bluuebunny/crossref_metadata_2025_split huggingface dataset:
6411 Ozempic - Oh no! Acute Renal Failure Associated with Initiation of Semaglutide
Authors: Barney K , Tahir D , Pannu A , Saeed R 
Published: October 2024

Abstract
Disclosure: K. Barney: None. D. Tahir: None. A. Pannu: None. R. Saeed: None.
Background: Semaglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist which has been proven to reduce weight in those with obesity and improve glycemic control in patients with type II diabetes mellitus. The effect of semaglutide on kidney function has not been well established. The phase 3b SUSTAIN trials revealed that when compared with other GLP-1 agonists, semaglutide exhibited more frequent acute kidney injuries [1-3]. The SUSTAIN 6 trial reported two instances of acute renal failure (ARF) in patients with chronic kidney disease, and one case of ARF in a patient with normal kidney function who was treated with semaglutide [3]. Despite these reports, the SUSTAIN 1-9 trials report no significant decline in kidney function associated with semaglutide [3-6]. Case: We present the case of a 58-year-old male with a past medical history of human immunodeficiency virus (HIV), type II diabetes mellitus, and hypertension who presented to the hospital with ARF after initiation of Ozempic (semaglutide) two months prior to presentation. On admission, vitals were stable and physical examination was benign. His pertinent labs were blood urea nitrogen (BUN) 55 mg/dL, creatinine 5.94 mg/dL (baseline 1.2 mg/dL), and urinalysis with 2+ protein. To determine the cause of his renal failure, urine sodium and creatinine were obtained to calculate his fractional excretion of sodium, which was found to be consistent with intrinsic renal disease. Further workup, including renal ultrasound, urine protein, urine eosinophils, complement and free light chain levels, and creatinine kinase, were unrevealing for cause of intrinsic renal injury. He was managed with intravenous fluids and his creatinine improved to 2.03 mg/dL. Given the acute onset of the patient’s renal failure and recent initiation of Ozempic, it was determined that this medication was the cause of his renal failure, and it was discontinued on discharge. He has since followed up with nephrology and endocrinology. He remains off Ozempic and is doing well. Conclusions: Our case highlights a rare but significant adverse effect of semaglutide on renal function. As the use of semaglutide has increased due to its rising popularity for weight loss and glycemic control in type II diabetes mellitus, the potential for renal injury should be considered and discussed with patients. Furthermore, it is imperative that semaglutide associated renal injury be considered as a cause for ARF in patients taking this medication. This case demonstrates that instances of ARF associated with semaglutide treatment are a cause for concern and further exploration.
Presentation: 6/1/2024
9334 Pancreatic Adenocarcinoma Presenting As Diabetic Ketoacidosis
Authors: Alvarez Julie , Horani Mohamad Hosam , Huynh Jacqueline , Huynh Jacqueline 
Published: October 2024

Abstract
Disclosure: J. Alvarez: None. M.H. Horani: None.
Background: Pancreatic adenocarcinoma is often diagnosed at an advanced stage due to late onset of clinical features including poor appetite, weight loss, weakness, epigastric pain, and rarely impaired glucose tolerance. In patients who present with impaired glucose tolerance or diabetic ketoacidosis without prior history of diabetes, pancreatic adenocarcinoma should be considered. Clinical Case: Patient is a 45-year woman with depression, HTN, irritable bowel syndrome who was found unresponsive by family and presented to the ED for acute encephalopathy. On exam, she was obtunded, tachypneic, with fruity-smelling breath and dry mucous membranes. Initial labs showed glucose of 950 mg/dL (70-99 mg/dL), lipase 539 U/L (8-78 U/L), lactic acid 4 mmol/L 0.5-2 mmol/L), ketone-BHB 170.75 mg/dL (0-2.81 mg/dL), A1c 16.5%. She had no prior history or family history of diabetes. She was admitted to hospital for DKA management.CXR to evaluate dyspnea showed bilateral opacities so CT chest/abdomen/pelvis without contrast was ordered. This showed bilateral multilobar pneumonia, trace pleural effusions, 6.7 x 3.8 cm lobulated fluid collection along pancreatic tail, 12.1 x 6.6 x 4.4 cm RLQ cystic lesion and 4.4 cm lesion vs loculation along the right pelvic sidewall.Initially, GI recommended repeat imaging of the pancreas in 4-6 weeks. OBGYN was consulted for pelvic masses and recommended IR-guided biopsy of right pelvic mass which showed rare mildly atypical mucinous epithelium present, cystic mucinous neoplasm cannot be excluded.CEA and CA125 tumor markers returned elevated. These biopsies showed adenocarcinoma (solid component) and rare atypical mucinous epithelium consistent with cystic mucinous neoplasm (cystic fluid). Patient was deemed medically stable for discharge with recommended follow-up to appropriate specialists. Following discharge, she was officially diagnosed with Stage III (cT4, cN0, cM0) pancreatic adenocarcinoma and started on appropriate chemotherapeutic regimen. Discussion: The current understanding is long-standing type 2 diabetes mellitus as a risk factor for pancreatic cancer based on previous studies.The inverse relationship of pancreatic cancer causing new onset diabetes is more rare, but if cancer is suspected in these patients it could potentially help in the diagnosis of early stage adenocarcinoma. Other case reports have suggested implementation of the enriching new-onset diabetes for pancreatic cancer (ENDPAC) score in addition to CT and EUS as screening for pancreatic cancer may help with earlier diagnosis. References: Menakuru, S. R., Priscu, A., Dhillon, V. S., & Salih, A. (2022). Diabetic Ketoacidosis as the Initial Presenting Symptom of Pancreatic Adenocarcinoma: A Discussion about Screening Utilizing ENDPAC Scoring Coupled with CT Scans and Endoscopic Ultrasound. Case Reports in Oncology, 15(3), 942-949. https://doi.org/10.1159/00052698
Presentation: 6/1/2024
8099 Pembrolizumab Induced Autoimmune Diabetes: An Abrupt Virulent Onset
Authors: Belal H F , Shaykh N , Rajesh A , Chehade J M 
Published: October 2024

Abstract
Disclosure: H.F. Belal: None. N. Shaykh: None. A. Rajesh: None. J.M. Chehade: None.
Background: Pembrolizumab is a programmed cell death protein 1 inhibitors (PD-1i) approved for the treatment of many solid cancers. Although thyroid abnormalities are among the most common endocrine adverse effects associated with PD-1i, insulin-dependent diabetes mellitus can also occur in up to 1% of patients treated with PD1-i.[1] Clinical Case: A 70-year-old female with past medical history of non-toxic multi-nodular goiter and surgical hypothyroidism was diagnosed with gastric cancer. She had no pancreatic abnormality on PET scan. Her management included four cycles of neo-adjuvant chemotherapy: fluorouracil, cisplatin, trastuzumab and pembrolizumab. She had no personal history of gestational diabetes. Prior to initiating neo-adjuvant chemotherapy her A1c was 5.9%. She was not prescribed any anti-diabetic medications. Her grandmother had type 2 diabetes mellitus. On exam her BMI was 23.73 kg/m². She had no acanthosis nigrans, skin tags or abdominal striae. Eighteen days after completing her second cycle of neo-adjuvant chemotherapy, she presented to the emergency department with nausea, vomiting, polyuria and confusion and was found to be in DKA. Her A1c during admission was 7.1%. Imaging revealed no pancreatitis. Labs showed suppressed C-peptide &lt;0.1 ng/mL (1.1-4.4) in the setting of blood glucose 283 mg/dL (71-99). Her GAD-65 antibody was elevated at 902 U/mL (0.0-5.0). She was diagnosed with PD-1i induced autoimmune diabetes mellitus (PD-1i DM) and subsequently treated with basal and prandial insulin. Conclusion: The mechanism of PD-1i DM is unclear. A proposed mechanism is aberrant T cell activation towards pancreatic islet cells. One study found that 59% of patients with PD-1i DM presented with DKA.[1] In this study, the median time of PD-1i DM onset was 20 weeks after the first treatment cycle. Additionally, 40% of these patient had at least one positive pancreatic autoantibody. A recent meta-analysis found the relative risk of PD-1i DM to be 1.56 (95% CI = 0.95-2.57, P = 0.08).2 This relative risk increased to 2.06 (95% CI = 0.48-8.86, P = 0.33) when PD-1i were combined with cytotoxic T lymphocyte antigen-4 inhibitors. References: 1. Stamatouli AM, Quandt Z, Perdigoto AL, Clark PL, Kluger H, Weiss SA, Gettinger S, Sznol M, Young A, Rushakoff R, Lee J, Bluestone JA, Anderson M, Herold KC. Collateral Damage: Insulin-Dependent Diabetes Induced With Checkpoint Inhibitors. Diabetes. 2018 Aug;67(8):1471-1480. doi: 10.2337/dbi18-0002. Epub 2018 Jun 24. PMID: 29937434; PMCID: PMC6054443. 2. Vardarli I, Tan S, Brandenburg T, Weidemann F, Görges R, Herrmann K, Führer D. Risk and incidence of endocrine immune related adverse effects under checkpoint inhibitor mono or combination therapy in solid tumors: a meta-analysis of randomized controlled trials. J Clin Endocrinol Metab. 2023 Nov 15:dgad670. doi: 10.1210/clinem/dgad670. Epub ahead of print. PMID: 37967245.
Presentation: 6/2/2024
12380 Point Of Care Microscale Magnetic Resonance (µNMR) Effectively Monitors Mitigation Of Oxidative Stress By GLP-1 Treatment In A Preclinical Model Of Diabetic Nephropathy
Authors: Alves Andre Topa , Thamarath Smitha Surendran , Fjordside Simone , Sassower Stan , Rohr Rodolfo , Chambers Adam Paul 
Published: October 2024

Abstract
Disclosure: A.T. Alves: ; co-founder. ; LarmorBio. S.S. Thamarath: ; co-founder. ; LarmorBio. S. Fjordside: Employee; Self; Novo Nordisk. S. Sassower, MS.EE: ; Co-founder. ; LarmorBio. R. Rohr: ; co-founder,CEO. ; LarmorBio. A.P. Chambers: Employee; Self; Novo Nordisk.
Oxidative stress is a major driver in the pathogenesis of diabetes, obesity, and related (cardio-renal) disorders. Early detection and prevention of an oxidative stress overload can improve and potentially modify the long-term harmful outcomes associated with chronic hyperglycaemia. A novel assay was developed, that uses µNMR technology to directly monitor oxidative stress from 5 µL of plasma at the point of collection in less than 10 minutes. This assay is highly sensitive to redox changes in the blood microenvironment, including increased ferric iron (Fe3+), protein oxidation and lipid peroxidation. Here, we show the oxidative stress profiling of three groups of ZSF1 rats in a twelve week (11th -23rd week of age) observational study. Vehicle lean, vehicle obese, and glucagon-like-peptide-1 (GLP-1) treated obese ZSF1 rats (n = 8/group) were studied with the assay along with conventional diabetic/metabolic markers, blood glucose (BG), HbA1c, Albumin Creatinine Ratio (ACR). The kidney (immuno)histology studies, alpha-smooth muscle actin (aSMA) and leucocyte common antigen (CD45) were performed at the termination phase of the ZSF1 rats (23rd week of age). The results demonstrated that the assay distinguished obese rats from lean rats with statistical significance (P ≤ 0.01) independent of other in-life diabetic/metabolic markers. Significant correlations with urinary Albumin Creatinine Ratio (ACR, ρ = 0.64, P ≤ 0.0001) were established throughout the study. A positive quantitative association is highlighted with classic histological end points of organ damage, kidney fibrogenesis (aSMA, ρ = 0.23), and inflammation (CD45, ρ = 0.45). Moreover, the assay detected significantly reduced oxidative stress levels (e.g., P ≤ 0.01) in the GLP-1 drug treatment group at five weeks of follow-up. In summary, the µNMR assay effectively monitored oxidative stress and captured disease-modifying therapeutics.
Presentation: 6/1/2024
8071 Prevention Of Acute Kidney Injury By Reducing Mitochondrial Dysfunction In Diabetic Mice
Authors: Kim Min-Ji , Oh Chang Joo , Khang Ah Reum , Jeon Jae-Han , Lee In-Kyu 
Published: October 2024

Abstract
Disclosure: M. Kim: None. C. Oh: None. A. Khang: None. J. Jeon: None. I. Lee: None.
Background: Acute Kidney Injury (AKI) significantly contributes to the pathogenesis of diabetic kidney disease, often exacerbating chronic kidney disease (CKD) and accelerating the need for dialysis. Mitochondrial dysfunction, induced by an increase in reactive Oxygen Species (ROS) and inflammation, plays a crucial role in AKI. This study investigates the prevention of AKI by reducing mitochondrial dysfunction through pyruvate dehydrogenase kinase (PDK) inhibition in an ischemia-reperfusion (IR)-induced AKI model using streptozotocin (STZ)-induced diabetic mice. Methods: We utilized an IR-induced AKI model in STZ-induced diabetic C57BL6/J mice, subjecting them to IR by clamping both renal pedicles. Mitochondrial function tests, cellular apoptosis, and inflammatory markers were evaluated in NRK-52E cells and mouse primary tubular cells after hypoxia and reoxygenation using a hypoxia workstation. Results: In diabetic mice experiencing AKI following IR injury, there was a significant increase in pyruvate dehydrogenase E1α (PDHE1α) phosphorylation. This correlated with a notable increase in mitochondrial damage - TEM images of mice with IR-induced kidney injury revealed distension, loss of cristae, and fragmentation of the mitochondria. We also observed a decrease in oxygen consumption rate (OCR) accompanied by increased ROS, as well as increased production of inflammatory markers. Remarkably, the pan-PDK inhibitor, sodium dichloroacetate (DCA), mitigated apoptosis, attributable to the reduction of PDHE1α phosphorylation levels as well as normalized mitochondrial morphology and function. DCA treatment lessened oxidative stress and decreased the production of inflammatory markers following IR-induced AKI or hypoxia-reoxygenation injury. Conclusion: Restoration of mitochondrial function by DCA effectively alleviated renal injury by decreasing ROS production and inflammation, highlighting its critical role in IR-mediated damage. These results suggest another potential target for renal protection during AKI; therefore, the prevention of acute kidney injury through the inhibition of PDK could be a promising therapeutic approach for treating Diabetic Kidney Disease (DKD).
Presentation: 6/1/2024
7442 Racial Disparities On Outcomes Of Hypoglycemia
Authors: Neupane Shila , Neupane Binita , Karki Sunita , Farooq Umer , Quartuccio Michael 
Published: October 2024

Abstract
Disclosure: S. Neupane: None. B. Neupane: None. S. Karki: None. U. Farooq: None. M. Quartuccio: None.
Introduction: Numerous studies have been conducted on the differences in racial and ethnic groups' access to healthcare; some groups face greater challenges when it comes to insurance coverage and other healthcare services compared to others. Risk factors that may contribute to hypoglycemia include advanced age, concomitant conditions, aggressive hyperglycemia therapy, etc. Research on racial differences in hypoglycemia is limited. Objective:To investigate potential disparities in mortality rates, length of stay (LOS), and overall hospitalization costs between the white and black populations with the diagnosis of hypoglycemia. Methods: Using the National Inpatient Sample (NIS) for the years 2017 through 2020, we carried out a retrospective cohort study of adult patients (age &gt;18) with a primary diagnosis of hypoglycemia. The disease and outcome codes were chosen using the International Classification of Diseases (ICD-10). The analysis was conducted using STATA. Adjusting for potential variables and calculating the adjusted odds ratio(aOR) were done using multivariate regression analysis. The student t-test was utilized to compare continuous variables, while the Fisher exact test was employed to compare proportions. Mortality was the primary outcome of the study; other secondary outcomes included LOS, total hospitalization costs, acute coronary syndrome (ACS), septic shock, pulmonary edema, acute respiratory failure (ARF), mechanical ventilation, acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and cerebrovascular accidents (CVA). Results: There was a total of 804,164 patients with the diagnosis of hypoglycemia; out of them, 515,264 were white, 200,955 were black, and the rest were from other races besides white and black. Blacks had increased LOS than whites by 0.53 days, (6.92 days vs. 7.87 days, p&lt;0.001) and rates of mechanical ventilation (11.96% vs.10.05%, p&lt;0.001). There were other significant outcomes in rates of acute coronary syndrome (1.59% vs.1.38%, p&lt;0.001), septic shock (10.07% vs. 9.90%, p=0.028), and ARF (16.10% vs. 15.27%, p&lt;0.001) on white compared to black population. There was no significant difference in the outcomes of mortality rates, total hospitalization costs, pulmonary edema, ARDS, AKI, and CVA in white compared to black population. Conclusion: In comparison to the black population, the white population had an increase in rates of ACS, septic shock, and ARF. The overall rate of LOS and mechanical ventilation was higher in the black population than in the white population. The rates of mortality, total hospital costs, pulmonary edema, ARDS, AKI, and CVA did not differ between the two groups. To prevent poorer outcomes, more research is needed to understand the pathophysiology and underlying reasons for racial differences in hypoglycemia.
Presentation: 6/1/2024
6700 Risk Of Dementia According To The Reproductive Factors In Postmenopausal Women With Diabetes
Authors: Yu Jin , Han Kyungdo , Yun Jae-Seung , Lee Seung-Hwan 
Published: October 2024

Abstract
Disclosure: J. Yu: None. K. Han: None. J. Yun: None. S. Lee: None.
Risk of dementia according to the reproductive factors in postmenopausal women with diabetes Jin Yu[1], Kyungdo Han[2], Jae-Seung Yun[3], Seung-Hwan Lee[1],[4] [1]Division of Endocrinology and Metabolism, Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea[2]Department of Statistics and Actuarial Science, Soongsil University[3]Division of Endocrinology and Metabolism, Department of Internal Medicine, St. Vincent’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea[4]Department of Medical Informatics, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea Background: Previous studies have suggested a possible association between endogenous estrogen exposure and decreased risk of cognitive impairment or dementia. We aimed to investigate the impact of reproductive factors on the risk of dementia in women with diabetes. Methods:166,245 postmenopausal women with type 2 diabetes aged over 40 who underwent health examination in 2009 were identified from the National Health Information Database. Information regarding reproductive factors were collected through self-administered questionnaires. Incident dementia was defined using diagnosis codes and anti-dementia drug prescription. Cox proportional hazards regression analyses were performed to evaluate the risk of all-cause dementia, Alzheimer’s disease, and vascular dementia according to reproductive factors including age at menarche, age at menopause, reproductive lifespan, parity, and use of hormone replacement therapy (HRT). Results: The mean age and reproductive lifespan were 64.5 ± 8.0 and 33.4 ± 4.7 years, respectively. During the median follow-up of 8.3 years, 25,330 cases of any dementia, including 20,817 cases of Alzheimer's disease and 2,756 cases of vascular dementia were developed. The hazard ratios (95% CI) of all-cause dementia were 1.28 (1.06-1.56) for age at menarche &gt;16 years compared with ≤12 years, 0.71 (0.66-0.77) for age at menopause ≥55 years compared with &lt;40 years, and 0.72 (0.68-0.76) for reproductive lifespan ≥40 years compared with &lt;30 years, respectively. The risk of all-cause dementia was decreased by 11% in women with parity ≥2 compared with 0, and by 16% in women with HRT for more than 5 years compared without HRT. Similar findings were observed for Alzheimer’s disease and vascular dementia. Conclusion: Longer reproductive lifespan was associated with lower risk of dementia in postmenopausal women with diabetes.
Presentation: 6/2/2024
12591 Screening For Metabolic Dysfunction-Associated Steatotic Liver Disease In Diabetes Clinics
Authors: D’Annibale D , Mimoto M , Lis R , Deioma A , Patton H 
Published: October 2024

Abstract
Disclosure: D. D'Annibale: None. M. Mimoto: None. R. Lis: None. A. Deioma: None. H. Patton: None.
Screening for Metabolic Dysfunction-Associated Steatotic Liver Disease in Diabetes Clinics Background: The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with Type 1 (T1D) or Type 2 diabetes (T2D) is elevated, ranging from 22% in T1D to &gt;55% in T2D. However, MASLD screening is not standard in diabetes clinics. The Fibrosis-4 (FIB-4) score and transient elastography (TE) are non-invasive tools to identify those at risk for MASLD and liver fibrosis. To identify at-risk individuals and determine the prevalence of undiagnosed MASLD in our Veterans with diabetes and elevated BMI, we developed a screening protocol using FIB-4 and TE. Methods: Veterans with T1D or T2D and elevated BMI seen in diabetes clinic were prospectively screened. Patients with prior TE or liver disease were excluded. In phase 1, patients were offered in-clinic TE during their visit. In phase 2, a FIB-4 determined referral to TE or hepatology. Results: 274 patients were screened over 8 months. Of 102 qualifying patients in phase 1, 28 had in-clinic TE; of these, 7 (25%) had a kPa of 8 or greater, indicating increased risk of fibrosis, and 16 (57.1%) had a CAP score &gt;280, indicating severe steatosis.In phase 2, a FIB-4 was ordered in 157 qualifying patients. Of 110 completed tests, the FIB-4 was &lt;1.3 (low risk), 1.3–2.6 (indeterminate risk) and &gt;2.6 (high risk) in 61 (55.5%), 44 (40%) and 5 (4.5%), respectively. Patients were referred to TE (indeterminate) or hepatology (high risk). To date, 21 patients have undergone TE, 5 (23.8%) had a kPa of 8 or greater and 11 (52.4%) had a CAP score &gt;280. Conclusions In Veterans with T1D or T2D and elevated BMI, both of our screening protocols identified those with severe steatosis (57.1% vs 52.4%) by TE at rates similar to those reported in the literature. Increased risk of fibrosis by TE was identified in ∼24-25% of our screened population. The high prevalence of undiagnosed MASLD in our Veteran population supports the need for screening in diabetes clinics. Increased provider awareness and point-of-care TE may increase access to screening and improve early diagnosis.
Presentation: 6/2/2024