bluuebunny/crossref_metadata_2025_split huggingface dataset:
THU373 Refractory Hypoglycemia In A Patient With Metastatic Cholangiocarcinoma: Abstract
Authors: Gabriela Fernandez Maria , Selen Daryl J 
Published: October 2023

Abstract
Disclosure: M.G. Fernandez: None. D.J. Selen: None.
Background: Nonislet cell tumor hypoglycemia is an uncommon but severe complication of cancer. It results from tumoral overproduction of insulin-like growth factor 2 (IGF-2), which inhibits hepatic glycogenolysis and the release of glucagon and growth hormone (GH). These three mechanisms can result in severe and refractory hypoglycemia. Clinical Case: We present a case of a 57-year-old female newly diagnosed with metastatic cholangiocarcinoma who was admitted to the hospital after an episode of syncope at home in the setting of hypoglycemia with a serum blood glucose of 17 mg/dL (N &gt;60 mg/dL). During the hospital admission, evaluation of hypoglycemia included a normal TSH of 1.170 (reference range [RR] 0.3-5.5 mIU/ml), fasting morning cortisol of 23.3 (RR &gt;14-15 μg/dL), and a negative sulfonylurea screen. In addition, the patient had an undetectable level of Insulin &lt;3.0 (RR 3-25 mU/L), Beta-hydroxybutyrate &lt;0.10 (RR 0.02-0.27 mMol/L), C-peptide &lt;0.1 (RR 0.5-3.3 ng/ml), and Pro-insulin &lt;1.6 (RR 3-20 pmol/L). CT of the abdomen revealed disease progression with innumerable bilateral enhanced hypoattenuating masses in the liver. Management for refractory hypoglycemia required nutrition optimization, nausea control, close glucose monitoring, IV dextrose infusion, and intermittent intravenous glucagon for episodes of severe hypoglycemia (&lt;40 mg/dL). During the hospitalization, the patient received the first cycle of chemotherapy with gemcitabine, cisplatin, and dexamethasone. On day 10 of admission, the IGF-2 resulted at 120 ng/ml (RR 180-580ng/ml) and IGF-1&lt;10 (RR 50-317 ng/ml) with an IGF-2/IGF-1 ratio greater than 100 (cut off&gt;10), diagnostic of a large nonislet cell tumor as the most likely cause of her severe hypoglycemia. Artificial nutrition did not align with this patient’s goals of care, so she was discharged from the hospital with a FreeStyle Libre 2 for continuous glucose monitoring. However, two weeks later, she returned to the emergency department with hypoglycemia (&lt;40 mg/dL), ultimately choosing to pursue hospice. Conclusion: Patients with large liver tumor burden can experience hypoglycemia due to low glycogen content in the liver. In addition, these patients can have decreased oral intake and weight loss, which confounds the clinical scenario and can delay diagnostic workup. Patients with refractory hypoglycemia and nonislet cell tumors require further evaluation for IGF-2 production, and alternative temporary nutritional options should be discussed with the patient immediately. Therapeutic options depend on the ability to treat underlying cancer. Palliative chemotherapy, surgery, or radiation can be considered to control the tumor and improve hypoglycemia for quality of life when the cancer is otherwise untreatable.
Presentation: Thursday, June 15, 2023
THU374 Fulminant Type 1 Diabetes Mellitus And DKA Secondary To Pembrolizumab
Authors: Iqbal Iqra , Alam Khan Muhammad Atique , Ahmad Mobeen , Mehreen Rameesha 
Published: October 2023

Abstract
Disclosure: I. Iqbal: None. M. Khan: None. M. Ahmad: None. R. Mehreen: None.
Introduction: Pembrolizumab is a programmed cell death receptor (PD-1) binder on T cells, which promotes their activation against cancer cells. It can also cause unwanted T cell activation against the body’s own cells, leading to type 1 diabetes mellitus (DM1), among other autoimmune phenomena. We are reporting a case of a new onset pembrolizumab-induced fulminant DM1 who presented with diabetic ketoacidosis (DKA). Despite the emerging data on immune checkpoint inhibitors (ICPI), fulminant DM1 with DKA in a previously nondiabetic patient is still uncommon. Case Presentation: A 66-year-old female with a history of recurrent metastatic non-small cell lung cancer (NSCLC) presented to the emergency room (ER) with an extensive itchy rash. She was enrolled in a clinical trial for NSCLC, where she received immunotherapy with pembrolizumab for five months. Rash was treated outpatient for scabies, with no improvement. She was then started on prednisone 40mg daily and betamethasone 0.05% cream. She applied the cream daily but took prednisone orally for only one day, after which she could not tolerate it due to anxiety and restlessness. She ran out of betamethasone three days before coming to ER. On admission, vitals were: Heart rate 90 beats per minute, blood pressure 119/95 mmHg, respirations 20/minute. The exam showed flushed cheeks, red and dry macules on the skin with excoriations, and dry mucus membranes. Random blood glucose levels (BSL) were 660mg/dl. Labs were; HCO3 16mmol/L, Beta-hydroxy butyrate 20mmol/L, anion gap 17mmol/L, Hemoglobin A1c: 5.6%. For DKA, we started an insulin drip. Workup revealed very low C-peptide levels of 0.2ng/ml, with a concomitant BSL of 500mg/dL. Anti-islet cell and anti-glutamic acid decarboxylase antibodies (anti-GAD) were positive with levels of 0.04 nmol/L and 0.07 nmol/L, respectively. Once she stabilized and the anion gap closed, she was transitioned to subcutaneous insulin and discharged on 42 units of Lantus, along with 12 units of premeal Lispro and sliding-scale insulin. She was removed from the clinical trial due to complications. Unfortunately, she got readmitted with influenza A, Staphylococcus aureus bacteremia, and another episode of DKA, complicated with respiratory failure, and she decided on hospice. The patient passed away after two days. Conclusion: Immune-related adverse event of new-onset fulminant DM1, leading to DKA, is a serious and potentially fatal complication of pembrolizumab. For patients receiving pembrolizumab, who have uncontrolled BSL, we suggest checking the anti-islet cell and anti-GAD antibody levels and DKA risk stratification to allow the timely initiation of insulin and prevent further complications.
Presentation: Thursday, June 15, 2023
THU384 Too Sweet To Digest; A Case Of Persistent Lactic Acidosis Secondary To Glycogenic Hepatopathy
Authors: Ayub Tooba , Alejandra Robles Lydia , Sami Faria , Saleem Sania , Guntupalli Saroja 
Published: October 2023

Abstract
Disclosure: T. Ayub: None. L.A. Robles: None. F. Sami: None. S. Saleem: None. S. Guntupalli: None.
Glycogenic hepatopathy (GH) is an under-recognized cause of persistent lactic acidosis and hepatomegaly in patients with uncontrolled DM and diabetic ketoacidosis (DKA). A 19-year-old female with history of type 1 DM with recurrent DKA presented with complaints of nausea, vomiting and abdominal pain for 1 week. Physical exam showed normal vitals and lower abdominal tenderness. Her initial labs showed glucose 250 mg/dl, high anion gap metabolic acidosis with beta hydroxy butyrate of 11.3 mmol/l, lactic acid 3.2mm/l, and mild transaminitis. She was diagnosed with DKA and started on insulin drip. Anion gap responded to IV insulin and fluid therapy and was transitioned to SQ insulin. However, she had increase in her lactic acid (8.2mm/l), without hemodynamic compromise, despite fluid resuscitation. Secondary work up including blood, urine, sputum cultures were non diagnostic for an infectious etiology. Abdominal imaging showed a liver span of 26 cm. There were no signs of end organ hypoperfusion, medication or toxin mediated insult as evident by normal transthoracic echo, iron studies, urine drug screen, alcohol level and negative hepatitis panel. Review of prior hospitalizations showed recurrent episodes of DKA with similar uptrend in lactic acid levels with negative secondary work up. Prior imaging revealed hepatomegaly during DKA episodes with resolution after strict glycemic control. Given uncontrolled DM type 1 with reversible and recurrent hepatomegaly, transaminitis, hyperlipidemia and elevated lactic acid, a clinical diagnosis of glycogenic hepatopathy was made. Patient declined liver biopsy due to concerns for complications. She was discharged on home insulin regimen with outpatient follow up. GH or hepatic glycogenosis is a reversible cause of lactic acidosis and hepatomegaly seen in uncontrolled DM type 1. Pathogenesis involves presence of fluctuating levels of hyperglycemia and insulin, concomitantly, that leads to glycogen storage. Insulin inhibits gluconeogenesis resulting in decreased conversion of pyruvate to glucose and high lactic acid levels, in the absence of any infectious, metabolic and hypoxic etiology. Lactic acidosis can be worsened when treated with high dose Insulin. Definite diagnosis of GH requires liver biopsy or gradient dual-echo MRI but can be made clinically in the setting of uncontrolled DM1, hepatomegaly, transaminitis and elevated lactic acid levels. Prompt recognition of GH can prevent unnecessary diagnostic testing and can decrease the duration of hospital stay. Treatment is strict glycemic control with resolution of condition and no long-term complications.
Presentation: Thursday, June 15, 2023
FRI626 Association Between Fasting Serum C-peptide Values And The Presence Of Chronic Kidney Disease In Patients With Type 2 Diabetes Mellitus
Authors: Leyva Figueroa Laura , Gomez-Perez Francisco J , Gonzalez-Valdivia Fernando , Cuevas-Ramos Daniel 
Published: October 2023

Abstract
Disclosure: L. Leyva Figueroa: None. F.J. Gomez-Perez: None. F. Gonzalez-Valdivia: None. D. Cuevas-Ramos: None.
Background: High C-peptide levels have been associated with microvascular complications, although there is controversial evidence in patients with T2DM. Objective: To correlate fasting serum C-peptide values in patients with T2DM with diabetic nephropathy. Hypothesis: In patients with type 2 diabetes mellitus there is a positive correlation of minimum r=0.3 between fasting C-peptide, albumin/creatinine ratio (ACR) and glomerular filtration rate (eGFR). Research Question: Is there a significant and independent correlation between fasting C-peptide values, ACR, and eGFR in patients with type 2 diabetes mellitus? Methods: Retrospective, cross-sectional, observational, real-world study, in 551 type 2 diabetic patients. Data was collected from the electronic clinical records. Microalbuminuria was defined as an ACR equal or greater than 30, and eGFR was calculated by CKD-EPI 2021. Fasting C-peptide was measured by immunochemiluminescence. Continuous variables were expressed as means +/− standard deviation, while categorical variables will be expressed as percentages. We used one-way ANOVA to compare continuous variables between groups, and Chi-square test to compare categorical variables. Multivariate logistic regression analysis was used to analyze the independent relationship between C-peptide quartiles, eGFR, and ACR, adjusted for weight, insulin, and disease duration. Results: 551 patients were evaluated (63% were women), with mean age of 62 ±11 years old, and a HbA1c of 8.4%. Median (interquartile range) of disease duration was 20 years (12-25), with a C-peptide median level of 1.6 (0.9-2.4 ng/ml), with no significant difference by gender. A statistically significant direct relationship was found between a higher C-peptide quartile and higher ACR (F=9.8, p= 0.03). A significant correlation was also found between C-peptide and ACR (r=0.16, p&lt;0.001), and also with eGFR (r=−0.11, p=0.01). Using a multivariate regression analysis we identified an independent association between C-peptide and ACR (beta=44.7, CI95%, 16-73, p=0.002), and also with eGFR (beta −2.7, CI95% −4.7 to −0.6, p=0.01). Conclusions: A significant and independent association was found between C-peptide levels and kidney function and albuminuria. Future studies may confirm that C-peptide can stand as an early marker for diabetic nephropathy.
Presentation: Friday, June 16, 2023
FRI640 Adherence To Diabetic Retinopathy Screening Guidelines In An Adolescent Patient Population
Authors: Sami Asra , Gurnurkar Shilpa , Vyas Neha 
Published: October 2023

Abstract
Disclosure: A. Sami: None. S. Gurnurkar: None. N. Vyas: None.
Diabetic retinopathy (DR) is a microvascular complication of diabetes mellitus (DM) and a major cause of vision loss. Risk factors for development of DR include duration of diabetes and poor glycemic control. Adolescents with diabetes face unique challenges in attaining glycemic control due to hormonal changes and transition from pediatric to adult care. The aim of this study was to determine the adherence to ADA DR screening guidelines in an ambulatory Endocrine clinic’s adolescent patient population, and to determine factors associated with non-adherence. Methods: A retrospective chart review was conducted on patients (ages 12-18) with type 1 diabetes (T1D) and type 2 diabetes (T2D) at Nemours Children’s Hospital between 2015 and 2022, with 142 charts included. Based on the ADA DR screening guidelines, patients with T1D were included if they had diabetes for at least 5 years and all patients with T2D between the ages of 12-18 were included. Patients were considered adherent if they met one of the following criteria: Recorded eye exam within the past 1 year (for T2D) or the past 2 years (for T1D) documented in chart OR attendance to an appointment with Nemours ophthalmology within a year of referral. Age, sex, ethnicity, race, insurance type, and HbA1c were recorded. Univariate binomial logistic regression analysis was completed to determine the association of the factors to DR guideline adherence. Results: Data analysis showed 69% adherence and 31% non-adherence to DR screening guidelines. The non-adherence rate was comparable to other studies in adult and youth populations. Patients with T2D were 58.3% less adherent to DR screening guidelines compared to patients with T1D (OR= 0.417, 95% CI 0.178-0.978). We did not find statistical significance with other factors. The results highlight adolescent patients with T2D as a target population for future studies aimed at improving adherence to DR screening guidelines.
Presentation: Friday, June 16, 2023
FRI643 Tirzepatide Associated Partial Small Bowel Obstruction: A Case Report
Authors: Mathew Anoopa , Hannoodee Hanan 
Published: October 2023

Abstract
Disclosure: A. Mathew: None. H. Hannoodee: None.
Glucagon-like peptide-1 receptor agonists (GLP1 RA) are quickly becoming an adjunctive treatment modality for people with type-2 diabetes and is approved for chronic weight management. Tirzepatide has a dual GIP/GLP-1 RA action and has a synergistic effect when administered together. GLP-1 RA are associated with improved cardiovascular and all-cause mortality outcomes in patients with type-2 diabetes. Tirzepatide is associated with gastrointestinal (GI) side effects like nausea, diarrhea, abdominal pain, decreased appetite, and constipation. This case report discusses a case of small bowel obstruction (SBO) that was noted after patient was changed from dulaglutide to tirzepatide. Mr. X is a 61 y/o male with PMHx of type-2 DM, HTN, and HLD who presented to ER for severe epigastric pressure- like 7/10 abdominal pain. No association with food intake. He had 1 episode of semi-loose stools. Denied any abdomen cramping, sick contacts, nausea/vomiting, fever/chills, or constipation. His previous endoscopy was only relevant for benign colonic polyps, which were removed. He had been on GLP1 RA for more than a year, and previously on dulaglutide 3mg, which was switched to tirzepatide 2.5mg 5 weeks ago. He was able to tolerate the medication without significant side effects and was recently up-titrated to 5 mg. Labs showed WBC 7.2, Hb 13.6, Cr 1.45, BUN 12, lipase 25, and normal LFTs. Abdominal X-ray and CT abdomen were noted to be significant for a partial vs evolving SBO without any identifiable small bowel intrinsic pathology. Mr. X was managed conservatively with fluids, NPO diet, and pain medications. Serial abdominal images were obtained, and he was eventually advanced to soft diet. Tirzepatide was discontinued on discharge. As a response to enteral nutrition, distal small bowel and colon release GLP-1 hormone. Exogenous and endogenous GLP-1 are associated with reduced gastric motility. GLP 1 RA and dual GIP/GLP-1 RA are advised to be used with caution in patients with established gastroparesis, as they can worsen the symptoms. GLP-1 effect on small intestinal motility is not extensively studied, however, small bowel motility inhibition was noted in animal models. Some of these actions were dose-dependent. There are some case reports of SBO due to GLP-1 RA. An observational cohort study noted an increased incidence of SBO with GLP1 RA when compared to SGLT2i. They noted most incidents of SBO happened early within the initiation of therapy (within 3 months). At the time of writing this abstract, there are no published SBO case reports associated with tirzepatide. Further large-scale clinical trials need to be conducted to explore the association of SBO in patients with GIP/GLP-1 and GLP-1 RA. These studies will help guide if these drugs should be contraindicated or used with caution in people with a previous history of SBO or colonic obstruction.
Presentation: Friday, June 16, 2023
FRI645 A Case Of Diabetic Ketoacidosis After Initiation Of Decitabine And Venetoclax Chemotherapy
Authors: Maini Rohan , Milosavljevic Jovan , Aleksic Sandra 
Published: October 2023

Abstract
Disclosure: R. Maini: None. J. Milosavljevic: None. S. Aleksic: None.
Background: Decitabine, a pyrimidine nucleotide analogue, and venetoclax, a Bcl-2 inhibitor (ABT-199), are chemotherapy agents used for the treatment of myelodysplastic syndromes. Clinical trials have shown hyperglycemia as an adverse reaction for both of these medications, but DKA has not been reported. Clinical Case: A 71-year-old woman with a history of T2D and myelodysplastic syndrome (MDS) presented with nausea, vomiting, and diarrhea for five days. Initial tests revealed blood glucose 839 mg/dL, an anion gap of 19 mEq/L (n 7-16), serum bicarbonate 14 mmol/L (n 20-30), venous pH of 7.24, and hydroxybutyrate &gt;4 mmol/L (n&lt; 0.3), consistent with diabetic ketoacidosis. Her anti-glutamic acid decarboxylase autoantibodies were negative. Chest CT showed bibasilar pulmonary opacities, concerning for multifocal pneumonia. She was placed on an insulin drip and fluids according to the institution's protocol and her anion gap closed within a day. She was transitioned to subcutaneous insulin. The patient had well-controlled T2D, with an HbA1c of 5.6% two weeks before her presentation and an admission fructosamine level of 377 umol/L (n 200-285). Her BMI was 25. Her only T2D medication was semaglutide 0.25 mg weekly but had not taken a dose in three weeks due to the national shortage. Five weeks prior to this presentation, she began weekly chemotherapy infusions of decitabine and oral venetoclax as part of a clinical trial (2021-13466) for MDS treatment, with her last infusion one week before her presentation. Conclusion: This is the first case to demonstrate DKA precipitated by decitabine and venetoclax treatment. While both agents have been linked to severe hyperglycemia in safety clinical trials, DKA has not been previously reported. Data from animal studies have shown that prolonged exposure of mouse islets to Bcl-2 antagonists increase levels of reactive oxygen species and induce pancreatic β cell apoptosis (1). Further research is needed to assess the benefits and risks of this chemotherapy regimen in patients with diabetes. References: 1.) Aharoni-Simon M, et al. Bcl-2 Regulates Reactive Oxygen Species Signaling and a Redox-Sensitive Mitochondrial Proton Leak in Mouse Pancreatic β-Cells. Endocrinology. 2016 Jun.
Presentation: Friday, June 16, 2023
FRI646 Dulaglutide-induced Acute Liver Injury - A Case Report
Authors: Shahid Maham , Hamza Ameer , Vather-Wu Daniel , Sultan Senan , Nabizadeh Payam 
Published: October 2023

Abstract
Disclosure: M. Shahid: None. A. Hamza: None. D. Vather-Wu: None. S. Sultan: None. P. Nabizadeh: None.
Introduction: Drug-induced liver injury (DILI) accounts for almost 10% of all cases of acute hepatitis and can occur within days to months of initiation of a medication. Outcomes can vary from spontaneous resolution on discontinuation of the offending agent to fulminant hepatic failure requiring transplant or even death. Dulaglutide is a GLP-1 receptor agonist that augments glucose-dependent insulin secretion and slows gastric emptying. It is a weekly injectable medication for management of type 2 diabetes mellitus (T2DM). Commonly reported side effects include nausea, vomiting, appetite suppression, and diarrhea or constipation. To date, there have been less than five published case reports of Dulaglutide-induced acute liver injury (ALI). Hereby, we present a case of Dulaglutide-induced ALI with coagulopathy that resolved with the use of N-acetylcysteine (NAC), steroids, and cessation of the medication. Clinical Case: A 38-year-old female with past medical history of T2DM, hypertension, dyslipidemia, and hypothyroidism presented with complaints of nausea, vomiting and epigastric discomfort for 5 days. She reported having malaise and lethargy for a month since she was started on Dulaglutide for management of her T2DM. Her physical examination was unremarkable. The laboratory workup showed AST &gt;6000 U/L, ALT &gt;3300 U/L, ALP 231 U/L, total bilirubin 3.3 mg/dL, direct bilirubin 2.3 mg/dL, indirect bilirubin 1.0 mg/dL, PT 40.3 seconds, INR 3.36 and negative toxicology screening. She was started empirically on intravenous NAC and methylprednisolone, and was followed by serial biochemical measurements. Further workup revealed no evidence of acute viral hepatitis, autoimmune hepatitis, metabolic (alpha-1-antitrypsin deficiency, Wilson disease, hemochromatosis) or alcohol-related ALI. There were no clinical or imaging findings suggestive of ischemic hepatopathy, venous outflow obstruction or biliary obstruction. After ruling out other causes, the ALI was attributed to Dulaglutide use. AST and ALT improved significantly within 7 days and subsequently normalized within 3-4 weeks. Hepatic synthetic function also normalized within 2 weeks without any sequelae. Conclusion: This report highlights the need for awareness regarding potential but not insignificant risk of dulaglutide as cause of DILI. Extensive testing for other causes of ALI was negative and Dulaglutide-induced ALI was the most likely etiology in our case. Given limited data on hepatotoxicity induced by GLP-1 receptor agonists, further research is needed to ascertain this potentially fatal adverse reaction. We hope to contribute to the current medical literature.
Presentation: Friday, June 16, 2023