bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-376 A Quality Improvement Project on Identification and Management of Primary Hyperparathyroidism in Patients Who Present with Osteoporosis to Reduce Morbidity from Bone Disease
Authors: Hatta Sharifah Faradila Wan Muhamad , Khine Aye Aye , Chopra Roopa , Chopra Amit , Talapatra Paulomi , Sapkota Hem , Buch Harit 
Published: May 2020

Abstract
Introduction:Individuals with Primary Hyperparathyroidism (PHPT); a common endocrine disorder are at increased risk of both vertebral and peripheral fractures.Meanwhile Normocalcaemic Primary Hyperparathyroidism (NPHPT),a recognised phenotype of PHPT with a prevalence of 0.4-3.1% in community-based cohorts were anticipated to be milder but most case series documented high rates of osteoporosis, fractures and kidney stones.
Objective:We proactively evaluated patients with a new diagnosis of osteoporosis to (a) identify the frequency of hypercalcaemic and normocalcaemic primary hyperparathyroidism in this cohort of patients and (b) to evaluate the benefit of deploying a proactive process for this evaluation as compared to the current arrangement in our Centre of devolving this to the primary care team.
Method:This cross-sectional study evaluated 194 patients whom were referred for dexa scan for newly diagnosed osteoporosis between January 2018 and December 2018. Patients whom had a secondary causes of osteoporosis, eGFR&lt;60mls/min, liver and malabsorptive conditions and taking medications that would interfere with bone metabolism were excluded from the study. A recommendation letter was sent to them and their General Practitioner to undertake the following investigations: serum calcium, PTH, phosphate, vitamin D, magnesium, liver function test, full blood count, coeliac screen and thyroid function test. Abnormal blood tests including new diagnosis of primary hyperparathyroidism and vitamin D deficiency were identified and treated accordingly. A second letter and telephone calls were made as a reminder if no response were received within 12 weeks of the first letter.
Results:After the first letter, only 83 (34.3%) patients complied with the request for the blood tests. After another 3 months a further 86 patients had the test done while 25(12.9%) did not have the test done despite the reminder.Mean age was 69.72 ± 13.01 and 90.2% were females. The commonest indication for bone density assessment was fragility fracture (46.2%). 69 (35.6%) had spinal, 77 (39.7%) femoral and 9 (4.6%%) wrist osteoporosis. 17(8.8%) patients were detected to have hypercalcaemic and 8(4.73%) patients had normocalcaemic primary hyperparathyroidism. 18(10.7%) patients had vitamin D deficiency and secondary PHPT with half of these patients (9(5.3%)) had severe deficiency (&lt;25 nmol/L).
Conclusions:A significant proportion of patients with osteoporosis without prior history of metabolic bone disease had PHPT but the proportion of these having NPHPT is low unlike what is reported in the literature.Proactive assessment of secondary causes is much more effective and should be routinely deployed
SAT-467 A Case of Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism
Authors: Alhumaidi Hebah , Rao Sarika , Kansal Dhruv 
Published: May 2020

Abstract
17 year old female presented for evaluation of galactorrhea of 3 months duration. Patient was diagnosed with papillary thyroid cancer and underwent total thyroidectomy in 2011. She was prescribed Synthroid 175 mcg but was not compliant with taking her medicine. In April 2019 she developed bilateral galactorrhea for which she was evaluated at an outside facility and was found to have a prolactin 143.7ng/mL (n 7.2-63) and TSH 996 mIU/L (n 0.5 -4.0). Pituitary MRI revealed pituitary macroadenoma measuring 1.5 x 1.4 x 1.2 cm with slight elevation of the optic chiasm and infundibulum. She was advised to restart Synthroid and was referred for the neurosurgery team at our facility for surgical resection of pituitary macroadenoma. Over the same period of time, she gained 25 lbs, developed headaches, excessive fatigue, constipation, hair loss, lower extremity swelling, and puffiness of her face. Her menstrual cycles were regular but this was only after she was placed on norelgestromin/ ethinyl estradiol transdermal patch. She denied visual changes. By the time she was seen at our clinic in June 2019, she was taking Synthroid daily for 1 month. TSH decreased to 1.0 mIU/L and prolactin improved to 68 ng/mL. IGF-1 was low at 98 ng/mL (n 149-509). ACTH, morning cortisol, and 24 hour urine free cortisol were within reference range. Visual field testing showed no visual defects. We advised patient to continue taking Synthroid and to follow up in 1 month. On the follow up visit in July 2019, TSH was 0.2 mIU/L, prolactin was 52 ng/mL and IGF-1 was 105 ng/mL. Pituitary MRI showed pituitary hyperplasia that has decreased compared to previous MRI, now measuring around 1 cm at the largest dimension without contact with the optic chiasm and the Infundibulum was at midline. Galactorrhea and headaches resolved and fatigue significantly improved.
MON-111 Plasma Insulin Measured with a Sensitive Immunoassay May Establish the Diagnosis of Congenital Hyperinsulinism Without Further Testing
Authors: Siersbæk Julie , Larsen Annette R , Nybo Mads , Christesen Henrik Boye Thybo 
Published: May 2020

Abstract
Background: The diagnosis of congenital hyperinsulinism (CHI) is often hampered by a plasma insulin (p-insulin) detection limit of 2-3 mU/L (14-21 pmol/L) by RIA methods.
Objective: To evaluate the diagnostic performance of a sensitive immunoassay for p-insulin and to find the optimal p-insulin cut-off for CHI versus other conditions with hypoglycaemia.
Design: Single centre retrospective cohort study.
Methods: Diagnostic tests with no medication, no i.v. glucose and under fasting conditions were performed in children with a clinical diagnosis of CHI. P-insulin concentrations determined at simultaneous p-glucose concentrations at least &lt;3.2 mmol/L (57.5 mg/dL) were included in the analysis (n=61).
The diagnosis of CHI was either clinical (n=61) or by gold standard criteria: hypoketotic hypoglycaemia plus disease-causing genetic mutations and/or diffuse, focal or atypical pancreatic histopathology (n=57). Samples from 15 children with idiopathic ketotic hypoglycaemia (IKH, diagnosis by exclusion, p-ketones &gt;1.5 mmol/L during hypoglycaemia) were used as controls.
P-insulin was measured by the high-sensitive assay (Cobas e411 immunoassay analyzer); lower detection limit 1.4 pmol/L (0.2 mU/L); normal range 18-173 pmol/L (2.57-24.7 mU/L). Concentrations &lt;18 pmol/L were considered suppressed; ≥18 pmol/L un-suppressed.
Receiver operating characteristics (ROC) curves with determination of area under the curve (AUC) values were performed for the diagnostic performance of p-insulin in the diagnosis of CHI. Results: In the 61 samples from CHI patients, the median (range) p-insulin was un-suppressed in all diagnostic samples [90; 20-758 pmol/L (12.9; 2.9-109.1 mU/L)], while p-insulin was suppressed in all 15 samples from IKH patients [1.5; 1.5-9 pmol/L (0.21; 0.21-1.3 mU/L)]. The ROC AUC was 1.0 (95%CI. 1.0-1.0) for the diagnosis of CHI defined both by the clinic and by gold standard. The optimal p-insulin cut-off was 14.5 pmol/L (2.1 mU/L) or 12.5 pmol/L (1.8 mU/L), for CHI patients by use of a simultaneous p-glucose cut-off of &lt;3.2 mmol/L (57.5 mg/dL; n=61), or 3.0 mmol/L (55 mg/dL; n=49), respectively.
Conclusions: The sensitive insulin assay performed excellent in diagnosing CHI with a ROC AUC of 1.0. The use of a p-insulin cut-off of 13 pmol/L (1.86 mU/L) during a diagnostic hypoketotic hypoglycaemia test may establish the diagnosis of CHI without further diagnostic testing.
SUN-284 Rare Case of Adipsic Diabetes Insipidus Post Astrocytoma Resection: Case Report
Authors: Alanazi Alanoud , Elamin Yasir , AlSaeed Zahra , Alabdrabalnabi Fatima 
Published: May 2020

Abstract
Background:
Adipsic diabetes insipidus (ADI) is a rare disorder triggered by injury to the hypothalamus impairing thirst osmoreceptors and the antidiuretic hormone syntheses leading to absence of thirst.
We are reporting a rare case of ADI Post astrocytoma resection who presented with a severe hypernatremia postoperatively.
Clinical Case:
A 16-year-old female known to have hypothalamic pilocystic astrocytoma post incomplete resection in 2014.
She presented in 2018 with one week history of sudden onset heachache, progressively worsen overtime, worst in the morning, there were no relieving factors. On examination she was conscious alert oriented GCS 15/15, Vital signs were normal, fundus exam within normal, pupil equal bilateral reactive to light, there was no focal neurological deficit. Systemic examination was unremarkable. Radiological imaging revealed interval size progression of previously seen suprasella region with extension into the floor of the third ventricle. Investigations: Renal profile & pituitary hormonal profile were normal. She underwent second stage resection.
Postoperatively, she developed asymptomatic hypernatremia with inability to sense thirst. On examination: Conscious, alert, BP:100/65, no postural drop, Pulse:95, Fluid balance negative 1L. Systemic examination was unremarkable. Laboratory investigations: Creat 0.77mg/dl (0.6–1), Na 173mEq/dl(136–145), K 3.3mEq/dl(3.5–5.1), Cl 134mEq/dl(98–107), Serum osmolality 363mOs/kg(285 -295), Urine osmolality 468mOs/kg(300 -1600), Urine Na 29mEq/L(20- 110) & Urine volume 1900. Diagnosis of ADI was made where she was treated with desmopressin. Her response was good with reduction in Na level of around 7- 9 mEq/L/Day. She was maintained on twice daily vasopressin, instructed to maintain her fluid intake 1–1.5 L/day and good urine output.
Conclusions:
Astrocytoma rarely linked with development of central diabetes insipidus and even fewer with adipsia. The absence of polydipsia and polyuria can be misleading. Long-term therapy should consider the benefits of vasopressin and fluid therapy against the risk of brain edema/herniation. Body weight and electrolytes monitoring essential & should be maintained a long with strict fluid intake.
SUN-048 Cardiometabolic Effects of Cross-Sex Hormone Therapy in Transgender Patients
Authors: Trebotic Lana Kosi , Deischinger Carola , Thomas Anita , Just-Kukurova Ivica , Trattnig Siegfried , Kaufmann Ulrike , Kautzky-Willer Alexandra 
Published: May 2020

Abstract
Background: Sex hormones are believed to play an important role in development and progression of cardiovascular disease. However, the gender gap in onset and mortality is not yet completely understood. Transsexuals undergoing hormone therapy are a promising collective for analysing the effects of sex hormones on cardiometabolic disease. Methods: Aim of this study is to identify gender specific cardiovascular changes attributed to high-dose cross-sex hormone therapy (HT) in male-to-female (MtF) and female to male (FtM) transgender patients by performing an oral glucose tolerance test (OGTT) and 3 Tesla magnet resonance spectroscopy for hepatic (HCL) and myocardial (MYCL) lipid content analysis. The control group (CON) is conducted by age, sex and BMI matched healthy individuals. Results: Until now we included 26 MtF,14 FtM patients and 12 age and BMI matched healthy controls. The mean age was comparable in all 3 groups (MtF 30.12±2.31, FtM 29.72±1,91, CON 30,23±1.22 as well as BMI (22.59±3.81, 21.62±2.53, 21.33±1.20 kg/m2, p=ns, respectively). The mean hormone therapy duration was similar in both groups (MtF 4.58±1.20 vs FtM 2.35±0,95, p=0,29). HOMA Index did not significantly differ between the groups (MtF 1,78±0,92 vs FtM 1,96±1.22 vs CON 1,8±1.01, p=0,3 vs 0,4 vs 0,3 respectively). HCL was significantly higher in MtF than FtM (1,50±0,41 % vs 0.54±0,33 %, p=0,022, respectively). We also found a significant correlation between ejection fraction (EF) and Testosterone levels (Spearmans Rho 0,80, p=0.002). Conclusio: These preliminary data could indicate a positive effect of Testosterone therapy on heart function. Contradictory to current data we found a higher HCL in MtF than FtM suggesting a not so protective estrogen effect when looking at the liver. Long-term studies are warranted to assess whether cross-sex HT results in different outcomes regarding cardiovascular disease.
MON-074 Ketotic Hypercalcemia; A Possible Side Effect of Managing Refractory Epilepsy with Ketogenic Diet
Authors: Dekelbab Bassem , Davydova Yafa , Levine Michael A 
Published: May 2020

Abstract
Background: Patients with epilepsy have multiple risk factors for low bone mass, including immobility, reduced muscle mass, and use of multiple anticonvulsant medications. The ketogenic diet (KD) has been used as an effective treatment of refractory epilepsy for decades, with multiple reports in medical literature describing adverse effects on bone and mineral metabolism including gradual loss of bone mineral density. There has been only one report of hypercalcemia in three children on the KD for refractory seizures. We now describe another case, highlighting the importance of considering the KD as a cause of hypercalcemia.. Case presentation: A 14-year-old girl with Rett syndrome, epilepsy, global developmental delay and gastrostomy tube dependency presented to the emergency room with marked dehydration. She had been on the KD for several years due to refractory epilepsy. Her parents had recently noticed thick oral secretions. The only change in her management plan was the recent change of her formula from Ketocal 3:1 to Ketocal 2.5:1. Lab studies showed hypercalcemia 15 mg/dL (ref 9.2-10.7) with ionized calcium of 7.99 mg/dL (ref, 4.8-5.2). She had normal serum calcium levels on multiple previous occasions, including 10.2 mg/dL 4 months prior to presentation. Other studies included increased BUN 37 mg/dL (ref, 7-21) and Creatinine 2.31 mg/dL (ref, 0.53-0.8). She had a low normal PTH 14 pg/ml (ref, 8-72), PTH-related peptide 0.6 pmol/l (ref, &lt; 4.2), and 25-hydroxyvitamin D 66 ng/ml (30-100). 1,25-dihydroxyvitamin D level was low at 12.5 pg/ml (ref, 19.9-79.3), with increased urine calcium/creatinine ratio 1.00 mg/mg creat (Ref, 0.02-0.26). Beta Hydroxybutyrate was 3.45 mmol/l (ref, 0.02 - 0.27), without major change over the last year. Renal US was normal. She received IV hydration with improvement in serum calcium, BUN, and creatinine and was discharged on increased intake of free water and adjustment of KD to maintain Beta Hydroxybutyrate around 2 mmol/l. Her serum calcium currently ranges 10.5- 12 mg/dl, and will soon begin therapy with subcutaneous calcitonin. Conclusion: The KD has adverse effects on bone and mineral metabolism, and can lead to severe hypercalcemia and/or hypercalciuria as well as decreased bone density. Agents that decrease bone resorption are highly effective. Providers caring for children on this diet should be aware of such potential association. Reference: Hawkes CP, Levine MA. Ketotic hypercalcemia: a case series and description of a novel entity.J Clin Endocrinol Metab. 2014 May;99(5):1531-6.
MON-644 Prevalence of Non-Alcoholic Fatty Liver Disease and Liver Fibrosis in Patients with Type 2 Diabetes Mellitus
Authors: Fanous Nada , Bril Fernando , Leiva Eddison Godinez , Kalavalapalli Srilaxmi , Cusi Kenneth , Lomonaco Romina 
Published: May 2020

Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. The more severe form is non-alcoholic steatohepatitis (NASH) which can progress to liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). NASH is more common in patients with type 2 diabetes mellitus (T2DM). However, its true prevalence in unselected patients with T2DM in the United States remains unknown. In 2019, the American Diabetes Association recommended screening for NASH and liver fibrosis in all patients with T2DM with steatosis and/or elevated ALT. Screening focuses on liver fibrosis as associated with increased risk of cirrhosis and HCC. Still, a liver biopsy remains the gold standard to accurately assess the severity of liver disease. The aim of this study was to determine the prevalence of liver fibrosis in unselected patients with T2DM presenting to primary care or endocrinology clinics at a university hospital in the US. Secondary outcomes were to assess the prevalence of steatosis controlled attenuation parameter (CAP) and performance of vibration-controlled transient elastography (VCTE) as a non-invasive tool to identify patients with significant liver fibrosis. Patients with T2DM between ages of 21-79 and without a history of alcohol intake or other causes secondary causes of NAFLD were recruited for the study. Participants underwent screening for NAFLD at the time of their clinic visit by means of point-of-care CAP and VCTE. Initial evaluation also included obtaining patient demographics, routine chemistries, and fasting samples (on visit #2 if not fasting initially) for metabolic measurements and fibrosis biomarkers. Liver biopsies were offered to patients with a liver stiffness measurement (LSM) ≥8.0 kPa (i.e., highly likely to have moderate-to-severe fibrosis or ≥F2), or those with ≥7 kPa if AST ≥20 and had an APRI and/or FIB-4 score suggestive of being at high-risk of liver fibrosis (i.e., at least mild-to-moderate fibrosis or ≥F1). A total of 469 patients were recruited (age 59±12; 56% females; 60% non-Hispanic whites, 30% African Americans, 4% Asian; BMI 33±6 Kg/m2; A1c 7.5±1.7%; FPG 143±60 mg/dL; AST 22±11 U/L; ALT 24±17 U/L; triglycerides 156±151 mg/dL; LDL-C 88±37 mg/dL; HDL-C 47±13 mg/dL). The prevalence of NAFLD by CAP (≥280) was 67% with a mean CAP of 305±3. The prevalence of any fibrosis was 24% patients. Among those with fibrosis, 15% had moderate-to-severe fibrosis or ≥F2. In those that underwent a liver biopsy, 61% had moderate-to-severe fibrosis (F2-3). Our ongoing study demonstrates the high prevalence of liver steatosis and fibrosis in patients with T2DM. NASH is a common but under-recognized complication of T2DM that requires greater awareness among clinicians taking care of patients with diabetes. While the optimal screening strategy remains unclear, an approach based on plasma biomarkers and CAP/VCTE deserves further exploration moving forward.
SUN-017 Developmental Programming: Prenatal Testosterone Treatment Induced Metabolic Defects May Involve Premature Cellular Senescence
Authors: Puttabyatappa Muraly , Ciarelli Joseph Norman , Padmanabhan Vasantha 
Published: May 2020

Abstract
Prenatal exposure to excess testosterone (T) programs peripheral insulin resistance and dyslipidemia along with tissue-specific increases in ectopic lipid accumulation, oxidative stress and insulin resistance in liver and muscle of the early adult female sheep. Prenatal T increased inflammation and oxidative stress in the visceral (VAT) but not subcutaneous (SAT) adipose tissue, with no effect on insulin sensitivity in both depots. These systemic and tissue-specific metabolic changes are reminiscent of defects such as non-alcoholic fatty liver disease (NFLAD) common among aged individuals. Because it is known that gestational insults can program premature aging of reproductive organs and chronic cardiovascular abnormalities, we hypothesized that programming of premature cellular senescence is one of the ways through which gestational T induces premature aging of metabolic systems during early adulthood. To test this hypothesis, mitochondrial oxidative phosphorylation (OXPHOS) and telomere length, as measure of cellular senescence, were assessed in liver, muscle, VAT and SAT collected from control and prenatal T- (100mg T propionate twice a week from days 30-90 of gestation) -treated female sheep at 21 months of age. Genomic DNA was subjected to TeloTAGG Telomere Length Assay (Sigma-Aldrich, St Louis, MO) and whole tissue protein lysates analyzed by immunoblot using Total OXPHOS Human WB Antibody Cocktail (ab110411, Abcam, Cambridge, MA). Data were analyzed by Student’s t test and Cohen’s effect size analysis. Prenatal T-treatment induced 1) a trend (p = 0.09) towards a large magnitude increase in shorter telomere fragments (0.08 -3.6 KB) in the liver and 2) a non-significant large magnitude decrease in shorter telomere fragments in muscle and SAT without having any effect in the VAT. Prenatal T also induced a large magnitude increase in mitochondrial OXPHOS protein complexes II and IV in liver, without having an effect at the level of the muscle, VAT and SAT. These findings are suggestive that prenatal T-treatment induced hepatic defects may involve premature cellular senescence. The relevance of parallel increase in mitochondrial OXPHOS in the liver is unclear and remains to be explored. The defects observed in the muscle and SAT may occur independent of cellular senescence or alterations in mitochondrial function. The lack of change in telomere length and mitochondrial OXPHOS in spite of increased inflammation and oxidative stress in the VAT is suggestive of a potential protective function in play, consistent with maintenance of the insulin sensitivity in this tissue. This study, therefore, raises the possibility that metabolic defects programmed by gestational insults may involve premature aging of metabolic organs in a tissue-specific manner and have translational bearing in conditions associated with hyperandrogenic states.
SAT-670 The Perfect Storm for Diabetic Ketoacidosis
Authors: Abushamat Layla A , Bhalla Rajat , Reusch Jane E 
Published: May 2020

Abstract
Background
Diabetic Ketoacidosis (DKA) is a life-threatening endocrine emergency characterized by metabolic acidosis occurring in the setting of hyperglycemia due to relative insulin deficiency leading to lipolysis and production of serum ketones. Clinical circumstances can potentiate this process, such as acute infection or insulin discontinuation. Additionally, patients on SGLT2-inhibitors are at risk for euglycemic DKA. In people with type 2 diabetes, DKA is uncommon; however, a combination of precipitating factors in these patients can lead to a greater risk of DKA, particularly in the setting of SGLT2-inhibitor use.
Clinical Case
A 63 year old male with past medical history significant for uncontrolled type 2 diabetes (10 year duration, HgA1c=11.2%, on insulins detemir and aspart, metformin, and empagliflozin), coronary artery disease, and treatment refractory antibody-negative polymyositis (baseline CPK levels ~1000-2000, on a burst of prednisone for flare) presented with fever (101.2F), fatigue, myalgias, and nausea with poor oral intake and insulin cessation after recent IV zoledronic acid infusion for prevention of steroid-induced osteoporosis. He was found to be acidemic with bicarbonate=16, AG=18, Cr=1.6 (baseline 1.1), lactic acid=2.9, glucose=245, glucosuria/ketonuria, serum osmolality=295, and CPK=3613. No infectious etiology was found. Differential diagnosis of precipitating factors of DKA includes: steroid-induced hyperglycemia with lipolysis and insulin resistance; starvation ketosis from poor oral intake due to bisphosphonate-induced flu-like illness; metformin-associated lactic acidosis in setting of acute kidney injury; ketone production secondary to insulin cessation in setting of febrile illness; and SGLT2-inhibitor use with dehydration secondary to decompensated hyperglycemia. He was treated for DKA with insulin and volume resuscitation. He was discharged with discontinuation of empagliflozin.
Conclusion
In people with type 2 diabetes and multiple medical problems, a collusion of clinical factors leading to acidemia can occur simultaneously and lead to a drastically increased risk of DKA, especially in the setting of SGLT2-inhibitor use. Clinicians should have heightened awareness of minor predisposing factors that in combination can increase risk of DKA in a patient with type 2 diabetes.