bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-083 Childhood Diabetic Ketoacidosis (DKA) in New-Onset and Established Patients in Central Illinois: Contributing Factors and Risk Stratification
Authors: Szymczuk Vivian , Dunneback James , Wang Yanzhi , Benavides Valeria C 
Published: May 2020

Abstract
Introduction: DKA is the leading cause of hospitalizations in children with type 1 diabetes mellitus (T1DM). Although most cases are preventable, DKA continues to occur in established patients.
Aim: To identify contributing factors and outcomes of DKA pediatric admissions in a tertiary referral center with a large rural catchment area to assess for actionable items to prevent DKA.
Methods: A retrospective, single-center chart review assessing children ˂19 years old admitted in DKA from October 2014 to May 2018. DKA was defined as a pH of ≤7.3 or bicarbonate of ≤15. Demographic data included gender, age, zip code, insurance type and ethnicity. Admission measures included HbA1c, DKA group (new-onset “NT1” or “ET1” established T1DM diagnosis), DKA severity (severe pH &lt;7.1, CO2 &lt;5mEq/L), contact with clinic, home insulin delivery. Outcomes included length of stay (LOS), total admission costs (TAC) and reimbursements amounts (RA).
Results: 272 patients were included (mean age 11.7 y, range 4.4-16; 60% female, 83% Caucasian, 14% African American). Of these, 33% were NT1 DKA. Compared to NT1 DKA, ET1 DKA patients were older (8.7 vs. 13.1 years, p &lt; 0.001), more likely female (49% vs. 65%, p 0.034) with public insurance (55% vs 63%, p 0.028); 73% didn’t contact the diabetes team prior to admission and 52% used an insulin pump. There were no significant differences in HbA1c or DKA severity.
LOS was similar between NT1 and ET1 DKA (p 0.051). Severe DKA was associated with longer LOS (RR 1.47, p &lt; 0.0001). Public vs. private insurance was associated with 1.28 times longer LOS (p &lt; 0.0001).
While there was no difference in TAC between NT1 and ET1 DKA groups (p 0.877), costs were higher with public vs. private insurance (&gt;$900, p 0.050) and severe DKA (RR 1.92; 95% CI 1.62-2.27; p &lt;0.0001). TAC were different between regions within central Illinois (RR 1.39; 95% CI 1.08-1.80; p 0.002).
Hospital RA was higher for NT1 vs. ET1 group (RR 1.26; 95%CI 1.03-1.54; p 0.0237) and higher DKA severity (RR 1.57; 95% CI 1.26-1.95; p &lt;0.0001); but lower for public vs. private insurance (RR 0.43; 95% CI 0.35-0.52; p &lt;0.0001).
Discussion: Established DKA patients tended to be rural teenage females, poorly controlled and public health insured. Severity of DKA and LOS did not differ between the groups. While TAC were similar among the groups, TAC were higher with public insurance and severe DKA. Lower hospital RA were seen for recurrent cases and public insurance. This study provides valuable information about non-metropolitan at-risk population characteristics to inform targeted preventive interventions. These findings suggest a significant difference in hospitalization RA, providing incentive for health care facilities / providers to invest in early outpatient interventions and QI initiatives.
SUN-371 Hyponatremia Correction Normalizes Bone Mineral Density and Bone Fragility in Rats
Authors: Xu Qin , Pillai Sambhu M , Barsony Julia , Herfat Safa , Verbalis Joseph G 
Published: May 2020

Abstract
Multiple epidemiologic studies have associated chronic hyponatremia with both osteoporosis and bone fractures. Studies in experimental animals and cultured cells have demonstrated that reducing the extracellular sodium concentration ([Na+]) causes bone loss primarily by increasing osteoclast formation and bone resorbing activity. In osteoclastic cell cultures, reducing [Na+] activated biochemical and functional changes in osteoclast activity, which appear to occur by direct sodium-sensing mechanisms on osteoclasts that are independent from changes in osmolality. Whether the pathological changes in bones induced by hyponatremia can be reversed by correction of hyponatremia has not been studied. The present studies were initiated to address this question. 22-month-old F344BN F1-hybrid rats were made hyponatremic using a desmopressin continuous infusion while fed a liquid diet. After 3 months of chronic sustained hyponatremia, a cohort of the hyponatremic rats were corrected to a normal [Na+] by removal of the desmopressin minipumps and allowed to recover for 2 months. Both bone density measurements by DXA and biomechanical testing were performed on excised bones from normonatremic control rats (NN, [Na+]=145±5.6 mmol/L, n=9), chronically hyponatremic rats (HN, [Na+]=114±4.7 mmol/L, n =9) and hyponatremic corrected rats (HC, [Na+]=139±1.4 mmol/L, n =9). The results confirm that chronic hyponatremia caused significant decreases in bone mineral density (BMD, g/cm2) in the L4 vertebra (NN=0.166±0.003, HN=0.151±0.002, P=0.002) and femur (NN=0.229±0.004, HN=0.213±0.005, P=0.024). Bone fragility as measured by ultimate load to fracture (UL, Newtons) was also increased in the L5 vertebra (NN=369.8±51.1, HN=262.9±29.4, P=0.0001), but only slightly in the femur (NN=295.4±57.5, HN=286.0±35.4, P=0.682). Following correction of hyponatremia, both BMD and UL recovered after 2 months to levels not significantly different than the normonatremic controls: L4 BMD (NN=0.166±0.003, HC=0.167±0.002, NS); femur bone density (NN=0.229±0.004, HC=0.226±0.003, NS); UL in the L5 vertebra (NN=369.8±51.1, HC=384.1±63.5, NS). These results show that bone fragility parameters are adversely affected by chronic hyponatremia in addition to the previously reported decreases in BMD in rats. Consistent with the BMD results, the trabecular bone in the spine was more severely affected than the cortical bone in the femur. Our results show that much of the bone pathology of hyponatremia-induced osteoporosis can be reversed following correction of the hyponatremia without using specific antiresorptive therapy. Our findings therefore raise the possibility that correction of hyponatremia may be effective as a therapy for treatment of hyponatremia-induced osteoporosis in selected patients.
SUN-509 Plasmapheresis Treatment of Thyrotoxicosis in Pregnancy for Preparation of Thyroidectomy
Authors: Horani Mohamad Hosam , Brooks Ryan M , Vazques Bianca , Arashahi Robert , Khan Mustapha 
Published: May 2020

Abstract
Introduction: Thyrotoxicosis in pregnancy presents the challenge of maintaining a normal level of maternal free thyroid hormone, while minimizing adverse drug effects, obstetric complications, and the risk fetal hypothyroidism.
Propylthiouracil is used for treatment in the first trimester with thyroidectomy typically performed in the second trimester if PTU/ MTZ are intolerable or if thyrotoxicosis persists. When thyroidectomy is indicated, thyroid hormone levels must be normalized prior to the operation, as there is risk of thyroid storm that can occur during and up to several hours postoperatively. In such cases, preoperative plasmapheresis may be considered.
Case Presentation: We present a 24 year old G2P0101 Hispanic female who reported to the ED with throat pain, chills, tachycardia, and shortness of breath who was found to have a TSH less than 0.005, free T4 3.15, elevated alkaline phosphatase, and an incidentally discovered early pregnancy approximately 4 - 6 weeks gestation. Medical history includes hyperthyroidism with over ten hospitalizations for thyrotoxicosis within the last three years and preterm delivery during her first pregnancy. A recent thyroid biopsy in 2017 showed a benign multinodular goiter. She had been taking methimazole and current CT of the neck demonstrated marked thyroid goiter with mild tracheal narrowing and mild tonsillitis. She was discharged on propylthiouracil 100 mg TID, metoprolol 25 mg TID, and augmentin 875 mg BID with the goal of decreasing her free T4 and T3 in preparation for thyroidectomy. Four days later, the patient returned to the ED with similar symptoms. Labs revealed TSH 0.001, free T4 3.70, FreeT3 15.1 WBC 3.1, platelets 103, and elevated total bilirubin, transaminases, and alkaline phosphatase. EKG demonstrated sinus tachycardia with minimal diffuse ST depression. Ultrasound showed a 0.34 cm round hypoechoic focus in the endometrial cavity without a fetal pole or cardiac activity. Chest X-ray demonstrated minor bibasilar atelectasis. The patient was admitted and PTU was discontinued due to leukopenia and elevated transaminases. Dexamethasone was started and metoprolol was continued.
Total thyroidectomy was planned for when free T4 less 2.0 The patient received two treatments of plasmapheresis, which decreased free T4 to 2.11 and then to 1.40. The thrombocytopenia and transaminitis resolved
A total thyroidectomy was performed and well tolerated. patient had full term pregnancy, uneventful delivery while on thyroid hormone replacement.
Conclusion : Preoperative plasmapheresis can be considered for the normalization of free T4 if thionamides fail or cannot be tolerated. This case demonstrates the successful management of thyrotoxicosis with plasmapheresis in the first trimester of pregnancy.to Our knowledge Plasmapheresis was not used before in Pregnancy in preparation for thyroidectomy.
OR30-03 Racial Differences in Technology Use Among Type 1 Diabetes in a Safety-Net Hospital
Authors: Wirunsawanya Kamonkiat , Rizo Ivania , Fantasia Kathryn 
Published: May 2020

Abstract
Objective: There is limited data regarding the use of diabetes technology such as continuous glucose monitor (CGM) and continuous subcutaneous insulin infusion (CSII) among patients with type 1 diabetes (T1D) in a minority serving and safety-net hospital. We examined racial differences in the use of CGM and CSII in this setting.
Methods: A retrospective review of 227 patients ≥ 18 years of age with T1D seen in the Endocrinology clinic at a safety-net hospital from October 2016 and September 2017 was completed. Statistical analysis assessed the likelihood of diabetes technology use among different races.
Results: The mean age was 39, 59% male, mean duration of diabetes was 21 years, 30% overweight, 22% obesity, 80% English speaking, and 50% had government insurance. In terms of the distribution of race/ethnicity, 43% were Caucasian, 25% African American (AA), 15% Hispanic, 15% defined as other, and 2% Asian. Mean HbA1c ± standard deviation (SD) of any technology (either CGM or CSII or both) and non-technology users were 8.27 ± 1.58 and 9.49 ± 2.04, respectively. Patients who had government health insurance were found to have lower odds of using technology (odds ratio [OR], 0.43; 95% confidential interval [CI], 0.25 - 0.74) compared to patients who had private health insurance. Overall, 26% of the patients used CSII with 43% of this population Caucasian, 10.5% AA and 14.2% Hispanic. The overall CGM use was 30% with 47% of users Caucasian, 14% AA and 22% Hispanic. In a multivariable logistic regression model that adjusted for insurance and language, AA or other were found to have statistically significant lower odds of using technology (AA OR 0.25 [95% CI 0.11 - 0.53] and other OR 0.33 [95% CI 0.12 - 0.89]) compared to the Caucasian group.
Conclusion: Our study showed that the use of technology in the Caucasian group was statistically significantly higher than in the non-Caucasian groups except for the Asian group. After adjusting for insurance and language, AA and other demonstrated statistically lower rates of technology use. Racial differences in diabetes technology use were observed in our study as well as the association between technology use and lowered HbA1c. Given diabetes technology is a useful tool in reducing HbA1c and hypoglycemia, the barriers to accessing diabetes technology in non-Caucasian individuals should be addressed to decrease health disparities.
SUN-019 Androgens Modulate Lipid Metabolism and Absorption in Control and Polycystic Ovary-Metabolic Syndrome Conditions
Authors: Vine Donna Faye , Lehner Richard , Watts Russell , Horkey Melanie , Ghosh Mahua , Proctor Spencer 
Published: May 2020

Abstract
Introduction: In polycystic ovary syndrome (PCOS) a high plasma level of androgens has been correlated with an adverse plasma lipid profile. At present we do not know the physiological or mechanistic pathways of how androgens regulate lipid metabolism under control or PCOS conditions. We have shown flutamide, an androgen receptor (AR) inhibitor, reduces the plasma concentration of triglycerides (TG) and apoB-lipoproteins, and intestinal secretion of TG. Aim: The aim of this study was to determine the direct physiological and mechanistic effects of androgens, Testosterone (T) and dihydrotestosterone (DHT), on lipid metabolism using a PCOS-prone rodent model. Methods: Control and PCOS-prone animals were administered vehicle, T or DHT for 7 days. PCOS-prone animals also present with the Metabolic Syndrome (MetS). Following treatment animals underwent a mesenteric lymphatic cannulation procedure to determine effects on intestinal chylomicron (CM-apoB48) and lipid secretion, and absorption using radiolabelled [³H]-cholesterol and [14C]-palmitic acid.
Results: Plasma LDL-C was increased with DHT treatment in control animals, and with both T & DHT treatment in PCOS. Intestinal absorption of TG and cholesterol were increased in T and DHT treated PCOS animals but not control animals. Whereas DHT reduced intestinal CM-apoB48 secretion in both control and PCOS groups. These effects were associated with changes in genes and protein expression in lipogenic (SREBP1a/c&2, SREBP1c, SREBP-2, ACC) and steroidogenic pathways (AR, ER and SRDA51) in the liver and intestine.
Conclusion: These results demonstrate androgens modulate lipid metabolism and absorption. T and DHT differentially affect intestinal chylomicron secretion and lipid absorption in PCOS-MetS and control conditions. In conclusion, these results suggest that androgens may directly cause or exacerbate lipid and lipoprotein metabolism in conditions of hyperandrogenemia and the MetS.
OR18-03 Functional TSH Receptor Antibodies Are a Biomarker for Graves’ Disease - a Prospective Trial
Authors: Kahaly George Jean , Diana Tanja , Kanitz Michael , Olivo Paul D 
Published: May 2020

Abstract
Objective
We aimed to evaluate the clinical utility and predictive value of stimulatory (TSAb) and blocking (TBAb) TSH receptor antibodies in the management of Graves’ disease (GD).
Methods
Hundred well-defined, consecutive, unselected, untreated hyperthyroid patients with GD were enrolled in a prospective two-year trial. Methimazole (MMI) was administered for 24 weeks according to baseline serum concentrations of free T3/free T4. Starting dose was 5–30 mg/day. Through a titration regimen, this dose was respectively tapered or increased at each subsequent study visit as the patient became euthyroid or remained hyperthyroid. Goals of therapy were to maintain normal fT4 and TSH levels. MMI therapy was stopped at week 24. The main outcome measure was clinical response versus non-response to a 24-week MMI treatment defined as biochemical euthyroidism versus persistent hyperthyroidism at week 24 and/or relapse at weeks 36, 48, and 96. TSAb was reported as percentage of specimen-to-reference ratio (cut-off SRR% &lt;140). Blocking activity was defined as percent inhibition of luciferase expression relative to induction with bovine TSH alone (cut-off &gt;40% inhibition).
Results
Forty-four patients responded to MMI of whom 43% had Graves’ orbitopathy (GO) while 56 were non-responders (66% with GO, p&lt;0.01). At baseline, undiluted serum TSAb but not thyroid binding inhibiting immunoglobulins (TBII) differentiated between thyroidal GD only versus GD+GO (p&lt;0.001). Further, at baseline responders demonstrated marked differences in diluted TSAb titers compared with non-responders (p&lt;0.001). All patients with a TSAb dilution titer above three did not respond to MMI treatment. In contrast, TBII dilution titers did not differentiate between responders and non-responders to MMI and serum samples became TBII negative already at low dilutions. During treatment, serum TSAb levels decreased markedly in responders (p&lt;0.001) but increased in non-responders (p&lt;0.01). In contrast, TBII strongly decreased in non-responders (p=0.002). All non-responders at week 24 and/or those who relapsed during the 72-week follow-up were TSAb positive at week 24. A shift from TSAb to TBAb was noted in eight patients during treatment and/or follow-up and led to remission.
Conclusions
Serum TSAb levels are a biomarker for and mirror severity of GD. Their increase during MMI treatment is a marker for on-going disease activity. TSAb dilution analysis had additional predictive value.
MON-524 Prospective Evaluation of Patients with Encapsulated Classical Variant of Papillary Thyroid Cancer and Noninvasive Follicular Thyroid Neoplasm with Papillary-Like Nuclear Features (NIFTP): Have They A Similar Prognosis?
Authors: Giani Carlotta , Torregrossa Liborio , Ugolini Clara , Ramone Teresa , Romei Cristina , Matrone Antonio , Viola David , Molinaro Eleonora , Materazzi Gabriele , Basolo Fulvio , Elisei Rossella 
Published: May 2020

Abstract
Background: Our previous retrospective study demonstrated that the absence of tumor capsule or, if present, its invasion were independent risk factors for the persistence of the disease (OR 6.75, CI 1.97-23.08 and OR 7.89, CI 1.78-34.94, respectively) in papillary thyroid cancer (PTC). This data was confirmed also analyzing separately the most frequent PTC variants [follicular variant (FVPTC) and classical variant (CVPTC)]. Moreover, we demonstrated that the absence of tumor capsule was significantly more frequent in FVPTC BRAF V600E mutated than FVPTC wild-type for BRAF gene or with rare-BRAF mutations (e.g., BRAF K601E, BRAF V600_K601delinsE). These data confirmed the importance of the integrity of the tumor capsule in FVPTC which led in 2016 to the definition of a new thyroid neoplasm entity named NIFTP. According to these retrospective data, we have assumed that the integrity of the tumor capsule in CVPTC could have a prognostic role similar to that confirmed in the NIFTP group.
Methods: we have prospectively collected data of patients (pts) underwent total thyroidectomy or lobectomy for encapsulated-CVPTC (E-CVPTC) or NIFTP. In both cases the tumor was accurately analyzed by the pathologists according to the criteria used for the NIFTP (in particular with one capsule sample every 1 mm). All pts performed at least one clinical control and neck US within 6 months from surgery.
Results: From January 2018 to June 2019, 144 E-CVPTC and 177 NIFTP were prospectively collected. 83/144 (57.6%) E-CVPTC and 106/177 (59.8%) NIFTP cases were included. The others were excluded due to the presence of other thyroid tumors associated in the same gland. No differences in epidemiological and pathological features were found between E-CVPTC and NIFTP except for the tumor size, significantly bigger in NIFTP than E-CVPTC [22±16mm (2-68) vs 8±11mm (1-80), p&lt;0.00]. A significantly higher rate of NIFTP’ pts underwent lobectomy respect to E-CVPTC pts (34%vs14.5%, p=0.02). After a mean of 9 months of follow-up all pts had an excellent response according to ATA guidelines.
Conclusions: These prospective data demonstrated that NIFTP and E-CVPTC have a similar clinical behavior in a short-term follow-up, thus suggesting that the presence of an intact tumor capsule is predictive of a good outcome. A longer follow up is needed to confirm these initial interesting findings.
SAT-137 The Effect of Hypertriglyceridemia on Triple Negative Breast Cancer Progression
Authors: Scully Tiffany , James Annie , Kang Chifei , Antoniou Irini M , Ettela Abora , Wong Nicholas J , Azeloglu Evren U , Kase Nathan G , Qiu Yunping , Kurland Irwin J , Gallagher Emily Jane 
Published: May 2020

Abstract
Obesity is associated with increased cancer risk and cancer-associated mortality1,2. Hypertriglyceridemia (HTG), a component of the metabolic syndrome which frequently co-exists with obesity, has been associated with increased breast cancer risk and mortality in triple negative breast cancer (TNBC)3,4. To determine if HTG is causally related to enhanced TNBC progression in the absence of other obesity-associated characteristics, TNBC growth and metastasis in a mouse model of HTG was examined. Mice overexpressing human apolipoprotein C3 (AC3) were backcrossed onto FVB/N background and crossed with recombination-activating gene 1 (Rag1) knockout mice to generate immunodeficient HTG mice. AC3 mice relative to wild-type (WT) littermates showed a 20-fold higher circulating triglycerides (p &lt; 0.0001) and elevated very low density lipoprotein (VLDL) cholesterol (p = 0.001). No differences in body weight, body composition, blood glucose or plasma insulin levels were observed between the two groups, allowing for investigation on the influence of HTG on TNBC without confounders such as hyperinsulinemia or hyperglycemia. AC3 mice orthotopically implanted with the mouse mammary tumor cell line, Mvt1, showed both increased tumor growth (AC3 vs WT: 1157.0 ± 84.2 vs 707.2 ± 58.6 mm3, p = 0.0009) and lung metastasis (AC3 vs WT: 57.3 ± 3.0 vs 32.9 ± 5.3 mm3, p = 0.001) relative to WT mice. Immunodeficient Rag1/AC3 mice likewise, showed increased tumor growth compared to WT controls when implanted with human TNBC MDA-MB-231 cells (AC3 vs WT: 363.2 ± 113.9 vs 92.95 ± 16.2 mm3, p = 0.038). To investigate how HTG affects tumor lipid metabolism, serum and tumors from both groups were analyzed by liquid chromatography/mass spectrometry. Total alkyl-acyl, di-acyl-phosphatidylcholines and sphingomyelin concentrations were higher in the serum of AC3 mice relative to WT. In contrast, no overall difference in tumor phospholipid or acylcarnitine content was noted between AC3 and WT mice, suggesting no difference in fatty acid oxidation in the setting of HTG. Mvt1 tumors from AC3 and WT mice were analyzed by RNA sequencing. Decreased expression of genes associated with cholesterol synthesis (Fdft1, Pvmk, Acss2) were found in tumors from AC3 mice. Tumors from AC3 mice also showed decreased protein expression of LDLR, which is associated with LDL cholesterol uptake. Overall, these findings suggest that HTG, independently of other obesity-associated characteristics such as hyperinsulinemia and hyperglycemia, leads to changes in intracellular lipid metabolism and promotes TNBC progression.
References: 1Chan, D. S. M. et al. Ann. Oncol. Off. J. Eur. Soc. Med. Oncol.25, 1901-1914 (2014). 2Pierobon, M. & Frankenfeld, C. L. Breast Cancer Res. Treat.137, 307-314 (2013). 3Lofterød, T. et al. BMC Cancer18, 654 (2018).4Goodwin, P. J. et al. Nutr. Cancer27, 284-292 (1997).