bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT238 Ionophore-based Chemical Sensors For At-home Blood Calcium Monitoring
Authors: Ghanbari Ghalehjoughi Nasrin , Adil Nafesa , Wang Xuewei 
Published: October 2023

Abstract
Disclosure: N. Ghanbari Ghalehjoughi: None. N. Adil: None. X. Wang: None.
At-home blood calcium monitoring may revolutionize the management of hypoparathyroidism similarly as glucose meters have done for diabetes management. Measurements of ionized calcium in whole blood via ion-selective electrodes and total calcium in plasma via chromogenic probes have been routinely performed in hospitals for decades. However, calcium monitoring in resource-limited settings such as at home remains challenging. One reason is that large volumes of blood (&gt; 95 μL) are needed for tests using current technologies, which are hard to collect from fingerpicks by patients. Another reason is that complicated and costly designs are used to handle fluids and perform on-site calibration. My group is developing two types of ionophore-based chemical sensors for highly selective detection of blood calcium via low-cost devices and less than 10 μL of capillary blood from the fingertip. In one direction, we develop highly sensitive colorimetric sensors that detect total calcium concentration in blood. Our novel biphasic sensing design does not suffer from optical interference from the colored and turbid blood and therefore tests blood without pretreatment processes. A smartphone with a color analysis app is used to acquire and analyze the colorimetric response to blood samples. In another direction, we develop electrochemical sensors that detect ionized calcium in blood without any fluid handling or on-site calibration. An innovative self-calibration method is designed to reduce the sensor-to-sensor variations and assure the accuracy of the calcium electrodes. The goal is that these methods will empower patients to self-monitor blood calcium and self-manage parathyroid disorders.
Presentation: Saturday, June 17, 2023
SAT253 A Rare Case Of Osteolytic Hypercalcemia Of Malignancy In Acute Myeloid Leukemia
Authors: Elahi Safiya , Baim Sanford 
Published: October 2023

Abstract
Disclosure: S. Elahi: None. S. Baim: None.
Introduction: Acute myeloid leukemia (AML) and other leukemias do not commonly induce hypercalcemia of malignancy (HCM). Limited previous reports of AML-related HCM have largely attributed cases to inflammatory-cytokine-mediated osteoclast activation, with rare reports of calcitriol-mediated HCM and ectopic parathyroid hormone (PTH) production. We describe an unusual case of AML-induced HCM caused by direct leukemic bone invasion, which responded to bisphosphonate therapy. Case Presentation: A 59-year-old female presented with spontaneous bruising and severe leukocytosis concerning for AML. The diagnosis was confirmed by flow cytometry and bone marrow biopsy. Imaging did not reveal any gross destructive bone lesions, but showed soft tissue nodules in the lumbar region which biopsy revealed to be myeloid sarcoma. Prior to initiation of chemotherapy, the patient developed severe hypercalcemia that was treated with aggressive intravenous hydration and zoledronic acid. Intrathecal chemotherapy and high-dose glucocorticoid therapy were initiated thereafter with normalization of serum calcium levels. PTH levels were suppressed. Calcitriol and PTHrP were below normal and undetectable, respectively. Bone turnover markers (C-telopeptide and bone-specific alkaline phosphatase) were significantly elevated prior to administration of zoledronic acid and normalized post-therapy. Calcium levels did not rebound after several interruptions in chemotherapy. Bone marrow biopsy showed focal areas of erosion in trabecular bone consistent with diffuse microscopic osteolytic disease. The patient developed bisphosphonate-induced hypocalcemia following treatment with zoledronic acid, which normalized with treatment with oral calcium carbonate. Discussion: Hypercalcemia of malignancy is a very unusual consequence of AML. No currently-published reports of this phenomenon have described biopsy-proven diffuse microscopic bone erosion associated with AML. We attribute our patient’s severe HCM to large-scale focal bone erosion by AML, independent of and/or associated with concurrent bone resorption mediated by inflammatory cytokines. A single dose of zoledronic acid, a potent suppressor of bone remodeling, achieved long term control of calcium for our patient despite interruption of chemotherapy. Bisphosphonate therapy should be considered an early treatment of HCM in patients with AML due to several potential mechanisms that result in direct calcium release from the skeleton.
Presentation: Saturday, June 17, 2023
SAT260 Asymptomatic Vitamin A Toxicity Causing Hypercalcemia
Authors: Seshan Nandini , Goswami Gayotri 
Published: October 2023

Abstract
Disclosure: N. Seshan: None. G. Goswami: None.
Background: Vitamin A toxicity is an overlooked cause of hypercalcemia. Most cases of hypercalcemia are secondary to primary hyperparathyroidism or malignancy. High levels of Vitamin A are thought to have a direct effect on the bone by stimulating osteoclast resorption or inhibiting osteoblastic formation, therefore increasing the fracture risk. Clinical Case: 56 year old female with history of alcoholic cirrhosis complicated by hepatic encephalopathy, acute kidney injury and now status post liver transplant five months prior that was admitted for asymptomatic hypercalcemia. Initially, hypercalcemia was thought to be secondary to cyclosporine, so medication was discontinued. Hypercalcemia resolved after hydration however she was again readmitted for hypercalcemia found on routine labs. She did not show any other signs of excess vitamin A. Lab work showed calcium 12.5 mg/dL (8.6 - 10.2mg/dL), albumin 4g/dL (3.4 - 4.8g/dL), normal 24 hour urine calcium excretion, eGFR 33mL/min, parathyroid hormone 16.9 pg/mL (8.7-77pg/mL), normal 1,25-OH and 25-OH vitamin D, PTHrP 25pmol/L, AM Cortisol 9mcg/dL, TSH 1.7 mIU/L (0.35 - 4.7mIU/L), serum protein electrophoresis unremarkable. Her vitamin A level was elevated to 113 ug/dL (30-75mcg/dL) and was diagnosed with hypercalcemia due to elevated vitamin A levels. Treatment involved hydration and discontinuation of her multivitamin containing vitamin A. Current limited literature suggests discontinuing vitamin A supplements will normalize vitamin A levels over time. Her vitamin A levels improved over several months. Incidentally, due to complaints of back aches from prior injury, imaging showed acute compression fracture deformities of two thoracic vertebrae. Bone density scan showed normal bone density. Bone turnover markers were elevated indicative of increased bone resorption. Clinical Lesson/Conclusion: Hypervitaminosis A is a rare etiology of hypercalcemia. Vitamin A toxicity may be due to excess ingestion of preformed vitamin A through supplements and animal sources. Though not well understood, the proposed mechanism of vitamin A actions on the bone involves stimulation of bone resorption through increase in osteoclastic activity and inhibition of bone formation through osteoblastic suppression, leading to high serum calcium and increasing the risk of fractures. We present a unique case in a patient who developed hypercalcemia secondary to hypervitaminosis A.
Presentation: Saturday, June 17, 2023
SAT261 Hypervitaminosis A With Hypercalcemia Without Overtly Excessive Vitamin A Intake
Authors: Chiou Cho-Yen , Greck Beth 
Published: October 2023

Abstract
Disclosure: C. Chiou: None. B. Greck: None.
Background: Hypervitaminosis A (hypervitA) is an uncommon cause of hypercalcemia and is due to excessive intake of preformed vitamin A (vitA), i.e., retinoids, especially in emulsified form, a common preparation in supplement. In contrast, provitamin (carotenoids) does not cause hypervitA due to limit in absorption and conversion to vitA. The tolerable upper intake level (UL) and recommended dietary allowance (RDA) of vitA for adult are 3000 and 700 (female) - 900 (male) mcg retinoid activity equivalent (RAE) respectively. While daily intake of vitA &gt; UL carries risk of chronic toxicity, there are reports of hypervitA with chronic intake of vitA below UL. VitA is mainly stored in hepatic stellate cells (HSC). Liver injury can induce HSC to transform, releasing vitA, and losing capacity of vitA storage. Renal insufficiency is known with higher vitA levels in blood. Potentially, the threshold of vitA toxicity from supplement is much less in conditions with hepatic and/or renal disease. Here we report a case without history of excessive vitA intake developed hypervitA in relatively short period of time after hospitalization while in the acute and long-term care unit. Clinical Case: A 57-year male was hospitalized for alcohol related pancreatitis. It was complicated by sepsis, multi-organ failure requiring respirator, parenteral nutrition and/or tube feeding. Mild hypercalcemia was noted 4 weeks after admission, initially intermittently, then persistently and progressively higher, peak of 12.6 mg/dL at 4 months after admission. Prior calcium levels were low or normal up to 6 years before admission. Evaluation of hypercalcemia found low i-PTH, low 1,25-D, hypercalciuria, negative serum protein electrophoresis, and normal PTH-related protein. VitA was surprisingly elevated at 137 [38-98] mcg/dL. Nutritional intake was reviewed. No history of excessive vitA intake. Patient was on total parenteral nutrition (TPN) and/or tube feeding most of time, the range and average of daily preformed vitA supplement from admission to onset of hypercalcemia were 0-1309 and 1006 mcg RAE respectively; while from onset to peak of hypercalcemia, 0-3327 and 1891 mcg RAE respectively. The maximal daily preformed vitA via TPN is 1000 mcg RAE. All preformed vitA in tube feeding is from original formula without extra addition. After discovery of hypervitA, feeding formula was changed to one containing much less preformed vitA, and hypercalcemia slowly improved. Conclusion: HypervitA can develop relatively easily with tube feeding and/or parenteral nutrition with average daily preformed vitA above RDA but way below UL in a susceptible patient. In patients with liver disease and/or renal insufficiency, careful selection of feeding formula and/or nutritional supplement regarding content of preformed vitA, and alert to potential development of hypervitA are advisable.
Presentation: Saturday, June 17, 2023
THU597 Po2-guided Adrenal Vein Sampling In Primary Aldosteronism
Authors: Omata Kei , Tezuka Yuta , Ono Yoshikiyo , Satoh Fumitoshi 
Published: October 2023

Abstract
Disclosure: K. Omata: None. Y. Tezuka: None. Y. Ono: None. F. Satoh: None.
Background: Accurate laterality diagnosis of adrenal aldosterone over-secretion is crucial in determining specific treatment for primary aldosteronism. Although adrenal vein sampling (AVS) is considered as the gold standard method for lateralization, successful canulation to right adrenal vein (RAV) has been reported to be difficult since RAV usually empties directly into inferior vena cava (IVC). In addition, the entrance of RAV is close to that of hepatic vein (HV) or opens to a common trunk with HV in up to 20% of the patients with PA. Cortisol step-up and other proposed indices are not always available during the procedure. Method: AVS was performed in confirmed PA patients between January 2021 and March 2022 at Tohoku University Hospital. During AVS, a small portion (0.3mL) of the sampled veins (RAV, IVC and HV) were analyzed with a blood gas analyzer for partial pressure of oxygen (pO2) measurement. Result: A total of 113 AVS was performed. After excluding inappropriate samples, further analyzed were 113 samples of IVC, 100 of RAV, 109 of HV before cosyntropin stimulation, and 113 samples of IVC, 110 of RAV, 108 of HV after cosyntropin stimulation. We observed an average of 22 mmHg increase of pO2 in RAV than IPV, and 27 mmHg increase than HV before stimulation. The difference between RAV and IPV was 15 mmHg in average and that of RAV and HV was 21 mmHg after stimulation. Similar pO2 step-up was also observed between left adrenal vein and left inferior phrenic vein. Discussion: Here we first describe prominent pO2 step-up in both adrenal veins compared to neighboring non-adrenal veins and peripheral blood. pO2 measurement is easier, faster, less expensive, and requires a very small amount of sample, can be performed by routine equipments in angiography suite, compared to other selectivity indices of successful canulation in AVS. This could also contribute to reducing unnecessary blood sampling, radiation exposure and repeat AVS. pO2 step-up in adrenal vein suggests low oxygen consumption in adrenal glands, which potentially contributes to survival advantage in systemic hypoxic conditions. We propose the novel pO2-guided AVS especially in patients with difficult RAV anatomy and in unexperienced centers.
Presentation: Thursday, June 15, 2023
FRI087 Tuberous Xanthomas And Thrombocytopenia In A Patient With A New Diagnosis Of Sitosterolemia
Authors: Grigoryan Seda , Else Tobias 
Published: October 2023

Abstract
Disclosure: S. Grigoryan: None. T. Else: None.
Introduction/ Background: Sitosterolemia is a rare autosomal recessive disorder characterized by increased plasma sterol levels, that can lead to xanthomas, premature atherosclerosis, and hematologic abnormalities. It is most commonly caused by pathogenic variants in either ABCG5 or ABCG8 encoding sterol transporters that excrete sterols, leading to increased intestinal absorption and decreased biliary excretion of plan sterols. While patients with sitosterolemia have elevated LDL cholesterol levels, the pathophysiology of this process is still unclear. Clinical Case: A 46-year-old man presented with tuberous xanthomas and hyperlipidemia (HLD). In the past surgical removal had been attempted, but the lesions recurred. Prior labs: total cholesterol level was 235 mg/dL, triglycerides 85 mg/dL, HDL 61 mg/dL, LDL 157 mg/dL and mild thrombocytopenia (88 -127 K/uL) with giant platelets and anemia. Prior to the initial visit he started 40 mg atorvastatin with a subsequent increase to 80 mg daily.
Physical exam was notable for periocular xanthelasmas and tuberous xanthomas. Achilles tendons appeared thickened without nodules. There was no family history of premature cardiac disease. Initial labs: Total cholesterol was 206 mg/dL(ref 120-200 mg/dL), TG mg/dL 66 mg/dl (ref 40-200mg/dL), LDL 119 mg/dL (ref 70-130 mg/dL), HDL 62 mg/dL (ref &gt;40), platelets 111 K/uL (ref 150-400 K/uL) with 27.7% immature fraction, Hb 13.6 g/dL (13.5-17 g/dL). Plasma sterols were significantly elevated, campesterol 182.2 mg/L (ref &lt;8mg/L), cholestanol 20.6 mg/L (ref &lt;6 mg/L ), sitosterol 247.2 mg/L (ref &lt;15mg/L ), stigmasterol 11.5 mg/L (ref &lt;0.5 mg/L), indicative of a diagnosis of sitosterolemia. Coronary artery calcification (CAC) revealed a score of 15 which represents 50-75th percentile for age and gender, indicating CAD disease in the patient. Following the diagnosis of sitosterolemia, the patient started ezetimibe 10 mg daily, atorvastatin was decreased to 40 mg daily given the success at decreasing the LDL. Follow up LDL decreased to 58 mg/dL (48% decrease) and non-HLD to 71 mg/dL (53% decrease). Patient was counseled on dietary modification with a focus on avoidance of plant-based oils as well as referred to medical genetics and a dietician for more in-depth counseling. Genetic confirmation is pending. Conclusion: The global prevalence is estimated to be 1/1,000,000∼5,000,000. However, prevalence is likely underestimated due to the significant clinical and biochemical overlap with other hyperlipidemias and great variations in phenotype. Due to the differences in treatment and dietary counseling, it is important to consider this diagnosis, particularly in patients with typical concurrent hematological abnormalities.
Presentation: Friday, June 16, 2023
FRI098 Triglyceride Glucose Index Is Associated With Elevated Blood Pressure, Independent Of Body Mass Index: Analysis From NHANES Study
Authors: Ayesh Hazem , Dean Niswender Kevin 
Published: October 2023

Abstract
Disclosure: H. Ayesh: None. K.D. Niswender: None.
Introduction: Triglyceride glucose index (TyG) is a novel marker of insulin resistance. Elevated blood pressure is associated with significant morbidity and mortality. Early identification of individuals at-risk for cardiovascular disease is essential for effective prevention. There are multiple reports in the literature that triglyceride glucose index (TyG), is associated with elevated blood pressure. In this study, we determined the association of TyG with elevated blood pressure, independent of body mass index (BMI), age, and diabetes status. Methods: A sample of 6799 individuals from the NHANES study population (2011-2020) consisting of all individuals who are above 18 years of age and have serum glucose and serum triglyceride levels available to calculate TyG. Elevated blood pressure status was assigned based on the question“Ever told you had high blood pressure” from NHANES survey.”. TyG was calculated using the formula “ln[fasting TG (mg/dL) × fasting plasma glucose (mg/dL)/2]”. TyG values were divided into 4 quartiles as follow: 1st(&lt;4.36), 2nd (&lt; 4.56), 3rd(&lt; 4.77), 4th(&gt; 4.77). Logistic regression analysis was performed to assess the association between TyG and elevated blood pressure. The analysis was adjusted for age, BMI, and diabetes status. Results: The analysis revealed a significant association between elevated blood pressure and TyG independent of age, BMI and diabetes status. The odds of elevated blood pressure were higher in the 4th quartile TyG compared to the 1st quartile with an odds ratio of 1.39 (95% CI 1.21-1.59), P value &lt; 0.001. Discussion/Conclusion: These results indicate that TyG can serve as a screening tool to identify individuals at risk for elevated blood pressure. Serum triglyceride and glucose measurement are affordable and routine in clinical practice. Implementation of auto-calculation of TyG based on serum triglyceride and glucose values in electronic health records may provide helpful screening and monitoring tools to identify individuals at risk for elevated blood pressure, especially with normal BMI. Future high-quality prospective studies will be helpful to further understand the association.
Presentation: Friday, June 16, 2023
FRI107 Ketogenic Diet Prevents Development Of Atherosclerotic Plaques In Apolipoprotein E Knockout Mice
Authors: Marzolla Vincenzo , Armani Andrea , Mammi Caterina , Gorini Stefania , Camajani Elisabetta , Caprio Massimiliano 
Published: October 2023

Abstract
Disclosure: V. Marzolla: None. A. Armani: None. C. Mammi: None. S. Gorini: None. E. Camajani: None. M. Caprio: None.
Higher aldosterone (aldo) levels are associated with increased risk of cardiovascular ischemic events and mortality. It has been demonstrated that aldo accelerates the development of atherosclerosis in apolipoprotein E knockout mice (ApoE KO). Ketogenic diet (KD) positively impacts several cardiovascular risk factors, yet its effect on atherosclerosis is elusive. We hypothesize that KD protects from development of atherosclerotic plaques in ApoE KO mice, a murine model of atherosclerosis. Eight-week-old male ApoE KO mice were fed a KD (90,5% Kcal from fat, 0.4% Kcal from carbohydrate, 9.1% Kcal from protein) or a moderate high fat die (HFD) (42% Kcal from fat, 42.7% Kcal from carbohydrate, 15.2% Kcal from protein) and treated with aldosterone (aldo, 6 μg/mouse per day) or vehicle through osmotic mini-pumps. Cholesterol content was comparable in KD and HFD. After 4 weeks of treatment, in all experimental groups, intraperitoneal glucose tolerance test was performed, and peripheral blood samples were collected. We analysed cryosections of embedded aortic root to quantify the atherosclerotic plaque size, lipid and collagen content. We assessed vascular inflammation in speciments of thoracic aorta by analysing pro-inflammatory (ICAM-1, VCAM-1, IL-6, TNF-α, MCP-1) and anti-inflammatory (Arg-1, RETNLA, CCL5) genes. In ApoE KO mice treated with aldo, KD determined a significant improvement in glucose tolerance, compared to mice fed a HFD, without any significant effect on body weight. Beta-hydroxybutyrate levels were always significantly higher in KD-mice than in AD-mice, confirming nutritional ketosis in KD-mice. Analysis of aortic root showed that aldo treatment determined a significant increase in atherosclerotic plaque size and lipid content in HFD-mice. Such effects were significantly reduced in KD-mice, suggesting a favorable impact of ketosis in preventing atherosclerosis development. Plaque fibrosis did not differ among treatment groups. Finally, we observed a significant reduction in vascular inflammatory markers in KD-mice, when compared to HFD-mice. In particular, KD determined a significant reduction in gene expression of pro-inflammatory markers (ICAM-1, VCAM-1, IL-6, TNF-α, MCP-1) with the concomitant up-regulation of anti-inflammatory markers (Arg-1, RETNLA, CCL5), compared to HFD. The study suggests KD as a potential non-pharmacological approach to prevent the development of atherosclerotic disease in subjects with high cardiovascular risk.
Presentation: Friday, June 16, 2023