bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-901 Primary Amenorrhea, Growth Arrest and Metabolic Syndrome Due to an Unclassified Hepatocellular Adenoma
Authors: Huang Zhimin , Li Yuwen , Chen Wenfang , Deng Wanping , Liao Zhihong , Li Yanbing 
Published: May 2020

Abstract
Primary Amenorrhea, Growth Arrest and Metabolic Syndrome Due to an Unclassfied Hepatocellalar Adenoma.
Background: Hepatocellular adenoma is a rare benign neoplasm, seldom ascribed as the cause of endocrine and metabolic derrangement. We herein report a case of primary amenorrhea, growth arrest and metabolic syndrome due to huge hepatocellular adenoma. En bloc resection of the tumor normalized all the disturbances.
Clinical Case: A 16-year-old girl, who is one of the quintuplets, complained of primary amenorrhea and growth arrest for the past 2 years. Her height (150cm) and weight (40kg) was at the 3rd percentile, whereas waist circumference (75cm) was at the 90th percentile for chronological age. She was hypertensive (145/115mmHg) on admission. Plasma cholesterols (TC 6.3mmol/L, LDL-c 3.76mmol/L), triglyceride (2.66mmol/L) and uric acid (532μmol/L) were elevated. Evaluation of GH/IGF-1 axis showed normal GH (0.90–2.53 μg/L) with extremly low IGF-1 concentration (35.29–39.74 ng/mL), and the latter was unresponsive to hGH stimulation. Computer tomography identified a huge liver mass (18.2cm×13.7cm×21cm). The patient underwent an uneventful open right hepatic lobectomy and cholecystectomy, and the tumor was en bloc resected. Immunohistochemistry indicated an unclassified hepatocellular adenoma, which was confirmed by whole exome sequencing. Her menarche started 6 months later followed by regular cycles without hormone replacement. IGF-1 concentration (471 ng/mL), blood pressure (102/62mmHg), lipid profile (TC 4.2mmol/L, LDL-c 2.51mmol/L, TG 1.44mmol/L) were all nomalized 10 months after surgery, and the girl had a reduction in waist circumference by 5cm, and a small gain in height by 2cm.
Conclusion: We provide evidence that liver-derived IGF-1 has a direct effect on skeletal and pubertal development, blood pressure, viseral adiposity and dyslipidemia. Though rare, we propose the need to look into cases with heptocellular adenoma, for the existence of IGF-1 deficiency and its impact on endocrine and metabolic derangment.
SAT-336 An Unusual Case of Symptomatic Hypercalcemia from Graves’ Disease in a Young Filipino Female
Authors: Dimayuga Diana Colleen Mandocdoc , Villa Michael Lim 
Published: May 2020

Abstract
Hypercalcemia in hyperthyroidism is usually asymptomatic, and related to a concurrent primary hyperparathyroidism. In this report, we describe a case of symptomatic hypercalcemia secondary to Graves’ disease alone. Case Report. A 24-year-old Filipino female presented to the emergency department with generalized weakness, vomiting and abdominal pain. No other symptoms were noted. She was otherwise previously healthy. Family history was unremarkable. During physical exam, she was noted to have a non tender palpable thyroid gland without bruit. Her ECG showed sinus tachycardia. The complete blood count and electrolytes were normal however, ionized calcium was high at 1.6mmol/L (NV 1–1.3). Renal function was normal. Hydration with saline and Furosemide 20mg once daily was started though calcium levels remained elevated. Other causes of hypercalcemia were excluded as PTH was appropriate suppressed (8.8ng/L; NV 14–72), vitamin D was also suppressed (15.29nmol/L; NV &gt;30). CT scan of chest and abdomen and bone scan did not point to any underlying malignancy nor metabolic bone disease. Medication history was also unremarkable. She was hyperthyroid with a suppressed thyroid stimulating hormone level of 0.004pmol/L (NV 0.55–4.78), free T3 of &gt;20pmol/L (NV 2.3–4.2), free T4 of 8.4pmol/L (NV 0.89–1.76). Thyroid receptor antibody levels were raised at 41.07kU/L (NV &lt;1) supporting the diagnosis of Graves’disease. She was started on propylthiouracil 50mg four times daily, along with propranolol 40mg three times daily. She was subsequently seen after two weeks with normal repeat calcium level and thyroid function test. Conclusion. This report aims to highlight that thyroid disease should always be considered as a cause of hypercalcemia. A concomitant primary hyperparathyroidism should also be evaluated. The definitive treatment for the hypercalcemia is correction of thyroid function.
MON-532 Characterization of the Angiogenic Factor SFRP2 in Papillary Thyroid Carcinoma
Authors: Wofford Wyatt O , Mukherjee Rupak , Siegel Julie , Garcia Denise , Hilliard Eleanor , Nasarre Patrick , Klauber-DeMore Nancy , Javid Mahsa 
Published: May 2020

Abstract
Over the last decade, there has been an average annual increase of 3.1% in thyroid cancer diagnosis in the U.S. Papillary thyroid carcinoma (PTC) accounts for 80% of all thyroid cancer diagnoses. However, few molecular markers exist to identify clinically aggressive phenotypes. The angiogenic factor, secreted frizzled-related protein 2 (SFRP2), is associated with a poor prognosis in several malignancies including breast cancer and melanoma. The role of SFRP2 in PTC has yet to be investigated. The aims of this study were to determine the differential expression of SFRP2 in PTC, benign thyroid adenomas, normal thyroid tissue (from patients without cancer), and normal adjacent tissue (NAT) (non-cancerous tissue from patients with PTC) and investigate the role of SFRP2 in tumor development in two PTC cell lines, PTC classical variant (PTC-CV) and PTC follicular variant (PTC-FV), upon treatment with a humanized anti-SFRP2 monoclonal antibody (hSFRP2 mAb). Immunohistochemistry (IHC) was performed using human tissue protein microarrays including 226 PTC, 79 benign adenomas, 112 NAT, and 30 normal thyroid tissue samples. In-vitro proliferation and apoptosis experiments were performed on MDA-T41 (PTC-CV) and MDA-T68 (PTC-FV) cell lines by treating with hSFRP2 mAb, Xolair IgG control, and a vehicle control. SFRP2 expression was significantly higher in PTC compared with benign adenomas and normal thyroid (mean expression scores 9, 6, and 1, respectively; p&lt;0.05). SFRP2 expression was significantly higher in NAT than normal thyroid (mean expression score 4 and 0, respectively, p&lt;0.05). Apoptotic rates were increased by 40% and 62% in the PTC-CV hSFRP2 mAb treatment group compared with the Xolair and vehicle treatment groups, respectively (p&lt;0.05). Apoptotic rates were increased by 126% and 59% in the PTC-FV hSFRP2 mAb treatment group compared with the Xolair and vehicle treatment groups, respectively (p&lt;0.05). Treatment with hSFRP2 mAb had no significant effect on proliferation in either cell line. In conclusion, SFRP2 expression is significantly higher in PTC than in benign adenomas and normal thyroid tissue. SFRP2 expression in NAT is significantly higher than in normal thyroid tissue and not significantly different from benign adenomas. SFRP2 expression in nonmalignant tissue adjacent to PTC could be due to expression in the tumor microenvironment. Treatment with a novel hSFPR2 mAb increases apoptotic rates in two different PTC cell lines. These data suggest that SFPR2 is involved in tumorigenesis of PTC.
MON-397 Potential Relationship Between Hypothyroidism and Bone Loss at Dental Implants
Authors: Yerke Lisa Marie , Cohen Robert E 
Published: May 2020

Abstract
Introduction: Hypothyroidism (HT) is an endocrine condition with autoimmune and inflammatory etiologies. Studies have shown that both periodontal disease and peri-implant bone loss are bidirectionally influenced by systemic inflammatory conditions, such as diabetes, adverse pregnancy outcomes, cardiovascular disease, and osteoporosis.1 There also is evidence that HT is associated with decreased bone metabolism, depressed bone turnover, and a prolonged bone remodeling cycle.2 Consequently, the objective of this study was to determine if the severity of bone loss around dental implants is related to the presence of HT.
Methods: Following IRB approval, medical, dental, and radiographic records of patients who received dental implant placement at a university-based postgraduate program in periodontics from 2000–2017 were reviewed (1480 implants; 635 patients). Rate of bone loss in mm/year was calculated from surgical implant placement and subsequent re-evaluation radiographs, with correction for radiographic distortion. Presence of HT was confirmed by review of patient medical records, clinical diagnosis of HT, and history of thyroid hormone supplementation. Populations were adjusted for smoking, diabetes, use of systemic steroids, presence of autoimmune disease (other than HT), and systemic inflammatory conditions. Calculations were performed using IBM SPSS Statistics v25.
Results: Patients with HT had a decreased rate of crestal alveolar bone loss around dental implants. Specifically, patients with HT experienced peri-implant bone loss at a rate of 0.42 mm/year, while bone loss from patients without HT was 1.34 mm/year (68.7% decrease; mean difference = 0.92 mm/year, 95% confidence interval = 0.39–1.50 mm/year, P&lt;0.002). There were no significant differences in patient oral hygiene, or in implant service time, among any of the groups studied (P&gt;0.05).
Conclusions: The results suggest that the rate of marginal alveolar bone loss at dental implants is significantly decreased in patients with HT, and occurs independently of any of the systemic conditions noted above. The findings imply that potential changes in bone metabolism and remodeling associated with HT might result in less peri-implant alveolar bone loss following implant placement surgery. As a result, there does not appear to be an increased risk of peri-implant crestal bone loss in patients with HT.
References: 1Kim J., Amar S., Odontol. 94(1):10–21, 2006. 2Tuchendler D., and Bolanowski M.,Thyroid Res. 7:12, 2014.
SUN-183 Adrenalitis Induced by Nivolumab
Authors: Khan Muhammad Atique Alam , Iqbal Iqra , Dhillon Puneet , Ullah Waqas 
Published: May 2020

Abstract
Introduction: Tumor cells often express a programmed death-ligand 1 (PD-L1), which binds to the programmed death receptor-1 (PD-1) on activated T-cells to induce immune tolerance. Among the class of immune checkpoint inhibitors (ICI), Nivolumab is an anti-PD-1 antibody which blocks these tumor cell interactions. Although some endocrinopathies have been reported for other PD-1 inhibitors, the adverse event of adrenalitis with nivolumab has not been reported before. Clinical Case: A 65-year-old female presented to the hospital with complaints of nausea, vomiting, fatigue, and headache for five days. She was recently diagnosed with metastatic lung adenocarcinoma, complicated by cerebellar metastases, and the left cerebellar mass was resected. She was also started on Nivolumab. Her blood pressure was 98/65 mmHg on the presentation. Serum sodium was 122mEq/L (normal 135–145) and potassium was 5mEq/L (3.5–5). TSH, LH, and prolactin were all normal. Aldosterone was low: 23pmol/L (27.7–582.5) and renin was high: 11 ng/ml/h (0.167- 1.38). Morning cortisol levels were low: 2.2 ug/dl (5- 25) and concomitant ACTH was high: 78 pg/ml (7.2- 63.3). Upon standard high dose cosyntropin stimulation test, basal cortisol was 2.0 ug/dl (5- 25). Cortisol level 30 minutes post cosyntropin was 7.1 ug/dl, while Cortisol 60 minutes post cosyntropin was 12.2 ug/dl (normal &gt;18 -20 ug/dl). Considering the low cortisol levels with high ACTH, and an inadequate rise in cortisol after the ACTH stimulation test, adrenal insufficiency was suspected as a result of adrenalitis due to Nivolumab. Hyponatremia along with low aldosterone and high renin levels also reinforced this clinical diagnosis. A computerized tomographic scan of the chest abdomen and pelvis only showed calcified uterine fibroids. She was initially resuscitated with intravenous fluids. Hydrocortisone 100 mg every 8 hours was started and then gradually tapered down to 60mg every 12 hours. Fludrocortisone was also initiated at 0.2mg daily. Symptoms began to improve, and sodium levels normalized to136 mEq/dl. She was discharged on 30mg of hydrocortisone and 0.1 mg of fludrocortisone daily and is stable since then. Conclusion: This is a rare case of Nivolumab-induced adrenalitis. It highlights the importance of checking for adrenal insufficiency in a patient who presents with symptoms of hypotension and hyponatremia while being on ICI drugs, as unidentified adrenal insufficiency and adrenal crisis can be fatal.
MON-599 Post-Bariatric Hypoglycemia: A Clinical Vignette on an Increasingly Recognized Disease
Authors: Farahmand Abtin Kevin , Lawler Helen 
Published: May 2020

Abstract
Introduction: Previously referred to as late dumping syndrome, post-bariatric hypoglycemia (PBH) is thought to represent at least 1% of all hospitalizations for hypoglycemia and 10% of all clinically recognized hypoglycemia cases. However, through the advent of CGM and more strict criteria over the last decade these numbers are likely an underestimate. As obesity continues to remain prevalent and with rising bariatric centers to help deal with this epidemic, endocrinologists will play an increasing role in managing PBH patients.
Clinical Case: A 39-year female with a PMH of hypothyroidism and bariatric surgery (BS) in 2009 presented to our ER for a seizure. She has been having seizures nearly every 2 weeks for one year. Neurology started her on Keppra; however, no etiology was identified. EMS had documented a blood glucose of 40 mg/dL; the patient was given an amp of D50 with resolution of neuroglycopenic symptoms. TSH and cortisol levels were within normal range. A sulfonylurea panel in the ED was negative. The patient states the symptoms can occur while fasting but also mainly post-prandial. A 72-hr fast was conducted with the patient nadir POC glucose of 77. Subsequently, the patient had a mixed meal tolerance performed and after 2 hours had a seizure and was found to have a BG of 50 mg/dL with an insulin level of 49 uIU/mL and a c-peptide of 18.8 ng/mL. The patient was diagnosed with PBH, and was discharged with a CGM, started on acarbose and was seen by nutrition to discuss dietary modifications. She is now seen in our clinic with control of her symptoms with the addition of diazoxide.
Conclusion: Altered anatomy after bariatric surgery, particularly after gastric bypass and sleeve gastrectomy is thought to play a major role in developing PBH. By bypassing normal anatomy, gastric emptying is increased 2–3 x, which leads to a higher and more rapid appearance of glucose in the distal foregut. This subsequently leads to an amplified incretin response leading to a hyperinsulinemic response in patients who have had bariatric surgery; however, for unclear reasons some patients develop an even more amplified hyperinsulinemic response that leads to subsequent hypoglycemia. History of neuroglycopenic symptoms 1–3 hours after eating in a patient who had a gastric bypass &gt; 6–12 months and with relief of symptoms with carbohydrates should raise an endocrinologist’s suspicion of PBH. Fasting hypoglycemia is an atypical feature that should raise one’s suspicion of a broader differential. Altered nutrition habits is the cornerstone of therapy with which the primary aim is to reduce post-prandial glucose spikes in these patients after they eat carbohydrates. These spikes in turn lead to hyperinsulinism leading to subsequent hypoglycemia. Primary diet modifications include controlled carbohydrate consumption of less than 30g per meal, avoiding high glycemic carbs, and always taking in ample fat and proteins with every meal.
SUN-940 Carney Complex: A Case of a Rare Multiple Endocrine Neoplasia Misdiagnosed as Peutz-Jeghers Syndrome
Authors: Vaid Sonal , Hasnain Fawaz , Morgan Rachel 
Published: May 2020

Abstract
Carney Complex (CNC) is an extremely rare multiple endocrine neoplasia caused by germline inactivating mutation in protein kinase A type I-alpha regulatory subunit (PRKAR1A gene). Mode of inheritance is mostly autosomal dominant; 25% of cases are due to de novo mutations. Only 750 world-wide cases have been reported. Most patients are diagnosed in the second or third decade. Clinical features include cutaneous myxomas, angiomyxoid nodules, lentiginous skin pigmentation, cardiac myxomas, and benign and rare malignant endocrine tumors. These endocrine tumors include and are not limited to prolactinomas, thyroid tumors, primary pigmented nodular adrenocortical disease (PPNAD), and large cell-calcifying Sertoli cell tumors (LCCSCT). Diagnosis is often challenging as disease manifestations can occur sporadically over a large span of time, and patients may present with various conditions such as Cushing syndrome, like our case. We present a case that demonstrates the importance of early recognition of this rare disorder.
A 28-year-old Caucasian male with PMH of HFrEF, HTN, Sertoli cell tumor status post orchiectomy, vertebral fractures, and surgical removal of lip angiomyxoma presented to clinic for hypogonadism. Physical examination revealed marked Cushingoid features and facial lentigines above his eyes and on his lips. His eclectic medical history and unique exam findings lead to finding of a unifying diagnosis. His labs revealed severe Cushing syndrome, and computed tomography (CT) of his abdomen was performed due to ACTH independent hypercortisolism, demonstrating a bilateral lobular appearance of the adrenal glands.
Combination of labs and physical exam findings of lentigines, skin myxomas, cushingoid features, rare angiomyxoma, LCCSCT and hypercortisolism lead to diagnosis of Carney Complex. He was misdiagnosed with Peutz-Jeghers in his adolescence due to LCCSCT and mucosal lentigines; therefore, hormonal screening was not routinely performed. Untreated Cushings led to severe osteoporosis with vertebral fractures and heart failure. Treatment included bilateral adrenalectomy. Pathology report confirmed rare PPNAD. PPNAD and LCCSCT are extremely rare tumors almost exclusively linked to Carney Complex. Interestingly, family history did not reveal endocrine disorders, cancers, or severe illnesses. Genetic testing returned positive for the PRKAR1A gene mutation. Given the consequences of untreated hormonal aberrations seen in this disorder, an early and accurate diagnosis is imperative.
SUN-083 Screening of Vitamin D and Calcium Concentrations in Neonates of Mothers at High Risk of Vitamin D Deficiency
Authors: Kozgar Sheikh Arif Maqbool , Chay Paul , Munns Craig Frank 
Published: May 2020

Abstract
Objective: The aim of this study was to determine, retrospectively, the serum 25OHD and calcium concentrations of screened neonates of mothers at high risk of 25OHD deficiency (maternal 25OHD &lt; 25 nmol/L or unknown vitamin D concentrations and risk factors for vitamin D deficiency) and critically analyse whether their measurements contributes to the management of these neonates.
Methods: Serum 25OHD and calcium concentrations from 600 samples of umbilical cord blood or venous blood collected from neonates over a 12-month period were analysed. 25OHD concentrations were reported for all while both the corrected calcium concentrations and vitamin D concentrations were available for 569 samples.
Results: There was little or no evidence of association between neonatal 25OHD concentrations and gender, gestational age or birth weight. There was a high prevalence of vitamin D insufficiency (27.6%, 30–50 nmol/L) and deficiency (21.3%, &lt; 30 nmol/L) in neonates from high-risk maternal groups. There was a statistically positive but weak correlation (ρ = 0.22, P &lt; 0.0001) between serum calcium and 25OHD concentrations. Only 7 neonates out of 569 (1.2%) had calcium levels in the hypocalcaemic range; however, a significant number (47.6%) were reported to be in the hypercalcaemic range. Nearly all of these were venous samples collected in first 24 hours after birth. We calculated the reference interval for corrected calcium from our data of venous samples in first 24 hours and the upper limit was significantly higher (2.38–3.04 mmol/L) than the standard reference range used.
Conclusion: Vitamin D deficiency is prevalent in neonates of high-risk mothers but the risk of hypocalcaemia due to vitamin D deficiency at birth is low. Screening neonates entails blood testing which can cause distress to neonates and their parents, substantial impost on staff and financial burden on the health care system. 25OHD deficiency is corrected relatively easily in neonates with supplementation and vitamin D supplementation of neonates from birth without routine screening appears to offer better value of care. Also, the data from this study suggest that the paediatric reference range for corrected calcium concentrations in neonates is higher and the paediatric reference range should be reconsidered.
SUN-161 Primary Aldosteronism and Klinefelter’s Syndrome: Two Cases
Authors: Seki Yasufumi , Morimoto Satoshi , Yoshida Naohiro , Bokuda Kanako , Sasaki Nobukazu , Yatabe Midori Sasaki , Yatabe Junichi , Watanabe Daisuke , Morita Satoru , Keisuke Hata , Yamamoto Tomoko , Nagashima Yoji , Ichihara Atsuhiro 
Published: May 2020

Abstract
Background: Primary aldosteronism (PA) is more common than expected. Aberrant adrenal expression of LH receptor in patients with PA has been reported, however, its physiological role on the development of PA is still unknown. Herein, we report two unique cases of PA in patients with untreated Klinefelter’s syndrome, characterized as increased serum LH, suggesting a possible contribution of the syndrome to PA development. Clinical Cases: Case 1 was a 39-year-old man with obesity and hypertension since his 20s. His plasma aldosterone concentration (PAC) and renin activity (PRA) were 220 pg/mL and 0.4 ng/mL/h, respectively. He was diagnosed as having bilateral PA by confirmatory tests and adrenal venous sampling (AVS). Klinefelter’s syndrome was suspected as he showed gynecomastia and small testes, and it was confirmed on the basis of a low serum total testosterone level (57.3 ng/dL), high serum LH level (50.9 mIU/mL), and chromosome analysis. Case 2 was a 28-year-old man who had untreated Klinefelter’s syndrome diagnosed in his childhood and a two-year history of hypertension and hypokalemia. PAC and PRA were 247 pg/mL and 0.3 ng/mL/h, respectively. He was diagnosed as having a 10 mm-sized aldosterone-producing adenoma (APA) by AVS. In the APA, immunohistochemical analysis showed co-expression of LH receptor and CYP11B2. Conclusion: Our cases of untreated Klinefelter’s syndrome complicated with PA suggest that increased serum LH levels and adipose tissues, caused by primary hypogonadism, could contribute to PA development. The possible complication of PA in hypertensive patients with Klinefelter’s syndrome should be carefully considered.