bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-386 Treatment Outcomes of Intravenous Zoledronic Acid vs Oral Alendronate in Postmenopausal Women with Osteoporosis
Authors: Pyone Zar Chi , Aung Moe Wint , Myint Thein , Khin Than Saw , Hlaing Thinn Thinn 
Published: May 2020

Abstract
In real practice, many patients with osteoporosis are poorly compliant with oral bisphosphonate, partly due to gastrointestinal side effects and partly due to medication procedure leading to premature termination of treatment. Once yearly intravenous zoledronic acid is well tolerated; little or no gastrointestinal effects and effective drug in treatment of postmenopausal osteoporosis with favourable dosing regimen to improve compliance of patients. So this study aims to study treatment outcomes of intravenous zoledronic acid vs oral alendronate in postmenopausal women with osteoporosis. This study was a randomized open label comparative study and included 94 postmenopausal women with osteoporosis. In this study, once yearly zoledronic acid (ZOL) infusion provided a greater reduction of serum procollagen type 1 N propeptide (P1NP) at 3 months than once weekly oral alendronate (ALN). Percentages of P1NP change in ZOL group was -70.25±17.51% and ALN group was -60.61±18.87% (P= 0.012). A decrease of P1NP ≥40% was observed in the majority of patients in both groups (89.4% in ZOL group and 85.1% in ALN group) (P= 0.536). ZOL was non-inferior to ALN in terms of BMD change at lumbar spine (4.8±5.5% in ZOL versus 4.9±4.5% in ALN treated patients) with P value of 0.922 and also at total hip (3.8±8.0% in ZOL versus 3.8±7.5% in ALN group) (P= 0.970). Two cases (4.3%) of new fractures was observed in ZOL group whereas 4 cases (8.5%) of new fractures occurred in ALN group over one year of study. The overall frequencies of treatment related adverse effects were similar between ZOL group (57.4%) and ALN group (42.6%) (P= 0.149). ZOL group showed significantly increased frequencies of musculoskeletal pain (57.4%) and acute phase reaction (12.8%) and 12.8% of participants in ALN group complained of heartburn. The overall preference to continue current medication was higher in ZOL group than ALN group (P= 0.002). The participants treated with ZOL were tend to have more satisfaction (P= 0.026) and willing to receive it longer period (P&lt; 0.001).Compared to weekly oral alendronate therapy in treatment of postmenopausal osteoporosis, yearly infusion of 5 mg zoledronic acid infusion produced a significant greater response in serum P1NP at 3 months and similar change in BMD at one year of treatment and overall frequencies of adverse effects were similar between two treatment groups with excellent patient preference and satisfaction after zoledronate treatment. Reference: (1) Al-Bogami et al (2015) Favorable therapeutic response of osteoporotic patients to treatment with intravenous zoledronate compared with oral alendronate. Saudi Med J. 36(11):1305-1311. (2) Saag et al (2007) A single zoledronic acid infusion reduces bone resorption markers more rapidly than weekly oral alendronate in postmenopausal women with low bone mineral density. Bone. 40:1238-1243.
OR22-04 Relationship of TSH Levels with the Components of Metabolic Syndrome in a Nationally Representative Population of Youth in the United States
Authors: Chen Xinlei , Deng Shuliang , Thaker Vidhu V 
Published: May 2020

Abstract
Introduction: Subclinical hypothyroidism (SH) is defined as elevated TSH with normal thyroid levels, and is often associated with obesity. SH has been linked to cardiometabolic risk factors such as abnormal lipids, elevated blood pressure, atherosclerosis and fatty liver. This study sought to elucidate the association of TSH level with the components of metabolic syndrome independent of BMI in children from the National Health and Nutrition Examination Survey (NHANES).
Methods: NHANES surveys 1999-01 and 2007-12 that measured thyroid function tests were included in the study. Youth aged 2-18 years with TSH levels &lt; 10 uU/mL and normal Total T4 (TT4) levels were included in the analysis. The components of metabolic syndrome were defined as abdominal obesity (waist circumference &gt; 95th %tile), hypertriglyceridemia (TG &gt;=100 for 0-9 years and &gt;=130 mg/dL for &gt; 10 years), low HDL cholesterol &lt; 40 mg/dL), elevated blood pressure (&gt; 95th %tile for age/sex/height) and hyperglycemia (FBG &gt; 100 mg/dL, or diagnosis of diabetes). The association of these components with quartiles of TSH were examined by logistic and linear regression controlling for age, sex, race/ethnicity and BMI. All analyses were performed in R v3.5.1.
Results: After excluding youth with TSH &gt;10 uU/mL and TT4 levels &lt; 12.4 mcg/dL, 2377 subjects (50% female) were included in the study. The mean age of the cohort was 15 ± 1.7 years; 28.2 % were non-hispanic whites and 38.5 % hispanic/latino. Obesity (BMI &gt;95 %tile) was seen in 21.7% individuals. There were 44 subjects with TSH levels &gt;4.5 uU/mL that was not different by BMI (2.5% in BMI &gt;95%tile and 1.7% BMI &lt; 95%tile, p = 0.29). Based on the distribution in the population, TSH levels were divided into 4 quartiles: Q1= 0.01-0.97, Q2= 0.98-1.42, Q3=1.43-2.0, Q4 = &gt; 2.01 uU/mL. A statistically significant association of the Q4 TSH was seen with abdominal obesity, OR 2.44 (1.38-4.39), p=0.002 and elevated BP, OR 1.6 (1.06-2.44), p = 0.02 but not with high TG, OR 1.58 (0.93-2.75), p=0.09, low HDL, OR 0.84 (0.6-1.17), p = 0.31 or those with hyperglycemia and/or diabetes, OR = 1.25 (0.78-2.05), p = 0.36. Linear regression models showed statistically significant association of abdominal obesity, hypertriglyceridemia, elevated BP and hyperglycemia (and/or diabetes) with increase in TSH level.
Conclusions: In children from a representative US population, the prevalence of SH defined as TSH level &gt;4.5 uU/mL is low, even with BMI &gt;95th %tile. The association of measures of metabolic syndrome with linear increase in TSH suggests that the current reference range may require modification.
MON-684 Neuroglycopenia: Avoiding Bias in Patients with Acute Psychosis
Authors: Otuonye Gene Chibuchim , Gibbs Otto , Sittol Rani Delraj , Tavares Matthew V , Abuaisha Munder , Kim Christian 
Published: May 2020

Abstract
Introduction
The neurogenic response to hypoglycemia (HG) is well established. In contrast, neuroglycopenic (NG) manifestations are widely variable and have been erroneously attributed to other diagnoses. Compounding diagnostic uncertainty is the incidence of these symptoms in a patient with a psychiatric illness.
Clinical Case
A 51 year old male with hypertension and schizophrenia maintained on amlodipine, risperidone and benztropine was transported to the ER psychiatric unit by law enforcement. He was detained after he was found wandering the streets demonstrating increased verbal and physical aggressiveness. He was known to the unit, with previous admissions for psychosis secondary to schizophrenia. On presentation vitals were solely significant for tachycardia. Physical and mental status examination revealed a disheveled, agitated and combative male who was disoriented to time, person and location. He was actively experiencing visual and auditory hallucinations with psychomotor agitation, intermittent loosening of association, circumstantial speech and persecutory delusions. Initially given one dose of i.m. haloperidol and benztropine, his psychosis persisted. Biochemical investigations were significant for a glucose of 37 mg/dL; All others including alcohol level, toxicology and TSH were normal. Head CT was unremarkable. His HG was treated with i.v. dextrose with complete resolution of psychotic symptoms within one hour of normoglycemia. He needed no further antipsychotic doses save his maintenance risperidone. Further historical enquiry revealed a recent diagnosis of type 2 DM managed on metformin and glimepiride with poor oral intake. He was discharged on metformin and sitagliptin post extensive DM self-management education, h; glimepiride was discontinued.
Discussion
NG manifestations of hypoglycemia are the direct result of central nervous system glucose deprivation. Uncommonly, they can be the sole presenting complaint in the HG patient. In one study, 27% of patients with insulinomas had only NG symptoms [1]. Interestingly, some case reports suggest acute psychosis may be an important NG feature [2]. Psychiatric patients, particularly those with primary psychotic disorders often face a labyrinthine process when seeking emergent medical care including but not limited to anchoring and ascertainment physician bias. If unrecognized, HG can lead to neuronal death. Clinicians must maintain a high index of suspicion of HG in patients presenting with acute psychosis even in the presence of functional illness so as to reduce morbidity, mortality and medicolegal risk.
References
Dizon AM., Kowalyk S., Hoogwerf BJ. Neuroglycopenic and other symptoms in patients with insulinomas, Am J Med. 1999 Mar; 106(3):307-10.
Klemen P., Grmec S., Cander, D. Hypoglycemia masquerading as acute psychosis in young age. Crit Care. 2000; 4(Suppl 1): P172. doi: 10.1186/cc892.
MON-450 Prophylactic Thyroidectomy in a Patient with Codon 891 Mutation of the RET Proto-Oncogene
Authors: Swami Janya , Howell Nicole R 
Published: May 2020

Abstract
Background: Medullary thyroid cancer (MTC) is a neuroendocrine tumor of the parafollicular or C cells of the thyroid gland, accounting for 1-2% of thyroid cancers in the United States. About 25% MTCs are familial as a part of the MEN2 syndrome or familial MTC (FMTC). Germline mutations in codon 891 are predominantly associated with FMTC. Case: 65-year-old Caucasian male was referred to the Endocrinology clinic after bilateral thyroid nodules were found on thyroid US. The patient had requested an ultrasound of his thyroid after his brother was diagnosed with MTC following fine-needle aspiration for an incidental thyroid nodule prompting total thyroidectomy and genetic testing. The patient’s brother was found to be heterozygous for RET mutation (c.2617T&gt;G;pSer891Ala). This resulted in screening of the other siblings including this patient, also found to be heterozygous for this mutation. Both parents were deceased, and their clinical history is not known. Only one of the remaining two siblings had genetic testing; one brother refused testing for the mutation and one sister was positive for the mutation but had no thyroid nodules on ultrasound. She underwent prophylactic thyroidectomy. Neither the patient, nor his siblings, have any progeny. The patient screened negative for primary hyperparathyroidism and pheochromocytoma. Calcitonin (739, normal &lt;/=14.3 pg/mL)and CEA levels (31.7, 0-3.0 ng/mL) were elevated. Thyroid ultrasound (US) showed two solid hypoechoic nodules with lobulated margins and internal coarse calcifications in the right and two in the left thyroid lobe; 1.5 cm and 1.2 cm in maximum diameter, and 1.2 cm and 3 mm in maximum diameter, respectively. Based on elevated calcitonin and CEA levels, known RET mutation and evidence for thyroid nodules, we recommended a total thyroidectomy and central neck dissection. Pathology revealed multifocal, bilateral medullary carcinoma (largest focus of 1.5 cm), with 4/4 lymph nodes positive for metastasis. This was classified as mpT1bN1aM0 (Stage III). Patient was started on levothyroxine with plans to repeat calcitonin and CEA levels and neck ultrasound, 3 months following surgery. CT chest, abdomen and pelvis did not reveal any distant metastasis. Conclusion: Inherited MTCs are rare. Early diagnoses by screening of at-risk family members in MEN2 kindreds is important because MTC can be life-threatening and can be cured and prevented by early thyroidectomy. While our suspicion for FMTC in this patient and his siblings is high, FMTC is now considered a variant of MEN2A and ongoing screening for pheochromocytoma and primary hyperparathyroidism is recommended.
SAT-459 A Grave Complication: Pulmonary Arterial Hypertension
Authors: Butt Wajeeha Saeed , Srinivasan Vijay 
Published: May 2020

Abstract
There is currently emerging evidence that thyroid disease can have an impact on pulmonary pathologies but a direct causation, as opposed to correlation, is yet to be established. We present a unique case of newly diagnosed Graves’ disease with pulmonary sequalae.
69 year old non-smoking female with no known medical history presented to the hospital with acute onset of chest tightness, shortness of breath and palpitations. She had been experiencing night sweats and 10 lbs weight loss in the 3 weeks preceding hospitalization. She did not endorse any pertinent family history. On exam, she presented with tachycardia. The rest of the physical exam remained unchanged. Complete blood count and comprehensive metabolic panel did not reveal any abnormalities. Her TSH was suppressed below lab capability of measurement (&lt;0.015). Free T4 was 5.97 ng/dL, and total T3 was 492 ng/dL. Subsequently obtained TPO antibody level was &gt; 1000 IU/ml and TSI was 29.3 IU/L. EKG showed atrial fibrillation with RVR. Thyroid U/S showed that the thyroid gland was diffusely enlarged to the upper limit of normal but no nodules. CT chest showed diffuse ground glass opacities.
She was treated with propranolol, and methimazole after resolution of acute symptoms. She was placed on diuretics to treat symptoms of pulmonary edema secondary to uncontrolled atrial fibrillation and high output heart failure. On outpatient follow up she continued to have mild shortness of breath on exertion. She had normal systolic and diastolic function of heart but an elevated PAP of 38mm Hg on a transthoracic echocardiogram, and her pulmonary function tests were within normal limits for her age. A follow up CT chest, 6 weeks after discharge, showed no resolution of ground glass opacities.
Current literature shows that there might be pulmonary effects of hyper-thyroidal diseases; such as ventilation disorders, OSA, CSA, and pleural effusions. A 2002 study revealed a strong association of hyperthyroidism with pulmonary hypertension. A 2016 literature review established that there is specifically an association of Graves’ disease with pulmonary arterial hypertension. Both of these studies have had a small patient group. Our case perhaps adds credence to the fairly less known affiliation of hyperthyroidism with pulmonary disease. A unique finding in our patient - unresolving ground glass opacities, suggests a possible thyroid related interstitial lung disease. As with our case, there needs to be an increased awareness in the among clinicians to further work up both thyroid related pulmonary hypertension and interstitial lung disease possibly related to uncontrolled thyroid pathology. Increased vigilance to include hyperthyroidism as a differential for pulmonary hypertension can lead to better clinical outcomes for patients, with less possible invasive and expensive testing of other causes of pulmonary hypertension.
MON-467 A Case of Inoperable Substernal Goiter
Authors: Papaioannou Garyfallia , Sifontes Erick Perez , Manivel Gnanambal , Eswaran Manivel Kumaran 
Published: May 2020

Abstract
Introduction: Goiter is abnormal growth of the thyroid gland. When goiter extends into the mediastinum it is called retrosternal or substernal. Substernal goiter can cause compression of the great vessels, trachea, and esophagus. When it compresses trachea it can result in airway obstruction. In that case treatment of choice is thyroidectomy and Radio Iodine Ablation (RIA). But some patients are considered to be high risk for operation due to multiple comorbidities. We are presenting this case where we tried experimental therapy with airway stent and external beam radiation. Case: An 81 year old female presented to the hospital complaining of chest pain. She also reported dysphagia to solids and liquids and weight loss during one month. Past medical history included congestive heart failure, atrial fibrillation, chronic obstructive pulmonary disease with home oxygen support. On physical exam thyroid was palpable to the level of sternal notch. Arterial blood gases showed hypoxemia (PO2 63), thyroid function tests showed an abnormally suppressed TSH (&lt;0.005 IU/ml), elevated free T4 (2.48 ng/dl) and normal T3. Thyroid stimulating immunoglobulin, IgG, IgM and IgA levels were normal. Thyroglobulin and thyroid peroxidase antibodies were negative. Chest X-ray revealed an upper mediastinal mass. Chest CTA showed a very large substernal goiter with left thyroid lobe of 7.4 x 3.4 x 7.8 cm that extended to the level of the carina causing compression of the upper to mid trachea and of the upper esophagus. The smallest diameter of the trachea was 6 millimeters. Ultrasound revealed an enlarged heterogeneous thyroid with a solid lesion in the left side inferiorly. Due to administration of IV contrast for the CTA, iodine uptake scan was not performed. Patient was determined to be of high surgical risk due to her comorbidities and she did not consent for thyroidectomy. She was treated with methimazole 20mg daily and IV hydrocortisone 50mg TID. Due to the administration of IV contrast she was not candidate for RIA either. Short term beam radiation was started. For the acute relief of respiratory distress the lesion was transversed through flexible bronchoscopy and a 16 mm by 80 mm covered ultraflex tracheobronchial stent was placed in the trachea. The post-stent lumen size was 80% of normal. Patient’s respiratory status improved and the treatments with external beam radiation were continued. Conclusion: The treatment of choice for substernal goiter that causes airway obstruction is surgery. RIA can be an alternative when surgery is contraindicated. Since surgery as well as RIA was not an option for this patient we attempted external beam radiation to reduce the size of goiter. Because this treatment takes several weeks to be effective, temporary airway opening via an airway stent is the option for acute relief of symptoms.
MON-698 Association of Sleep Quality and Painless Diabetic Peripheral Neuropathy in Type 2 Diabetes
Authors: Choi Dughyun , Kim Bo Yeon , Jung Chan-Hee , Kim Chul-Hee , Mok Jioh 
Published: May 2020

Abstract
Aims
Diabetic peripheral neuropathy (DPN) is one of the most common and early manifested complication in T2D. Previous reports have shown that painful sensation of diabetic peripheral neuropathy (DPN) results in sleep problems in type 2 diabetes (T2D)1, 2. However, it is not known that subtype of DPN, the painless DPN also is associated with poor sleep quality in T2D. The purpose of the current study was to investigate the association between painless DPN and poor sleep quality in T2D.
Methods
A total of 146 patients of T2D who did not previously diagnose with symptomatic DPN were recruited into the study. Among the patients, painless DPN was diagnosed by using the current perception threshold (CPT) test. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) questionnaire.
Results
The percentage of painless DPN was significantly higher in the poor sleep quality group than the good sleep quality group (70.0% vs. 35.5%, P&lt;0.001). In the subscale results, stimulus values in 2000 Hz, hypoesthesia and hyperesthesia were significantly higher in the poor sleep quality group, than in the good sleep quality group (45.7% vs. 25.0%, P=0.009; 34.3% vs. 18.4%, P=0.029; 40.0% vs. 19.7%, P=0.007, respectively). The association of painless DPN and poor sleep quality remained significant after adjustment for significant variants (odds ratio, 3.825; 95% confidence interval, 1.674-8.742; P&lt;0.001).
Conclusions
The current study showed that painless DPN was associated with poor sleep quality. Future studies are required to clarify the pathophysiologic causal relationship between painless DPN and sleep quality.
References
1. Gore M, Brandenburg NA, Dukes E, Hoffman DL, Tai K-S, Stacey B. Pain severity in diabetic peripheral neuropathy is associated with patient functioning, symptom levels of anxiety and depression, and sleep. Journal of pain and symptom management. 2005;30(4): 374-385.
2. Zelman DC, Brandenburg NA, Gore M. Sleep impairment in patients with painful diabetic peripheral neuropathy. Clin J Pain. 2006;22(8): 681-685.
SAT-129 Interactions Between Macrophages and Cancer Stem-Like Cells Promote Mammary Tumor Angiogenesis Under Obesity
Authors: Hillers-Ziemer Lauren , McMahon Rachel , Hieptas Margaret , Paderta Gretchen , McCready Jessica , LeBeau Jennelle , Arendt Lisa 
Published: May 2020

Abstract
Obesity is a growing health concern worldwide and increases the incidence of multiple types of cancer, including breast cancer. Obese breast cancer patients often develop more aggressive tumors than lean patients and have increased risk for metastasis, tumor recurrence and mortality. Here, we sought to address how obesity alters the biology of breast cancer to promote aggressive tumors. To induce obesity, we fed mice either a control diet (CD) or high fat diet (HFD) for 16 weeks, then transplanted Met-1 tumor cells into mammary fat pads and monitored tumor growth. At end stage, tumors from HFD-fed mice were significantly larger than tumors from CD-fed mice, suggesting obesity promotes tumor growth. To investigate how obesity promotes tumor aggression, we dissociated the tumors from CD- and HFD-fed mice and plated isolated tumor cells in tumorsphere and invasion assays to test for cells with cancer stem-like cell (CSC) properties. Tumor cells from HFD-fed mice demonstrated increased tumorsphere formation and increased capacity for invasion compared to tumor cells from CD-fed mice, suggesting that obesity selects for tumor cells with CSC properties. Next, to address how obesity impacts the tumor microenvironment, we evaluated tumor necrosis and blood vessel formation through CD31 staining. Tumors from HFD-fed mice had significantly less necrosis and greater CD31 staining than those from CD-fed mice, suggesting that obesity promotes tumor angiogenesis. Since obesity promotes chronic, macrophage-driven inflammation within adipose tissue of the mammary gland, we stained tumors for the macrophage marker, F4/80. As with obese mammary glands, tumors from HFD-fed mice had significantly greater macrophage recruitment than tumors from CD-fed mice, together suggesting that obesity alters the tumor microenvironment. To determine how obesity stimulates tumor angiogenesis, we performed an in vitro assay by culturing dissociated tumor cells from HFD or CD-fed mice alone or with macrophages. Conditioned media (CM) isolated from tumor cells from HFD-fed mice cultured with macrophages enhanced the ability of endothelial cells to form networks in vitro. In contrast, CM from HFD tumor cells alone, macrophages alone, or those from CD-fed mice did not promote network formation. Together, these results suggest that cooperation between macrophages and tumor cells from HFD-fed mice promotes angiogenesis. Next, to investigate how macrophages and tumor cells interacting in obesity, we depleted macrophages using anti-F4/80 antibodies in CD-fed and HFD-fed tumor-bearing mice. In HFD-fed mice, macrophage depletion significantly reduced tumor volume and CD31 staining while increasing tumor necrosis compared to controls. Obesity promotes interactions between tumor cells and macrophages to enhance tumor angiogenesis and progression.