bluuebunny/crossref_metadata_2025_split huggingface dataset:
RF18 | PSAT146 Bone Quality in Lean Adults with Metabolic Syndrome
Authors: Ferri-Guerra Juliana , Badour Sanaa , Garg Rajesh , Valderrãbano Rodrigo J 
Published: November 2022

Abstract

Purpose
Metabolic syndrome (MetS) comprises a constellation of risk factors for cardiovascular disease, which are thought to be derived from truncal obesity. Adipose tissue can have positive effects on bone density through mechanical stimulation on weight bearing sites and can have hormonal influences which affect bone cells, however in obesity this relationship is inversed as the deleterious effects of excess fat mass predominate. It is unclear how MetS and the regional distribution of fat relate with bone density and bone quality in lean individuals who do not benefit from increased weight bearing.

Methods
We performed a cross sectional analysis of adults who underwent bone density and body composition by dual energy x-ray absorptiometry (DXA) at a university health system bone clinic, and had laboratory and demographic data available in the electronic medical record. We included adults with BMI below 24.9 kg/m2 in the analysis. Individuals were classified as being metabolically unhealthy lean (MUL) when they fulfilled at least 2 of the following criteria: blood pressure &gt; 130/85, triglyceride &gt;150 mg/dL, HDL &lt; 50 mg/dL for women and &lt; 40 mg/dL for men, fasting plasma glucose &gt;100mg/dL (or HbA1c &gt;=5.7), and metabolically healthy lean (MHL) when they did not fit the criteria. Linear regression was used to evaluate the association of body composition fat parameters with trabecular bone score (TBS), and bone mineral density (BMD) at the total hip (TH).

Results
Among the 119 (100%) lean adults, 50 (42%) were classified as being MUL. Mean age was 62 ±14 years old and mean BMI was 22 ±1.9kg/m2. The population was mostly white 105 (88%) and 70 (41%) were Hispanics. Additionally, 43 subjects (40%) had a history of a previous fracture. Total body fat was similar between the two groups (mean,%) MHL 33.5, MUL 34.1 (p=0.32), as were age (mean, years) MHL 62.3 vs MUL 62.5 (p=0.48), BMI (mean, kg/m2) MHL 22.2, MUH 22.2 (p=0.49), TH BMD (mean, g/cm2) MHL 0.74, MUL 0.72 (p=0.140) and TBS (mean, unitless) MHL 1.34, MUL 1.33 (p=0.308). However, visceral adipose tissue area (VAT) (mean, cm2) was statistically significantly different between the groups (MHL 69.0, MUL 86.7, p=0.004). In linear regression analyses total body fat had negative association with TBS (B=-0.44, p&lt;0.001) and TH BMD (B= -0.37, p&lt;0.001) while VAT had negative association with TBS (B=-0.26, p=0.02) but not TH BMD (B=-0.17, p=0.08).

Conclusion
In our sample of older lean individuals body fat distribution varied by classification of metabolic health. Total body fat amount was associated with decreasing bone density and quality, while higher truncal fat as measured by VAT area was associated with decreasing bone quality. Our findings suggest that excess body fat may have deleterious effects on bone health even in lean individuals
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Sunday, June 12, 2022 1:06 p.m. - 1:11 p.m.
RF30 | PSAT148 Bone Mass and Body Composition Analysis in Transgender Men: A 1 Year Follow Up
Authors: Orozco Bruno , de Oliveira Otavio Lima , Haddad João Victor Magliari , de Macedo Luciana Pereira , Nurse Graduate , de Amorim Alessandra Toledo , Nurse Graduate , Alvares Leonardo Azevedo Mobilia , dos Santos Livia Marcela 
Published: November 2022

Abstract

Introduction
Sex steroid hormones play a key role in bone health, however medical therapies for gender dysphoria lead to hormonal changes.

Purpose
Understanding the changes in bone mass and body composition is extremely important, because this treatment will be carried out over a long period of time.

Methods
In a prospective study, we included 19 transgender men (female-to-male transgender persons) before treatment and after 1 year of treatment with undecanoate (1000 mg i.m./12 weeks). Bone densitometry model Hologic-Discovery performed at baseline and after 6, 12 months of therapy. All participants signed the TCLE, project approved by CEP-CAAE: 36823220.6.0000.0062.

Results
Analysis of 19 transgender men with a mean age of 24 years +/- 10 years. LS-BMD (lumbar spine) at initial time (0m) 1,075±0,238 g/cm2 and after 6 months (6m) 1,044±0,117 g/cm2 and 12 months (12m) after 1,052±0.122 g/cm2, p=0.21; FN-BMD (Femur Neck) 0m= 0.904±0.121 g/cm2; 6m= 0.918±0.108 g/cm2 and 12m= 0.905±0.107 g/cm2; p=0.90. TH-BMD (Total Hip) 0m=1.017±0.139 g/cm2; and 6m= 1.023±0.134 g/cm2; 12m= 1.032±0.136g/cm2; p=0.05. About body composition: the percentage of body fat: 0m=38.8±6.7%, 6m=34.5±7.1%; 12m=34.9±9.0; p=0.09; android/gynecoid ratio: 0.93±0.16, 6m=0.94±0.17; 12m=0.94±0.18 p=0.06, VAT mass (cm3) 431.8±262.1, 6m= 401.8±298.6, 12m= 455.5±322.7 and Lean/Height2 (kg/m2) 0m= 15.52±3.24 6m= 16.15±2.19 kg/ m2; 12m= 15.86±2.22 kg/m2; p&lt;0.01 and Appen. Lean/Height2 (kg/m2) 6.92±1.74, 6m= 7.32±1.22 and 12m= 7.31±1.07; p&lt;0.01

Conclusion
In 1 year of hormone therapy with testosterone, we did not observe significant differences in bone mass, but in body composition there was a gain in appendicular lean mass.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m., Monday, June 13, 2022 1:00 p.m. - 1:05 p.m.
LBODP029 Pseudohypobicarbonatemia In The Setting Of Diabetic Ketoacidosis And Severe Hypertriglyceridemia
Authors: Lamb Seth , Wee Erica , Halpin Kelsee 
Published: November 2022

Abstract

Background
Severe hypertriglyceridemia is a rare complication of diabetic ketoacidosis (DKA); however, the resulting spuriously low measurements of serum bicarbonate ("pseudohypobicarbonatemia") are less well known.

Clinical Case
A healthy 15-year-old female presented to the emergency department with polydipsia, polyuria, and abdominal pain. She had a normal BMI and a sibling with type 1 diabetes (T1D). Labs demonstrated serum glucose of 351 mg/dL, serum ketones of 3.4 mmol/L, serum bicarbonate of &lt;5 mmol/L, anion gap of &gt;23 mmol/L, and triglycerides of &gt;21,000 mg/dL. Serum lipase was normal at 70 units/L. She was admitted for protocolized DKA treatment with intravenous fluids and regular insulin drip. Hospital day 2, serum bicarbonate remained very low (7 mmol/L) despite declining ketones (1.9 mmol/L), decreasing anion gap (15 mmol/L), normal chloride (112 mEq/L), and normal lactic acid (1.3 mmol/L). A spurious lab was suspected, so bicarbonate was calculated from a venous blood gas (VBG) which showed a pH of 7.28 and a bicarbonate of 16.2 mmol/L at a time when serum bicarbonate was 7 mmol/L. Serial BMPs and VBGs were trended, with the serum bicarbonate consistently 7-10 mmol/L lower than the blood gas bicarbonate. Her ketoacidosis resolved, yet she remained hospitalized for continued IV regular insulin drip (max 0.3 units/kg/h) for treatment of severe hypertriglyceridemia. On hospital day 7, triglycerides fell below 500mg/dL. She never developed pancreatitis. She was discharged home on multiple daily injection insulin and a low-fat diet. Her triglyceride level two weeks later was 173 mg/dL. Diabetes autoantibodies returned positive, confirming a diagnosis of T1D.

Clinical Lessons
This case demonstrates that very high triglycerides can occur with pediatric DKA and cause a falsely low serum bicarbonate level, also known as "pseudohypobicarbonatemia". This is due to chemistry panel analyzers using absorbance to estimate bicarbonate levels, which makes them susceptible to triglyceride interference. In contrast, blood gas analyzers use the Henderson-Hasselbalch equation to calculate bicarbonate, thus, are not vulnerable to the same triglyceride interference. This is especially relevant in pediatrics, as triglyceride levels may not be routinely checked for patients in DKA, so massive elevation may be missed. It is also pertinent for centers where serum bicarbonate levels may be trended to monitor for DKA resolution, instead of blood gases. If the serum bicarbonate level remains low in a patient with DKA and resolving ketosis, a blood gas may be obtained as another way of looking at the acid/base status. If there is a discrepancy between the two measurements, triglycerides should be assessed, as this could change management and prevent complications such as pancreatitis.
Presentation: No date and time listed
ODP138 Age-related Associations of LDL Cholesterol and Atherosclerotic Cardiovascular Disease: A Nationwide Population-based Cohort Study
Authors: Kim Min-Ju , Kim Min-Seon , Min Se Hee , Na Jung Han , Jung Chang Hee , Kim Ye-Jee 
Published: November 2022

Abstract

Background
No completed randomized trial exclusively incorporating the elderly has addressed the benefit of statin treatment for primary prevention until now. Therefore, consensus of major international lipid management guidelines has not been made upon lowering LDL cholesterol (LDL-C)to prevent primary atherosclerotic cardiovascular disease (ASCVD)in the older population. Question: This study aimed to investigate whether ASCVD risk according to increasing LDL-C differs between age groups.

Methods
Data was provided by the Health Screening Cohort of the Korean National Health Insurance Service, which is a nationwide health screening program covering the whole population with alow attrition rate. Subjects with preexisting cardiovascular disease or taking lipid-lowering drugs were excluded. Participants were followed up from January1,2011 to December31, 2015. Multivariable Cox proportional hazard regressions were performed to evaluate the relationship between LDL-C and ASCVD. Subgroup analyses were also conducted in patients with T2DM.

Results
The final cohort was composed of 285,119 participants with a mean age of 58.4 years and 55.2% of men. The average baseline LDL-C level was 121.5 mg/dL (standard deviation, 36.4). The proportion of individuals was 2.4% (n =6,718),9. 0% (n = 25,687), 26.6% (n = 75,981), 37.2% (n = 105,952), 20.2% (n = 57,562), and 4.6% (n = 13,219) in LDL-C ≥190, 160–189, 130–159, 100–129, 70–99, and&lt;70 mg/dL, respectively. Patients with T2DM comprised 7.5% (n = 21,258) of the entire population. During a median follow-up of 6.44 years, the first ASCVD developed in8,996 participants (3.2%). All age groups showed positive associations between LDL-C and ASCVD risk, mostly with statistical significance from LDL-C of 160 mg/dL onward. ASCVD risk did not differ significantly between the age groups (P for interaction =0.62). Compared with ASCVD risk in LDL-C of 70–99 mg/dL, the risk in the highest LDL-C(≥190 mg/dL)was similar between groupsaged&lt;50 and ≥70 years (adjusted hazard ratio [aHR], 1.90 [95%confidence interval (CI),1.52–2.38] and aHR, 1.86 [95% CI, 1.30–2.68], respectively). Subgroup analysis in patients with T2DM showed that 7.2% of subjects experienced incident ASCVD. Age-specific association of ASCVD risk and LDL-C in T2DM patients displayed no difference in line with the total participants(P for interaction = 0.31).

Conclusions
A large-scale, population-based cohort study of adults who had no previous CVD history and were not prescribed lipid-lowering drugs demonstrated that elevated LDL-C was significantly correlated with a greater risk of ASCVD in people aged≥70 years, which was comparable with the risk in younger adults. This finding spotlights the necessity of settling intensive guidance on LDL-C levels for primary CVD prevention in the elderly.
Presentation: No date and time listed
ODP143 Cushing Syndrome - A Potential Risk Factor For Atrial Fibrillation
Authors: Konindala Navya , Park Kyeeun , Enriquez Leidy Plaza , Aung Pyi Phyo 
Published: November 2022

Abstract

Introduction
Cushing syndrome (CS) is a systemic disorder characterized by prolonged exposure to high cortisol hormones. Our study analyses the association of Cushing syndrome as a risk factor for atrial fibrillation (A-fib), its effect on associated complications and mortality.

Methods
We conducted a retrospective analysis of 3 years of the National Inpatient Sample (NIS) data base from 2016 to 2018. Patients with Cushing syndrome, in association with/without A-fib were selected using ICD-10 diagnosis code. Discharge-level weight analysis was used to produce a national estimate. We conducted multivariate regression analysis to calculate odds ratio. RESULTS: During the study period 107,024,275 patient met inclusion criteria. 35,309 patient was diagnosed with CS. Mean age of Cushing patients was 52 and non-Cushing patients was 49. History of hypertension, congestive heart failure (CHF) and obstructive sleep apnea (OSA) were more prevalent in CS population (42. 03% v 29.34%, 20.99% vs 14.18, 17.29% v 5.86). Cushing patients had less prevalence of ischemic heart disease (5.10% v 5.91%). After adjusting with age, hypertension, CHF, ischemic heart disease, race and OSA, CS is related with higher prevalence of A-fib (OR 1.13, 1. 03-1.24, p = 0. 014). However it doesn't increase the complications of A-fib. While 3.70% patients with both CS and A-fib developed ischemic stroke, 3.81% patients without Cushing had the ischemic strokes. No arterial embolic events were detected in CS patients with A-fib, but 0.41% of patients without CS had arterial embolism. Univariate regressions demonstrated no significant association between CS and ischemic stroke associated with A-fib (p = 0.898). Our study also demonstrated that CS is related with high in-hospital mortality. When it was adjusted to age, sex, congestive heart failure, ischemic stroke and chronic kidney disease, CS with concomitant A-fib is associated 1.8 times higher mortality (OR 1.8, 1.27- 2.60, p = 0. 001).

Discussion
Several studies have demonstrated a possible association between serum cortisol level and the risk of A-fib. To our knowledge, this is the first study to demonstrate CS's clinical significance on A-fib. In our analysis, a statistically significant association was found between A-fib and CS with higher in-hospital mortality reported in patients with CS and concomitant A-fib. Patients with CS tend to have higher CHA2DS2-VASc Score but there is no association with higher risk of complications from A-fib. Our study prompts the need for further research to establish CS as an important risk factor for atrial fibrillation.
Presentation: No date and time listed
ODP145 Epigenesis of 11beta-hydroxysteroid dehydrogenase 1 in the adipose tissue of aldosterone-producing adenoma
Authors: Aono Daisuke , Demura Masashi , Karashima Shigehiro , Kometani Mitsuhiro , Konishi Seigo , Sawamura Takashi , Takeda Yoshimichi , Takeda Yoshiyu , Yoneda Takashi 
Published: November 2022

Abstract

Objective
11Beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) is the key enzyme of metabolic syndrome. The transcript-specific epigenetic regulation of 11b-HSD1 (HSD11B1) is reported. We examined the HSD11B1 mRNA level and methylation status of the promoter region of the HSD11B1 in the adipose tissue of patients with aldosterone-producing adenoma (APA).

Methods
We evaluated 10 adipose tissue specimens from patients with primary aldosteronism due to aldosterone-producing adenoma (APA) and 7 tissue specimens from patients with non-functioning adrenal adenoma (NFA). Primary aldosteronism was diagnosed according to the guideline of the Japanese Endocrine Society. The expression levels of HSD11B1 mRNA were quantified using a real time PCR. Isolated DNA was treated with bisulfite and amplified using primers specific for the humanHSD11B1promoter region.

Results
The glycohemoglobin level was significantly higher in patients with APA compared with those with NFA (p&lt;0. 05). Blood pressure was significantly elevated in patients with APA compared with those with NFA (p&lt;0. 01). TheHSD11B1 mRNA level and the enzyme activities were significantly increased in the adipose tissues of APA compared with NFA patients (p&lt;0. 05). The methylation ratio was not significantly different between APA and NFA patients.

Conclusion
These results may suggest that adipose11beta-HSD1 contributes to metabolic abnormalities in APA. The pathophysiological significance of epigenetic control of 11beta-HSD1 gene in the adipose tissue should be further studied.
Presentation: No date and time listed
ODP151 Hypothyroidism and Cardiac Remodeling in Ischemic Strokes
Authors: Rashid Hytham , Brown Jonathan , Pansuriya Tusharkumar , Khalaf Khaled , Raza Syed 
Published: November 2022

Abstract
Hypothyroidism has been shown to increase the risk of developing cardiovascular disease (CVD), yet the mechanism is not well described. Previous studies correlated hyperlipidemia, diastolic hypertension, and smoking with impaired thyroid function, which serve as independent risk factors for CVD. Our study seeks to understand the prevalence of hypothyroidism in ischemic strokes. We hypothesize that hypothyroidism may exacerbate the severity of co-morbidities accelerating cardiac remodeling and risk for ischemic strokes. Our multi-center retrospective study constructed a database of 646 patients who were admitted over a three year period for a primary diagnosis of ischemic stroke. Detailed chart review excluded patients with known risk factors for ischemic strokes including: atrial-fibrillation, atrial-flutter, prior stroke, carotid artery stenosis, thromboembolic disease, and an active cancer diagnosis. Cardiac remodeling was identified by the hallmark finding of left atrial enlargement (LAE) on transthoracic echocardiogram (TTE) with severity determined as a composite measurement of either left atrial diameter (LAD) or left atrial volume index (LAVI). Inclusion criteria were met by 482 patients (75%), where 349 (54%) were female, 435 (67%) were Caucasian, 390 (60%) had hypertension, 360 (56%) had hyperlipidemia, 291 (45%) were previous or current tobacco users, and 199 (31%) had diabetes. Our preliminary analysis found that 83 (13%) of patients had a diagnosis of hypothyroidism. Of note, TTE reports available for 225 (35%) of patients, wherein 74 (33%) of patients met at least one criteria for LAE. Our initial findings support further subgroup analysis to characterize the significance of hypothyroidism as a comorbidity in the development of ischemic strokes. Further research may identify the individual contribution of hypothyroidism to the severity of cardiac remodeling, as well as the impact of treatment for hypothyroidism in stroke risk reduction. Our preliminary analysis found 74 (48%) of patients met at least one criteria for LAE.
Presentation: No date and time listed
LBODP032 Case Report Of A 13 Years Old Female With A Novel Pathogenic Variant In The Hnf1b Gene
Authors: Griffing Emily , Tsai Sarah J L 
Published: November 2022

Abstract

Background
MODY5 results from mutations in the gene encoding hepatocyte nuclear factor 1 homeobox B (HNF1B), a transcription factor critical in development of the pancreas, liver, intestines, and the urogenital tract (1). We report the case of a pediatric patient with a novel frameshift variant (p. Phe309SerfsTer18) in the HNF1B gene accounting for the co-occurrence of diabetes mellitus and structural renal abnormalities. Clinical case: A 13-years-old female with chronic kidney disease stage 3 (eGFR = 48 ml/min/1.73m2) secondary to congenital dysplastic-appearing left kidney and surgical removal of a cystic dysplastic right kidney was referred to our diabetes clinic for hyperglycemia. She reported long-standing polyuria and polydipsia previously attributed to her kidney disease. She required laparoscopic right nephrectomy at age 5 years due to increasing cyst size. Her left kidney also has small renal parenchymal cysts which have been monitored over time. There is no known family history of kidney disease, and grandparents have a history of diabetes. Laboratory investigation revealed a random blood glucose of 478 mg/dL and a hemoglobin A1c of 12.2%. She was not in diabetic ketoacidosis. She had a detectable insulin level of 5.1 mcIU/mL and C-peptide was 3.4 ng/mL. She was initially presumed to have Type 1 diabetes based on a relatively low insulin level and started on basal-bolus insulin (up to 0.59 units/kg of weight/day). Glycosylated hemoglobin was 8.7% one month after diagnosis. Glutamic acid decarboxylase, zinc transporter, islet cell, and insulin autoantibodies were not detected, however, and she was then suspected to have either Type 2 diabetes or MODY. Approximately one year later, she was taken off insulin due to hypoglycemia and managed only with metformin 500 mg twice daily. Next-generation sequencing revealed a de novo pathogenic variant in HNF1B causing a frameshift deletion (p. Phe309SerfsTer18). Genetic testing of parents was negative. Once her diagnosis of MODY5 was made, she was started on glipizide 2.5 mg once daily which has been titrated up to a dose of 5 mg with some success. However, she has since been re-started on insulin (up to 0.2 units/kg/day) due to hyperglycemia keeping in line with the MODY5 phenotype likely causing destruction of beta cells over time (1).

Conclusion
We report a case of MODY5 with a novel frameshift mutation (p. Phe309SerfsTer18) in the HNF1B gene. This case highlights the importance of screening for HNF-1B mutations in those patients with structural renal abnormalities and hyperglycemia, as diagnosis can guide management decisions and provide prognostic information. Reference Bellanné-Chantelot C, Chauveau D, Gautier JF, et al. Clinical spectrum associated with hepatocyte nuclear factor-1beta mutations. Ann Intern Med. 2004;140(7): 510-517. doi: 10.7326/0003-4819-140-7-200404060-0000
Presentation: No date and time listed