bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-031 Megestrol Acetate for Bodybuilding Resulting in Abrupt Hypothalamic-Pituitary Dysfunction
Authors: Lessard Kimberly Kochersperger , Miller Jeffrey L , Arzeno Luis 
Published: May 2020

Abstract
Introduction: Megestrol acetate (MA) is a synthetic progestin often used for appetite stimulation and weight gain in patients with cachexia related to AIDS, cancer or terminal illness. MA is frequently implicated in development of both glucocorticoid excess and adrenal insufficiency (AI) in a somewhat unpredictable manner. Less commonly reported adverse effects of MA include dysfunction of the hypothalamic pituitary axis. Few cases in literature exist regarding the use of MA in young, healthy patients and the potential clinical severity of pituitary dysfunction in this population.
Case : A 24-year-old male was previously healthy but frustrated by an inability to gain muscle mass. Evaluation one-year prior was unrevealing and included a total testosterone of 1100ng/dL (264-916ng/dL). In the interim, he was prescribed MA 625/5mg for 2 months with rapid development of abdominal adiposity, depressed mood, low libido and erectile dysfunction. Repeat evaluation revealed a precipitous drop in total testosterone to 66 ng/dL at which point he self-discontinued MA. He then began to experience palpitations, sweats, poor concentration, and undesirable weight loss along with worsening symptoms of sexual and erectile dysfunction.
Three months after MA discontinuation, he appeared well with physical examination and vital signs within normal limits. Surprisingly, repeat studies revealed total testosterone &lt;3, free testosterone &lt;0.2 (9.3 -26.5 pg/mL), LH 1.3 (1.7-8.6 mIU/mL), FSH 2.2 (1.5-12.3 mIU/mL), Prolactin 33.4 (4.0-15.2 ng/mL) as well as 8AM cortisol 2.2 ug/dL and ACTH 22.7 pg/mL. A basic metabolic panel, thyroid function studies and pituitary MRI were unremarkable. The patient was empirically placed on prednisone 5mg daily pending ACTH stimulation testing for HPA axis reassessment. Topical testosterone replacement therapy was initiated due to intolerance of hypogonadal symptoms.
Discussion: MA, by virtue of affinity for glucocorticoid receptors, has the potential to cause hyperglycemia and Cushing’s syndrome. Secondary AI often results from withdrawal of MA however central AI can also occur with active administration by unclear mechanisms. Hypogonadism and hyperprolactinemia are additional under-reported adverse effects of MA with symptoms often masked by AI or elements of chronic illness. In study of men age 60-85 year on MA, a mean percentage change of ACTH -89.5%, LH -49%, TSH -14.7% and Prolactin +150% were seen from baseline after 12 weeks of therapy as was decreased cortisol. Limited data exists in young patients such as ours given limited indications for the agent’s use. Importantly, MA should be prescribed with understanding that weight gain is predominantly adipose rather than muscle mass and that its safety is limited by potential HP axis dysfunction, namely adrenal and gonadal deficiencies.
SUN-697 Importance of Immunosuppressive Therapy for Managing Insulin Resistance Type B
Authors: Amankwah Samuel , Silpasuvan Artit 
Published: May 2020

Abstract
Background: Autoimmune Antibodies against insulin receptors leading to refractory hyperglycemia is known as Type B insulin resistance. In addition to insulin management, immunosuppressive therapy appears to be an essential part for successful management. Clinical Case: A 20 year old African American woman with no significant past medical history presented to the Emergency Department with worsening nausea and vomiting for 5 days and shortness of breath. She admitted to polyuria, unintentional weight loss of 15 pounds in the last six months, decreased appetite, and hyper-pigmented rashes mostly on her back. The patient was not on any medications at home. No known drug allergies, no past surgical history. Family history was significant for Grandmother with Type 2 Diabetes Mellitus and Lupus on father’s side of family. The patient denied use of alcohol, tobacco, illicit and IV drug use. T: 37.2 °C, HR: 124, RR: 25, BP: 105/74, SpO2: 100%. Weight 45kg. Physical exam significant for Tachycardia but normal rhythm. Initial work up revealed new onset diabetes HbA1c 9.6% and massive pericardial effusion on echocardiogram s/p pericardiocentesis. Due to developing complaints of intermittent cyanosis of fingertips and intermittent joint pain of fingers, Rheumatology work up was ordered and positive for mixed connective tissue disease. Patient was treated with Cellcept 1500 mg BID, Plaquenil Sulfate 300 mg daily, and prednisone 12.5 mg BID. Hospital course was complicated due to hyperglycemia in 300s-400mg/dL requiring high amounts of insulin. Diabetes work up was negative for GAd-65 and islet cell antibodies. C-peptide was elevated at 16.1 ng/mL (0.8-3.1 ng/mL) and anti-Insulin an antibodies was 20uU/mL. Patient was euthyroid. Hyperglycemia persisted despite increasing doses of long and short acting insulin subcutaneously. The patient eventually required Insulin intravenously at 50 units/hour plus 50 units of short acting Insulin every 4 hours subcutaneously. The patient was transferred to a facility to begin Combined Immunosuppressive Therapy plus insulin to manage hyperglycemia due to insulin resistance. After six months of rituximab, high-dose pulsed steroids, cyclophosphamide, plus insulin therapy, glycemic index improved with HbA1c reduced to 5.6%. Conclusion: Combined Immunosuppressive Therapy in addition to insulin management of refractory hyperglycemia due to type B insulin resistance has been shown to not only be effective in controlling refractory hyperglycemia but preventing against recurrences as well. Reference: 1) Klubo-Gwiezdzinska J, Lange M, Cochran E, Semple RK, Gewert C, Brown RJ, Gorden P. Combined Immunosuppressive Therapy Induces Remission in Patients With Severe Type B Insulin Resistance: A Prospective Cohort Study. Diabetes Care. 2018 Nov;41(11):2353-2360.
SAT-466 Hashimoto’s Glomerulonephritis: A Reality or Just a Coincidence?
Authors: Gomez Noronha Andres Alberto , Sedó Isabel Pulgar 
Published: May 2020

Abstract
Background: Glomerulonephritis is a common health problem surrounding nephrologists, mainly characterized by nephrotic range proteinuria, low serum albumin level and edema. There are several causes such as infections, cancer or autoinmune disorders, like Hashimoto’s thyroiditis. This is a chronic inflammation of the thyroid gland caused by high serum thyroid autoantibodies leading to hypothyroidsm. In the last years, many authors worldwide have found an uncommon association between Hashimoto’s disease and nephrotic syndrome. This may be attributed to cross-reacting antigens, such as thyroglublin, that become deposited in the glomeruli. Clinical Case: A 40-year women was admitted to our hospital with typical symptoms of nephrotic syndrome. The patient has a history of hypothyroidsm two years ago, treated with levothyroxine 200 mcg. Initial tests were congruent with glomerular impairment: low serum albumin 2.8 g/dl (NR &gt; 3.5 g/l), hypercholesterolemia 300 mg/dl, (NR &lt;200 mg/dl) and nephrotic-range proteinuria (9g/24h). Viral infections such as HIV, hepatitis B and C, herpes virus and rubella were discarded. Moreover, autoantibodies such as ANA, ANCAc and ANCAp were studied with no contributory results. Tumor markers were also tested and a complete body CT scan was performed looking for some occult cancer, but nothing contributory was found. Thyroid hormones levels were out of range (TSH: 20.04 mIU/l, NR: 0.27-4.20 mIU/l; FT4: 5 pmol/L, NR: 12-22 pmol/L). ATPO and ATG were performed, which were positive and in several fold higher levels than expected. (ATPO: &gt;600 U/ml, N&lt;34 U/ml; ATG: 195 U/ml, N &lt;115 U/ml)
During hospitalization a kidney biopsy was performed. The anatomic pathology report was compatible to membranous glomerulonephritis. Since there was no clear etiology of the nephrotic syndrome, we assumed that Hashimoto’s disease had an important role in this particular case, having already discarded the most common causes. We decided to optimized levothyroxine dose (from 200 mcg qd to 250 mcg qd) and ACE inhibitors (losartan 50 mg qd) were added to the therapeutic plan. During the follow up (one year later), we observed an improvement in thyroid hormone levels (TSH: 0.94 mIU/l, FT4: 14.17 pmol/L) and a decreased in proteinuria (3g/24h); however, ATPO and ATG levels persisted high (ATPO: &gt;600. ATG: 170.6). No immunosuppressive therapy was used at all. Conclusion: This is the first case in our hospital demonstrating the possible association between Hashimoto’s disease and membranous glomerulonephritis. Santoro et al. strongly believe that there is a trully relationship connecting both entities, suggesting that similar imnunological abnormalities ought to be the key point in the pathogenesis of the two conditions. Reference: (1) Santoro, D., Vadalà, C., Siligato, R., Buemi, M., & Benvenga, S. Autoimmune thyroiditis and glomerulopathies. Frontiers in endocrinology, 8, 119. (2017)
SUN-010 Efficacy of High Intensity Intermittent Training for Improving Cardio-Metabolic Health in Women with Polycystic Ovary Syndrome: A Pilot Study
Authors: Patten Rhiannon Kate , McIlvenna Luke , Moreno-Asso Alba , Stepto Nigel Nigel , Hiam Danielle 
Published: May 2020

Abstract
Polycystic ovary syndrome (PCOS) is a common and complex endocrinopathy with reproductive and metabolic manifestations, carrying a major health and economic burden. Exercise training has consistently been found improve clinical outcomes in women with PCOS, but shortfalls with exercise prescription are evident. Research suggests that high intensity intermittent exercise (HIIT) is feasible, well tolerated and enjoyable for people with or at risk of chronic disease and can address many of the shortfalls and barriers to exercise participation. To investigate the effects of high intensity exercise, twenty-four reproductive aged, overweight and obese, previously sedentary women with PCOS were recruited from the community and randomised to complete either 12 weeks of moderate intensity continuous cycling exercise (MOD; 50-60% of maximal heart rate [HRmax]; n=11) or HIIT (90-95% HRmax; n=13). All exercise was supervised by an exercise physiologist and completed 3 times per week on a cycle ergometer. Baseline and post testing measures consisted of peak oxygen consumption (VO2peak) determine by a graded maximal exercise test, insulin sensitivity determined by hyperinsulinaemic-euglycaemic clamp, body composition outcomes and anti-mullerian hormone (AMH). Enjoyment was also measured throughout the intervention using feeling scales. Significant improvements were seen for VO2peak after HIIT with an average increase of 5.6 ± 2.5 mL.kg-1.min-1 (P=0.013) and non-significant increases in the MOD group (3.4 ± 2.1 mL/kg/min; P=0.20). Body composition, fasting insulin and AMH values remained unchanged in both groups. Non-significant improvements in glucose infusion rate (3.3 ± 2.8 mg.lbmkg-1.min-1; P=0.06) and insulin sensitivity index (M-to-I ratio; 3.0 ± 3.8 mg.lbmkg-1.min-1[mU/I]-1 x 100; P=0.17) were found as a result of HIIT compared to no changes after moderate intensity exercise. Importantly, HIIT was also found to be more enjoyable than moderate intensity continuous exercise. The present study is the first to compare current exercise recommendations of moderate and vigorous intensities in women with PCOS. The results of this study provide preliminary validation of HIIT and should be considered for improving cardio-metabolic health in women with PCOS.
SAT-181 Pheochromocytoma Masquerading as Acute Coronary Syndrome. To Cath or Not to Cath?
Authors: Khatri Krish , Haas Richard Allen 
Published: May 2020

Abstract
Background
Pheochromocytoma had been known as the “Great Mimic” as it can present with signs and symptoms consistent with numerous differentials [1]. Cardiac ischemia is one in particular which creates a diagnostic dilemma and poses significant risk for misdiagnosis.
Clinical Case
62-year-old female with recent onset hypertension and type II diabetes(HbA1C of 6.9%) presented to the ER with new episodes of nausea, vomiting, and substernal chest pain. During the preceding four months she also experienced episodic headaches, palpitations, and flushing.
Initial vital signs were significant for blood pressure 157/81 mm Hg. Physical exam was unremarkable. An Electrocardiogram showed normal sinus rhythm with right axis deviation and ST segment depressions in the inferior leads II, III and aVF.
Labs revealed a troponin peak at 2.95 (&lt;0.04 ng/mL) and d-dimer of 403 (&lt;400 ng/mL). Serum chemistry, TSH, and complete blood count were within normal limits. A CT Chest with angiography was negative for pulmonary emboli. However, it did note a heterogenous 7.6 cm right adrenal mass. At this juncture there was clinical concern for pheochromocytoma and serum free metanephrines was ordered.
Prior to receiving medical treatment for her pheochromocytoma, she underwent cardiac catheterization which showed no evidence of coronary artery disease. The procedure was uncomplicated. However, post-procedurally she did develop worsening paroxysms and severe hypertensive episodes with heart rate up to 140 beats per minute and systolic blood pressure up to 220 mm Hg. She was subsequently started on alpha blockage with phenoxybenzamine 10mg twice daily to which she responded favorably. Her initial serum free metanephrine was 6087(&lt; 57 pg/mL) and free normetanephrine 2489 (&lt;148 pg/mL).
Conclusions
This case highlights the importance of maintaining a high index of suspicion for pheochromocytoma for all patients with acute chest pain and hypertension. Her untreated pheochromocytoma could have been fatal during or immediately after the cardiac catheterization. Given the suspicion for pheochromocytoma in this case, it would have been most appropriate to have begun alpha blockade after blood was drawn for metanephrines and before attempting any invasive procedures. Pheochromocytoma should be included in the differential diagnosis of acute coronary syndrome because it can mimic an ischemic episode.
References:
1. Soltani A, Pourian M, Davani BM. Does this patient have Pheochromocytoma? a systematic review of clinical signs and symptoms. J Diabetes Metab Disord. 2016 Mar 17;15:6. doi: 10.1186/s40200-016-0226-x. Erratum in: J Diabetes Metab Disord. 2017 Oct 16;16:42. PMID: 26998444; PMCID: PMC4797176.
SAT-306 Muscarinic and Adrenergic Receptor Cooperativity in a Human Adrenocortical Carcinoma Cell Line
Authors: Malaiyandi Latha , Meyer Alice , Surachaicharn Nuntida , Pelchat Dominic , Gilchrist Annette , Kopf Phillip , Dineley Kirk 
Published: May 2020

Abstract
The role of autonomic receptors in the regulation of the adrenal cortex is poorly understood. We recently showed that activation of M3 muscarinic receptors stimulates intracellular calcium oscillations, aldosterone production, and expression of CYP11B2 (1). The present study explores the relationship between muscarinic and adrenergic receptors in corticosteroid production. Using live-cell fluorescence imaging of HAC15 adrenocortical cells with the calcium-sensitive probe Fluo-4, we have shown that stimulation of adrenergic receptors with the endogenous, non-selective adrenergic agonist norepinephrine (10μM) enhances intracellular Ca2+ oscillations caused by the cholinergic agonist carbachol (1μM). However, Ca2+ is not affected by norepinephrine alone. Adrenergic enhancement of carbachol-induced Ca2+ oscillations is blocked by the ⍺ adrenergic receptor antagonist phentolamine, but not by the β adrenergic receptor antagonist propanolol. Specifically, ⍺2 and β2 antagonists (such as yohimbine and butoxamine, respectively) significantly suppressed the norepinephrine effect, but ⍺1 and β1 antagonists (such as tamsulosin and metoprolol, respectively) had no effect. RT qPCR identified ⍺2A receptors as the most abundant adrenergic receptor in HAC15 cells. Saturation experiments using 3H-NMS and 3H-Rauwolscine confirmed the presence of muscarinic M2 and M3 receptors as well as ⍺2A receptors. Using competition radiolabeled binding assays we explored the cooperation between M2/M3 and ⍺2A adrenergic receptors. Our results suggest that autonomic regulation of intracellular Ca2+ depends on an interplay of M3 and ⍺2A receptors. Additional experiments will use ELISA methods to determine the functional impact of autonomic receptor cooperativity on steroid synthesis and secretion.
References: (1) Malaiyandi et al., Mol Cell Endocrinol. 2018 478: 1-9.
SAT-369 Parathyroid Microadenomas as a Cause of Normocalcemic Primary Hyperparathyroidism (PHPT) and a Surgical Challenge
Authors: Nguyen Tiffany , Coltrera Marc D , Chao Jing H 
Published: May 2020

Abstract
Background: Patients with normocalcemic primary hyperparathyroidism (PHPT) share similar risks of osteoporosis and nephrolithiasis with patients having hypercalcemic PHPT. The prevalence and natural history of normocalcemic PHPT is not well defined. Parathyroid microadenomas weighing &lt; 100 mg may present as special clinical challenges in both the diagnosis and surgical resection.
Clinical Case: A 55-year-old woman presented for an evaluation of osteoporosis following a non-traumatic L1 compression fracture at the age of 50 years. Noting an initial serum calcium of 10 mg/dL, we diagnosed her with normocalcemic PHPT based on a concurrent parathyroid hormone (PTH) level of 112 pg/mL (12-88 pg/mL) and a lack of other causes for an elevated PTH, including a normal eGFR, serum 25-hydroxyvitamin D, 24-hour urine calcium, and autoantibodies for celiac disease. Initial dual-energy x-ray absorptiometry (DXA) scan from 2015 showed normal bone mineral density (BMD) and T-scores in the L-spine, total hip, and femoral neck. Neck imagings, including ultrasound, sestamibi scan, and 4D CT, failed to localize a parathyroid adenoma. In the absence of a target and indications for parathyroidectomy other than osteoporosis, she was treated with bisphosphonates. While her serum calcium remained normal (9.6-10.2 mg/dL) despite an elevated PTH level (92-116 pg/mL) over a two-year period, subsequent DXA scans showed a significant loss in BMD on the bisphosphonates, prompting a peripheral DXA scan, which revealed severe osteoporosis at the distal third of the forearm (BMD 0.450 g/cm2, T-score -3.7), consistent with PTH-associated bone resorption. Following a 4-gland exploration with removal of 2 parathyroid microadenomas (63 and 100 mg), intra- and post-operative PTH levels normalized. She now awaits a repeat DXA scan at 1 year after a successful parathyroidectomy.
Conclusion: Although many patients with normocalcemic PHPT may progress to develop hypercalcemia, some remain normocalcemic over an extended period. We report a patient who maintained normocalcemia for over 2 years. To correctly establish the diagnosis of normocalcemic PHPT, a comprehensive evaluation must be performed to exclude secondary causes of an elevated PTH (renal insufficiency, hypovitaminosis D, hypercalciuria, and malabsorption). Since significant osteoporosis may be preferentially seen in the cortical bone, BMD at the distal 1/3 of forearm should be evaluated in addition to the L-spine, hips and femoral necks. When a parathyroid adenoma cannot be localized in patients with normocalcemic PHPT, a careful 4-gland exploration for parathyroid microadenoma(s), paying special attention to the size, texture, and shape of the glands, and guided by intraoperative PTH levels, ensures the successful removal of the culprit gland(s).
SAT-565 Familial Homozygous Lipoprotein Lipase Defect Presenting with Recurrent Chylomicronemia Syndrome: Making a Case for Elective Plasmapheresis as an Adjuvant Treatment Modality
Authors: Shaka Hafeez , Edigin Ehizogie , Yap Sara Elizabeth , Asemota Iriagbonse 
Published: May 2020

Abstract
Background
The chylomicronemia syndrome is a disorder characterized by severe hypertriglyceridemia and fasting chylomicronemia. Type Ia hyperlipoproteinemia is an extremely rare genetic disorder that results from homozygous deficiency in LPL activity. It is characterized by eruptive xanthomas, lipemia retinalis, memory disturbances, hepatosplenomegaly and frequent episodes of pancreatitis. Pharmacologic agents including fibrates, fish oils and statins have been used for treatment. Patients who fail pharmacologic therapy are usually treated with plasmapheresis. This case showed a patient in which joint decision making led to elective plasmapheresis to avoid chylomicronemia syndrome as an adjunct to medical therapy.
Clinical case
A 35-year-old lady without known medical co-morbidity presented with 2 weeks of dull abdominal pain radiating to the back. She developed nausea and vomiting which led to her presentation. There was no history of alcohol use, gall stones, diabetes mellitus or thyroid dysfunction. She was not on any medications. Physical examination was significant for BMI of 18, moderate abdominal tenderness, splenomegaly and an indurated rash in her legs. Laboratory investigation showed elevated lipase and triglyceride level of 3313 (normal 30-50) mg/dL. CT of the abdomen was consistent with acute interstitial pancreatitis. She was managed with insulin drip and fenofibrate and discharged 3 days later on fenofibrate, atorvastatin and long acting insulin. She developed another episode of acute pancreatitis while on medical therapy requiring readmission and initiation of insulin drip 2 months later. However, triglycerides trended upwards when the drip was stopped and symptoms of acute pancreatitis worsened. She subsequently underwent plasmapheresis which led to resolution of symptoms. Despite maximally tolerated pharmacologic therapy, she persistently has triglycerides above 4000s and persistent abdominal discomfort. Genetic testing confirmed homozygous defect in LPL gene. Following an outpatient Endocrinology visit, a decision was made to pursue elective plasmapheresis as an adjunct to therapy. She had on average 2 sessions monthly for 3 months with overall improvement in abdominal discomfort as well as significant improvement in triglyceride levels.
Conclusion
Familial chylomicronemia syndromes often require multimodal therapeutic approaches to prevent morbidity and complications. These include diet and pharmacologic therapy. Although plasmapheresis is often used during hospitalizations for hypertriglyceridemia induced pancreatitis refractory to diet and pharmacologic therapy, it was used in our patient electively and efficaciously to control hypertriglyceridemia and improve symptoms of chylomicronemia syndrome.