bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-364 Severe Postoperative Encephalopathy in a Patient with Oncogenic Osteomalacia and Neurofibromatosis Type 1
Authors: Sarkar Sauradeep , Singh Amteshwar , Krug Esther Irina 
Published: May 2020

Abstract
Background: Acute hypophosphatemia superimposed on chronic phosphate depletion results in decline in intracellular ATP and 2,3-diphosphoglycerate levels, affecting virtually all organ systems. It can lead to metabolic encephalopathy, impaired myocardial and diaphragmatic contractility, skeletal and smooth muscle dysfunction, increase in erythrocyte rigidity leading to hemolysis, and increased risk for postoperative morbidity and mortality. Risk of symptomatic hypophosphatemia may be greater in patients with urinary phosphate wasting syndromes hospitalized for intercurrent illness. Tumor-induced (oncogenic) osteomalacia (TIO) is a rare paraneoplastic disorder associated with mesenchymal tumors caused by tumor production of fibroblast-derived growth factor-23 (FGF-23). FGF-23 impairs transport of phosphorus in renal tubules, inhibits renal 25(OH)-1-α-hydroxylase activity, causing decreased levels of calcitriol, leading to hyperphosphaturia, hypophosphatemia and osteomalacia. We present a case of a patient with underlying TIO who presented with acute hypophosphatemia following hip surgery.
Case: 50-year-old woman with Neurofibromatosis type-1(NF-1) complicated by TIO, presented after a fall resulting in left femur fracture requiring surgery. During her initial management in an outside hospital for 4 days and following transfer her home calcitriol and phosphorus replacement regimen was not administered leading to treatment interruption of 7 days. On postoperative day 1 she became hypotensive, tachycardic with non-specific ST-T changes and encephalopathic requiring ICU care. At the time of endocrinology consultation, she was non-verbal, not following simple commands, had severe hypophosphatemia, transaminitis, hyperbilirubinemia, elevated LDH, anemia and elevated troponin. She required aggressive phosphate and calcitriol replacement reaching 4 doses of 20mEq IV Na- Phos daily, Na-KPhos Q6H and Calcitriol IV 0.5mcg Q8H over the course of 72 hours. After 4 days in the ICU, once phosphorous levels normalized, she had dramatic improvement in mental status and gradual resolution of laboratory abnormalities.
Discussion: To our knowledge, this is the first report of a patient with TIO associated with NF-1 presenting with severe symptomatic hypophosphatemia causing metabolic encephalopathy and multiple organ dysfunction following surgery. It underscores the fact that abrupt interruption of calcitriol and phosphorus supplementation in such cases can cause acute hypophosphatemia carrying high morbidity. High phosphate replacement requirements are indicative of severity of phosphate depletion. This case illustrates importance of recognition of presence of urinary phosphate wasting syndrome in hospitalized patients in order to minimize risk of preventable complications and morbidity.
SAT-640 Glycemic Profile of Intravenous Glucocorticoid Induced Hyperglycemia Using Continuous Glucose Monitoring
Authors: Zhang Fan , Goldberg Zoe , Karam Jocelyne Georges 
Published: May 2020

Abstract
Background: Intravenous (IV) steroids are widely used in critically ill patients and with chemotherapy. It is well known that glucocorticoid-induced hyperglycemia (GCIH) occurs within 3 hours following oral administration of steroids with typical postprandial glycemic excursions lasting 24-36 hours. The recent increased availability of Continuous Glucose Monitoring (CGM) has allowed a detailed description of glycemic fluctuations in patients receiving steroids in different settings, however there is no reported observation of CGM findings following a single dose of IV Dexamethasone in a patient with diabetes. We present a case of glycemic pattern documented on CGM of a patient with type 2 diabetes, who had received 11 cycles of a single dose Dexamethasone-containing chemotherapy. Clinical Case: The patent is 70 years old female with history of type 2 DM of 19 years duration and metastatic pancreatic adenocarcinoma, diagnosed in November 2018, and treated with Fluorouracil and Dexamethasone 6mg IV on every other Wednesday since December 2018. Her diabetes was fairly controlled on Metformin, Repaglinide, Pioglitazone and Detemir insulin. Premeal Lispro was added while Metformin and Repaglinide were discontinued with the beginning of chemotherapy. She started using Freestyle Libre CGM in January 2019. During her visit in March 2019, the patient was taking Detemir Insulin 50 units in AM and 30 units at night, and Lispro 15 units before meals, in addition to correction insulin based on an Insulin Sensitivity Factor (ISF) of 1:25 for Blood Glucose (BG) above 200mg/dl. Unlike the reported postprandial hyperglycemic excursions associated with oral steroids, the patient’s CGM data showed a reproducible triphasic glycemic pattern following IV Dexamethasone, consisting of a steady state of hyperglycemia reached within 3 hours and lasting around 18-30 hours, followed by a transient BG improvement for 18-20 hours, and ending with another hyperglycemic plateau of 10-16 hours on day 3 post chemotherapy, with no association to meal intake. Given this recurrent pattern, the patient was advised to increase her bedtime Detemir insulin from 30 to 45 units and her correction ISF from 1:25 to 1:18 on days 1 and 2 after chemotherapy, with subsequent attenuation and shortening of GCIH. Conclusion: Our case report is the first one to describe CGM documented glycemic profile following a single dose of IV Dexamethasone in a patient with type 2 diabetes treated with insulin. The CGM data reveals a consistent steady GCIH, lasting around 48 hours, and reflecting the prolonged action of Dexamethasone. The transient BG improvement seen on day 2 is likely due to the Detemir dose self-increase and the carbohydrates intake decrease in response to day 1 hyperglycemia. A 48 hours modified insulin regimen based on higher dose of long acting and correction insulin improved Dexamethasone induced hyperglycemia.
SAT-453 Delayed TSH Elevation in Small for Gestational Age Infants: A Need for Second Screening?
Authors: Kang Seok-Jin , Lee Ga-Hyun 
Published: May 2020

Abstract
The incidence of CH with a delayed TSH elevation was higher in ELBW and VLBW infants compared with infants weighing ≥1500 grams. Second screening should be considered in preterm neonates, low birth weight (LBW) and very low-birth weight (VLBW) neonates, ill and preterm newborns admitted to NICU, specimen collection within the first 24 hours of life, and multiple births (particularly same-sex twins). Purpose of this study was to determine incidence of delayed TSH elevation with or without congenital hypothyroidism in SGA infants and to Investigate necessity for second screening. Retrospective analysis was performed. 66 SGA newborns with 34-40 weeks’ gestation born at Keimyung University Dongsan Medical Center from 2015 to 2018 were enrolled. Primary screening was performed 48 hours - 7 days after birth. Second screening including venous TSH and venous free T4 at postnatal 8-40 days. Exclusion criteria were infants with congenital hypothyroidism at primary screening (NBS), descendants of mothers with immune thyroid disease, congenital malformations, renal, hepatic, and metabolic diseases, history of steroid or dopamine usage. Initial NBS were collected onto pre-printed filter at the age of 2-7 days by heel prick. (normal TSH &lt; 10 mIU/L). Second sample was obtained at the age of 8-49 days by venous sampling (normal TSH &lt; 5 mIU/L). TSH and free T4 were measured on venous samples with Cobas 8000 e801 (electrochemiluminescence, Roche, Diagnostics, Basel, Switzerland) using standard methods.
Incidence of delayed TSH elevation was 27% (18/66). Of them number of transient hyperthyrotropinemia was 13. Mean TSH at initial elevation was 7.56 mIU/L and median age at initial TSH elevation was 18.6 days. Median age at resolution of TSH elevation was 41.5 days. Number of hypothyroidism undergoing l-thyroxine medication was 5. Mean TSH at initial elevation was 22.1 mIU/L. Median age at initial TSH elevation was 14 days. Mean peak TSH was 23.4 mIU/L.
The presence of delayed TSH elevation was not related to very low birth weight. SGA infants might be at a risk of delayed TSH elevation. Considering 2nd screening test within 1 month. Further study with more SGA infants are needed. Limitation of this study was relative small number of patients and iodine status was not considered
MON-377 Fracture Site in High-Energy Trauma Is Associated with Osteoporosis Risk
Authors: Chourpiliadis Charilaos Paulos , Bantouna Dimitra , Hourpiliadi Hara , Karvounis Evangelos , Jaume Juan Carlos , Paparodis Rodis 
Published: May 2020

Abstract
Background: In our recent studies, we noted that patients with history of high energy fractures commonly have underlying endocrine abnormalities and low bone mineral density (BMD). In this expanded patient population, we aimed to investigate whether the fracture site can better predict the risk of abnormal BMD.
Methods:We prospectively enrolled adult patients of both genders, with any history of high energy fracture. We measured serum PTH, vitamin-D and calcium and we performed BMD measurements with a DEXA scan. We split our subjects’ BMD, based on the lowest T- or Z-score in “Normal” (≥-0.9), “low bone mass” (LBM) (-1.0 to -2.4) and “Osteoporosis” (OST) (≤-2.5). We classified our patients according to fracture site, in vertebral, humeral, hip, tibial, malleolar-carpal, radial-ulnar and others, including rib fractures. Ratios were compared with χ 2 test, and continuous variables with one-way ANOVA.
Results: We enrolled 444 consecutive subjects with 543 fractures. n=315 (71.0%) subjects had low BMD: OST 25.9% and LBM 45.1%. Among subjects &lt;50 years of age, 43.1% had LBM and 9.2% OST, while in those &gt;50, 46.3% had LBM and 36.6% OST (p&lt;0.0001). The cohort’s mean lowest T/Z score was -1.6±1.2. Subjects with &gt;1 fracture had more frequently low T/Z score (p=0.015). History of vertebral fractures provided the lowest mean T/Z score overall (-2.4±1.1), in females (-2.5±0.9) and subjects &gt;50 (-2.5±1.1). The same holds true for hip fractures in males (-1.9±1.2) and subjects &lt;50 (-2.1±1.4). Subjects with vertebral fractures had the lowest Hip (-1.7±1.2) and Spine (-2.3±1.2) T/Z scores, while those with tibial fractures had the lowest Radius T/Z score (-1.8±1.3). History of vertebral fractures was associated with the highest rate of OST (65.9%) in our overall population, males (50%), females (67.5%), subjects &gt;50 (70.0%), while subjects with history of tibial fractures had the highest rate of normal BMD (46.2%), in males (80%) and females (50.4%), and those &lt;50 (75.0%). Vitamin-D deficiency was present in 81.4% of all subjects. PTH was significantly higher in patients with OST compared to LBM or normal BMD (p=0.0006).
Discussion: Patients with history of high energy fractures need to be screened with DEXA scan early, as they have high likelihood to suffer from osteoporosis.
MON-113 The Effect of Body Mass Index on the Peak Growth Hormone Level After Growth Hormone Stimulation Test in Children with Short Stature
Authors: Lee Nayeong , Cho Wonkyoung , Lee Yoonji , Kim Seulki , Lee Seonhwa , Choi Yujung , Ahn Moon Bae , Kim Shinhee , Cho Kyoungsoon , Jung Min-Ho , Suh Byung-kyu 
Published: May 2020

Abstract
Objective: The aim of this study is to evaluate the effect of body mass index (BMI) on peak growth hormone (GH) response after GH stimulation test in children with short stature.
Methods: Data was obtained from retrospective review of medical records who visited the pediatric endocrinology at St. Vincent hospital of catholic university for short stature from January 2010 to June 2019. We studied 115 children (aged 3-17 years old) whose height was less than 3percentile for one’s age and sex and who underwent GH stimulation test {GH deficiency (GHD) = 47, Idiopathic short stature (ISS) = 68)}. Peak GH response was stimulated by dopamine (n=111), clonidine (n=7), glucagon (n=19), insulin (n=56) and arginine (n=32). Birth weight, parental height, chronologic age, bone age, height SDS (standard deviation score), weight SDS, BMI SDS hemoglobin, fT4, T3 TSH, cortisol, ACTH, GH, IGF-1 SDS, IGF-BP3 SDS and peak stimulated GH were analyzed.
Results: In the characteristics of subject, weight SDS and BMI SDS in GHD group were increased than ISS group (p&lt;0.000, p=0.000). Free T4 was decreased in GHD group than ISS group (p=0.012). In total group, BMI SDS was associated negatively with peak GH level stimulated by dopamine (r=-0.419, p&lt;0.000), insulin (r=-0.271, p=0.044) and arginine (r=-0.368, p=0.038), but did not showed correlation with peak GH level stimulated by glucagon. In GHD group, BMI SDS showed negative correlation with peak GH level using dopamine (r=-0.356, p=0.015) and arginine (r=-0.509, p=0.022). In ISS group, BMI SDS was correlated negatively with peak GH using dopamine (r=-0.330, p=0.007). In multivariate regression analysis of GHD group, weight SDS and BMI SDS were the only two significant predictors of peak GH response in stimulation test stimulated by dopamine (ß=-0.576, p=0.015) and arginine (ß=-0.097, p=0.022). In ISS group, only mother’s height (ß=0.474, p=0.000) and TSH (ß=-2.251, p&lt;0.000) were demonstrated statistically significant predictors of peak GH stimulated by dopamine in multivariate regression analysis. In case of using insulin as a stimulant in ISS group, there is nothing which has statistical significance as a predictor of peak GH response in multivariate regression analysis.
Conclusion: BMI was associated negatively with peak GH response after GH stimulation test in children with short stature, especially in GHD group.
MON-366 X Linked Hypophosphatemic Rachitism: Case Report in Adult Patient
Authors: Medina Adriana , Vargas Juan José , Romero Andres Florez , Coy Andres 
Published: May 2020

Abstract
BACKGROUND: X linked hypophosphatemia (XLH) is a rare genetic disorder, with an estimated prevalence of 1: 20,000 live births resulting from a mutation in the PHEX gene (phosphate regulatory endopeptidase), which causes increased levels of circulating fibroblast growth factor 23 (FGF23), reducing both renal reabsorption of phosphate and serum levels of 1,25-dihydroxyvitamin D3, causing chronic hypophosphatemia, rickets and osteomalacy. CLINICAL CASE: a 34 year old female with a height of 1.34 meters whose past medical history began at the age of three years old with a diagnosis of short stature, associated with genu varum and low serum phosphate levels. She received treatment with phosphate salts and calcitriol until eleven years old. During childhood, she underwent several surgical procedures to correct the genu varum. After stopping the treatment, she has presented four fractures in the lower extremities: bilateral femur, tibia and fibula that have required six surgical interventions (osteotomy, osteosynthesis and external fixation); the last surgery was performed in June of 2019; in addition, she has had multiple dental abscesses that required several oral surgeries. Current laboratory tests report: calcium 8.89 mg/dL (8.6-10), 24-hour urine calcium 72.17 mg (100-300) with urinary volume 1470 ml/24 h, serum creatinine 0.44 mg/dL (0.51-0.95), urine creatinine 43.72 mg/dL (29-226), serum phosphate 1.78 mg/dL (2.5-4.5), urine phosphate 17.75 mg/dL (40-136) PTH 86 pg/mL (15-65), alkaline phosphatase 134 ug/ dL (35-104), 25OH vitamin D 23 ng/mL (30-40). Tubular resorption of phosphate corrected for glomerular filtration rate (TmP/GFR:) 1.6 mg/dL (&lt;2.8), Tubular Reabsorption of Phosphate (TRP) 89.96% (&gt;80). Densitometry revealed a normal bone mineral density (BMD) in lumbar spine and hip. Radiographs of the lower limbs showed a difference of 19 mm of the right lower limb in anatomical length and 13 mm in functional length. A HLX genetic panel was performed, with a result of a definitely pathogenic Gene PHEX linked to chromosome X, with a pathological mutation 22 151 705 G&gt; A p Trp456. The patient started treatment with calcitriol and dibasic phosphorus one month ago because of bone and muscle pain, stiffness, functional limitation, periodontal disease, recent hip fracture and indication of left hip replacement. She is candidate for burosumab (Anti-FGF23 Monoclonal Antibody) treatment.CONCLUSIONS: We present the case of adult patient with X-linked hypophosphatemia. Early treatment with phosphate is essential to avoid bone deformities. In adult patients, identifying pain, fractures or requirement of bone surgery, are indications for continuing treatment to improve quality of life, either with phosphate and calcitriol or with the new option, burosumab for pain control, improving functionality and stiffness.
SAT-440 Phthalates Expose and Thyroid Parameters in Euthyroid Patient with Type 2 Diabetes: Sex Specific Associations
Authors: Chen Yi , Chen Chi , Chen Jingsi , Zhang Wen , Wang Yuying , Wan Heng , Wang Ningjian , Chen Bo , Lu Yingli 
Published: May 2020

Abstract
Phthalates are ubiquitous in different environmental exposure media around the world. Recent years, issues on the relationships of phthalates and endocrine disorders raise attention. Evidence of thyroid disruption as a result of phthalates expose among euthyroid participants with diabetes is very limited. We aimed to evaluate the association between phthalate and thyroid function, and to explore whether thyroid autoimmunity mediated this association. Concurrent urine and blood samples were collected from 538 participant in METAL study. We measured urinary concentrations of ten phthalate metabolites (urinary creatinine adjusted), along with serum levels of thyroid-stimulating hormone (TSH), free thyroxin (FT4), free triiodothyronine (FT3), thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb). Euthyroidism was defined as TSH within normal range. After adjusting for age, sex (only with the entire sample), BMI and smoking status, linear regression analyses showed exactly opposite directional results among men and women. TSH levels were negatively associated with mono-2-ethyl-5-carboxypentylphthalate (MECPP), mono-2-ethyl-5-hydroxyhexylphthalate (MEHHP), mono-2-ethyl-5-oxohexylphthalate (MEOHP), mono-2-carboxymethyl-hexyl phthalate (MCMHP) and sum of di (2-ethylhexyl) phthalate metabolites (ΣDEHPm) in men, but positively associated with monoisobutylphthalate (MiBP) and mono-n-butylphthalate (MnBP) in women. Meanwhile, FT4 was positively associated with mono-2-ethylhexylphthalate percentage (%MEHP) in men, but negatively associated with MnBP, MEOHP and MCMHP in women. Further, in women, TPOAb was increasing along with the increased level of MEHP and %MEHP. In the mediation analysis, TPOAb demonstrated a mediating effect whereby MEHP or %MEHP had a positive effect on TSH and a negative effect on FT4 only in women (all P&lt;0.05). We got a conclusion that among euthyroid participants with diabetes, urinary phthalate metabolites maybe associated with altered TSH, FT4 and TPOAb levels in different direction in men and women. Further, our present study maybe the first to suggest that TPOAb might be a potential mediator of the association between phthalate metabolites and thyroid function in women.
SUN-715 IIM May Influence Matured Oocytes’ DNA Methylation of PCOS Patients
Authors: Li Congru , Yu Yang 
Published: May 2020

Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of childbearing age and is the main cause of anovulatory infertility. To increase the number of oocytes obtained, controlled ovarian stimulation (COS) has become a routine choice for in vitro fertilization-embryo transfer (IVF-ET), which is one of the common assisted reproductive technologies for PCOS patients. However, for these patients, there is a high risk of ovarian hyperstimulation syndrome (OHSS). Obtaining in vitro maturation (IVM) of immature oocytes, and then in vitro fertilization and embryo transfer of mature oocytes provides a possible way for people to solve the above problems. Since the IVM technology will expose oocytes to in vitro conditions for a longer period of time, theoretically increasing the risk of the oocytes being affected by the culture environment, further research and explorations are needed for study in gene programming, epigenetics, etc. Therefore, to explore the impact of IVM operation on embryonic development is of great significance for further clarifying assisted reproductive safety and improving IVM operation conditions. Here we focused on DNA methylation reprogramming process which was essential for embryonic development. We tested the DNA methylation of sperm, IVM oocytes and IVM generated early stage embryos including pronucleus, 4cell, 8cell, morula, inner cell mass, trophoectoderm (TE) as well as six-week embryos by Nimble Gen Human DNA Methylation 3x729K CpG Island Plus RefSeq Promoter Array and compared the data with our published genome-wide DNA methylomes of human gametes and early embryos generated from in vivo maturation oocytes. We showed that IVM embryos show abnormal DNA methylation reprogramming pattern. By analyzing the abnormally reprogrammed promoters, we further found that IVM may affect the functions of demethylation related genes. Oocytes from IVM manipulation were tested with higher DNA methylation levels, and their abnormal methylated promoters mainly enriched in immune and metabolism pathways. Furthermore, we investigated the DNA methylation of TE, which was directly related with implantation process and revealed the abnormal methylated promoters were related with metabolism pathway too. Our data support that IVM may influence the DNA methylome of oocytes, which in turn affects the methylome of their embryos. However, due to the limited number of samples and the inability of the chip to cover all CpG sites, the results of this study require further research and validation.