bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT-628 Risk Factors Associated with 30-Day and 90-Day Readmission in Persons with Diabetic Foot Ulcers
Authors: Dawkins Makeda , Baskaran Inthuja , Izard Stephanie , Elzanaty Mohammed , Zhang Meng , Bissoonauth Aditya A , Oropallo Alisha , Kaplan Sally , Rao Amit , Myers Alyson K 
Published: May 2020

Abstract
Background Diabetic foot ulcers (DFU) are the leading cause of lower-extremity amputations among patients with diabetes (DM)1. 15% of patients with DM develop DFU, with the potential for progression to osteomyelitis or gangrene with suboptimal glycemic control. Repeated readmissions are not only a negative prognostic indicator for these patients, but also contributes to increasing healthcare costs.
Areas of Uncertainty Previous studies have examined associations among demographics, comorbidities and DFU, and the value of Hemoglobin A1c (HbA1c) and C-reactive protein (CRP) as a prognostic indicator and monitoring tool for progression and regression, respectively3,4. However, no studies to date have examined medical or pharmaceutical factors contributing to 30-day and 90-day readmission.
Methods A retrospective chart review was conducted examining 397 patients with type 2 diabetes readmitted for DFU between 2014 and 2019. Variables were summarized using descriptive statistics, t-tests, chi-square, and logistic regressions.
Results Majority of patients were white males with a BMI over 30 and HbA1c &gt;7%. Patients with 30-day readmission were more likely to be using anticoagulants (30.00% vs. 17.24%, p= 0.0493). Patients with 90-day readmission were more likely to be discharged home with healthcare services (55.67% vs. 39.85%, p=0.0341) or to a skilled nursing facility (7.22% vs. 6.02%, p=0.0341). Although not statistically significant, patients with both 30-day and 90-day readmissions were also more likely to have HbA1c &gt;7, while those with a 90-day readmission had higher CRP levels.
Conclusions DFU patients with suboptimal glycemic control were more likely to experience a 30-day and 90-day readmission. Predicators for readmission in this population include: anticoagulation use, discharge to a skilled nursing facility or discharge home with healthcare services. As a result, patients not on anticoagulation, as well as those discharged home without services or to rehabilitation facilities have a reduced risk of readmission.
1.
Lazzarini PA, Clark D, Derhy PH. What are the major causes of lower limb amputations in a major Australian teaching hospital? The Queensland Diabetic Foot Innovation Project, 2006 – 2007. 2011;4(1):O24. doi:10.1186/1757-1146-4-S1-O24
2.
Vella L, Gatt A, Formosa C. Does Baseline Hemoglobin A1c Level Predict Diabetic Foot Ulcer Outcome or Wound Healing Time? Journal of the American Podiatric Medical Association. https://www.ncbi.nlm.nih.gov/pubmed/28880596. Published July 2017. Accessed September 28, 2019.
3.
King DE, Mainous AG, Buchanan TA, Pearson WS. C-Reactive Protein and Glycemic Control in Adults With Diabetes. Diabetes Care. https://care.diabetesjournals.org/content/26/5/1535. Published May 1, 2003. Accessed September 28, 2019.
OR25-05 Increased Overall Mortality and Cardiovascular Morbidity in Patients with Adrenal Incidentalomas and Autonomous Cortisol Secretion: Results of the ENS@T NAPACA-Outcome Study
Authors: Deutschbein Timo , Reimondo Giuseppe , Dalmazi Guido Di , Bancos Irina , Falhammar Henrik , Tsagarakis Stylianos , Newell-Price John , Kastelan Darko , Stigliano Antonio , Scaroni Carla Maria , Letizia Claudio , Prete Alessandro , Morelli Valentina , Ivocic Miomira , Kaltsas Grigorios , Pazaitou-Panayiotou Kalliopi , Hanzu Felicia Alexandra , Loli Paola , Yener Abdullah Serkan , Shafigullina Zulfiya , Langton Katharina , Zacharieva Sabina , Kocjan Tomasz , Terzolo Massimo , Fassnacht Martin 
Published: May 2020

Abstract
Objective. Several smaller studies on adrenal incidentalomas (AI) suggested an association between autonomous cortisol secretion (ACS) and mortality (Di Dalmazi Lancet Diabetes Endocrinol 2014, Debono J Clin Endocrinol Metab 2014, Patrova Endocrine 2017). However, a recent meta-analysis (9 studies, 1356 patients) could not confirm these findings (Elhassan Ann Intern Med 2019). Aim. To investigate the effects of ACS on mortality, prevalence of cardiovascular (CV) risk factors, and (CV) morbidity, in a representative cohort of AI. Design. Retrospective observational study conducted at 27 ENS@T centers from 15 countries. Methods. Inclusion criteria: AI diagnosed 1996-2015, 1 mg dexamethasone suppression test, follow-up (FU) of ≥36 months, known survival status. Exclusion criteria: clinically relevant adrenal hormone excess (i.e. Cushing’s syndrome, pheochromocytoma, primary hyperaldosteronism), known malignancy. Patient stratification: serum cortisol after dexamethasone (&gt;5 µg/dl, ACS; 1.9-5 µg/dl, possible ACS (PACS); ≤1.8 µg/dl, non-functioning adenoma (NFA)). Definition of CV events (CVE): hospitalization due to myocardial infarction and related interventions (PTCA, surgical bypass), stroke, deep vein thrombosis, pulmonary embolism. Results. 3640 patients (57% NFA, 36% PACS, 7% ACS) were considered eligible: 64% females; median age 61 years (range 18-91); median FU 84 months (36-277) (distribution between subgroups n.s.). 352 patients died during FU. Age- and sex adjusted overall survival was significantly reduced in patients with PACS (HR 1.55; 95%CI 1.24-1.94) and ACS (1.84; 1.29-2.61). Prevalence of CV risk factors were significantly higher in PACS and ACS than in NFA (hypertension: 72, 73, 57%, p&lt;0.0001; dyslipidemia: 42, 49, 35%, p&lt;0.0001; diabetes: 22, 25, 17%, p&lt;0.0001) When adjusted to relevant confounders (i.e. age, sex, CV risk factors), time to first CVE was shorter in PACS (HR 1.36; 1.07-1.73) and ACS (HR 1.62; 1.10-2.40) compared to NFA. Conclusion. PACS and ACS are associated with increased overall mortality and CV morbidity. However, to prove causality a large randomized intervention trial is required.
SUN-699 Canagliflozin Induced Severe Hyponatremia- a Rare Life Threatening and Poorly Understood Complication- a Case Report
Authors: Dhanasekaran Maheswaran , Mehta Suchita 
Published: May 2020

Abstract
Background: Sodium-glucose cotransporter-2 (SGLT2) inhibitors induce osmotic diuresis by inhibiting the proximal renal tubular reabsorption of the filtered glucose load. This can occasionally lead to severe dehydration, hypotension and in some cases, severe hyponatremia. The effects of SGLT2 inhibitors on sodium and water handling by the renal tubules is not well studied.
Clinical Case: A 49-year-old male with history of type 2 diabetes mellitus on canagliflozin, an SGLT2 inhibitor, who was brought to the Emergency Room following a motor vehicle accident from acute onset of confusion and altered mental status. Initial trauma workup was negative. He was found to have severe hyponatremia to 118 mEq/ L (n 135–145 mEq/ L) and was also noted to be in euglycemic ketoacidosis with positive serum ketones (qualitative assessment) along with acute onset urinary retention. Urine toxicology was negative including negative blood alcohol level. Thyroid function was normal 1.080 mIU/ L (n 0.47- 6.90mIU/L). His total urine osmolar excretion was ~ 2400 mOsm in 12h (n 500–800 mOsm/kg of water/ 24 hours), confirming the diagnosis of his ongoing massive osmotic diuresis. On admission, his antidiuretic hormone (ADH) level was noted to be elevated to 9.1 pg/mL (n &lt;4.3pg/ mL). This severe degree of hyponatremia was postulated to be secondary to canagliflozin causing massive osmotic diuresis resulting in severe intravascular volume depletion with reflex increase in antidiuretic hormone (ADH) compounded by increased free water intake by the patient.
Conclusion: With more widespread use of this relatively new hypoglycemic medication with protective metabolic and cardiovascular benefits that include weight loss and reduction of BP in T2DM patients, it is equally important to understand the physiology of potentially life-threatening adverse effects associated with severe volume depletion by massive osmotic diuresis and electrolyte abnormalities that include hypernatremia (even hyponatremia), and the timely recognition of euglycemic ketoacidosis.
SAT-011 Prevalence of Menstrual Disorders and Hormonal Control Use in Elite Female Athletes in New Zealand
Authors: Heather Alison K , Ogilvie Megan , Beable Sarah , Coleman Lynne , Thorpe Holly , Schofield Katie , Sims Stacy , Milsom Stella Ruth , Hamilton Bruce 
Published: May 2020

Abstract
Menstrual disorders are frequent in female athletes, especially those participating at the elite level. Factors which may contribute to impaired ovarian function in athletes include high training volumes, eating disorders and/or low body weight, which in turn may interrupt GnRH signaling. Hormonal contraception may disguise underlying menstrual disorders, and athlete use of such approaches is common, despite limited data on whether hormonal control has positive, neutral or negative effects on athletic performance. To determine the prevalence of hormonal contraceptive use, as well as the prevalence of menstrual disorders, in New Zealand elite female athletes, we completed a national internet-based survey of 219 participants being supported by High Performance Sport New Zealand. The survey aimed to characterize the demographics, health and athletic performance history, the training load and contraceptive use. We found that athletes were training intensely, with 38% reporting training volumes of &gt;70 hours/month. At the youngest age represented (15-19 years), 72% had been in competitive sports for more than 5 years, suggesting a young gynecological age is represented by the cohort. More than half (58%, 127/219) of the surveyed athletes reported diagnosed illness or injuries. Stress fractures (39% 50/127), concussion (31%, 39/127) and asthma (26%, 33/127) were the most common diagnoses, followed by oligo/amenorrhea (20%, 26/127), reduced energy deficit syndrome (9%, 17/194), endometriosis (8%, 16/194), and polycystic ovary syndrome (5%, 9/194). Oligomenorrhea was significantly associated with stress fracture (p=0.018) and disordered eating (p=0.009). More than 50% of athletes tracked their menstrual cycle, and self-reporting showed even higher rates of oligo/amenorrhea 37% (29/79) in athletes not using hormonal contraception. Self-reporting also indicated a high prevalence of other menstrual disorders including delayed menarche (21%,43/207), menorrhagia (30%, 60/203), and dysmenorrhea (32%, 66/203). In athletes reporting menorrhagia, there was a significant association with iron deficiency (p=0.026). Of the 219 athletes, 37% were currently using hormonal contraception, of which the oral combined pill was the most popular (64%). The most commonly cited reason for hormonal contraception was birth control, however athletes used hormonal control to manipulate either the frequency (38%) or the symptoms (29%) of menstruation, particularly around competition. The data clearly suggests that there is likely to be significant undiagnosed gynecological pathology in elite female athletes. Hormonal contraception can mask gynecological health issues and themselves can lead to side effects that affect performance. It remains that health issues, especially those related to gynecological health, need to be considered by athletes, their coaches and medical support staff.
MON-026 Estradiol Triggering Extracellular Matrix Degradation Leading Signalling Cascades Succeeding a Feedback Loop as Contributing Factor to Develop Endometriosis in Females of Reproductive Age
Authors: Malik Arif , Qamar Iram , Waquar Sulayman 
Published: May 2020

Abstract
INTRODUCTION: Endometriosis is common gynaecological disorder that leads to infertility in females of reproductive age. It is characterized by endometrial glands and stromal tissues outside the wall of uterus. Upregulation of estradiol is responsible for the cell proliferation, adhesion and invasion in endometriosis. It enhances prostaglandins (PGE-2) that triggers the formation of matrix metalloproteinases (MMPs), Tumor necrosis factor-α (TNF-α) and nuclear factor kappa B (NF-kB). Whereas, levels of progesterone are reported to be decreased in the patients with endometriosis. Less production of progesterone activity of 17β-hydroxysteroid dehydrogenase-II (17β-HSD-II) decreases that converts estradiol to less potent estrone. Intake of excess trans-fats and deficiency of vitamin D raises level of arachidonic acid and converts PGE-2 by the action cyclooxygenase (COX-2). PGE2 in theca cells of ovaries increases cAMP and activity of liver receptor homologue-1/steroidogenic factor-1(LRH-1/SF-1) thus leading to the stimulation of aromatase enzyme. MATERIALS AND METHODS: Two hundred eighty-eight (n=288) females with endometriosis and hundred (n=100) controls were enrolled. Informed consent was obtained before the collection of samples. Levels of estradiol, progesterone, aromatase enzymes, 17β-HSD-II, COX-2, PGE-2, MMPs (2, 7, 9), vitamin D and lipopolysaccharides (LPO) were estimated by respective protocols. RESULTS: Findings suggests significant increase in the levels of estradiol, aromatase enzymes, COX-2, PGE-2, MMPs (2,7,9) and LPO (67.08±5.55 pg/ml, 7.16±1.28 ng/ml, 1.56±0.144 ng/ml, 4.89±0.61 pg/ml, 995.2±8.15 ng/ml, 105.2±7.19 ng/ml, 109.2±12.25 ng/ml and 125.25±11.26 pg/ml) in patients as compared to (21.08±3.65 pg/ml, 2.08±0.15 ng/ml, 0.61±0.056 ng/ml, 1.158±0.18 pg/ml, 388.26±14.26 ng/ml, 66.29±5.26 ng/ml, 38.29±15.2 ng/ml and 17.25±1.26 pg/ml) controls respectively. Whereas, levels of progesterone, 17β-HSD-II and vitamin D remained significantly low in the endometrial patients (3.07±1.08 ng/ml, 0.183±0.024 ng/ml and 17.17±2.3 ng/ml) as compared to healthy females (29.22±3.29 ng/ml, 1.43±0.153 ng/ml and 36.26±3.09 ng/ml). CONCLUSION: Current study suggests the role of estradiol in triggering ECM degradation and initiating signalling cascades that following a feedback loop enhances the levels of estradiol and contributes in the development and progression of endometriosis. Hence, therapies with supplementation of vitamin D and progesterone may help in regressing the role estradiol and other contributing factors that are involved in the development and progression of endometriosis in the patients. Keyword: Endometrial glands, Stromal tissues, Estrogen, Progesterone, Endometriosis, Vitamin D
SAT-454 A Novel Role of Thyroid Hormone Receptor in Synaptic Plasticity in Cerebellar Purkinje Cells
Authors: Ninomiya Ayane , Hosoi Nobutake , Kokubo Michifumi , Amano Izuki , Haijima Asahi , Miyazaki Wataru , Hirai Hirokazu , Koibuchi Noriyuki 
Published: May 2020

Abstract
Thyroid hormone (TH) is essential for the development and the maintenance of the brain function. TH action is mediated by TH receptor (TR). TR binds to a specific DNA sequence on TH-target genes and thus functions as a ligand-dependent transcription factor. In thyroid diseases such as congenital hypothyroidism or resistance to TH (RTH), TH-TR binding is dominantly disrupted, leading to the various symptoms such as motor deficits. However, in such cases, all the cells that express TR get affected by the disrupted TR signaling; thus, the specific mechanism has not been cleared. It has been well known that proper motor coordination is deeply related to long term depression (LTD) of synaptic transmission from parallel fiber (PF) to Purkinje cell (PC) in the cerebellum (Ito, 1989). Therefore, we examined the involvement of TR in synaptic plasticity at PF-PC synapses by using transgenic mice (Mf-1 mice) which express dominant-negative TR specifically in PCs. Since Mf-1 display the impairment of motor coordination and motor learning, a decrease in TR signaling in PCs may alter synaptic plasticity and contribute to motor incoordination. A whole-cell patch clamp recording of Mf-1 PCs revealed the inhibition of LTD but instead the induction of long term potentiation (LTP) of the synaptic transmission at PF-PC synapses. This indicates that the intracellular calcium dynamics may be disrupted in Mf-1 PCs since LTD requires a higher elevation of the intracellular calcium concentration in PCs than LTP does. Indeed, single-PC qPCR showed that the mRNA levels of some important molecules for the intracellular calcium dynamics in PCs (SERCA2, IP3R, and P/Q-type calcium channel) are downregulated in Mf-1 PCs. This result suggests those genes as possible TH-target genes. Taken together, the present study suggested a novel possible role of TR in synaptic plasticity at PF-PC synapses by regulating the expression of some important genes for LTD occurrence in the cerebellum. This finding could give a new insight into the mechanism of motor deficits in thyroid diseases.
SUN-422 Risk Factors Associated with Thyroid Nodules in Type 2 Diabetes
Authors: Gonzales Sonia Gisella Chia , ruiz victor noriega , Pinto Miguel Eduardo , zárate eduardo pretell , Santisteban Segundo Seclen 
Published: May 2020

Abstract
Objective: To determine risk factors associated with the presence of thyroid nodules in patients with type 2 diabetes
Material and methods: A case control prospective study, matched 1:1, according to age, sex and smoking habit was conducted. Patients with type 2 diabetes were recruited from the Endocrinology Service of Cayetano Heredia Hospital, Lima-Perú. Clinical evaluation, laboratory tests and thyroid ultrasound were performed to indentify patients with type 2 diabetes with and without thyroid nodules. The association was evaluated by calculating Odds ratios (OR) by conditional multivariate logistic regression techniques.
Results: 83 patients with type 2 diabetes and thyroid nodule and 83 patients with type 2 diabetes without thyroid nodule; were obtained. The risk factors associated with the presence of thyroid nodules in patients with type 2 diabetes were HbA1c (OR= 4.12, P= 0.002), BMI (OR= 1.13, P 0.030) and TSH (OR= 3.27, P= 0.0001), with cut-off points according to ROC curve of HbA1c ≥ 8%, TSH in the normal upper limit ≥ 2.3 μIU / mL and BMI ≥ 27 kg / m2. Patients with type 2 diabetes and thyroid nodule had higher values of blood glucose, thyroid volume, abdominal and neck circumference; greater frequency of acantosis nigricans and acrochordons compared to controls.
Conclusions: The risk factors associated with the presence of thyroid nodules in patients with type 2 diabetes were HbA1c, BMI and TSH, with cut-off points according to ROC curve of HbA1c ≥ 8%, TSH in the normal upper limit ≥ 2.3 μIU / mL and BMI ≥ 27 kg / m2.
MON-080 Unusual Association Between Congenital Hyperinsulinism and Neurofibromatosis Type 1
Authors: Marinescu Andreea S , Suarez Elizabeth A 
Published: May 2020

Abstract
Background: Neurofibromatosis type 1 (NF1) is an autosomal dominant multisystemic disorder characterized by an increased risk of benign and malignant tumor formation affecting skin, bone and nervous system. In children with NF1, endocrine manifestations include central precocious puberty, growth hormone deficiency and growth hormone hypersecretion, resulting from complications of optic pathway gliomas involving the hypothalamic and sellar region. A few reports of adults with NF1 have been described to have hypoglycemia due to insulinoma. However, hypoglycemia due to hyperinsulinism has not been described in children with NF1. We present a case of NF1 diagnosed during neonatal period associated with congenital hyperinsulinism.
Case: Patient was delivered at 36 weeks by C- section with birthweight of 2780 grams which was appropriate for her gestational age. There was no maternal history of diabetes. Pertinent exam findings included microcephaly and multiple café-au-lait spots. She developed hypoglycemia at DOL1 with blood glucose of 26 mg/dl which normalized with IV dextrose at a glucose infusion rate of 6 mg/kg/min. At DOL8, an attempt to wean IV dextrose failed and she developed hypoglycemia with blood glucose of 47 mg/dl. Critical sample showed insulin level 3.3 uU/ml, betahydroxybutyrate 0.08 mg/dl (0.2-2.8), cortisol 18.1 mcg/dL and GH 13.2 ng/mL. A glucagon stimulation test showed an increase in glucose of 30 mg/dl. She was diagnosed with hyperinsulinism and started on Diazoxide (8 mg/kg/day) with improvement of blood glucose with prefeed glucose of &gt; 70 mg/dl. She had normal 8- hour fasting tolerance with all BG &gt; 70 while on Diazoxide. Genetic test for known mutations causing hyperinsulinism was negative. Microarray confirmed a 1.42Mb interstitial deletion at chromosome 17q11.2 which encompasses NF1 gene confirming the diagnosis of NF1. Additionally, she has an Xp22.33 duplication of uncertain clinical significance.
Conclusion: Our patient presented with an unusual association between congenital hyperinsulinism and NF1. Further testing needs to be performed to determine whether this association is coincidental or whether congenital hyperinsulinism is a rare manifestation of NF1.
OR21-02 Impact of Nodule Size on the Probability of Hurthle Cell Carcinoma and Other Cancers in Thyroid Nodules with Multiple Chromosomal Copy Number Alterations
Authors: Nikiforova Marina N , Nikitski Alyaksandr , Tebbets Jessica , Tolino Lindsey , Manroa Pooja , Yip Linwah , Nikiforov Yuri E 
Published: May 2020

Abstract
Fine-needle aspiration (FNA) of thyroid nodules yields indeterminate cytological diagnosis in ~20% of cases, confounding patient management. This includes Hurthle cell nodules, which typically yield Bethesda IV and III cytology. Chromosomal copy number alterations (CNA) are known to occur in thyroid tumors, particularly in Hurthle cell carcinomas (HCC) as well as in other typically follicular-patterned tumors including papillary thyroid carcinomas (PTC) and poorly differentiated thyroid carcinomas (PDTC). The aim of this study was to evaluate thyroid nodules tested positive for CNA but negative for all other genomic alterations using ThyroSeq v3 NGS assay in order to establish the probability of cancer in these nodules and find whether it is influenced by the pattern of CNA and nodule size. We evaluated 111 nodules with multiple CNA detected by ThyroSeq in FNA samples and available surgical pathology outcome. Of those, 69 (62%) nodules showed CNA changes consistent with genome near-haploidization (GNH) whereas 42 (38%) nodules had multiple chromosomal losses and gains (CLG). Nodule size ranged from 0.5-10.2 cm; cytology was Bethesda III in 54%, Bethesda IV in 43%, and Bethesda V-VI in 3% of cases, with Hurthle cells mentioned in the cytology report in 64% of cases. On surgical pathology, 38 (34%) of these nodules were malignant (including 24 HCC, 8 PTC, and 5 oncocytic PDTC) and 73 (66%) were benign (including 43 Hurthle cell and 18 follicular adenomas). No significant difference was observed in probability of malignancy between the two patterns of CNA (p=0.41). However, a significant correlation between the nodule size and probability of cancer was found (p=0.006). In specific CNA groups, correlation between cancer and nodule size remained significant for nodules with GNH pattern (P=0.0002), but not with CLG pattern (p=0.449). Specifically, cancer probability in nodules with GNH pattern and &lt;2 cm in size was 14% (all cancers minimally-invasive), 2.0-2.9 cm was 33%, 3.0-3.9 cm was 50%, 4-4.9 cm was 67%, and ≥5 cm was 80%. Among high-risk cancers (widely-invasive or angioinvasive HCC, PDTC), all 10 tumors had the GNH pattern (p=0.01) and average nodule size of 4.9 cm (range, 2.1-8.5 cm). These findings suggest that CNA of both types are frequently found in Hurthle cell tumors, and probability of cancer in nodules with CNA and no other mutations increases with larger nodule size. This may help to refine the pre-operative assessment of cancer probability and risk of more aggressive disease and offer more tailored management to these patients.