bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUN-304 Hypophisitis in Patients with and Without Autoimmune Rheumatological Disease
Authors: Vázquez Aguirre Marlon Vladimir , Godoy-Alonso Juan Pablo , Cruz Germán González-de la , Rocha-Haro Andrea , Ordaz-Candelario Karla Krystel , Balbuena-Álvarez Juan , Martínez-Jiménez Angélica , Flores-Cárdenas Romina , Roldan-Sarmiento Paola , Gómez-Sámano Miguel Ángel , Gómez-Pérez Francisco Javier , Higuera-Calleja Jesús , Hinojosa-Azaola Andrea , Martin-Nares Eduardo , Cuevas-Ramos Daniel 
Published: May 2020

Abstract
Background: Hypophysitis is an inflammatory process of the pituitary gland with different origins. Infundibulum may be also involved, called infundibulum-hypophysitis. Sometimes, enlargement of pituitary gland causes mass effect and anterior or posterior hormonal dysfunction, including hypopituitarism, and diabetes insipidus (DI), respectively. Hypophysitis is a rare autoimmune disease, however, the number of cases have been recently increasing due to higher detection related with more magnetic resonance imaging (MRI) studies. In addition, hypophysitis may be related with autoimmune rheumatologic disease (ARD) such as generalized lupus erythematosus (GLE), granulomatosis with polyangeitis (GPA), IgG4-related disease, and rheumatoid arthritis (RA). Aim: to compare the clinical and biochemical findings among patients with hypophysitis grouped depending on the presence of coexistent ARD activity. Methodology: it is a comparative and cross-sectional study. We registered all data from cases followed-up in Neuroendocrinology and Rheumatology units, from January 1987 to July 2019. Results: 24 patients showed confirmed diagnosis of hypophysitis. Majority of them (n=17, 71%) do not have coexistent diagnosis of ARD. However, 7 cases (29%) presented pituitary involvement with coexistent activity of GPA (n=4, 17%), GLE (n=1, 4%), RA (n=1, 4%) and IgG4-related disease (n=1, 4%). Female gender predominate in hypophysitis cases with and without ARD (p=0.9). Interestingly, age of hypophysitis diagnosis was significantly younger in cases without (38±14) vs. with (49±5) ARD (p=0.01). MRI results showed similar and typical findings related with hypophysitis independently of the presence of ARD. Hypopituitarism was present in the majority of cases, however, none of cases with hypophysitis and ARD showed hypogonadism (p=0.02). DI was present in 15 patients (63%), three of them with ARD (all with GPA). All cases received only medical therapy (i.e., glucocorticoids, rituximab, or azathioprine). Surgery or radiotherapy was not necessary in any case. Conclusions: Almost a 30% of cases with hypophysitis may have coexistent ARD. Pituitary function should be evaluated in cases with previous ARD diagnosis. However, hypogonadism was not present in cases with ARD and hypophysitis. Patients with ARD presented hypophysitis at older age. The remaining clinical and radiological data were similar between groups.
References: 1) Clinical Diabetes and Endocrinology. December 2016;2(1). 2) Clin Rheumatol. 2019 Aug 24. doi: 10.1007/s10067-019-04735-7
SAT-643 Predictors of Technology Success in Cystic Fibrosis Related Diabetes
Authors: Jain Ashna , Kaminski Beth Anne , Kutney Katherine 
Published: May 2020

Abstract
Background: As patients with cystic fibrosis live longer, cystic fibrosis related diabetes (CFRD) is becoming a more common complication. CFRD has a negative impact on lung function, nutrition, and survival. The ADA guidelines recommend that patients with CFRD be treated with insulin and monitor their glucose at least three times a day. Continuous glucose monitors (CGM) allow glucose to be measured by scanning a reading device or by automatic updates every 5 minutes. Little is known about factors predicting successful CGM use in patients with CFRD.
Methods: We completed a retrospective chart review of all patients with insulin-treated CFRD at a single center. Successful CGM implementation was defined as CGM use for 3 months or more. Patient characteristics (age, BMI, ppFEV1, HbA1C, diabetes duration, insurance type) were compared between the CGM and no CGM groups. For the CGM group, HbA1C, ppFEV1, and BMI, were compared before and after CGM implementation. Paired and unpaired t-tests were used to evaluate continuous variables and fisher’s exact test was used to evaluate dichotomous variables.
Results: Of the 55 patients eligible for inclusion, 12 patients (22%) had successfully implemented CGM in their diabetes routine. Age, BMI, ppFEV1, HbA1C, and insurance type were not significantly different between the CGM and no CGM groups. CGM users appeared to have a slightly longer duration of diabetes than non-implementers but this did not meet statistical significance (6.6 vs. 4.8 years, p=0.08). Among CGM users, BMI, ppFEV1, and hemoglobin A1C did not change significantly after implementation of CGM. The documented number of glucose checks did increase at the CFRD visit immediately after implementing CGM (1.9 vs. 3.3 checks per day, p=0.002).
Conclusions: No patient factor was found to predict successful CGM implementation in our cohort. Our small study suggests that longer duration of diabetes may be associated with successful CGM implementation. Longer follow-up is needed to determine whether CGM therapy improves A1C, BMI, or ppFEV1 in patients with insulin-treated CFRD.
MON-037 Vitamin D Levels in Women with Polycystic Ovary Syndrome: Influence of Obesity
Authors: Maidana Patricia Nieves Amelia , Fernández Gladys Isabel , Fritzler Analy , Ropelato María Gabriela , Eugenia Lamas-Majek , Lopez Mariana , Gonzalez Diego , Rosales Mónica , Leiderman Susana Mabel , Fabre Bibiana , Mesch Viviana 
Published: May 2020

Abstract
Introduction: Polycystic ovary syndrome (PCOS) is the most frequent cause of hyperandrogenism in women of reproductive age. Among its metabolic complications, vitamin D deficiency has been described in relation with insulin resistance’s pathophysiology and other metabolic risk factors. However, it is not clear if this deficiency is inherent to PCOS or it depends on adiposity degree. As well, it is also suggested that vitamin D could regulate leptin levels and high leptin levels should be associated with vitamin D defiency in obesity. Our aim was to evaluate the relationship between vitamin D, leptin and obesity degree in PCOS patients.
Subjects and methods: In 84 PCOS women (19 -37 years) and 49 controls (22-45 years), 25 hidroxi-vitamin D (25 OH-D) was measured by direct chemoluminiscence. Body mass index (BMI) was calculated; 20% of PCOS women were overweight and 46% were obese. Waist circumference (WC) was measured as an indicator of abdominal obesity. The lipid accumulation product (LAP) index, a secondary marker of insulin resistance, was calculated (LAP: [waist (cm) - 58] x triglycerides (mmol/l)). In a subgroup of 26 patients, leptin levels were determined by ELISA method. Statistical analysis was performed through SPSS 22.
Results: Variables are expressed as mean ± SD or median (range) according to distribution. The following parameters were higher in PCOS women than in controls, BMI: 29.3 (18.6-48.2) vs 22.4 (18.1-37.4) kg/m2; WC 95 ± 16 vs 82 ± 11 cm and LAP: 47.9 (1.1-198.2) vs 17.5 (6.8-93.4) cm.mmol/L, p&lt;0.0001 in all cases. 25 OH-D was lower in PCOS: 14.5 (10.0-39.0) vs 17.0 (10.0-38.8) ng/ml, p=0.024. Leptin levels in PCOS women were 10.1 ± 5.4, 26.4 ± 7.0 and 33.8 ± 16.9 ng/ml in normal weight, overweight and obese patients, respectively. After a logistic binary regression analysis, differences in 25 OH-D between groups were lost when BMI and WC were considered (p=0.556; RR=0.978; IC95% [0.909-1.063]). 25 OH-D levels were negatively associated with WC (r=-0.286, p=0.006), LAP (r=-0.333, p=0.002) and leptin (r=-0.462, p=0.017).
Conclusions: although 25 OH-D levels were lower in PCOS women than in controls and negatively associated with LAP, an insulin resistant marker, the fact than differences between groups was lost after correction by BMI and WC, in addition to the correlation found between 25 OH-D and leptin levels, indicates that obesity degree and abdominal fat distribution should be responsible of decreased vitamin D levels in PCOS.
MON-194 Phaeochromocytoma-Paraganglioma (PPGL): Post-Operative Hypotension Is a Vanishing Phenomenon
Authors: Osher Esther , Tordjman Karen Michele , Klausner Joseph , Nachmany Ido , Sagie Boaz , Stern Naftali , Lahat Guy , Wolf Ido , Zac Lilach , Otremski Sorina , Barnes Sophie , Aizic asaf , Zohar Naomi Even , Greenman Yona 
Published: May 2020

Abstract
Background: Treatment of hemodynamic instability in patients with PPGL in the intra-and postoperative periods is challenging. Persistent postoperative hypotension is a common and serious complication, reportedly occurring in 30-60% of PPGL patients. This phenomenon reflects 1) high doses of pre-operative antihypertensive drugs; 2) low intravascular volume secondary to chronic catecholamine-induced vasoconstriction with pressure natriuresis; 3) the sudden drop in circulating catecholamines after surgery. It has been shown that tumor size and preoperative levels of catecholamines are directly related to the need for treatment with vasopressor agents in the early period after tumor removal. The aim of this study was to evaluate the efficacy and safety of the current perioperative treatment protocol for PPGL used in our Institute. Methods: We retrospectively reviewed the rate of hemodynamic instability and postoperative hypotension in relation to catecholamine levels, and the efficiency of preoperative pharmacological preparation in consecutive patients with PPGL treated between 2000-2019. Results: There were 39 patients (F/M 19/20; mean age 50.4 ±16.5 years) 33 of which had adrenal lesions and 6 had extra-adrenal tumors. Mean tumor size was 3.9 ±2.2 cm. Median metanephrine and normetanephrine levels were 5 and 10 fold the upper limit of the normal range respectively. All patients were treated with α-blockade (phenoxybenzamine-17, mean dose 60±38 mg/day; doxazosin-22; mean dose 9.6±6.1mg/day) along with β- blockade, and high sodium diet and IV saline 24 hours before the operation. The length of the preoperative preparation period was 3.4±2 weeks. Within the first 24-48 hours from surgery, no episodes of hypotension (&lt;90 mmHg systolic pressure) were recorded. Mean systolic BP was 121 ±14 (range 95-150) with a mean diastolic BP of 70 ±11 (range 89-46). In contrast, intraoperative hypotension occurred in 22% of the patients; and BP surge occurred in 36% of patients, mostly during tumor manipulation. There were no differences between subjects with and without such BP rises/falls in terms of pre/post- surgical BP, catecholamine levels or type of medical treatment. Conclusion: In contrast with older literature and previous reports, the patients in our cohort did not experience postoperative hypotension. This is most likely due to tight BP control while avoiding pre-operative hypotension, and adequate volume control. We propose that proper preoperative management in the modern era can drastically minimize intraoperative hemodynamic instability and post-operative hypotension.
OR05-06 The Androgen Receptor Is a Tumour Suppressor in Estrogen Receptor Positive Breast Cancer
Authors: Hickey Theresa E , Selth Luke , Chia Kee Ming , Milioli Heloisa , Roden Daniel , Laven-Law Geraldine , Jindal Shalini , Hui Mun , Ebrahimie Esmaeil , birrell Stephen , Stelloo Suzan , Caldon Elizabeth , Findlay-Schultz Jessica , Abdel_Fatah Tarek , Ellis Ian , Zwart Wilbert , Palmieri Carlo , Sartorius Carol Ann , Swarbrick Alex , Lim Elgene , Carroll Jason S , Tilley Wayne D 
Published: May 2020

Abstract
There is strong interest in targeting the androgen receptor (AR) in estrogen receptor (ER) positive breast cancer, but widespread confusion exits as to what therapeutic strategy - agonism or antagonism - is appropriate. Current understanding of AR predominantly stems from the field of prostate cancer, where AR is the key oncogenic driver and therapeutic target. An ensuing assumption is that AR promotes malignancy in breast cancer and should be therapeutically antagonised. However, compelling pre-clinical data to support this assumption is lacking. Since estrogen stimulates and androgen inhibits the development of normal breast tissue, we hypothesized that AR acts as a tumour suppressor in the breast and that AR agonism is the appropriate therapeutic strategy for ER-driven breast cancer. We tested this hypothesis using a large suite of cell line and patient-derived explant (PDE) and xenograft (PDX) models of breast cancer, including those that were resistant to current therapies and those harbouring genomic anomalies of ESR1 associated with treatment-resistant disease. Across the diverse models we found compelling evidence that AR agonism, but not antagonism, potently and durably inhibited tumour growth. A signature of AR activity derived from the xenograft models positively predicted disease survival in multiple large clinical cohorts of ER+ breast cancer, out-performing other breast cancer-specific prognostic signatures. We also show that an AR agonist can be combined with current ER target therapies such as Tamoxifen or a CDK4/6 inhibitor to maximize growth inhibition. Mechanistically, agonist-bound AR opposed ER signalling by repositioning ER and the co-activator p300 in the chromatin landscape, resulting in down-regulation of cell cycle genes. Introduction of an AR DNA binding mutant had no effect on ER signalling or estrogen-stimulated growth in breast cancer cells. As part of this study, we have generated consensus AR cistromes representing ER+ breast cancer cell lines and ER+ tumours that provide a new understanding of AR activity and clearly show differences to those associated with prostate cancer cell lines and tumours. In conclusion, our data provides a compelling biological rationale for AR agonism as a therapeutic strategy in multiple, clinically relevant contexts of ER-positive breast cancer. These findings should dispel widespread confusion over the role of AR in ER-driven breast cancer, an issue that currently hinders progress in leveraging modern AR-targeted therapies (e.g. selective androgen receptor modulators) that lack the undesirable side-effects of androgens for clinical benefit.
SAT-477 Melanoma Treated with Pembrolizumab Leading to Thyroiditis and Subsequent Hypothyroidism
Authors: Fishel Heather 
Published: May 2020

Abstract
Background: Pembrolizumab (PD-1) is an immune checkpoint inhibitor used for treating melanoma and has been associated endocrine immune-related adverse events.
Case Presentation: 76-year-old Caucasian male presented for evaluation of abnormal thyroid labs. Significant co-morbidities included recurrent melanoma, heart failure, atrial fibrillation, coronary artery disease, type 2 diabetes, hypertension. Patient’s melanoma was being treated with Pembrolizumab. Further history revealed no family/personal history of thyroid disease but a history of mouth cancer treated with radiation over 30 years ago. He denied any recent glucocorticoid or biotin use. Symptoms included worsening fatigue, weight loss, and diarrhea. He was afebrile and vitally stable. Physical exam was unremarkable. Prior to this year, patient had normal thyroid labs. Recent thyroid labs showed TSH of 0.01 uIU/mL (normal 0.34-4.94 uIU/mL), confirmed with repeat labs a week later (TSH: &lt; 0.01, Free T4: 2.23 ng/dL, normal Free T4: 0.7-1.48 ng/dL). There was a high suspicion that these labs were related to Pembrolizumab, but other etiologies were evaluated. Completed thyroid uptake and scan showed no evidence of increased activity (4-hour uptake: 1.6%, 24-hour update: 1.2%). Repeat thyroid labs indicated recovering thyroid function with a TSH: 0.14 uIU/mL, Free T4: 0.49 ng/dL, Free T3: 1.5 pg/mL (normal Free T3 2.3-4.2 pg/mL), TSI: 96% (normal &lt; 140%), TPO Ab: 111 IU/mL (normal TPO Ab &lt; 9 IU/mL). One month later thyroid tests resulted as TSH: 72.81 uIU/mL, Free T4: &lt; 0.40. He was started on levothyroxine, which was titrated over several weeks.
Discussion: Pembrolizumab (PD-1) is an IgG4 programmed cell death 1-directed monoclonal antibody, whose mechanism of action is to inhibit cancer cells ability impede T-cell activation. However, because of this mechanism, some T-cells, will remain activated, leading to autoimmune diseases. PD-1 has been associated with thyroid dysfunction, with an incidence rate as high as 14-20%. The clinical presentation varies from isolated thyrotoxicosis to overt hypothyroidism. In our patient, he developed thyrotoxicosis with subsequent development of hypothyroidism. Generally, the timing of thyroid dysfunction after the initiation of PD-1 ranges from 3 to 40 weeks, with the median onset at week 6. Baseline TSH and free T4 should be obtained with rechecking of these labs monthly for the first 6 months. For patients who present with thyrotoxicosis, Grave’s disease should be ruled out, and initial treatment should include beta-blockers. Hypothyroidism should be treated with levothyroxine with titration to normal thyroid function tests. What remains to be determined is the mechanism in which PD-1 causes thyroid dysfunction and if specific patient characteristics, such as thyroid antibodies, can be used to risk stratify the likelihood of a patient developing thyroid dysfunction.
SUN-700 Fournier’s Gangrene and Diabetic Ketoacidosis Caused by Canagliflozin
Authors: Stamatiades George Alexiades , Kasbawala Kinjal , Gugger Aristea Sideri , Elahee Mehreen , Majumdar Sachin K 
Published: May 2020

Abstract
Introduction
Sodium glucose co-transporter 2 (SGLT2) inhibitors have become an appealing treatment for diabetes due to their favorable cardiac and renal outcomes. However, reports continue to emerge describing potentially life-threatening adverse events such as Fournier’s gangrene (FG) and diabetic ketoacidosis (DKA) associated with their use. Herein, we report a case of simultaneous FG and DKA in a patient taking canagliflozin.
Case Presentation
A 37-year-old woman with a history of type 2 diabetes mellitus, peripheral neuropathy, and morbid obesity (BMI of 45.8 kg/m2) presented to the hospital with left gluteal pain associated with dysuria despite 5-day treatment with trimethoprim/sulfamethoxazole for a presumed urinary tract infection. Approximately 1 month prior, sitagliptin and canagliflozin were added to her regimen due to poor glycemic control on metformin (HbA1c 9.8%). On examination her temperature was 36.9oC, pulse 117 beats/minute, blood pressure 144/79 mmHg and respiratory rate was 19 bpm. She appeared lethargic and had suprapubic tenderness and induration in the left gluteal region extending to the perineum. Laboratory findings revealed an arterial pH of 7.23 and PCO2 of 34 mmHg, a blood glucose of 402 mg/dL, serum bicarbonate 12mmol/L (20-30mmol/L), an elevated anion gap of 24mmol/L (7-17mmol/L) and a lactate of 1.8 mmol/L. Urinalysis showed 4+ glucose and 1+ ketones. Serum β-hydroxybutyrate was 2.49 mmol/L (0.02-0.27mmol/L). A CT scan of the abdomen and pelvis showed marked inflammatory changes with subcutaneous edema and air within the medial left gluteal soft tissues and locules of air extending into the presacral soft tissues suggestive of Fournier’s gangrene. The diagnoses of Fournier’s gangrene and DKA were made. The patient was started on empirical antibiotic treatment and required six surgical explorations with debridement. Interestingly, initial DKA management included only subcutaneous insulin. Only when serum ketones were identified and the anion gap persisted, insulin infusion with aggressive fluid resuscitation was initiated with successful resolution of anion gap metabolic acidosis. She was discharged with a urinary catheter, vacuum dressing, colostomy with instructions to start insulin glargine 18U and discontinue the oral anti-diabetic medications.
Discussion
To the best of our knowledge, this is the first case describing the simultaneous occurrence of two potentially fatal adverse effects of SGLT2 inhibitor therapy; Fournier’s gangrene and DKA. In light of the FDA’s warnings and the growing popularity of SGLT2 inhibitor therapy it is important to be mindful of their more serious and potentially fatal complications. It is also important to promptly terminate SGLT2 inhibitors when harmful adverse effects are suspected to prevent further progression.
MON-319 Impact of Tumor Characteristics and Preoperative IGF-1 Levels on Postoperative Hormonal Remission Following Endoscopic Transsphenoidal Surgery in Patients with Acromegaly: A Single-Surgeon Series
Authors: Cardinal Tyler , Rutkowski Martin , Patel Tanu , Shiroishi Mark , Carmichael John David , Zada Gabriel 
Published: May 2020

Abstract
Introduction:
Acromegaly is a potentially fatal neuro-endocrinopathy caused by a growth hormone (GH)-secreting pituitary adenoma (PA). A lack of consensus on factors that reliably predict patient outcomes in acromegalic patients following endoscopic endonasal approaches (EEA) warrants additional investigation.
Methods:
Pre- and postoperative tumor and endocrinological characteristics from 55 acromegalic patients who underwent EEA for resection of a GH-secreting PA were evaluated as potential predictors of postoperative hormonal remission (defined as age- and sex- normalized IGF-1 levels).
Results:
The 55 patients included had a mean age of 50.1 ± 13.5 years and a mean follow-up time of 18 ± 17.4 months. Fifty-three patients (96%) presented with dysmorphic craniofacial features, with 22 (40%) presenting with prognathism, 22 (40%) exhibiting frontal bossing, and 18 (33%) presenting with macroglossia. Ten (18%) had microadenomas and 45 (82%) had macroadenomas. Five (9.4%) had giant adenomas. Forty-five (92%) tumors were invasive, with 44 (83%) exhibiting infrasellar invasion, 17 (32%) extending above the sella, and 9 (18%) with cavernous sinus invasion. Thirty-three patients (66%) underwent gross total resection (GTR; mean maximal tumor diameter = 1.52 cm), and 17 (34%) underwent subtotal resection (STR; mean maximal tumor diameter = 2.77 cm). Invasive tumors were significantly larger and Knosp scores were negatively correlated with GTR. Thirty-three patients (65%) achieved hormonal remission after EEA resection alone, which increased to 80% with adjunctive medical therapy. Additionally, 90% of patients who underwent GTR and 63% of patients who underwent STR demonstrated postoperative remission. Six patients (11%) exhibited biochemical remission after postoperative medical therapy with an average time to remission of 5.2 months. These patients all had significantly higher preoperative IGF-1 levels and larger tumors than patients who remitted immediately postoperatively. In all patients preoperative IGF-1 levels were inversely correlated with hormonal remission.
Conclusions:
This study indicates that endoscopic transsphenoidal resection of growth hormone secreting pituitary adenomas is a safe and highly effective management strategy for achieving hormonal remission and tumor control for patients with acromegaly. When combined with postoperative medical therapy, we observed endocrinological remission rates of 80% based on normalized IGF-1 levels. Our results support the conclusions of current literature that smaller and less invasive tumors are more likely to be fully resected. We additionally suggest that patients with lower preoperative IGF-1 are more likely to undergo postoperative biochemical remission, irrespective of tumor size and invasion.