bluuebunny/crossref_metadata_2025_split huggingface dataset:
THU347 Diffusion Tensor Imaging Of The Tibial Nerve Can Detect Peripheral Neuropathy In Type 2 Diabetes
Authors: Park Hyeong-Kyu , Oh Eunsun , Joon Park Sang , Jung Kim Hye , Byun Dongwon 
Published: October 2023

Abstract
Disclosure: H. Park: None. E. Oh: None. S. Park: None. H. Kim: None. D. Byun: None.
Magnetic resonance imaging (MRI) has played little role for the study of peripheral nerve disease. However, recent technological advances in MRI have provided us more information about neural microstructure and higher resolution in peripheral nerves. The aim of this study is to evaluate whether diffusion tensor imaging (DTI) parameters in MRI can detect peripheral neuropathy in type 2 diabetes (T2D). In this prospective, single-center study, eight T2D patients (mean age, 62.1 ± 10.8 yr; 5 M/ 3F) with peripheral neuropathy and seven healthy controls (65.0 ± 3.3 yr, 7 F) were included. All T2D patients underwent Michigan Neuropathy Screening Instrument questionnaire and quantitative sensory testing. MRI including DTI and axial T2-weight Dixon sequence was performed for each participant. Region of interest analysis was independently performed by one radiologist on each side of tibial nerve at two levels: lower margin of adductor magnus muscle insertion (level 1), and quadriceps femoris tendon at patellar attachment (level 2). DTI parameters including cross-sectional areas (CSA), fractional anisotropy (FA), as well as diffusivity (mean (MD), axial (AD), and radial (RD)) were calculated.
FA was significantly lower in T2D patients with peripheral neuropathy than healthy controls at both level 1 (396 ± 74 vs. 541 ± 141, P&lt;0.05) and level 2 (422 ± 65 vs. 565 ± 108, P&lt;0.05). AD was significantly lower in T2D patients with peripheral neuropathy than controls at level 2 (2,207 ± 492 vs. 2,884 ± 497, P&lt;0.05). RD was significantly higher in T2D patients with peripheral neuropathy than controls at level 1 (1,156 ± 313 vs. 867 ± 147, P&lt;0.05). No difference in the CSA of the tibial nerve was seen in both levels between two groups.
Our results have shown that DTI parameters can detect nerve abnormalities of the tibial nerve in T2D patients, suggesting DTI may be useful as a biomarker in diabetic peripheral neuropathy.
Presentation: Thursday, June 15, 2023
THU354 Enfortumab Vedotin Induced Refractory Hyperglycemia
Authors: Hussein Marwah , Makadsi S , Samantray J 
Published: October 2023

Abstract
Disclosure: M. Hussein: None.
Introduction: Immunotherapy has transformed the treatment landscape of cancer therapy and has created promising hope for cancer patients. While immunotherapy has dramatic efficacy it also has unique toxicity profile. A spectrum of adverse events known as endocrinopathies have been reported with immune checkpoint inhibitors. One of the newer medications is Enfortumab Vedotin, an antibody-drug conjugate. This drug is approved for use in advanced urothelial carcinoma. Case: We present a 68-year-old male with advanced urothelial carcinoma who was started on Enfortumab vedotin after he progressed on a different chemotherapy/immunotherapy. His medical history was significant for prediabetes and morbid obesity.2 weeks after the first cycle of treatment he presented to emergency room with worsening dyspnea and fatigue. Vital signs: Temp: 37.3, HR: 90, BP: 122/65, RR 18, SPO2 95% on 3L O2 through nasal canula. BMI 44 kg/m. Biochemical workup revealed elevated Glucose level of 310 and anion gap of 12. He was started on subcutaneous insulin. He continued to be uncontrolled and was transferred to the ICU and switched to intravenous insulin due to hyperglycemia. His total daily insulin dose was close to 900 units to achieve blood glucose &lt;180. It took 48-72 hours of Intravenous insulin use to get controlled blood glucose. Hgba1c was 7.3%. Insulin antibody, GAD65 and Islet cell antibodies were negative, C peptide 38 for a glucose of 428. Unfortunately, the patient developed multiorgan failure, and passed away on day 7 of the admission. Discussion: The mechanism of this drug inducing hyperglycemia is not well understood as of yet. But the presumed theory here is the patient developed severe acute insulin resistance that led to this refractory hyperglycemia, as evident by the high c peptide level. Absence of beta cell antibodies and elevated c peptide go against an autoimmune destructive beta cell pathway. The other theory is that there is a malfunction in the signaling pathway at the cellular level that led to hyperglycemia. Risk of developing hyperglycemia as a side effect to this medication increase with patient’s personal risk factors for developing diabetes mellitus (prediabetes and obesity). In phase 3 trial of Enfortumab vedotinEV301, treatment related hyperglycemia was reported in 6.4 % of patients. Hyperglycemia occurred more frequently in patients with hyperglycemia at baseline or with a body-mass index of 30 or higher. Conclusion: We are in need for further studies to understand the mechanism of refractory hyperglycemia induced by this drug. Patients on this type of therapy should be monitored very closely for developing a new onset of diabetes mellitus or worsening of established diabetes mellitus.
Presentation: Thursday, June 15, 2023
THU372 Finasteride Induced Hyperglycemia
Authors: Bose Vivek , Santos Martinez Dorothy 
Published: October 2023

Abstract
Disclosure: V. Bose: None. D.S. Martinez: None.
Objective: Finasteride is a 5-alpha reductase inhibitor that is often prescribed to treat benign prostatic hyperplasia in men. It prevents the conversion of testosterone to dihydrotestosterone. Dihydrotestosterone has numerous physiological actions including having effects on physiological function of liver and pancreatic β-cells. While the medicine does not have hyperglycemia as an adverse effect on its profile, this is a case presentation of worsening hyperglycemia in a diabetic patient who was started on 5-alpha reductase inhibitor. Methods: The patient’s clinical course with laboratory data is presented. Results: The patient is a 69 year old obese male presented for hyperglycemia management. He had been treated with GLP1 agonist, SGLT2i and NPH. He noted that since starting finasteride in 2018, his fingerstick glucose levels were higher compared to prior readings. His hemoglobin A1c was also noted to have increased from 7% to 8.2%. He also reported some weight gain. Conclusion: In this case, one can see that the use of 5-alpha reductase inhibitor precipitated worsening hyperglycemia. The inhibition of androgens to their various metabolites may result in pathophysiological states that present as hyperglycemia via insulin resistance and liver disturbances. In patients with diabetes, the addition of finasteride or dutasteride should be cautiously monitored and if possible, avoided to limit worsening hyperglycemia and diabetic complications. Reference: Traish AM. Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. World J Mens Health. 2020 Jul;38(3):323-337. doi: 10.5534/wjmh.200012. Epub 2020 Mar 20. PMID: 32202088; PMCID: PMC7308241.
Presentation: Thursday, June 15, 2023
THU378 Presentation Of Autoimmune Destruction Of Pancreatic Beta Cells By Pembrolizumab In The Setting Of Existing Type 2 Diabetes
Authors: Seidenberg Jacob , Uddin Ansari Mohammad Jamal 
Published: October 2023

Abstract
Disclosure: J. Seidenberg: None. M.J. Ansari: None.
Background: Prembrolizumab, like other immunotherapies, have become a commonplace treatment for certain cancers. Its method of action is binding of the programmed cell death I receptor that blocks the binding of the programmed cell death ligand 1. PD1-1 receptors have been reported to cause autoimmune endocrinopathies including type 1 diabetes. Many patients who present with the adverse reaction of autoimmune diabetes type 1 present with ketoacidosis. However, patients already diagnosed with diabetes type 2 on insulin could have this strong initial presentation masked. Clinical Case: Patient is a 76 year old female who was recently diagnosed with bladder cancer and started on Pembrolizumab. She presented to the endocrinology clinic due to new onset poor blood sugar control with self-tested glucose levels ranging from 300-400. This patient was previously diagnosed with diabetes type II and was taking metformin, Levemir 18 units daily, Humalog 6 units AC. A C peptide level was obtained during euglycemia, which was undetectable, indicating autoimmune destruction of pancreas. Patient was continued on Pembrolizumab due to her clinical response to it and a low probability of pancreatic beta cells functioning again. Patient’s C peptide continued to be undetectable 1 year after her presentation. Conclusion: Autoimmune destruction of pancreatic beta cells from Pembrolizumab is a rare but important adverse effect. Pembrolizumab has been reported to be associated with autoimmune-related pancreatitis leading to type 1 diabetes in only 0.1% of all patients in clinical trials. We present this patient, who was already being treated with insulin for type 2 diabetes and thus was being tested for elevated glucose regularly. She was able to notice a significant change in glucose control prior to onset of symptoms. All patients who take Pembrolizumab, especially those with underlying diabetes, should be regularly evaluated for interference with pancreatic beta cells with regular glucose labs and if hyperglycemia occurs, with a C peptide level should then be ordered.
Presentation: Thursday, June 15, 2023
THU386 Non-diabetic Ketoacidosis As A Rare Complication Of Colitis And Gastritis
Authors: Bosques-Lorenzo Jaymilitte , Irizarry-Garcia Jose J , Baez-Torres Joedali , Colon-Castellano Janet 
Published: October 2023

Abstract
Disclosure: J. Bosques-Lorenzo: None. J.J. Irizarry-Garcia: None. J. Baez-Torres: None. J. Colon-Castellano: None.
Background: Starvation ketoacidosis is a rare cause of metabolic acidosis that is often under-recognized. To our knowledge, no cases of starvation ketoacidosis secondary to colitis and gastritis have been reported. Clinical Case: A 91 y/o male presented to the ER with nausea, vomiting, left lower quadrant abdominal pain, and anorexia that progressed for the previous two days. Physical examination was remarkable for a fragile man, acutely over chronically ill, with reduced skin turgor, dry oral mucosa, but a benign abdominal examination. Vitals signs upon arrival were stable. Basic laboratories showed hypoglycemia at 64 mg/dL (70 - 99 mg/dL), low CO2 17.7 mEq/dL (24 -32 mEq/dL), Na 137 mEq/dL (135 - 145 mEq/dL), Cl 94 mEq/dL (100- 110 mEq/dL). High anion gap metabolic acidosis was demonstrated (25 mEq/L). Renal function was preserved and within the patient's baseline, lactic acidosis was ruled out with normal levels in the laboratory, and CBC was negative for leukocytosis. Patient denied alcohol ingestion upon questioning. There were no suspected infectious foci. Abdomino-pelvic CT scan with oral contrast demonstrated colonic, rectal, and gastric inflammation. Case reevaluation and assessment of the data and history of present illness, led to B-hydroxybutyrate measurement. Surprisingly, ketones levels came back markedly elevated at confirming starvation ketoacidosis in the setting of colitis and gastritis. Patient was treated with aggressive intravenous fluids with normal saline for the first 24 hours, IV glucose to correct hypoglycemia, electrolytes were replaced as needed, and stomach antacids for symptomatic relief of abdominal discomfort. We slowly progressed diet as tolerated and electrolytes were carefully monitored for refeeding syndrome. Few days later the patient was discharged home with full resolution of symptoms. Conclusion: Metabolic acidosis secondary to ketoacidosis is mostly visualized to be exclusive for diabetic patients, leading to under-recognition of starvation ketoacidosis. This is the first case of starvation ketoacidosis secondary to colitis and gastritis. Understanding its association can lead to prompt recognition and treatment, especially in the non-diabetic population.
Presentation: Thursday, June 15, 2023
THU387 Euglycemic Diabetic Ketoacidosis And SGLT-2 Inhibitor Use
Authors: Abrahimi Nora , Abrahimi Aryan , Terrigno Nicole 
Published: October 2023

Abstract
Disclosure: N. Abrahimi: None. A. Abrahimi: None. N. Terrigno: None.
Background: Diabetic ketoacidosis (DKA) is a known adverse effect of SGLT-2 inhibitors. (1) Incidences of euglycemic diabetic ketoacidosis in patients on SGLT-2 inhibitors are reported on less. Clinical Case: A 39-year-old male past medical history of uncontrolled, non-insulin dependent diabetes mellitus and pancreatitis who presented with abdominal pain, nausea and coffee ground emesis. On initial work up, basic metabolic panel showed blood glucose level of 175 mg/dL with an elevated anion gap of 22 mmol/L. Initial differentials included suspicion for euglycemic diabetic ketoacidosis or acute intraabdominal pathology. Venous blood gas showed metabolic acidosis, with a pH of 7.21 and bicarbonate of 9.7 mmol/L, beta hydroxybutyrate was elevated at 7.83 mmol/L. CT abdomen pelvis found a small hiatal hernia, gastric wall thickening, likely gastritis, and was negative for other intraabdominal pathology. Home medications of the patient included dapagliflozin, semaglutide, metformin, gabapentin, and pantoprazole. Patient was admitted with the diagnosis of suspected euglycemic diabetic ketoacidosis and was started on an insulin drip along with D5 0.45 normal saline. Patient’s anion gap was monitored with basic metabolic panel orders every two hours. The insulin drip was discontinued once the patient had two consecutive normal anion gaps and the patient was subsequently started on a subcutaneous insulin regimen. Conclusion: SGLT-2 inhibitors may cause euglycemic diabetic ketoacidosis based on the physiology of the SGLT-2 transporter and the pharmacology of the SGLT-2 inhibitors. (2) Clinical importance of this case report is to consider euglycemic diabetic ketoacidosis in patients on SGLT-2 inhibitors presenting with nausea, vomiting with normal blood glucose to not delay in the diagnosis and treatment of this life-threatening condition. References: (1) Liu J, Li L, Li S, Wang Y, Qin X, Deng K, Liu Y, Zou K, Sun X. Sodium-glucose co-transporter-2 inhibitors and the risk of diabetic ketoacidosis in patients with type 2 diabetes: A systematic review and meta-analysis of randomized controlled trials. Diabetes Obes Metab. 2020 Sep;22(9):1619-1627. doi: 10.1111/dom.14075. Epub 2020 May 21. PMID: 32364674. (2) Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab. 2015;100(8):2849. Epub 2015 Jun 18
Presentation: Thursday, June 15, 2023
THU390 Case Report On Hirata Syndrome: A Rare Cause Of Hypoglycemia
Authors: Pranala Maanasi , Kuttiyil Oommen Varghese Tharakan , Sanker Vivek , Harshitha Vallabhaneni Sree , Ajith Krithika , Thomas Anil 
Published: October 2023

Abstract
Disclosure: M. Pranala: None. V. Kuttiyil Oommen: None. V. Sanker: None. S. Vallabhaneni: None. K. Ajith: None. A. Thomas: None.
Introduction: Hirata's disease, also known as insulin autoimmune syndrome (IAS), is a rare cause of hypoglycemia that is characterized by episodes of spontaneous hypoglycemia and insulin autoantibodies in patients who have not received exogenous insulin. IAS has been associated with rheumatoid arthritis and Graves' disease in 96% of Japanese IAS patients, and it has also been associated with other autoimmune disorders like Graves' disease. Case History: We report a case of 73-year-old male presented with the complaints of episodes of profuse sweating, palpitation and numbness over his head. Patient was initially treated symptomatically and since the symptoms were not resolving further evaluation was done. Two hourly GRBS, c- peptide, insulin levels and serum cortisol of our patient was monitored. Patient had extremely high serum insulin levels. Serum insulin antibodies level was also high (&gt;300 U/ml). CT abdomen ruled out pancreatic pathology. It has been speculated that hypoglycemia occurring in IAS is due to dissociation of insulin from its antibodies in the post absorptive state. Our patient was diagnosed with IAS based on the criteria of Hirata. The age at onset, sex, and duration of hypoglycemic attacks, outcome or treatment, medication taken prior to the onset of IAS and background disease were all taken into consideration. In our patient, hypoglycemia occurred spontaneously in the post-absorptive state 4–6 hours after meal rather than after a 72-hour fast test. Extremely high levels of insulin (&gt;200 µIU/mL) and Serum insulin antibodies found to be &gt;30 U/ml were constructive in the diagnosis of IAS. The patient improved on dietary management alone consisting of frequent small meals. Conclusion: In order to facilitate early recognition and prevent unnecessary investigations, this could be the most significant syndrome in the differential diagnosis of endogenous hyper-insulinemic hypoglycemia (EHH). In such patients with a high index of suspicion, insulin autoantibodies should be examined. IAA prevents insulin to bind its receptor in the postprandial phase, possibly resulting in mild hyperglycemia; thereafter, insulin is released from the complexes irrespective of blood glucose concentrations, thus inducing hypoglycemia
Presentation: Thursday, June 15, 2023
FRI614 Rescuing Aging-associated CD4+ T Cell Dysfunction Via Mitochondrial Transplantation
Authors: Headley Colwyn A 
Published: October 2023

Abstract
Disclosure: C.A. Headley: None.
Mitochondrial dysfunction alters cellular metabolism, increases oxidative stress, and may be principal to the dysregulated signaling and function of CD4+ T lymphocytes in the elderly. In this proof of principle study, we investigated whether the transfer of functional mitochondria into CD4+ T cells that were isolated from old mice and elderly humans, could abrogate aging-associated mitochondrial dysfunction and improve the functionality of aged CD4+ T cells. Our results show that the delivery of exogenous mitochondria to aged T cells led to cellular and mitochondrial reprogramming. This was evidenced by significant mitochondrial proteome alterations that coincided with improved aerobic metabolism and decreased mitoROS in non-activated CD4+ T cells from old mice that received healthy mitochondria. Compared to non-manipulated CD4+ T cells, CD4+ T cells that received functional mitochondria (i.e. mito-transferred CD4+ T cells from old mice) showed improvements in activation-induced TCR-signaling kinetics that correlated with increased frequencies of CD4+ T cells that displayed markers of activation (CD25), increased IL-2 production, as well as enhanced proliferation ex vivo. Immunodeficient mouse models (RAG-KO and TCR-KO) showed that the adoptive transfer of mito-transferred naive CD4+ T cells, protected recipient mice from influenza A and M. tuberculosis infections and promoted effector memory T cell differentiation. Further, mito-transfer improved CD4+ T cell activation in human T cells by decreasing activation-induced senescence. These findings support mitochondria as targets of therapeutic intervention in aging.
Presentation: Friday, June 16, 2023
FRI617 Targeting Unc119b For Insulin Sensitization
Authors: Mittal Ayushi , Buscaglia Paul , Sebag Julien A 
Published: October 2023

Abstract
Disclosure: A. Mittal: None. P. Buscaglia: None. J.A. Sebag: None.
Using high-throughput screening, we identified a new insulin sensitizer, C59, which enhances insulin-stimulated GLUT4 translocation and glucose uptake in glucose storage tissues. C59 treatment improves glucose tolerance in rodent models of insulin resistance. Using Proteome Integral Stability Assay we identified Unc119B as the molecular target of C59. Interaction of C59 with Unc119 was further confirmed by solving the crystal structure of C59 bound Unc119. Unc119B, a protein involved in intracellular trafficking of lapidated cargos, has not previously been implicated in the regulation of glucose homeostasis. Here, we show that deletion of Unc119B protects mice from high fat diet induced insulin resistance compared to DIO WT mice despite similar weight gain, thus, further suggesting an important role of this protein in glucose handling. To understand the mechanism through which Unc119b may inhibit insulin-stimulated GLUT4 translocation, we tested its interaction with TC10α, a prenylated small G-protein that plays a critical role in GLUT4 translocation. Co-immunoprecipitation in CHO cells revealed that Unc119B forms a complex with TC10α. Our results identify Unc119B as a new important regulator of GLUT4 translocation and suggest that it may be acting through the regulation of TC10α activity. This work also identifies Unc119b as a new promising target for the treatment of pre-diabetes and type II diabetes.
Presentation: Friday, June 16, 2023
FRI623 Beta Cell Primary Cilia Mediate Somatostatin Responsiveness Via SSTR3
Authors: Elizabeth Adamson Samantha , Li Alex , Hughes Jing 
Published: October 2023

Abstract
Disclosure: S.E. Adamson: None. A. Li: None. J. Hughes: None.
Somatostatin is an important modulator of beta cell function, but communication between beta and delta cells is not well-understood. Primary cilia are membrane organelles that act as signaling hubs due to their enrichment in certain G-protein coupled receptors and other signaling proteins. We show that somatostatin modulates insulin secretion via somatostatin receptor 3 (SSTR3) located on beta cell primary cilia in mouse islets. SSTR3 and the presence of primary cilia are required for normal beta cell response to somatostatin. Somatostatin signaling leads to beta cell calcium changes, which we characterize here using a beta cell specific genetically-encoded GCaMP6f calcium reporter. Our findings show that ciliary SSTR3 mediates delta to beta cell paracrine crosstalk.
Presentation: Friday, June 16, 2023