bluuebunny/crossref_metadata_2025_split huggingface dataset:
MON-003 Uterine Contractility in Pregnancies Complicated by Obesity: The Effects of Adipokines on the in Vitro Functional Contractility of Isolated Uterine Samples
Authors: Mustafa Hiba J , Upchurch Weston , Vogel Rachel , Iaizzo Paul , Lisa Gill 
Published: May 2020

Abstract
Objectives: The onset of parturition in pregnant women with obesity is frequently delayed. Without induction, these women are nearly twice as likely as normal-weight to have prolonged pregnancy (≥41 weeks gestation) which is concerning because of associated two-fold increased risk of third-trimester stillbirth. Data from vascular studies have shown that different adipokines have different effects on smooth muscle contractility; either as relaxants or constrictors. However, only few studies have investigated their role in uterine contractility, a relationship that we sought to investigate. Materials and Methods: Total of 22 pregnant women scheduled for term cesarean delivery (CD) were recruited. Strips from the first two participants were used to identify dose response effects for each adipokine, and 20 participants’ data were included in the final analysis. Study groups consisted of normal-weight (N=10) and women with obesity (N=10). Myometrial strips were obtained from the hysterotomy incision at the time of the CD. Muscle strips were mounted within experimental recording baths. Both spontaneous and oxytocin induced contractions were recorded by a custom-build data acquisition software. Adipokines of interest included adiponectin, TNFα, resistin, and omentin. Adipokines were added to the muscle baths after muscle equilibration was achieved. Contractions outcomes of interest included forces, durations, and frequencies. Data comparisons were conducted using Wilcoxon Rank-Sum tests; medians and ranges are presented. Results: Forces of contractions in normal-weight participants were double those studied from participants with obesity (13.9 [9.3-34.3] vs. 8.9 [4.8-23.6], p=0.05). There were no statistically significant differences between contractility outcomes of interest after adding adiponectin, TNFα, and resistin to the muscle baths within and between the study groups. In participants with obesity, compared to baseline, omentin significantly reduced the force of spontaneous induced contractions (p=0.002) and prolonged the period between contractions (p=0.01). Importantly, that effect was not seen in normal-weight participants or in oxytocin induced contractions. Omentin also significantly reduced the forces of spontaneous induced contractions (2.9 [2.2-4.6] vs. 14.4 [4.8-33.6]; p=0.01) and prolonged the period (790.6 [753.0-832.0] vs. 611.4 [128.3-702.7]; p=0.04) in participants with obesity compared to normal-weight participants. Differences were no longer observed after adding oxytocin. Conclusion: In vitro, uterine contractions were reduced in muscle samples prepared from pregnant women with obesity compared to normal-weight counterparts. Omentin may have a role in reduced uterine contractility in pregnant women with obesity and that effect may be corrected by oxytocin administration.
SUN-426 The Impact from AJCC 8Th Edition Staging System on Thyroid Cancer Outcomes by Race And Ethnicity
Authors: Santamaria-Barria Juan Antonio , Graff-Baker Amanda N , Chang Shu-Ching , Khader Adam , Scholer Anthony J , Kledzik-Garland Mary , Goldfarb Melanie 
Published: May 2020

Abstract
Background. Previous studies have demonstrated racial and ethnic outcome disparities among differentiated thyroid cancer (DTC) patients. However, the impact of the 8th edition of the American Joint Committee on Cancer staging system (AJCC8) on these disparities is unknown.
Methods. DTC patients with sufficient tumor and survival data were identified in the National Cancer Database from 2004-2013. The 7th edition of the staging system (AJCC7) and AJCC8 criteria were compared. Multivariable logistic regression was used to evaluate the association between AJCC7 to AJCC8 staging change and race and ethnicity. Cox-proportional hazards regression was then used to evaluate the association between AJCC7 to AJCC8 staging change and overall survival.
Results. Of 33,323 DTC patients, 76.7% were White/Non-Hispanics, 7.6% Blacks, 6.7% Hispanics, 5.4% Asian/Pacific-Islanders, and 3.6% Native-American/Other. Most were female (77%) with papillary DTC (90%). After adjusting for demographic, tumor, and treatment characteristics, Hispanics and Asian/Pacific-Islanders were 27% and 12% less likely to be AJCC7 to AJCC8 downstaged than White/Non-Hispanics (OR=0.73, 95%CI: 0.66-0.81; and OR=0.88, 95%CI: 0.79-0.99, respectively); Blacks had no significant downstaging difference compared to White/Non-Hispanics (OR=0.99, 95% CI: 0.90-1.09, p=0.79). Although AJCC8 was a better survival prognosticator than AJCC7, Cox-proportional hazards regression showed that all AJCC7 to AJCC8 downstaged patients had an increased risk of death compared to patients with unchanged staging, regardless of race and ethnicity: White/Non-Hispanics (HR=2.64, 95%CI: 2.34-2.98), Blacks (HR=1.77, 95%CI: 1.23-2.54), Hispanic (HR=3.27, 95%CI: 2.05-5.22), Asian/Pacific-Islanders (HR=2.31, 95%CI: 1.35-3.98), and Native-American/Other (HR=5.26, 95%CI: 2.10-13.19). However, based on two way interaction, the magnitude of negative change in survival from downstaging was only different between White/Non-Hispanics and Blacks (HR=2.64 vs. HR=1.77, respectively; p=0.04).
Conclusions. Racial and ethnic outcome disparities persist with AJCC8. The proportion of downstaged DTC patients with AJCC8 varies by race and ethnicity, with the least impact found in Hispanics and Asian/Pacific-Islanders. Downstaged patients across all racial and ethnic groups had a decreased survival than those with unchanged stage, with the least impact in Blacks. These disparities should be taken into account when counseling patients about their prognosis with the new AJCC8.
MON-677 A Neuro-Radiological Stroke Mimicker: Non-Ketotic Hyperglycemia Induced Occipital Lobe Hyperdensity Presenting with Seizures
Authors: Pansare Rahul Shashikant , Castillo Mariana Marrero , Scrogin Andrew 
Published: May 2020

Abstract
Background: Acute hyperglycemia in absence of DKA or HHS is a common cause for hospitalization and is termed as Non-Ketotic Hyperglycemia (NKH). NKH-related occipital lobe seizure activity is a rare entity and it’s neuroradiological findings can be confused for acute stroke. We describe a case of NKH-related seizure activity presenting with distinct MRI findings.
Clinical Case: 19-year-old male with DM-1 presented with complaints of burning and numbness involving the left side of face, left upper and lower extremity. These lasted for a few hours and had resolved upon arrival to the ER. At the time of presentation, vitals were stable. Physical examination was significant for flat affect with delayed response to questions without any focal deficits. History obtained from his father revealed that he has had similar episodes of decreased responsiveness during periods of acute hyperglycemia. Laboratory values were significant for glucose of 779mg/dl and sodium of 126mMol/L. Absence of ketones or acidosis ruled out DKA. Normal serum osmolality of 295 ruled out HHS. HbA1c &gt;15% confirmed his non-compliance to insulin use. UDS was negative. Patient was admitted and started on insulin basal/bolus regimen. On the second day of hospitalisation, rapid response was called for seizure-like activity characterised by twitching of left side of face, staring into space and deviation of eyes to left upper corner. This resolved with IV lorazepam without any residual focal deficits. Glucose at the time of seizure was 425mg/dl. He was started on levetiracetam and EEG thereafter revealed no seizure-like activity. CT head and CT angiogram of the head and neck were negative. However MRI showed T2 hyperintensity and restricted diffusion with edema throughout the right occipital lobe. Neurology suspected stroke. However, extensive stroke workup for infectious, autoimmune and hypercoagulable states remained negative. Glucose control was achieved and patient was subsequently discharged on a strict insulin regimen and outpatient follow up with an endocrinologist.
Conclusion: NKH is known to manifest as seizure activity and thus, should be considered an endocrine emergency requiring prompt diabetic management. The suggested pathophysiology for seizures is prolonged hyperglycemia leading to oxidative stress and cellular edema. Furthermore, this may contribute to the unique MRI findings and should not be confused for an acute stroke.
References: Hung WL1, Hsieh PF, Lee YC, Chang MH. Occipital lobe seizures related to marked elevation of hemoglobin A1C: report of two cases.Seizure. 2010 Jul;19(6):359-62. doi: 10.1016/j.seizure.2010.05.006. Epub 2010 Jun 16.
SAT-545 Diabetes Mellitus Is the Risk Factor of Cardiovascular and Cerebrovascular Events in Primary Aldosteronism
Authors: Otsuki Michio , Saiki Aya , Tamada Daisuke , Kitamura Tetsuhiro , Shimomura Iichiro , Naruse Mitsuhide 
Published: May 2020

Abstract
The prevalence of diabetes mellitus (DM) in primary aldosteronism (PA) patients is higher than essential hypertension patients and general population. Though both DM and PA play an important role in the progression of cardiovascular and cerebrovascular (CCV) diseases, the relationship between DM and these diseases in PA patients have not been evaluated.The aim of this study was to investigate whether DM was involved in the risk of CCV events and the progression of renal disorder in PA patients. This study was conducted as a part of the Japan Primary Aldosteronism Study/ Japan Rare Intractable Adrenal Diseases Study (JPAS/JRAS) study and retrospective cross-sectional analysis. The nationwide PA registry in Japan was established at 29 centers, including 15 university hospitals and 14 city hospitals. Patients, who were diagnosed PA between January 2006 and October 2016 and had available data of CCV events and DM, were enrolled (n=2,524). Logistic and liner-regression analysis for CCV events and renal parameters were performed. DM significantly increased the odds ratio of CCV events (OR 1.59, 95% CI: 1.05-2.41). DM also significantly increased the odds ratio of proteinuria (OR 2.25, 95% CI: 1.59-3.16) and had significant positive correlation with declines in eGFR (β=0.05, p=0.02). In conclusion, DM is an independent risk factor for CCV events and proteinuria in PA patients. We should pay attention to whether DM coexists with PA and treat both DM and PA to prevent the exacerbation of CCV diseases and kidney disease. (Supported by AMED grants No. JP17ek0109112/ JP19ek0109352; National Center for Global Health and Medicine, Japan (27-1402/ 30-1008)).
MON-123 Underdiagnosis of Primary Hyperparathyroidism in the Outpatient Setting of an Academic Health Care System
Authors: Dawood Nardeen , Nguyen Dalena , Tseng Chi-Hong , Livhits Masha Jean , Leung Angela M , Yeh Michael W 
Published: May 2020

Abstract
Background: Primary hyperparathyroidism (PHPT) is the leading cause of hypercalcemia in the outpatient population and is associated with nephrolithiasis, osteoporosis, and further end-organ effects. When indicated, parathyroidectomy is an effective intervention. The aim of this study was to assess the prevalence of patients with hypercalcemia resulting from undiagnosed PHPT within a large, urban, academic healthcare system.
Methods: The study population comprised all patients within UCLA Health. The electronic medical record was queried between 01/01/2016-12/31/2018 to include patients with at least two elevated serum total calcium concentrations (&gt;10.4 mg/dL) within a six-month period in the outpatient setting. Causes of secondary and tertiary PHPT were excluded. In concordance with the PHPT diagnostic criteria outlined by the Fourth International Workshop, we evaluated the proportion of patients with hypercalcemia who were further assessed with a serum intact parathyroid hormone (iPTH) test. The study identified cases of PHPT as defined by confirmed elevated serum total calcium concentrations and elevated or inappropriately normal iPTH concentrations.
Results: There were 7102 patients with a single elevated serum total calcium result who never received a repeat assessment within the study period. Although there were 5617 patients with confirmed hypercalcemia, only 2773 (51%) had an iPTH level assessed within six months of the repeated calcium measurement. Of those who underwent iPTH testing, 1931 (69%) were biochemically confirmed to have classic (34.2%) or normohormonal (35.4%) PHPT; the remaining 31% had an appropriately suppressed iPTH concentration relative to the hypercalcemia.
Conclusions: In a large, academic, tertiary healthcare center, over half of the ambulatory patients with confirmed hypercalcemia did not receive further work-up to assess for possible PHPT. Efforts to improve diagnosis of PHPT and expand curative treatment have the potential to decrease the prevalence of nephrolithiasis, bone loss, and further end-organ effects associated with the disease.
SUN-494 A Case of Hyperthyroidism with Multiple Recurrences of Neutropenia After Stopping Methimazole
Authors: Gil Susana Mallea , Sankowicz Silvina , Aparicio Marta , Latorre-Villacorta Laura , Palazzo Adriana , Sosa Maria de los Angeles , Ballarino Carolina 
Published: May 2020

Abstract
Background: The adverse effects of methimazole usually occur in the first 6 months of treatment and they usually are dose dependent. The most severe ones are hepatotoxicity and agranulocytosis, the frequency of the latter is 0.1-0.5% and with a high mortality rate.
Clinical case: A 15-year-old female patient was sent to Endocrinology in May 2017 because of a 4-month history of tremor, palpitations and heat intolerance. Lab tests: WBC: 6,800, neutrophils: 36% (2,448/l), TSH: &lt; 0.06 uU/ml (0.27- 4.7), T4: &gt; 25 ug/dl (4.5 -12), FT4: &gt;7.7 ng/dl (0.93 -1.7), TPO &gt;1,000 UI/ml (&lt;10), TRAb &gt; 40 UI/L (&lt;1.75) which confirmed Graves’ disease. Propranolol 80 mg/day and methimazole 30 mg/day were prescribed. Two months later methimazole dose was increased to 40 mg/d, hematologic lab test was normal. Seven months after starting methimazole the patient presented with febrile neutropenia, methimazole was stopped, methylprednisolone 20 mg/d was prescribed and we increased propranolol to 120 mg/d, neutropenia improved. A month after the first episode of neutropenia, she presented a second episode with a pharyngeal infection, WBC: 6,300, neutrophils: 1%. In December 2017 radioiodine therapy was performed: 15 mCi. Hyperthyroidism was not resolved, she continued with methylprednisolone 20 mg/d and propranolol 120 mg/d, and 6 drops/d of Lugol solution was prescribed. From December 2017 to July 2018, the patient presented 9 episodes of febrile neutropenia, she had a good response to Granulocyte-colony stimulating factor. Serology tests for CMV, VDRL, HIV, Epstein Barr, Toxoplasmosis, hepatitis B and C were all negative. Lab tests for rheumatologic diseases: rheumatoid factor, C3 and C4, electrophoretic proteinogram, antiestreptolysin O, anti-DNA, ANA, anti-Ro/SSA, anti-La/SSB were all negative, and immunoglobulins were normal. Bone marrow aspiration was normal. We could not perform flow cytometry of anti-neutrophil cytoplasmic antibodies (C-ANCA). Hyperthyroidism persisted and a second I-131 treatment was performed (20 mCi) in June 2018. A month later she presented hypothyroidism, levothyroxine was indicated. She continued with episodes of febrile neutropenia until March 2019, 23 months after the diagnosis of hyperthyroidism, 16 months after stopping methimazole and 8 months after having initiated levothyroxine treatment and having normal thyroid levels.
Conclusion: We presented a young female patient with persistent and recurrent neutropenia despite having stopped methimazole, and regardless of her thyroid hormone levels. Although neutropenia usually appears in the first months of treatment, it seldom occurs much later and almost never after stopping the drug. We could not reach an etiological diagnosis of neutropenia, but it is probable that methimazole had triggered an immune-hematological illness associated to Graves’ disease.
MON-924 Susceptibility Genetic Testing and Functional Imaging Modalities in the Management of Bladder Paragangliomas
Authors: Anandappa Samantha , Joshi Mamta , Breen Louise A , Thurairaja Ramesh , Christodoulou Dimitra , Jacques Audrey , McGowan Barbara Maria Cristina , Izatt Louise , Velusamy Anand , Carroll Paul V 
Published: May 2020

Abstract
Introduction: Bladder Paragangliomas (PGLs) are rare neuroendocrine tumors derived from sympathetic paraganglionic tissue within the bladder wall, accounting for &lt;1% of all Pheochromocytomas and Paragangliomas (PPGLs). &gt;40% of PPGLs are associated with inherited syndromes through mutations affecting citric acid cycle enzymes (commonly SDH). Susceptibility gene identification has important implications for long-term care and facilitates targeted cascade genetic screening. Functional imaging using MIBG, Gallium DOTATATE and FDG-PET have become important tools in both diagnosis and treatment (Peptide Receptor Radionuclide Therapy).
Clinical Cases: We report the demographics, clinical characteristics and novel features of 7 patients with bladder PGLs. The series includes 2 females and 5 males, median age 38 years (range 14-68). 5 presented with hematuria and 2 were detected incidentally (1 found on radiological imaging and the other during cystoscopy surveillance). Other symptoms reported were headaches, sweating and palpitations which were relieved by urination. Only 1/7 had a known family history of PGLs. 5/7 patients had elevated plasma normetadrenaline levels and 2 had non-elevated catecholamine metabolites (these 2 patients were asymptomatic).
6/7 patients had genetic testing performed and pathogenic variants were identified in 4 (Fumarate hydratase (FH), SDHA, SDHB*2 genes) and no pathogenic variant identified in 2 patients in our genetic panel of 10 PPGL genes. All primary tumors demonstrated MIBG avidity and in 2 patients assessed there was PGL FDG-PET avidity. Metastatic disease was present in 2 patients (2 SDHB mutations; with 1 MIBG avid bone and 1 FDG-PET avid nodal metastasis). SDHB immunostaining on resected histology was available for 3 cases - absent SDHB immunostaining in the patient with SDHA mutation and strongly positivity in 2 patients (1 with no genetic mutation and in 1 with FH mutation).
Conclusions: The majority (&gt;65%) of patients with bladder PGL have a germ line mutation in a susceptibility gene involving the citric acid cycle. An extended gene panel should be performed in all patients diagnosed with bladder PGLs including SDHA and FH gene mutations. SDH immunostaining of tumour can indicate SDHx gene defects but can be normal in FH mutations. SDHB is associated with increased risk of malignant/metastatic behavior. All 3 modalities of functional imaging (Ga DOTATATE, FDG PET, & MIBG) have a role in the assessment and treatment decision making in the management of bladder PGLs.
SUN-518 Graves’ Disease Newly Diagnosed in the Setting of Hypokalemic Periodic Paralysis in an HIV+ Patient
Authors: Nosova Emily V , Japp Emily , Brown Sheldon T , Cohen Alan J , Greenberg Pietra D 
Published: May 2020

Abstract
Relevance: A rare yet distinct cause of sudden onset paralysis is severe hypokalemia associated with thyrotoxicosis. This is thought to be associated with mutations in genes encoding cellular potassium channels. We report a case of acute onset paralysis with profound hypokalemia and a new diagnosis of Graves’ thyrotoxicosis in a previously asymptomatic African American, HIV+ man on highly active antiretroviral therapy (HAART) for over 8 years.
Clinical case: A 49-year-old man with hypertension and HIV presented with acute paralysis of his bilateral upper and lower extremities. His initial potassium was 1.8 mEq/L (3.5-5.0). Prior to sudden onset loss of motor strength, he denied any preceding palpitations, tremor, anxiety, diaphoresis, hyper-defecation, weight loss, heat or cold intolerance, neck pain, increase in neck girth or difficulty swallowing, proptosis or other ocular symptoms. He has no family history of thyroid disease. He had an enlarged palpable thyroid without nodules and no audible bruit. There was no periorbital edema or proptosis, and no signs of dermopathy. A thyroid ultrasound showed a hyperemic and diffusely enlarged thyroid gland without nodules. Labs included a TSH of 0.007 mCU/mL (0.43-3.8), Free T4 2.1 ng/dL (0.71-1.85), Total T3 229.6 ng/dL (58-194), and thyrotropin receptor antibody 2.6 IU/L (0-1.75). The CD4+ count was 146 in 2010 with a slow gradual rise to 673 in 2019, and HIV viral load was undetectable. There were no offending medications or supplements identified. With aggressive potassium repletion, the serum potassium improved to 4.6 mEq/L and he regained normal strength within several hours. He was started on Methimazole 10mg daily and propranolol 10mg TID. At one month, the thyroid function tests normalized. Methimazole 10mg daily was continued and propranolol was tapered off. He remains euthyroid. Genetic testing is pending.
Conclusions: Graves’ disease is the most common thyroid disease triggered by immune reconstitution in HIV + individuals on HAART. The incidence of thyroid disease in HIV patients on HAART is higher in women and Africans with a 1.5-2 fold increase compared with the general population [Muller et. al, Eur Thyroid J 2019;8:173-185]. Despite a higher incidence of hyperthyroidism in women, over 95% of cases of hypokalemic periodic paralysis have been reported in men, with a 10-fold higher incidence among Asians compared to Westerners. There has been one prior case report of Thyrotoxic Periodic Paralysis in an HIV + patient and this was in a Polynesian male (Brown JD et al. Hawaii Med J 2007). To our knowledge, this is the first case report of an African American HIV+ patient with this disorder. An association with mutations in the Kir2.6 gene (encodes a potassium channel, is expressed in skeletal muscle, and is transcriptionally regulated by thyroid hormone) has been proposed [Ryan et. al, Cell 2010 January 8; 140(1):88-98].