bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-050 Isolated Hyperprolactinemia Caused by Chest Binding in a Transgender Male
Authors: Cunningham Hayley E , Coviello Andrea D , Kelley Carly E 
Published: May 2020

Abstract
Background: Prolactin levels are routinely measured in patients evaluated for PCOS. Compared with the general population, PCOS is more common among transgender men, with prevalence estimates as high as 30 to 50%1,2. Nipple stimulation is a recognized cause of hyperprolactinemia, and many transgender men engage in chest binding, which involves compressing the breast tissue to produce a more masculine appearance. Clinical Case: A 22-year old natal female with gender dysphoria, who presented to our clinic for initiation of masculinizing hormone therapy, revealed a history of irregular menstrual cycles, hirsutism, and moderate acne. The patient was on a combination OCP to regulate menstrual cycles but no other medications or supplements. Laboratory evaluation revealed normal TSH, creatinine, 24-hour urine cortisol, testosterone, 17 hydroxyprogesterone, and DHEA-S. LH was 2.4 mIU/mL, FSH was 6.0 mIU/mL, and prolactin was elevated at 55.6 ng/mL (4.8-23.3 ng/mL). Polycystic ovaries were not present on pelvic ultrasound. Pituitary MRI was ordered for further evaluation of hyperprolactinemia and no pituitary adenoma or other structural abnormality was seen. The patient denied nipple discharge and tenderness but endorsed chest binding. In the absence of another explanation, nipple stimulation through chest binding was hypothesized to be the cause of hyperprolactinemia. After withholding chest binding for one week, the patient’s prolactin level normalized to 13.95 ng/dL. The patient was diagnosed with PCOS according to Rotterdam criteria after exclusion of alternative etiologies. It was presumed that five years of consistent OCP use had normalized androgen levels and suppressed the appearance of polycystic ovaries on ultrasound. The patient was initiated on testosterone cypionate for gender affirmation. Prolactin increased again to 29.33 ng/mL one year later after resumption of continuous chest binding. Conclusion: This is the second reported case of hyperprolactinemia induced through chest binding.3 Transgender men are at increased risk for irregular periods due to underlying PCOS and therefore more likely to undergo an evaluation that includes prolactin measurement. By recognizing chest binding as a cause of isolated hyperprolactinemia, physicians can minimize unnecessary testing and anxiety in patients who engage in this practice.1. Baba, T. et al. Hum Reprod. 2007;22;1011-16. 2. Becerra-Fernandez, A. et al. Endorinol Nutr. 2014;61; 351-8.3. Patel, S., & Abramowitz, J. (2019, April). Hyperprolactinemia in a Transgender Male. Poster session presented at the Annual Scientific & Clinical Congress of the AACE, LA, CA.
SUN-501 Grave’s Disease Concealing the Diagnosis of Pancreatic Carcinoma
Authors: Unjom Zubina S , Nandu Nitish , Gilden Janice L 
Published: May 2020

Abstract
Background: Hyperthyroidism is a disease that presents with various nonspecific symptoms. Unintentional weight loss can often be the presenting complaint. We present a patient with unexplained weight loss that was attributed to Grave’s hyperthyroidism, but was later discovered to be secondary to pancreatic carcinoma. Case Description: A 58-year-old man with no significant medical history, was referred to the endocrine clinic for weight loss, low energy, and abnormal TFT’s. He reported 45 lb. weight loss over the past one year. Past Medical history was notable for opioid use, and is enrolled in the Methadone program for the past 10 years. Family history is significant for type 2 diabetes. He smokes ½ a pack of cigarettes, denies alcohol or drug use. On exam, heart rate was 84 bpm with fine tremors on outstretched upper extremities, no proptosis, lid lag, thyromegaly, or pretibial edema, normal reflexes. His labs were TSH=0.01; (n=0.270 - 4.20 uIU/mL), FT4=2.1; (n= 0.55 - 1.60 ng/dL), FT3=283;(n=2.52 - 4.34 pg/mL) Thyroglobulin Ab 4 IU/ml, Thyroid peroxidase Ab &gt; 900 IU/ml, TSI 358(n=&lt;140%). He was diagnosed with Grave’s disease and was started with Methimazole and Propranolol, which were titrated to an optimal range over the next few months. However, the patient was lost to follow up, and presented one year later to the ED with complaints of abdominal pain, jaundice for one-week, greasy diarrhea for 6 months, also reporting noncompliance with thyroid medications during this time. On examination, he was icteric and jaundiced with hepatomegaly, trace pedal edema. Although LFT’s were previously normal, the labs now showed alkaline phosphatase=533, (n=40-129 IU/L); AST=107 units (n= 0-32 IU/L), ALT=213units (n= 0-40 IU/L), total bilirubin 11.4 (n= 0-1.0 mg/dl), TSH=0.01, FT4=0.6, FT3=3.2. Ultrasound showed gallbladder sludge, CT abdomen-dilatation of the pancreatic duct in neck and body of pancreas, MRCP- marked pancreatic ductal dilatation and soft tissue fullness within the pancreatic head. CA 19-9= 64.8, he underwent ERCP, and was later diagnosed with adenocarcinoma of the Pancreatic head. He was discharged with referrals to GI and Oncology for further treatment. Discussion:Although weight loss and diarrhea are nonspecific, and can often result from hyperthyroidism, this case highlights the importance of further investigation for other causes and avoiding attribution to a single diagnosis. Other diagnoses were only looked into when the patient presented with painless jaundice and hepatomegaly several months later. The effects of autoimmune hyperthyroidism on the pancreas function remain unclear. However, patients with Grave’s hyperthyroidism have a higher number of islet cell antibodies, as compared to controls. Further studies are required in this regard. We also emphasize the importance of patient education and compliance which can lead to earlier diagnosis, and overall better outcomes.
SAT-165 Sterol O-Acyl Transferase 1 as a Prognostic Marker of Adrenocortical Carcinoma
Authors: Lacombe Amanda Meneses Ferreira , Soares Iberê Cauduro , Charchar Helaine da Silva , Brondani Vânia Balderrama , Neto João Evangelista Bezerra , Tanno Fabio , Srougi Victor , Chambo José Luiz , de Freitas Ricardo Miguel Costa , Hoff Ana Oliveira , Almeida Madson Q , Zerbini Maria Claudia Nogueira , Kroiss Matthias , Fragoso Maria Candida Barisson Villares 
Published: May 2020

Abstract
Background: Adrenocortical carcinoma (ACC) is a rare endocrine malignancy with an unfavorable prognosis. Despite the poor prognosis in the majority of patients, no improvements in treatment strategies have been achieved, largely due to the rarity of these tumors. Therefore, the discovery of new prognostic biomarkers that could guide and improve the management of patients with ACC is of enormous interest. Sterol-O-Acyl Transferase 1 (SOAT1) is involved in cholesterol esterification in adrenocortical cells. Recently, it was demonstrated that SOAT1 inhibition leads to impaired steroidogenesis and cell viability in ACC [1]. There are no studies so far addressing the impact of SOAT1 protein expression in ACC prognosis and clinical outcomes.
Methods: We evaluated SOAT1 protein expression by immunohistochemistry (ab39327; 1:4000; Abcam, EUA) in a tissue microarray of 107 adrenocortical carcinomas (Weiss score ≥ 3) from adult patients treated in a single tertiary center in Brazil. Immunohistochemistry results were evaluated through a semiquantitative approach by two independent pathologists. We aimed to evaluate the correlation of SOAT1 protein expression with clinical and biochemical parameters, surgical specimen histological characteristics, recurrence free-survival, progression free-survival and overall survival.
Results: SOAT1 protein expression was heterogenous in this cohort; 38% of ACCs demonstrated strong SOAT1 protein expression while 62% demonstrated weak or absent SOAT1 protein expression. Strong SOAT1 protein expression correlates with known features of high aggressiveness in ACC, such as excessive tumor cortisol secretion (p= 0.007), advanced disease stage [ENSAT 3 and ENSAT 4 (p= 0.009)] and high Ki67 index (0.008). On multivariate analysis, strong SOAT1 protein expression was an independent predictor of lower overall survival (HR 1.71, CI 95% 1.05-2.92; p= 0.04) when considering all cases (n= 107) and of lower progression free survival (HR 3.05, CI 95% 1.05-8.85; p= 0.04) in patients with metastatic disease at diagnosis (n= 22).
Conclusions: Our findings demonstrated that SOAT1 protein expression has prognostic value in ACC and reinforce the importance of investigating SOAT1 as a possible therapeutic target for patients with ACC. Multicentric prospective studies including a larger number of patients are needed in order to validate and consolidate the results found in this cohort.
References:
1.
Sbiera S, Leich E et al. Mitotane inhibits Sterol-O-Acyl Transferase 1 Triggering Lipid-Mediated Endoplasmic Reticulum Stress and Apoptosis in Adrenocortical Carcinoma Cells. Endocrinology. 2015; 156 (11):3895-908.
SAT-397 Characteristics and Outcomes of Severe Hypercalcemia Related Admissions - a Single Centre 5 Years’ Experience
Authors: Ponce Jo-Anne , Lee Myron , Caswell Amanda , Parsons Mclaine O , Acharya Shamasunder 
Published: May 2020

Abstract
Introduction: Severe hypercalcemia (corrected calcium ≥3.5mmol/L) is typically associated with multi-organ dysfunction and increased mortality. We audited 47 consecutive patients who were admitted to a single tertiary referral center over 5 years period (2014-2019) with severe hypercalcemia. Results: The median age 69 years (10-97yrs); 55% females, and median length of stay was 9 days (1-120). Most patients (30%) were admitted under general medicine and 53% received endocrinology consultation. Renal dysfunction (91%) dominated the clinical presentation, but gastrointestinal abnormalities (70%), neuropsychiatric manifestations (53%), and musculoskeletal involvement (45%) were also very common. PTH was measured in 43/47 patients with 37 PTH independent (calcium level 3.82 mmol/L) and 6 PTH dependent (calcium level 3.70mmol/L) hypercalcemia. Recurrence of the condition within five years was recorded for 5 patients (11%), ten (21%) patients died during the admission, and 4 patients (9%) required ICU admission in PTH independent severe hypercalcaemia, majority are due to malignancy; while none of these outcomes were observed in PTH dependent severe hypercalcaemia. The length of hospital stay is longer in PTH independent (15.5 days) as compared to PTH dependent severe hypercalcaemia (12 days). The most common cause of severe hypercalcemia was malignancy (47%) with multiple myeloma as the most common in 32% followed by lung cancer at 27%. The other non-malignancy causes are calcium supplementation, vitamin D toxicity, and hyperparathyroidism implicated in 13% each. Twenty eight patients (65%) were managed by fluid and antiresorptive agent with 26 patients able to decrease calcium level to &lt;3mmol/L (93%). Eight patients (19%) were managed by fluid alone (not effective in 37%), 9% by antiresorptive agent alone (not effective in 25%), and 16% did not receive any fluid nor antiresorptive agent (not effective in 43%). Conclusion: Similar to previous studies, severe hypercalcaemia is commonly seen in patients with malignancy and associated with significant symptoms, recurrence in 5 years, ICU admission and mortality. Calcium and vitamin D supplementation and hyperparathyroidism are also found to commonly cause severe hypercalcemia. The most effective management is combination of fluid resuscitation and antiresorptive agent to decrease the calcium level to &lt;3mmol/L.
SAT-221 50-Year-Old Fungus Suddenly Flourishes in Adrenal Glands: A Case of Sudden-Onset Bilateral Adrenal Masses Due to Latent Disseminated Histoplasmosis
Authors: Carrillo Maritza Elide , Chang Amy , Walsh Christopher L 
Published: May 2020

Abstract
Histoplasma capsulatum is endemic to Africa, Asia, Central and South America, and within the US, to the Ohio and Mississippi River Valley. Disseminated histoplasmosis is less commonly seen in immunocompetent individuals, who usually present with asymptomatic self-limited acute pneumonitis. Time to involvement of the adrenals is unknown. Adrenal insufficiency occurs in 45% of cases involving the adrenals, and is thought to be irreversible even in patients in remission.
A 76-year-old man with no significant past medical history was incidentally found to have large bilateral adrenal masses during routine surveillance of a 7 mm pulmonary nodule on annual Chest CT, which showed normal adrenal glands the year prior. He was asymptomatic. A lifetime non-smoker native to California, whose only significant travel history was in his 20s to Ecuador and Puerto Rico, areas endemic to Histoplasma.
Abdominal CT showed large bilateral adrenal masses with intermediate density and low washout values (right: 4.9 cm, HU 45, absolute washout 30%; left: 4.8 cm, HU 30, absolute washout 25%).
On exam, vital signs were stable with normal orthostatics. Labs revealed normocytic anemia, normal chemistry panel, normal cortisol after 1-mg dexamethasone overnight test 2.6 mcg/dL (n&lt;5 mcg/dL), plasma metanephrine &lt;0.10 nmol/L (n &lt;0.50 nmol/L), plasma normetanephrine 0.89 nmol/L (n &lt;0.90 nmol/L), aldosterone 4.0 ng/dL (n &lt;31 ng/dL), PRA 2.0 ng/ml/hr (n 0.5-4 ng/ml/hr) and random free cortisol 0.38 ug/dL (n 0.022-0.254ug/dL). HIV antigen and antibody, and Histoplasma urinary antigen were negative.
Left adrenal mass biopsy revealed necrotizing granulomatous inflammation with fungal culture revealing budding yeast morphologically consistent with Histoplasmosis, with DNA probe confirming Histoplasma capsulatum.
Treatment with itraconazole was initiated and the patient is tolerating the treatment well.
To our knowledge, this is the first case demonstrating rapid development of large bilateral adrenal masses within a year due to latent disseminated histoplasmosis in an asymptomatic individual, which highlights the need for appropriate testing in patients with known exposure or travel history to endemic areas, regardless of time since exposure.
1.Singh M, Chandy DD, Bharani T, Marak RSK, Yadav S, Dabadghao P, et al. Clinical outcomes and cortical reserve in adrenal histoplasmosis- a retrospective follow-up study of 40 patients. Clin Endocrinol 2019 Jan 17
SAT-450 Essential Role of GATA2 in the Negative Regulation of the Prepro-Thyrotropin-Releasing Hormone Gene by Liganded T3 in the Rat Paraventricular Nucleus
Authors: Kuroda Go , Sasaki Shigekazu , Matsushita Akio , Ohba Kenji , Sakai Yuki , Shinkai Shinsuke , Nakamura Hiroko , Oki Yutaka 
Published: May 2020

Abstract
T3 inhibits thyrotropin-releasing hormone (TRH) synthesis in hypothalamic paraventricular nucleus (PVN). Although T3 receptor (TR) β2 is known to mediate the negative regulation of prepro-TRH gene, its molecular mechanism remains unknown. Our previous studies on the T3-dependent negative regulation of the thyrotropin β subunit (TSHβ) gene indicate the tethering mechanism, where T3-bound TRβ2 interferes with the function of the transcription factor GATA2, which is essential for TSHβ expression. Interestingly, the transcription factor Sim1, a determinant of PVN differentiation in hypothalamus, is reported to induce the expressions of TRβ2 and GATA2. Indeed, our immunohistochemistry revealed the expression of GATA2 in the TRH neuron of the rat PVN. According to the experimental report with transgenic mice, the DNA sequence from nt. -547 to nt. +84 is sufficient for the expression of the prepro-TRH gene in PVN. Using the CAT reporter gene harboring this region, we found that this promoter is activated by GATA2 approximately 6-fold in CV1 cells. The deletion and mutation analyses identified a functional GATA-responsive element (GATA-RE) between nt. -357 and nt. -352. When TRβ2 was co-expressed, T3 reduced GATA2-dependent promoter activity to approximately 30%. T3-dependent repression was maintained after the mutation of the putative negative T3 responsive element (site4). Although the melanocortin 4 receptor signaling is known to stimulate the prepro-TRH promoter via protein kinase A pathway in the PVN, inhibition by T3 was dominant over the 8-bromo-cAMP-induced activation. We observed the in vivo recognition of GATA-RE by GATA2 using chromatin immunoprecipitation assay with CA77 cells, which express endogenous TRH. The electrophoretic mobility shift assay also demonstrated that GATA2 bound to oligonucleotide containing the GATA-RE. These results suggest that, as in the case of the TSHβ gene, GATA2 transactivates the prepro-TRH gene and that T3-bound TRβ2 interferes with its function, resulting in the negative regulation of this gene.
SUN-652 Progesterone Receptor Membrane Component 1 Suppresses Type II Diabetes (T2D) Progression via Induced Insulin Signaling in Muscle
Authors: Lee Sang R , Hong Eui-ju 
Published: May 2020

Abstract
Type II diabetes (T2D) is characterized for insulin resistance in muscle, liver, and fat (1). Progesterone receptor membrane component 1 (Pgrmc1) is novel cell surface receptor which is associated with insulin receptor beta (IRβ) (2). Therefore, we speculated Pgrmc1 might be related to T2D. Using Pgrmc1 KO mice reported in our previous study (3), we observed the decrease of body weight (BW) and increase of muscle weight per body weight. When blood glucose level in post-prandial state was lower, Pgrmc1 KO mice showed improvements in glucose tolerance test (GTT) and insulin tolerance test (ITT). Though insulin level was low, insulin signaling genes were up-regulated in post-prandial Pgrmc1 KO mice, especially in muscle. Regulations of blood glucose level and insulin signaling gene levels by Pgrmc1 were also similarly observed in insulin-deficient state. To induce T2D, C57BL/6 mice were fed with high-fat diet for 8 weeks and injected by low dose of streptozotocin (30mg/kg). As a result, T2D-induced Pgrmc1 KO mice increased lean mass per BW, decreased the blood glucose level, and improved GTT and ITT. The insulin signaling genes were also up-regulated, while cytoplasmic GLUT4 was decreased, but membrane GLUT4 was increased in T2D-induced Pgrmc1 KO muscle. Glycolysis, TCA cycle, and oxidative phosphorylation genes were increased, suggesting energy metabolism was increased in T2D-induced Pgrmc1 KO muscle. Present study suggests that Pgrmc1 loss increases insulin signaling through induction of cytoplasmic IRβ and pAKT, and induces glucose uptake of muscle, thereby showing improvement in T2D progression. This has important clinical value because Pgrmc1 modulation will evade hypoglycemia caused by classic insulin therapy for T2D (4).
References: (1) Fernandez, A. M., Kim, J. K., Yakar, S., Dupont, J., Hernandez-Sanchez, C., Castle, A. L., Filmore, J., Shulman, G. I., and Le Roith, D. (2001) Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes. Genes & development 15, 1926-1934. (2) Hampton, K. K., Anderson, K., Frazier, H., Thibault, O., and Craven, R. J. (2018) Insulin Receptor Plasma Membrane Levels Increased by the Progesterone Receptor Membrane Component 1. Mol Pharmacol 94, 665-673. (3) Lee, S. R., Kwon, S. W., Kaya, P., Lee, Y. H., Lee, J. G., Kim, G., Lee, G. S., Baek, I. J., and Hong, E. J. (2018) Loss of progesterone receptor membrane component 1 promotes hepatic steatosis via the induced de novo lipogenesis. Scientific reports 8, 15711. (4) Zammitt, N. N., and Frier, B. M. (2005) Hypoglycemia in type 2 diabetes: pathophysiology, frequency, and effects of different treatment modalities. Diabetes care 28, 2948-2961.
SUN-418 Patterns of Thyroid Disease in Basrah, Iraq. Retrospective Study
Authors: Mansour Abbas Ali , Ali Alhamza Ali Hussain , Abdullah Almomin Ammar Mohammed Saeed , Zaboon Ibrahim Abbood , Alibrahim Nassar Taha Yaseen , Hussein Rudha Naser , Kadhim Muayad Baheer , Mohammed Adel Gassab , Jabbar Al-Waeli Dheyaa Kadhim , Nwayyir Hussein Ali , Alidrisi Haider Ayad Yassin , Hussein Ibrahim Hani , Odhaib Samih Abed , Altemimi Mahmood Thamer Jallod , Imran Husam Jihad 
Published: May 2020

Abstract
Background: Data on thyroid disease epidemiology in the Middle East are scanty and anecdotal. This study aimed to assess the pattern of thyroid disease seen in Faiha Specialized Diabetes, Endocrine and Metabolism Center (FDEMC) in Basrah,Southern Iraq.
Methods
Retrospective observational study of database retrieval from the FDEMC a tertiary care Center in Basrah for the period of September 2008 to January 2019. Included all adults non pregnant 18 years or older.
Results
Total enrolled patients 17878; of them 4174(23.3%) men and 13705(76.7 %) women. There were 2229(12.5%) patients with hypothyroidism (83.0% women), with subclinical hypothyroidism observed in 364 out of 2229 with hypothyroidism(16.3%).
We found 1087 (6.1%) patients with hyperthyroidism (67.7% women) and subclinical hyperthyroidism observed in 92 of 1087 hyperthyroidism (8.4%).
Thyroid nodularity was seen in 944 (5.2%) patients (807 women in 85.5%). Thyroidectomy was done in 776(4.3%). Differentiated thyroid cancer was seen in 77 (0.4%).
Conclusion: Hypothyroidism was double that of hyperthyroidism. Cross-sectional community-based study can give more information on the epidemiology of thyroid disease in Iraq.Iodine status needed studded in the future.
Keywords: Hyperthyroidism, hypothyroidism,autoimmune thyroid disease, Iraq.