bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT-359 Hypercalcemia - Is This Sarcoidosis, Hyperparathyroidism, or Both?
Authors: Veeramachaneni Ravali , Sandhu Harjyot , Gilden Janice L 
Published: May 2020

Abstract
Hypercalcemia (HC) is a common clinical problem. Among all causes of HC, primary hyperparathyroidism (HPT) and malignancy are the most common, accounting for &gt;90 % of cases. We present a case of HC in a patient attributed to long-standing history of Sarcoidosis (SC) and later found to also have HPT with Parathyroid Adenoma (PA) and Vitamin D Deficiency.
A 64-year-old female presented to the emergency room for social needs. She had not received medical care for the past 10 years and had known history of SC, previously treated with prednisone and methotrexate. She also noted a long-standing history of elevated calcium (Ca) up to 11 mg/dL. She was fasting for the past 1 month for spiritual reasons and was not taking any medications or supplements. Initial labs were significant for Ca of 13.2 mg/dL, Albumin 4.4 g/dL, ionized Ca 1.43 mmol/L. Creatinine was 1.1. EKG revealed T-wave inversions in V1, 2, 3. She received IV fluids and Ca improved to 11 mg/dL. HC was attributed to known history of SC. However further evaluation revealed parathyroid hormone (PTH) level high at 156 pg/mL, 25-OH Vit D level low at 8.5 ng/mL with normal 1,25 hydroxy Vit D levels at 46 pg/mL. Parathyroid sestamibi scan revealed a left parathyroid adenoma. Surgery was deferred because patient was asymptomatic and did not meet criteria for parathyroidectomy. On discharge, Ca levels remained stable and she was started on Ergocalciferol 50,000 units weekly.
HC can be either parathyroid mediated, non-parathyroid mediated, or due to medications. In primary HPT, the elevated PTH levels cause increased bone resorption through activated osteoclasts and increased intestinal Ca absorption. Malignancies involving solid tumors and leukemias can lead to HC through osteolysis and osteoclasts or PTH-related peptide. Thiazide diuretics increase renal Ca absorption that lead to mild HC which can be reversed when the medication is discontinued. Other endocrine disorders that can lead to HC include thyrotoxicosis-induced bone resorption, adrenal insufficiency and pheochromocytoma.
Management of hypercalcemia depends upon the level of Ca. Mild HC (Ca &lt; 12mg/dL) is usually asymptomatic and improves with hydration. Asymptomatic or mildly symptomatic patients with chronic moderate HC (Ca 12-14 mg/dL) may not require immediate treatment. Severe HC (Ca &gt;14mg/dL) is treated with IV hydration with normal saline (NS), calcitonin and zolendronic acid. Administration of calcitonin and NS results in substantial reduction in Ca within 12-48 hours.
Although, HC was initially attributed to SC, primary HPT and low 25-OH Vit D levels also contributed to HC in this patient. Thus, it is important to evaluate patients with known HC from sarcoid for other etiologies.
MON-478 Impaired Sensitivity to Thyroid Hormone - A Diagnostic and Therapeutic Challenge
Authors: Pedro Jorge , Gorito Vanessa , Ferreras Cristina , Maria Ferreira João Silva , Ferreira Sofia , Costa Carla , Silva Rita Santos , Correia Cíntia Castro , Fontoura Manuel 
Published: May 2020

Abstract
Background: Impaired sensitivity to thyroid hormone refers to any process that negatively affects its action, including defects in its transport, metabolism and action on the receptor. Resistance to thyroid hormone due to beta-receptor mutations (RTH-beta) is the most common form of this entity and is characterized by reduced response of peripheral tissues to the action of thyroid hormone. The genetic variability of cofactors involved in the action of thyroid hormone explains the heterogeneity of resistance among affected individuals. Generally, patients with this disorder, have increased levels of free T4 and free T3 in association with normal or high TSH. Clinical case: 11-year-old boy, with personal history of Attention-deficit/hyperactivity disorder (ADHD). A pediatric endocrinology consultation was requested to evaluate abnormalities in his thyroid function tests. A few months earlier, his father was referred to endocrinology consultation because of thyroid function tests abnormalities: TSH - 3.01 μIU / mL (N: 0.35 - 4.94); Free T4 1.7 ng / dL (N: 0.7-1.48); Free T3 4.77 pg / mL (N: 1.71-3.71). Initially, two diagnostic hypotheses were considered: central hyperthyroidism or impaired sensitivity to thyroid hormone. The adult underwent pituitary magnetic resonance, which raised the hypothesis of a pituitary microadenoma, and TRH stimulation test, whose result was strongly suggestive of the second diagnostic possibility. A genetic study was requested and the presence of the c700 G&gt; A variant (p. Ala 324 trh) in the THRB gene was identified, which confirmed the most likely hypothesis. At the time of the pediatric endocrinology consultation, the 11-year-old boy had the results of his lab tests: TSH - 6.67 μIU / mL (N: 0.35 - 5); T4L 2.27 ng / dL (N: 0.88-1.58); T3L 7.79 pg / mL (N: 2-4.20). Given his perfect height and weight evolution and the absence of symptoms suggestive of hypo or hyperthyroidism, it was decided not to start any medication, keeping only periodic surveillance. Conclusion: This case exemplifies unusual thyroid function tests. This discordance between serum thyroid hormone and TSH concentrations should raise the possibility of impaired sensitivity to thyroid hormone. In this condition, patients may present with symptoms of hypo or hyperthyroidism and the etiology of thyroid function tests abnormalities are not easily recognized. This can lead to misdiagnosis and consequently unnecessary treatment.
SUN-575 Levels of Nesfatin-1 in Adolescents, and Its Association with Body Mass Index and Risk of Cardiovascular Disease
Authors: Gutierrez Karla Paola , Kornhauser Carlos , Gómez Armando , Luevano-Contreras Claudia , Fafutis-Morris Mary , Gugliucci Alejandro , Garay-Sevilla Ma Eugenia 
Published: May 2020

Abstract
Nesfastin-1 is a recently discovered anorexigenic neuropeptide, which seems to follow the signaling pathway of melanocortin, and is involved in cardiovascular regulation (1). It is expressed in several tissues, including pancreatic islet cells, the central nervous system, In subcutaneous and visceral fat tissue, among others (2). There are few and controversial data that assess the levels of nesfatin-1 and its relationship with the cardiovascular disease. The aim of this study was to evaluate the serum levels of nesfatin-1 in adolescents with different metabolic status and BMI and its association with cardiovascular risk factors (glucose, lipid profile).
Material and methods: This cross-sectional study included adolescents between 15 and 19 years old, classified in 3 groups according to BMI and HOMA-IR: adolescents with normal weight without metabolic alterations (n ​​= 30), metabolically healthy obese (MHO) n = 30 and metabolically unhealthy obese adolescents (MUO) n = 42. Anthropometric measurements were performed, a fasting blood sample was taken to quantify glucose, lipid profile and creatinine. Insulin and nesfatin-1 concentrations were measured by ELISA. Statistical tests employed were Kruskal Wallis, Spearman correlation.
Results: the group of adolescents MUO had higher levels of total-C (p&lt;0.0002); triglycerides (p&lt;0.00001) compared to the control and MHO; higher levels of nesfatin-1 (p=0.0002) and lower levels of HDL-C (p&lt;0.002) compared to the control group. A positive correlation was between nesfatin-1 and BMI (p&lt;0.001), triglycerides (p&lt;0.027), and HOMA-IR (p&lt;0.025) and negative correlation with HDL-C (p&lt;0.026)
Conclusion: Our results show that metabolically unhealthy obese adolescents have higher concentrations of nesfatin-1, showing an association with traditional cardiovascular risk factors, which could lead to the development of cardiovascular disease.
Nothing to disclose GK, KC, GOA, LCC, FMM, GA, GSME
Sources of research support: Grant University of Guanajuato (DAIP 302/2018)
References: (1) Oh-I et al., Nature. 2006; 443:709–712. (2) Stengel A et al., Regulatory Peptides. 2010; 163:18–23
SAT-276 Co-Secreting TSH and Growth Hormone Pituitary Adenoma
Authors: Eid Hatem 
Published: May 2020

Abstract
Introduction: Secreting pituitary adenoma is exceedingly rare. Less than 15 cases having been reported. Its clinical presentation and diagnosis is challenging. We report a case of pituitary macroadenoma, with features of acromegaly and hyperthyroidism. Case report: A 75 years’ old man presented with new onset atrial fibrillation. He had high FT4 with normal TSH. His ultrasound scan of the neck showed a solitary nodule. He had ablation twice and was started on bisoprolol and anticoagulant. He had MRI scan for headaches and this showed a pituitary macroadenoma. He had high IGF-1. His oral glucose tolerance showed failure of GH suppression. His FT4 was persistently high with normal TSH and he had high a subunits. This suggested the diagnosis of TSH and GH secreting pituitary adenoma. Discussion: TSH-secreting pituitary adenomas are rare and not uncommonly, they co-secrete other pituitary hormones including growth hormones. Somatotrophs and lactotrops share common transcription factors with thyrotrophs. TSH-secreting adenomas are benign but 60% of them are locally invasive. TSH-secreting pituitary adenomas typically present with either symptoms of tumor growth like headache or visual field disturbance or symptoms of hyperthyroidism. Thyroid nodules are common in patients with TSHomas. In patients with TSH-secreting pituitary adenomas, majority will need only surgery and radiation. The medical treatment used to normalize TSH and FT4 levels is somatostatin analogs. This is effective in about 90% of patients with TSH secreting pituitary adenomas TSHoma should be differentiated from resistance to thyroid (RTH). The main difference between TSHoma and RTH is the presence of signs and symptoms of hyperthyroidism in patients with TSHoma, absence of a family history, normal thyroid hormone levels in family members, and the presence of an elevated glycoprotein α-subunit in patients with pituitary tumor. Reference: H Adams and D Adams. A case of a co-secreting TSH and growth hormone pituitary adenoma presenting with a thyroid nodule. EDM case reports 2018 Hatem.eid1@nhs.net
MON-680 Might Podocyturia Be an Early Marker for Diabetic Nephropathy in Males
Authors: Durcan Emre , Korkmaz Ozge Polat , Murt Ahmet , Saygi Halil Ibrahim , Sahin Serdar , Dincer Tamer , Ozkan Serbay , Bakir Alev , Ozkaya Hande Mefkure , Trabulus Sinan , Meydanli Emine Elif Guzel , Seyahi Nurhan , Gonen Mustafa Sait 
Published: May 2020

Abstract
Renal involvement can develop before detection of microalbuminuria in type 2 diabetes. There is an interest in finding biomarkers to detect diabetic nephropathy (DN) earlier and identify progression risk. Podocyturia emerge as a marker for early kidney damage however standardization problems hamper its widespread use. We aimed to investigate the value of podocyturia for the detection of early DN. Herein we report our preliminary results.
Our study population was composed of three type 2 diabetic patient groups and a healthy control group. Diabetic groups were defined as follows; group 1: patients without microalbuminuria who had HbA1c &lt;7%; group 2: patients without microalbuminuria who had HbA1c&gt; 8.5%; group 3: patients with diabetic retinopathy who had proteinuria &gt;1g/day and/or microalbuminuria &gt;300 mg/day and group 4: healthy volunteers without any known disease. Patients with glomerular filtration rate (GFR) below 30 ml/min were excluded.
GFR was calculated using the abbreviated MDRD formula. Microalbuminuria was measured in 24 hour urine. Number of podocytes in the urine was determined by immunocytochemical staining of podocalyxin. Due to the known expression of podocalyxin in the female genital tract, only males were included. Statistical analyses were carried out using Statistical Package for the Social Sciences version (SPSS) 24.0 and statistical significance was set as p&lt;0.05.
We examined a total of 119 patients (mean age 57.35 ± 12.75 yrs.). Patient distribution in each group was as follows; group 1: 24(20%); group 2: 26(22%); group 3: 24(20%) and group 4: 45(38%) patients. There was no significant difference in mean age (p=0.582) and duration of diabetes (p=0.517) between the diabetic groups. The mean GFR was significantly lower in group 3 than in group 1 and 2 (p&lt;0.001, p:0.007; respectively). The median podocyte measurement in urine was 0,25 (IQR: 0- 2.68) podx/ml in group 1; 0,37 (IQR: 0-2.12) podx/ml in group 2; 1,37 (IQR: 0.56-5.18) podx/ml in group 3; 0.0 (IQR: 0-0.75) podx/ml in group 4. The mean number of podocytes in urine was significantly different between the 4 groups (p=0.001). In posthoc analysis with Bonferoni correction, the mean podocytes measurement was significantly higher in group 3 than in group 1 and 4 (p=0.033, p=0.001; respectively).
According to our preliminary results; podocyturia assessed by podocalyxin immunostaining does not seem to be increased in male diabetic patients without proteinuria. Further studies on larger patient groups and using different podocyte markers might clarify the value of podocyturia as an early marker of DN.
SAT-346 Hypercalcemia Secondary to Calcitriol and PTHrP Cosecretion Only Responsive to Hydroxychloroquine
Authors: Panvelker Samir S , Khan Amna Nabeel 
Published: May 2020

Abstract
Background: Hypercalcemia of malignancy mediated by concurrent elevations in both 1,25-dihydroxyvitamin D (calcitriol) and parathyroid hormone (PTH)-related protein (PTHrP) is a rare phenomenon previously only reported with solid tumors. The preferred treatment for calcitriol-mediated hypercalcemia is glucocorticoid therapy and second-line therapy is traditionally ketoconazole. Hydroxychloroquine has previously been reported as efficacious only in cases of calcitriol excess related to sarcoidosis.
Clinical case: A sixty-two year-old female with a history of diffuse large B cell lymphoma, complicated by disease progression despite multiple treatment regimens over the preceding five years, developed acute hypercalcemia to a corrected value of 14.7 mg/dL (8.9-10.3). Work-up revealed a suppressed PTH, PTHrP &lt;2.0 pmol/L (0.0-3.4), and calcitriol elevation of 136.0 pg/mL (19.9-79.3). She was treated with zolendronate with rapid normalization of calcium levels. Upon recurrence of hypercalcemia six months later, repeat calcitriol was 176.0 pg/mL with a new PTHrP elevation of 7.0 pmol/L. Repeat dosing of zolendronate was less efficacious. She was prescribed prednisone 60 mg daily with subsequent addition of denosumab 120 mg weekly with continued hypercalcemia. Given rising levels of calcitriol and PTHrP (up to 285.6 pg/mL and 43.5 pmol/L, respectively) and potential drug interactions between ketoconazole and her chemotherapy, she was started on hydroxychloroquine 400 mg daily. Her calcium normalized and calcitriol dropped to 61.1 pg/mL despite imaging evidence of continued lymphoma progression. Three weeks later, she developed septic shock and was transitioned to hospice.
Conclusion: In reviewing the literature, this appears to be the first reported case of a hematologic malignancy with pathologic levels of both calcitriol and PTHrP. It is also the first reported efficacy of hydroxychloroquine in malignant hypercalcemia. Interestingly, PTHrP secretion occurred months after the initial development of hypercalcemia. Control of both calcitriol and calcium levels did not occur until initiation of hydroxychloroquine despite preceding use of high-dose glucocorticoids and anti-resorptive therapy. Our case suggests that hydroxychloroquine should be considered in cases of calcitriol-mediated hypercalcemia resistant to glucocorticoids, particularly as it has less drug interactions and a more favorable side effect profile when compared to ketoconazole.
SAT-233 Primary Adrenal Diffuse Large B-Cell Lymphoma in HIV Patient: A Rare Case Report
Authors: Ibrahim Safa , Thibodeaux Rachel , Mathew Mini 
Published: May 2020

Abstract
Introduction: Primary adrenal lymphoma is remarkably rare type of extra-nodal lymphomas, accounting for &lt;1% of non-Hodgkin lymphomas. For unclear reasons, HIV population appear to have an increased risk of developing non-Hodgkin lymphoma. We are presenting a rare case of bilateral primary adrenal non-Hodgkin lymphoma in HIV patient.
Case Presentation: A 65-year-old man with history of HIV, presents with nausea and generalized weakness for the past month. Other symptoms include, fever and unintentional weight loss of 10 kg also reported.
On admission, patient was found to have low sodium value of 124 mmol/L. He was worked up for hyponatremia; Labs were suggestive of primary adrenal insufficiency. Other endocrinology labs including; TSH, metanephrines, renin, and aldosterone were within normal values.
CT of the abdomen showed bilateral adrenal masses. The right lesion measured 10.6 cm. The left lesion measured 10.1 cm. Fungal work up was negative. Epstein Barr virus (EBV) panel was suggestive of convalescent versus reactivated disease.
CT guided biopsy of the adrenal mass confirmed Diffuse Large B-cell Lymphoma, activated B Cell Phenotype. Bone marrow biopsy showed no evidence of lymphoma.
Following oncology recommendations, patient was started on R-CHOP therapy. Currently, patient received two cycles of chemotherapy which he is tolerating well.
Discussion: Primary adrenal lymphoma is a rare type of non-Hodgkin lymphomas (NHL). Diffuse large B cell lymphoma (DLBCL) is the most common histologic subtype of NHL that present in the adrenal glands. Approximately one hundred cases reported of primary adrenal DLBCL in the literature with only two previously reported cases in HIV patients. It is considered an AIDS defining malignancy. HIV population are at higher risk of developing NHL than general population. The pathogenesis of the development of NHL in adrenal glands, which lack lymphoid tissue, particularly in HIV patients is yet to be determined, but impaired cellular immunity and chronic B cell stimulation and T cell immunodeficiency leading to loss of control of transforming viruses, particularly EBV are thought to play essential roles.
Because of the rarity of this tumor, diagnosis can be challenging. As exemplified in our patient, most cases have nonspecific presentation, including; fever, weight loss, night sweats, nausea, vomiting, adrenal insufficiency, and hyprecalcemia.
The recommended treatment for primary adrenal DLBCL is chemotherapy, with R-CHOP being the typical treatment. This disease appears to have a poor prognosis, and the median survival is approximately 1 year. Young age, good performance status, and early diagnosis and treatment can improve the outcome.
Conclusion: Primary adrenal DLBCL are rare tumors that has been associated in the literature with impaired cellular immunity. Our patient is the third case reported of primary adrenal DLBCL in HIV positive patient.
MON-669 Diabetic Macular Edema Thickness in Asians and Caucasians: Is There a Difference?
Authors: Leung Brian , Wu Gloria , Luu Shannon , Momen Donia , Lau Chap-Kay K 
Published: May 2020

Abstract
Background: Diabetic macular edema (DME) is a manifestation of diabetic retinopathy (DR) which can result in vision loss. DME affects over 750,000 US adults over the age of 40, costing 33% more in Medicare dollars than those patients without DME. Ethnicity plays a role in the development of DR but there are no studies about DME and HbA1c in Asians versus Caucasians. As Asians are the fastest growing ethnic group in the US and are at an increased risk of developing Type 2 Diabetes Mellitus (T2DM), there is a need for more knowledge about DME compared to Caucasians.
Purpose: Evaluation of diabetic macular edema thickness between Asian and Caucasian Diabetic patients.
Methods: A retrospective chart review (2017-2019) of consecutive diabetic patients were performed at California Retina Clinic. Inclusion criteria: DME thickness was measured by Optical Coherence Tomography (OCT) (Heidelberg Spectralis, Heidelberg, Germany), OCT +/- 3 months of their HbA1c lab test, control (C) non-diabetic patients=HbA1c &lt;6.0%; For T2DM patients diagnosed by primary care physician: HbA1c ≥6.0%. Exclusion criteria: Age under 18 or over 90 years. Data analysis: R Project version 3.6.1 (R Foundation for Statistical Computing, Vienna, Austria). Two-way ANOVA was used to determine the difference between the four groups. The post-hoc test, Tukey’s HSD was used for p-values (&lt;0.05).
Results: Of 500 consecutive patients: 80 patients met inclusion criteria: T2DM Asian (ADM), T2DM Caucasian (CDM), C Asian (CA), C Caucasian (CC). n=80 pts, avg age=59.187 years (sd=15.42, range 23-89 years), Female=44, Male=36;
ADM: n=20, avg age=60.90 years (sd=11.22, range 37-79 years), Female=10,Male=10, HbA1c range = 6.7-11.9%, Avg HbA1c = 7.59%, Avg DME=276.28 um (sd=25.93 um, range = 238.5-342 um);
CDM: n=20, avg age=68.05 years (sd=10.54, range 46-87 years), Female=9, Male=11, HbA1c range = 6.0-11.5%, Avg HbA1c = 7.52%, Avg DME=298.68 um (sd=33.84 um, range = 253.5-397.5 um); HbA1c in ADM v CDM: p=0.8(ns)
CA: n=20, avg age=52.85 years (sd=16.81 years, range 34-84 years), Female=10, Male=10, HbA1c range = 4.8-5.5%; Avg DME=267.05 um (sd=21.09 um, range = 230-310 um).
CC: n=20, avg age=62.95 years (sd=13.47 years, range 40-89 years), Female=14, Male=6, HbA1c range = 4.8-5.6%, Avg DME=285.68 um (sd=16.58 um, range = 248.5-312.0 um).
ADM v CDM and DME [F(1, 76)=13.267, p = 0.00049]. Tukey’s HSD post hoc tests were carried out. CDM v ADM had a significantly higher avg DME: 22.4 um (p=0.031). Body Mass Index (BMI): ADM patients (avg= 25.6) compared to CDM patients (28.5):(p=0.05, t-test).
Conclusion: In this small study, T2DM Asians had less macular edema thickness than T2DM Caucasians with similar HbA1c. T2DM Asian patients had lower Body Mass Index than T2DM Caucasians. Body Mass Index may be an additional factor to consider in the evaluation of diabetic macular edema in Asians and Caucasian Diabetic patients.