, qRT-PCR data showed absence of Kiss1 expression in the liver of AAV-CRE mice compared to AAV-GFP mice with no changes in kisspeptin gene expression were noted in the ovary, testes, spleen, pancreas, arcuate or AVPV. Estrous cyclicity was also not affected by viral ablation of hepatic Kiss1. Elevated fasting glucose and glucose intolerance in the GTT were found in AAV-CRE compared to AAV-GFP females (P &lt; 0.05). No differences in AAV-CRE and AAV-GFP male mice were found, indicating the importance of Kiss1 in glucose homeostasis in females. The insulin tolerance test was not statistically different between groups or treatments. Further research is required to elucidate the mechanism by which hepatic kisspeptin alters glucose metabolism in mice in a sexually-dimorphic fashion.
SAT-627 Racial and Ethnic Differences in Metabolic Disease in Obese Adolescents with Polycystic Ovary Syndrome
Authors: Andrisse Stanley , Reyes Yesenia Garcia , Pyle Laura , Nadeau Kristen , Kelsey Megan Moriarty , Cree-Green Melanie 
Published: May 2020

Abstract
Background: Polycystic ovary syndrome (PCOS) affects up to 15% of women and is associated with a multitude of metabolic complications including insulin resistance, type 2 diabetes, cardiovascular disease, and hepatic steatosis. In the general population, metabolic disease rates vary by race and ethnicity. The interaction of race and ethnicity with PCOS-related metabolic disease in adolescent youth has not been extensively examined. Methods: Secondary analysis of data from overweight and obese (&gt;90 BMI%ile) adolescent (12-21 years) female participants with PCOS enrolled across 4 protocols. Measurements included fasting hormone and metabolic measures, a 2-hour oral glucose tolerance test and MRI for hepatic fat. Groups were compared by ANOVA, with and without correction for BMI or chi-square tests for proportions. Results: Participants included 39 white (NHW 15.7±0.2 years; 97.7±0.2 BMI%ile), 50 Hispanic (15.2±0.3 years; 97.9±0.3 BMI%ile) and 12 black (NHB 16.0±0.6 years; 98.6±0.4 BMI%ile) adolescents. BMI%ile was different between groups (p=0.04), but age of menarche, free testosterone and hirsutism severity were not. Hepatic markers of insulin resistance were worse in Hispanic youth, including lower sex hormone binding globulin and TG/HDL ratio (p&lt;0.001), although HOMA-IR was worst in NHB (p=0.009) and Hispanic (p=0.036) compared to NHW youth. There were no significant differences in insulin concentrations—either fasting or during the OGTT—although fasting C-peptide was higher in Hispanic (p=0.008) compared to NHW youth. Fasting and 2-hour glucose concentrations were not different between groups. HbA1c was highest in NHB (5.7±0.4%, p&lt;0.001 vs. NHW, p=0.026 vs. Hispanic), then Hispanic (5.5±0.3, p&lt;0.001 vs. NHW), then NHW (5.2±0.3) youth. Fasting triglycerides differed between groups (p=0.029), being highest in Hispanic youth (129 [105,167] mg/dL). The frequency of hepatic steatosis (NHW 42%, Hispanic 62% NHB 25%, p=0.032) and the metabolic syndrome components HDL &lt;40 mg/dL (NHW 61%, Hispanic 82% NHB 50%, p&lt;0.001) and HbA1c 5.7-6.4% (NHW 5%, Hispanic 36% NHB 50%, p&lt;0.001) were different between the groups. Conclusions: Adolescents with PCOS appear to show similar racial and ethnic variation to the general population in terms of metabolic disease components.
SAT-173 SAMD9 (Sterile Alpha Motif Domain-Containing 9) Expression in Adrenocortical Tumors
Authors: Bueno Ana C , Santos Carlos H , More Candy CB , Stecchini Monica F , Ramalho Leandra NZ , Ramalho Fernando S , Moreira Ayrton C , Brandalise Silvia R , Yunes Andres , Castro Margaret De , Antonini Sonir RR 
Published: May 2020

Abstract
Introduction: SAMD9 variants are associated with colon, breast and lung tumors. SAMD9 mutations result in adrenal hypoplasia, suggesting its importance in adrenal development. We investigated the contribution of abnormal expression of SAMD9 and its homologous, SAMD9L, to the pathogenesis of pediatric adrenocortical tumors (pACT) Objective: To evaluate the involvement of SAMD9 and SAMD9L in normal human adrenal cortex development and adrenocortical tumorigenesis, as well as to evaluate their association with tumor presentation and patient outcome. Methods: pACT samples (n= 72), normal pediatric adrenal cortices (n= 11), and normal fetal and post-natal adrenals (20 weeks of gestation to 10 years of age; n= 51) were enrolled. Protein expression of SAMD9 (immunohistochemistry) and SAMD9/SAMD9L mRNA levels were evaluated (qPCR). The associations between SAMD9/SAMD9L expression in pACT with tumor presentation (P53 p.R337H genotype and metastasis occurrence) and patient outcome (Overall (OS) and Disease-Free Survival) were analyzed. In silico, publicly available data from pediatric patients with ACT available in the Gene Expression Omnibus were used to evaluate the aforementioned associations with SAMD9 (GSE76021) and SAMD9L (GSE76019) mRNA levels. In vitro, SAMD9 subcellular localization pattern was investigated in the ACT cell line NCI-H295R (immunofluorescence). Results: Nuclear and cytoplasmic SAMD9 expression was observed throughout all different phases of adrenal development evaluated. However, in pACT samples, 26% presented nuclear and 86% cytoplasmic immunostaining. In line, NCI-H295R cells presented mostly cytoplasmic SAMD9 immunostaining under basal conditions. No differential expression was observed between SAMD9 or SAMD9L mRNA levels in pACT and in normal pediatric adrenals. Moreover, no association between SAMD9 immunostaining, SAMD9 or SAMD9L mRNA levels, tumor presentation and patient outcome were observed in our cohort, nor in the in silico evaluation. Conclusion: SAMD9 is nuclear and cytoplasmic expressed during adrenal cortex adrenal development and its loss of function is associated with adrenal hypoplasia. On the other hand, SAMD9 is mostly cytoplasmic expressed in pACT and immortalized NCI-H295R cells. No differential expression of SAMD9 nor its counterpart SAMD9L mRNA were associated with tumor presentation and pediatric patient outcome.