Glucose Monitoring Research Articles

The Diabetes Technology Society Error Grid and Trend Accuracy Matrix for Glucose Monitors.

An error grid compares measured versus reference glucose concentrations to assign clinical risk values to observed errors. Widely used error grids for blood glucose monitors (BGMs) have limited value because they do not also reflect clinical accuracy of continuous glucose monitors (CGMs). Diabetes Technology Society (DTS) convened 89 international experts in glucose monitoring to (1) smooth the borders of the Surveillance Error Grid (SEG) zones and create a user-friendly tool-the DTS Error Grid; (2) define five risk zones of clinical point accuracy (A-E) to be identical for BGMs and CGMs; (3) determine a relationship between DTS Error Grid percent in Zone A and mean absolute relative difference (MARD) from analyzing 22 BGM and nine CGM accuracy studies; and (4) create trend risk categories (1-5) for CGM trend accuracy. The DTS Error Grid for point accuracy contains five risk zones (A-E) with straight-line borders that can be applied to both BGM and CGM accuracy data. In a data set combining point accuracy data from 18 BGMs, 2.6% of total data pairs equally moved from Zones A to B and vice versa (SEG compared with DTS Error Grid). For every 1% increase in percent data in Zone A, the MARD decreased by approximately 0.33%. We also created a DTS Trend Accuracy Matrix with five trend risk categories (1-5) for CGM-reported trend indicators compared with reference trends calculated from reference glucose. The DTS Error Grid combines contemporary clinician input regarding clinical point accuracy for BGMs and CGMs. The DTS Trend Accuracy Matrix assesses accuracy of CGM trend indicators.

7296 Gestational Diabetes RT-Continuous Glucose Monitoring Users Utilized Fingerstick less in Pregnancy than Recommended Compared to Fingerstick Monitoring Alone with No Difference in A1c Outcomes

Abstract Disclosure: N.M. Ehrhardt: Advisory Board Member; Self; Bayer, Inc., Novo Nordisk, Dexcom. Grant Recipient; Self; Novo Nordisk. Research Investigator; Self; Novo Nordisk, Dexcom. P. Mandava: None. E. Fay: None. G. Abdalla: None. S. Fonda: None. Background: The Federal Drug Agency recently approved continuous glucose monitoring (CGM) use in gestational diabetes (GDM). However, self-monitoring of blood glucose (SMBG) with fingersticks is still recommended as an adjunct to CGM use. Here we report on SMBG with and without CGM and A1c, as part of a randomized controlled trial (RCT) of CGM for women with GDM. Methods: This is an RCT of 104 participants with GDM who were randomized to real-time CGM (RT-CGM) (N=48) or SMBG alone (control group; N=56). Sixty-one percent in the control group (N=34) withdrew after randomization because they desired a CGM device. Data collection was completed remotely given COVID-19 pandemic. A1c data was collected at baseline and 36 weeks gestation. Fingerstick data was collected at each of 4 study visits (2 weeks apart) until 38 weeks or delivery. All participants were advised to perform SMBG by fingerstick as instructed by their obstetric provider. This analysis is of participants who completed the study (control N=22; RT-CGM N=47). Results: The average age was 33.77 (+/- 5.26) years, 68.11% had a college degree or greater, 69.57% had an income of >$50,000, 95.65% had health insurance, 30.43% reported being Asian and 42.03% reported being white. Baseline mean A1c (+/- SD) was 5.39 (+/- 0.39) in the RT-CGM group and 5.41 (+/- 0.37) in in the control group. Mean A1c at ∼36 weeks of pregnancy was 5.44 (+/-0.43) in the RT-CGM group and 5.37 (+/- 0.44) in the control group. In the RT-CGM group, 20/47 (42.55%) provided SMBG data for ≥3 study visits, 18/47 (38.30%) had data for 1-2 visits, and 9/47 (19.15%) provided no SMBG data at all 4 visits. The mean (+/- SD) tests/day for the RT-CGM group who provided any meter data was 1.31 (+/- 1.89). In the control group, 16/22 (72.73%) provided SMBG data for ≥3 visits, 2/22 (9.09%) had data for 1-2 visits, and 4/22 (18.18%) never provided SMBG data. The mean (+/- SD) tests/day for the control group was 3.4 (+/- 0.73). For the RT-CGM group, simple correlation analyses found no association between number of visits in which fingerstick data were provided and A1c at visit 3 (r=-0.14; p=0.40) or average fingerstick tests/day and A1c at visit 3 (r=0.10; p=0.40). For the control group, there was no association between number of study visits in which fingerstick data were provided and A1c at visit 3 (r=0.38; p=0.11). However, for the control group, more fingerstick tests/day was associated with lower A1c at visit 3 (r=-0.45; p=0.07). Conclusions. Data is limited by missing data as participants did not always supply fingerstick data. Overall A1c in both groups remained stable, despite less SMBG testing in the CGM group. This suggests that SMBG data may add little in GDM management in conjunction with CGM use. More data is necessary to remove the recommended requirement for fingerstick with CGM in pregnancy. Presentation: 6/2/2024

6923 Case Report: Long Standing Type 2 Diabetes with TOFI Phenotype Successfully Weaned Off One Hundred Units of Basal-Bolus Insulin Therapy With Glucagon-Like Peptide 1 Receptor Agonist Therapy

Abstract Disclosure: Y.C. Kon: None. A 60-year-old Indian male was diagnosed with type 2 diabetes in 1997. In July 2017, his fasting blood glucose level (FBGL) was 10.3 mM, paired C-peptide 719 pM, eGFR measured as more than 60 ml/min. Since Sep 2017, he had been compliant on the same stable regimen of sc insulatard 20 units om and 20 units at 10 pm, sc actrapid 20 units t.i.d premeal, PO metformin 850 mg t.i.d and PO dapagliflozin 10 mg om. In the past, he had suffered myocardial infarction, with left ventricular ejection fraction 35%, and had left anterior descending coronary artery stenting. In 2017, he had automatic cardioverter defibrillator implanted for primary arrhythmia prevention. His cardiac medications included bisoprolol fumarate 5 mg om, losartan 25 mg om, spironolactone 25 mg om, aspirin 100 mg om and high intensity statin therapy. Since 2020, his HbA1c had measured 8% to 9% with FBGL at 6 mM to 11 mM. Hence he was referred by his cardiologist in Oct 2022 to optimize glycaemic control. Once every few months, he experienced hypoglycaemic symptoms with corresponding low capillary blood glucose (CBG) of 3 mM, reversed with glucose intake. On physical examination, he weighed 81.6 kg, BMI was 25.4 kg/m2, BP 110/67 mmHg, pulse rate 69/min regular, waist circumference 106 cm. There was no acanthosis nigricans. He did not appear Cushingoid nor acromegalic. As he had “thin outside, fat inside (TOFI)” type 2 diabetes phenotype, he was started on sc liraglutide 1.8 mg om. His actrapid dose was halved to 10 units premeal, and insulatard dose halved to 10 units bid. His dapagliflozin was switched to subsidised empagliflozin 25 mg om. Subsequently, his premeal CBG measured 4 to 7 mM, bedtime CBG 4-6 mM, with occasional minor hypoglycaemic episodes with CBG at 3-4 mM. In July 2023, HbA1c measured 6.3%, FBGL was 5.5 mM and paired C-peptide measured as 554 pM. Basal insulatard was discontinued and he was switched from liraglutide to sc dulaglutide 1.5 mg once weekly. In Oct 2023, his FBGL was 5.2 mM and HbA1c had improved markedly to 5.7%. His weight had reduced from 81.6 kg to 70.0 kg, BMI decreased from 25.4 kg/m2 to 22.9 kg/m2 and waist circumference reduced from 106 cm to 97 cm. As he continued to experience occasional minor hypoglycemic episodes, actrapid insulin was discontinued. On his current therapy of sc dulaglutide 1.5 mg once weekly, PO empagliflozin 25 mg om, PO metformin 850 mg tid, and PO acarbose 50 mg t.i.d, his fasting CBG measured 6.7-7.7 mM, premeal CBG 6.4 to 10.1 mM, off all insulins and without further episodes hypoglycaemia. Conclusion: Patients with long standing “TOFI” type 2 diabetes and robust C-peptide may be trialled on GLP1-receptor agonist therapy to wean off high daily doses of insulin, thus avoiding hypoglycaemia, achieving weight and abdominal fat loss, whilst maintaining glycaemic control. This is especially important in patients with established coronary artery disease. Presentation: 6/3/2024

6692 Proarrhythmic Risk Of Hypoglycemia; A Case Of Insulin-Induced Hypoglycemia Provoking Torsade De Pointes-Cardiac Arrest

Abstract Disclosure: A.M. San Hernandez: None. A. Adelkhanova: None. H. Ashraf: None. J. Aguayo Herrera: None. M.F. Siddiqui: None. Introduction: Torsade de Pointes is a life-threatening polymorphic ventricular tachycardia which is associated with QTc prolongation caused by medications, metabolic and electrolyte abnormalities. Very few cases of hypoglycemia causing QTc prolongation and Torsades de Pointes have been reported in the literature. Although the mechanism is unclear, the effects of low blood glucose have been proposed to induce a sympathetic response, hypokalemia and calcium disturbances. We report a case of an insulin-induced hypoglycemia causing Torsades de Pointes cardiac arrest, highlighting the proarrhythmic risk of hypoglycemia. Case presentation: A 57-year-old female with a history of Insulin-dependent Type 2 Diabetes Mellitus (DM) was brought in by EMS due to severe symptomatic hypoglycemia (POC blood glucose of 30 mg/dL), requiring treatment with dextrose. Patient reported reduced oral intake due to vomiting for 1 week and continued insulin administration without self-monitoring of blood glucose. Laboratory work up on presentation revealed severe hypoglycemia VBG= 55 mg/dL and mild hypomagnesemia Mg=1.4mg/dL (Ref Range 1.7-2.2mg/dl) which was treated. There was no hypokalemia or hypocalcemia. ECG showed sinus rhythm with prolonged QTc interval of 573ms and non-specific ST changes.Few hours later, patient developed torsades de pointes, requiring ACLS resuscitation. ROSC was achieved after two rounds of CPR. Patient received dextrose infusion to maintain euglycemic state. She was not taking any QTc prolonging medication. There was no history of autoimmune disease. Except for hypoglycemia, no other metabolic abnormality could be identified. Cardiac and pulmonary etiologies of cardiac arrest were ruled out. Post-ROSC ECG showed sinus tachycardia with normalization of QTc to 454ms. Thus, Insulin-induced hypoglycemia was appointed as the main culprit for her cardiac arrest, in the setting of QTc prolongation. Patient received diabetes self-management and hypoglycemia education. Conclusion: Several studies support strong correlation between hypoglycemia and arrhythmic events during bedtime in people with diabetes “The dead in bed syndrome”. Hypoglycemia causes an acquired long QT syndrome independent of other risk factors such as cardiac autonomic neuropathy. Possible mechanisms include; sympathoadrenal activation, which regulates potassium, calcium and chloride channels or altered autonomic regulation caused by hypoglycemia itself regardless of the effect of insulin or hypokalemia. QT prolongation is a risk factor for sudden cardiac death by causing torsades de pointes ventricular tachycardia (VT).People with insulin dependent diabetes are at high risk of hypoglycemia and should be cautioned about the proarrhythmic risk of hypoglycemia. Education is crucial, and Continuous glucose monitor (CGM) is a valuable tool to be use in such a patient population. Presentation: 6/3/2024

8132 Prolonged Refractory Hypoglycemia For Seven Days After Discontinuation Of Neutral Protamine Hagedorn (NPH) Insulin And Injectable Semaglutide

Abstract Disclosure: A. Musleh: None. M.T. Rauf: None. E. Afroze: None. S. Al-Bacha: None. A 75-year-old male with Type 2 Diabetes was brought to the emergency department (ED) by emergency medical services (EMS) due to altered mentation. The patient’s wife found him unresponsive with seizure-like activity. EMS was called to the scene and obtained a capillary blood glucose reading of 31 mg/dL. Despite initial treatment with 50% dextrose the patient’s capillary blood glucose came down to 21 mg/dL in the ED and was confirmed by venous glucose. Workup including Computed Tomography (CT) imaging was inconsistent with a cerebrovascular accident. Given refractory hypoglycemia and delirium, the patient was started on a dextrose 10% infusion at 150 milliliters per hour. He was admitted to the intensive care unit for closer monitoring. His wife states that the patient had a few episodes of mild hypoglycemia overnight for the past several weeks, which improved after eating. His home medications included NPH insulin 46 units twice daily, empagliflozin 25 mg once daily, and injectable semaglutide 2 mg once weekly. The last dose of NPH insulin was the night before the presentation and the last dose of semaglutide was 5 days prior to admission. Serum creatinine levels were stable at 1.3-1.5 mg/dL throughout the hospitalization, which was below his baseline creatinine of 1.7 mg/dL. Laboratory results were as follows: hemoglobin A1c 5.9%, c-peptide level was 0.3 ng/mL (normal range 0.8-3.9 ng/mL) with a glucose of 68 mg/dL (normal range 70-100 mg/dL), insulin 203.8 mcIU/mL (normal range less than 24 mcIU/mL), proinsulin 3.2 pmol/L (normal range less than or equal to 8 pmol/L), beta-hydroxybutyrate 0.06 mmol/L (normal range 0.02-0.27), cortisol 66.6 mcg/dL (normal range 6.7-22.6 mcg/dL), insulin-like growth factor 1 123 ng/mL (normal range 53-222), and hypoglycemic agent panel was negative. On ICU Day 2, his mentation improved, he was allowed to eat but continued to require dextrose infusion to prevent hypoglycemia. Repeat fasting insulin levels even four days from prior showed an incremental decrease to 59.4 mcIU/mL with a glucose of 77 mg/dL. It took 7 days before the patient was able to maintain glucose above 70 mg/dL off of dextrose infusion. After which he had hyperglycemia requiring gradual reintroduction of his diabetes medicines other than insulin. It is rare to see such prolonged refractory hypoglycemia from an exogenous source of insulin as exhibited in this case. Notably, the patient was on semaglutide and had stable chronic kidney disease without acute kidney injury. Although multiple mechanisms explain the prolonged insulin duration of action in kidney disease, the effects of semaglutide on insulin action are unknown. Presentation: 6/3/2024

5104 Ectopic Insulinoma- a Rare Presentation of a Rare Tumor

Abstract Disclosure: O. Lavrynenko: None. A. DeMarsilis: None. C. Jiang: None. R. Middelbeek: None. H. Rosen: None. M.E. Patti: None. Background. Insulinoma is a rare, functioning neuroendocrine tumor (NET) typically localized within the pancreas, that secretes insulin, resulting in hypoglycemia. Ectopic insulinoma is even more rare than pancreatic insulinoma and is more difficult to diagnose. Case report. This 31-year-old previously healthy woman, who had an uncomplicated pregnancy and a healthy baby in October 2021, presented with intermittent hypoglycemia for more than 8 months. She denied any prior use of insulin or antidiabetic medications and was not currently taking any medications at all. There is no history of bariatric or other GI surgery. While nursing her baby in early 2022, she was noted to have a capillary blood glucose (BG) between 20-30 mg/dl, and reported both adrenergic and neuroglycopenic symptoms of hypoglycemia; these usually occurred in the morning or before lunch, especially if lunch was delayed. She wore a Libre CGM which revealed episodic hypoglycemia, which correlated with her timeline of symptoms. She reported weight gain of 8 lbs during this period. Laboratory data obtained after a 10-12 hour fast revealed hypoglycemia (venous glucose 39 mg/dL) with inappropriately high plasma insulin (42.3 mIU/ml), C- peptide (3.78 ng/ml), and proinsulin (99 pmol/L). Beta-hydroxybutyrate was 0.05 mmol/L (reference <0.28) and insulin autoantibody and sulfonylurea screen were negative. Various imaging modalities for localization revealed a solitary omental mass outside the pancreas consistent with extra-pancreatic insulinoma. No pancreatic lesion or other findings were observed with MRCP, CT C/A/P or endoscopic ultrasound. The patient underwent CT-guided biopsy of the omental mass, which confirmed a well-differentiated NET, consistent with insulinoma. Due to persistent hypoglycemia, she was started on corn starch and diazoxide. She subsequently underwent laparoscopic resection of the mass. Postoperative pathology revealed a well-differentiated NET staining positive for insulin, consistent with an extra-pancreatic insulinoma. Following surgical resection of the insulinoma, her hypoglycemia resolved even off corn starch and diazoxide. Conclusion. Ectopic insulinoma is a rare insulin-secreting NET. Only 28 ectopic insulinomas have been described in the literature to date1. We describe a patient with symptomatic hypoglycemia who was found to have an omental neuroendocrine tumor; hypoglycemia completely resolved after laparoscopic enucleation of the ectopic insulinoma. 1Fernando Guerrero-Pérez, Nuria Vialarrasa, Lidia V. Huanuco et. al. Ectopic Insulinoma: a systemic review: Reviews in Endocrine and Metabolic Disorders, 2023 Presentation: 6/1/2024

8255 Munchausen Syndrome After Partial Pancreatectomy for Insulinoma: A Case Report

Abstract Disclosure: C.R. de Macedo: None. T.D. Bertolacini da Silva: None. I.P. de Magalhães: None. M.A. Pereira: None. I.C. Marques: None. J.L. Pinheiro Filho: None. G.F. Darce: None. D.M. Lourenço Junior: None. Background: Insulinoma is a rare, insulin-secreting pancreatic neuroendocrine tumor, most commonly benign, solitary, sporadic, well differentiated and with a slight female predominance. The investigation of hypoglycemia requires a fasting test to exclude, among other causes, factitious hypoglycemia. Clinical Case: A 27-year-old woman was admitted to the emergency room after seizure by hypoglycemic crisis (capillary blood glucose < 55 mg/dL). She had recurrent episodes of adrenergic/neuroglycopenic symptoms since the age of 14, occurring during fasting, mainly in the morning, with improvement after eating. After confirming Whipple's triad, a fasting test showed hyperinsulinemic hypoglycemia (glycemia 53 mg/dL, normal value >55 mg/dL; insulin 11.5 mcU/mL, nv <3mcU/mL) and increased C-peptide (3.83 ng/mL, nv <0,6 ng/mL). Abdominal magnetic resonance showed a 1.4 cm nodule in the pancreas tail. During hospitalization, she experienced Raynaud's phenomenon, leading to the diagnosis of Raynaud's disease (RD). Distal pancreatectomy was performed, confirming the diagnosis of insulinoma by immunohistochemistry. There was brief remission of the hypoglycemic episodes once they recurred two weeks later. As imaging tests did not show new pancreatic lesions, somatostatin analogue was begun, resulting in improvement for a few more weeks. Due to recurrent hypoglycemia and new seizures, she required continuous intravenous infusion of glucose during hospitalization. A new fasting test revealed hyperinsulinemic hypoglycemia (glycemia 42 mg/dL, insulin 43.3 mcU/mL), low C-peptide (0.5 ng/mL) and normal proinsulin (2.39 pmol/L, nv <5 pmol/L) values. Due RD, auto-immune hypoglycemia was excluded by negative anti-insulin antibodies. Insulinomatosis was also considered, as potential etiology, but review of surgical specimen excluded this hypothesis. After 4 months of hospitalization, due suspicious behavior, a review of her personal belongings revealed insulin vials and needles for injection. The patient confessed to applying insulin to simulate the symptoms, also revealing a history of childhood trauma and previous suicide attempts. After psychiatric evaluation, borderline personality disorder was identified, and Munchausen syndrome was considered. Since then, the patient did not require intravenous glucose with no recurrence of hypoglycemia. Conclusion: The investigation of hypoglycemia can be challenging, requiring appropriate diagnostic protocols. Even in patients who appear to have a well-defined diagnosis, as in our case with anatomopathological confirmation of insulinoma, it is always important to rule out factitious hypoglycemia. The incorrect diagnosis can lead to inappropriate invasive and surgical procedures with definitive consequences, such as exogenous pancreatic insufficiency and insulin-dependent diabetes mellitus. Presentation: 6/1/2024

7148 Fake Fingerstick: Artifactual Hypoglycemia in a Hospitalized patient with Systemic Sclerosis

Abstract Disclosure: S. Shteyman: None. F. Mirza: None. Introduction: Artifactual hypoglycemia is a problem in hospitalized patients. It often leads to unnecessary use of resources and creates anxiety for the patient and medical team. We describe a case of a 60-year-old female with history of systemic sclerosis (Raynaud, telangiectasias, esophageal dysmotility, interstitial lung disease, pulmonary hypertension), rheumatoid arthritis, autoimmune hepatitis and hypothyroidism who initially presented to the hospital emergency department with bilateral lower extremity radiculopathy, and new onset urine incontinence. She underwent spine surgery initially, followed by emergent left upper extremity thrombectomy two days later. Postoperatively, she was noted to have fingerstick glucose of 34 mg/dL. Dextrose and juice were given, and endocrinology service was consulted. The patient was monitored with 2 hourly fingerstick glucose and was noted to have frequent hypoglycemia on fingerstick monitoring. Serum glucose in AM labs was consistently within normal limits. Patient denied both adrenergic and neuroglycopenic symptoms during periods of “hypoglycemia”. She was asked to fast till fingerstick glucose was noted to be at 43 mg/dl, when blood was drawn for serum glucose, insulin, proinsulin, C-peptide, B-hydroxybutyric acid, IGF-2, insulin AB, and sulfonylurea panel, prior to giving her any dextrose. She was asymptomatic at the time. All labs were within normal limits, with serum glucose at 119 mg/dL. At that point, artifactual hypoglycemia was suspected. Serum glucose was checked twice again when fingerstick glucose was noted to be <45mg/dL, and corresponding serum glucose was noted to be normal at both times (>100 mg/dL). Decision of artifactual hypoglycemia was made and fingerstick glucose monitoring was discontinued in this non-diabetic patient, with recommendation to check serum glucose only if symptoms of hypoglycemia occur, as fingerstick glucose values were not reliable. Fasting serum glucose continued to be normal for the remainder of the hospitalization. Discussion: There have been a handful cases of artifactual hypoglycemia reported in patients with CREST, systemic sclerosis, and Raynaud’s disease. It is thought to be due to abnormal small vasculature causing delayed transit of blood through capillaries, and increased uptake of glucose into the interstitial tissue. Some recommend using earlobe sticks as a replacement for fingerstick glucose monitoring in these patients. Future research can explore if continuous glucose monitoring can be used reliably in these patients. Presentation: 6/1/2024

12273 Do The First 48 Hours Of Hospitalization Require More Vigilance In Geriatric Patients At Risk Of Hypoglycemia?

Abstract Disclosure: S. Ravi: None. H. Afsana: None. Hypoglycemia (HG; blood glucose <70 mg/dL) is a commonly encountered problem in hospitalized patients and is associated with significant morbidity and mortality as well as increased healthcare costs. Elderly patients are particularly vulnerable to HG as they are more likely to have autonomic dysfunction, resulting in fewer discernible symptoms as well as an impaired counterregulatory response, making it more likely that events go undetected and uncompensated. A survey of the literature identifies a number of risk factors for developing HG, including nephropathy, liver disease, infection, cognitive dysfunction, as well as sulfonylurea and long-term insulin use. Given the significant risks posed by HG, we pose the question: how can we do better to identify geriatric patients at high risk of HG events? In this retrospective chart review, data was collected from charts of patients aged 65-99 years with HG, who presented to the ED and were hospitalized for various reasons at a community hospital. Patients were included if a diagnosis of HG was documented in the EMR during hospitalization regardless of diagnosis of Diabetes Mellitus (DM). In 219 total individuals, potential associated variables were analyzed using descriptive statistics, chi-square tests, and Fisher’s exact tests. When data was not complete for any individual variables, the incomplete data was excluded during respective analysis. Among 219 patients, 128 (58.45%) presented at the time of admission, 33 (15.07%) presented within 24 hours after, 15 (6.85%) presented between 24 - 47 hours after, and 43 (19.63%) presented ≥48 hours after admission. Overall, 80.37% of HG events occurred within the first 48 hours of hospitalization. Interestingly there was no significant relationship identified between severity of HG events and HbA1c. The percent distribution identified delayed or missed meals (33%), insulin use (26%), and infection (8%), as the most common potential causes. These findings suggest that it is beneficial to extend the suspicion of HG events to all geriatric patients, regardless of diagnosis of DM. While validated tools have been proposed to identify diabetic patients at risk for HG, fewer studies have been done to identify potential markers of HG risk in all geriatric patients. It may be that the first 48 hours pose a critical period to identifying and better managing these patients’ blood sugars. While use of continuous glucose monitoring in the inpatient setting has been proposed as a potential solution, other cost-effective methods include ensuring timely delivery of meals and food intake, as well as closer finger stick glucose monitoring in the first 48 hours. Higher powered studies across a wider variety of clinical settings are required to further investigate hypoglycemic events in geriatric patients and to synthesize validated assessment tools. Presentation: 6/2/2024

7252 Difference between interstitial and blood glucose during glucose loading is associated with the degree of insulin resistance in subjects with prediabetes and type 2 diabetes

Abstract Disclosure: D. Kim: None. S. Ryang: None. M. Im: None. J. Kim: None. Y. Kim: None. Y. kim: None. J. ha: None. J. Kim: None. S. Kim: None. Background and Aims: This study investigated the main factors responsible for the differences between blood glucose (BG) and interstitial fluid glucose (ISF) during glucose loading. Methods: A total of 204 Korean subjects without history of type 2 diabetes were enrolled. The subjects were categorized into three groups according to diabetes criteria by American Diabetes Association; NGT (normal glucose tolerance, n=36), PreDM (prediabetes, n=130) and T2D (undiagnosed type 2 diabetes, n=38). For glucose monitoring, a CGM (continuous glucose monitoring) system (Dexcom G6, Dexcom, San Diego, USA) was attached for 10 days. 75g oral glucose tolerance test (OGTT) was performed during applying CGM with stabilization (after wear of 3 days). Blood sample collected at t=0, 30, 60, 90 and 120 min for glucose and insulin concentration. Two parameters [insulin sensitivity (mIS) and beta-cell function (mBCF)] were derived novel mathematical model. Results: Among NGT, PreDM and T2D, there are heterogeneity in the difference and pattern between BG and ISF in this study. We identified the probability density function of BG - ISF across glucose tolerance, there is a trend that the means of BG - ISF with G60, 90, and 120 move to the right, as glucose tolerance status changes NGT to PreDM and DM. BG - ISF is significantly associated with insulin resistance (R=0.32, p<0.001), not diminished beta cell function. Conclusions: Because individuals vary in their degree of insulin resistance as a primary pathophysiology of type 2 diabetes, the caution should be needed in interpreting the glycemic response of CGM after a glucose load. Presentation: 6/3/2024

7437 Harnessing Diabetes Technology for Management of Immune Checkpoint Inhibitor Associated Diabetes

Abstract Disclosure: A. Knape: None. A. Kotwal: None. D. Rohlfsen: None. A. Patel: None. W. Goldner: None. Background: Immune checkpoint inhibitors (ICIs) are a key treatment modality for many cancers. One percent of patients who receive ICIs can develop insulin deficient ICI associated diabetes (ICI-DM). These patients often have complex oncologic therapy plans making treatment of newly diagnosed insulin deficient diabetes challenging which often results in additional healthcare-related burden for the patient. Methods: This is a retrospective case series of five adults who developed ICI-DM after receiving either PD-1, CTLA-4 or PDL-1 inhibitors or a combination. Data on demographics, medical history and labs were collected in addition to mode of glucose monitoring and treatment after diagnosis of ICI-DM. Results: Patients were age 44-72 at diagnosis of ICI-DM, three were female. Two were admitted to the hospital in DKA, one was diagnosed in the ER with severe hyperglycemia without DKA, two had outpatient hyperglycemia without DKA. Glucose at diagnosis ranged from 215-510 mg/dL. C-peptide was low for all patients. Fingerstick blood sugar (FSBS) monitoring and basal/bolus insulin was immediately initiated for all patients. All were transitioned from FSBS to continuous glucose monitor (CGM) and 2/5 ultimately transitioned to sensor-augmented insulin pump therapy (AID). Time in range on CGM improved in four patients with percent time in range improving between 10-48%. In two patients, hypoglycemia frequency declined by 6% and 3%. Hyperglycemia frequency declined by 13% and 48% in patients on AID therapy and by 14% and 25% in two of those on basal/bolus insulin therapy. All patients preferred CGM over FSBS and remained on CGM therapy. Those who chose AID preferred it over basal/bolus insulin therapy stating it was less complicated than basal/bolus insulin with CGM. Conclusions: We report successful treatment of five cases of ICI-DM with CGM + basal/bolus insulin or AID. 80% demonstrated improved time in range and decreased overall frequency of hyperglycemia. 40% had decreased frequency of hypoglycemia. CGM allows for dynamic adjustment of insulin therapy in a population with complex medical regimens resulting in fluctuating glucose levels. The integrated pump and sensor technology in AID was less burdensome than basal/bolus in those who chose it. Managing ICI-DM is complicated. The burden of this entity can be lessened by harnessing the power of diabetes technology. Presentation: 6/2/2024

8798 How Low Can You Go: Suspected Methadone-Induced Hyperinsulinemia

Abstract Disclosure: L. Ravindra: None. M.G. Fernandez: None. V. Cheng: None. Background: Studies have shown that methadone use can result in severe hypoglycemia. This is thought to be related to methadone having antagonistic activity at NMDA receptors, resulting in increased pancreatic insulin release, suppressed glucagon and epinephrine, and inhibition of hepatic glycogenolysis. These mechanisms affect the normal physiologic response to hypoglycemia and can result in hyperinsulinemic-induced hypoglycemia. Clinical case: We present a case of a 56-year-old male with complex regional pain syndrome managed with a high daily dose of methadone (345 mg) who presented to the hospital for evaluation of failure to thrive and hypoglycemia. During the hospital admission, evaluation of hypoglycemia included a serum blood glucose level of 41 mg/dL (normal >60 mg/dL), with an inappropriately normal level of insulin 10 (Reference Range (RR) 3-25 mU/L), C-peptide 2.9 (RR 0.5-3.3 ng/ml), Pro-insulin 2.9 (RR 3-20 pmol/L), an undetectable level of Beta-hydroxybutyrate <0.10 (RR 0.02-0.27 mMol/L) negative insulin antibodies <0.4 (RR 0.0 - 0.4 U/mL), and negative sulfonylurea screen. Additional labs included a normal TSH of 2.8 (RR 0.3-5.5 mIU/ml) and appropriate morning cortisol of 23 (RR >14-15 μg/dL). The abdominal CT and follow-up MRI did not reveal any definite abnormalities in the pancreas. Given persistent evidence of hyperinsulinemic-induced hypoglycemia, a PET Dotatate scan was performed, confirming the absence of a neuroendocrine tumor. While admitted, management included nutritional optimization, close glucose monitoring, and an intravenous dextrose infusion. Diazoxide was also initiated and gradually increased to 150 mg three times a day. Addiction Medicine assisted in tapering down the methadone dose from 115 mg to 105 mg three times a day. With these interventions, the patient had no further episodes of hypoglycemia. On discharge, the patient was provided with a continuous glucose monitor. On follow-up, the patient has continued to show improvement and the diazoxide dose has been decreased without recurrent hypoglycemia. Given this, a selective arterial calcium stimulation test was not pursued. Conclusion: Methadone is an uncommon cause of hyperinsulinemic-induced hypoglycemia. Suspicion should arise, particularly in patients on high doses. Current evidence suggests tapering methadone dosage as the primary intervention, as insulin levels can decrease drastically and improve hypoglycemia. This therapeutic approach should be considered before pursuing invasive and costly diagnostic testing. Presentation: 6/3/2024

6666 Asymptomatic Fasting Hypoglycemia After Sleeve Gastrectomy

Abstract Disclosure: K. Mitrollari: None. H.K. Deveaux: None. A. Gundeti: None. A.P. Calimag: None. T. Yasmeen: None. Introduction: Post-bariatric surgery hypoglycemia (PBSH), though previously considered rare, is increasingly recognized, occurring not only after Roux-en-Y gastric bypass (RYGB,) but also following various bariatric procedures. PBSH can manifest as postprandial or fasting hypoglycemia, requiring thorough investigation and prevention due to potential asymptomatic presentations that may lead to severe consequences, including coma and death. Case Report A 45-year-old female with a history of type 2 DM, ESRD on HD, gastric sleeve surgery, bilateral trans-metatarsal amputations, coronary artery disease, and congestive heart failure presented with bilateral lower extremity wounds. On admission her venous blood glucose was 71 mg/dL. Glycohemoglobin was 3.9% and fructosamine was 225 (205-285 umol/L). Her glycohemoglobin levels consistently remained below 6.4% status post sleeve gastrectomy off diabetes medications. Throughout admission, she experienced almost daily episodes of fasting asymptomatic hypoglycemia correlated with venous sample with lowest blood glucose reading 38 mg/dL. Initially, these episodes were attributed to NPO status for procedures or decreased PO intake. Her diet consisted of fast food brought by her family, which she reported was similar to her diet at home. Workup during a hypoglycemic episode (glucose 51 mg/dL,) revealed insulin 4 mUnits/L, proinsulin 7.1 pmol/L (<=7.2 pmol/L), C-peptide 25.7 ng/mL (0.8-3.9 ng/mL), and beta-hydroxybutyrate 0.5 mmol/L (0.0-0.3 mmol/L). Negative insulin antibodies and sulfonylurea panel, normal cortisol, and ACTH levels were noted. The patient was placed on a 10% dextrose infusion to avoid further episodes of hypoglycemia. However, she continued to experience hypoglycemia and was started on oral diazoxide. A CT pancreas with and without contrast was unremarkable, and endoscopic ultrasonography only revealed a 10 mm accessory spleen. The patient was discharged with counseling on glucose monitoring, dietary changes, and follow-up with endocrinology. Conclusion: PBSH should be considered as a differential diagnosis in patients with unexplained hypoglycemia and a history of bariatric surgery. PBSH mimics insulinoma or non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) with elevated insulin, proinsulin, C-peptide, and low beta-hydroxybutyrate during hypoglycemia, however NIPHS is exclusive to non-bariatric patients. Imaging is crucial to rule out insulinoma, and invasive tests such as endoscopic ultrasound aid diagnosis. PBSH is a diagnosis of exclusion; therefore, workup involves ruling out other causes of hypoglycemia. First-line treatment involves diet modification, with medications like diazoxide or acarbose considered if dietary changes prove insufficient. This case underscores the complexity of hypoglycemia, implicating bariatric surgery as a contributing factor. Presentation: 6/3/2024

5045 The Effects Of Non-functioning Adrenal Incidentalomas On Metabolic Comorbidities And Clinical Characteristics Changes: A Systematic Review And Meta-Analysis

Abstract Disclosure: X. Li: None. H. Lan: None. J. Wen: None. G. Chen: None. W. Lin: None. The Effects of Non-functioning Adrenal Incidentalomas on Metabolic Comorbidities and Clinical Characteristics Changes: A Systematic Review and Meta-analysis. Context: Adrenal incidentalomas (AI) are frequently detected during abdominal imaging, with non-functioning adrenal incidentalomas (NFAI) being particularly common, even in elderly individuals. This meta-analysis investigates the influence of NFAI on metabolic comorbidities, comparing non-surgical and surgical patient groups, and assessing alterations in NFAI characteristics. Design: Our comprehensive meta-analysis utilized data from multiple databases, encompassing studies from January 2000 to August 21, 2023.Setting: Data sources included PubMed, Embase, Cochrane Library, and Web of Science. Participants: The analysis comprises 24 articles involving 2,770 NFAI patients, categorized into non-surgical and surgical groups. Intervention: The non-surgical group underwent no surgery, while the surgical group underwent tumor resection. Main Outcome Measure: The study investigated changes in metabolic comorbidities (hypertension, diabetes, obesity, lipid metabolism disorders), tumor characteristics, and hormone production in NFAI patients during follow-up or after surgery. Results: In the non-surgical NFAI patient group (20 studies), metabolic comorbidities exhibited a discernible upward trajectory during follow-up. The initial hypertension prevalence of 58.3% increased by 4.2% over a 4-5 year follow-up period. Moreover, diabetes, obesity, and lipid metabolism disorders experienced significant increases of 5.8%, 2.2%, and 8.8%, respectively. In contrast, the surgical group (6 studies) demonstrated a notable reduction in hypertension, with 43.9% of initially hypertensive patients achieving hypertension-free status after surgery. As for tumor changes in the non-surgical group, they were generally inconsequential, with only 5% of patients witnessing tumor growth exceeding 10mm over approximately 3.3 years, and 8% undergoing functional changes. These findings underscore the divergent impact of non-surgical and surgical interventions on metabolic comorbidities in NFAI patients. Conclusion: The study advocates for regular monitoring of blood glucose and blood pressure in NFAI patients, especially those with metabolic comorbidities. When necessary, adenoma resection should be considered. Further investigation is warranted to elucidate the mechanisms connecting NFAI with metabolic factors. Presentation: 6/1/2024

7360 An Overlooked Cause of Hypoglycemia and Weight Loss: Phosphodiesterase-4 Inhibitors

Abstract Disclosure: J. Aurora: None. K. Cappetta: None. R.M. Lechan: None. Background: Phosphodiesterase-4 (PDE-4) inhibitors, apremilast and roflumilast, are anti-inflammatory agents used to treat psoriasis, psoriatic arthritis, and COPD. These agents are commonly associated with gastrointestinal intolerance. However, patients may also experience profound weight loss (>10%). We present a case of a patient with T2DM who developed significant hypoglycemia and weight loss on apremilast. Clinical Case: A 57-year-old female with T2DM, obesity, psoriasis, and postsurgical hypothyroidism due to papillary thyroid cancer developed symptoms of hypoglycemia and weight loss over 1 month. Prior to this, her A1c was 7.8% and weight 104 kg on stable doses of metformin, repaglinide, and insulin glargine. Insulin glargine and repaglinide were both discontinued given her symptoms, yet hypoglycemia persisted, and she continued to lose weight. Further investigations into the cause of this sudden change were carried out. Initial fasting labs: BG 53 mg/dL, C-peptide 4.48 ng/mL (RR 0.8-3.85 ng/mL), insulin 12.8 uIU/mL (RR <18.4 uIU/mL), proinsulin 29.8 pmol/L (RR <18.8 pmol/L), A1c 6.8%, cortisol 24.9 mcg/dL (RR 4-22 mcg/dL), IGF-1 95 ng/mL (Z-score -0.7), and IGF-2 434 ng/mL (RR 267-616 ng/mL). 1 month later, hypoglycemia symptoms improved but she continued to lose weight. Fasting labs were repeated: BG 84 mg/dL, C-peptide 5.62 ng/mL, insulin 24.3 uIU/mL, proinsulin 35 pmol/L, and beta-hydroxybutyrate (BHB) 0.17 mmol/L (RR <0.28 mmol/L); metformin was subsequently stopped. A MR abdomen revealed a 2 cm cystic pancreatic lesion that showed atypical mucinous epithelium by biopsy under endoscopic ultrasound guidance. Gallium-68 DOTATATE-PET scan was unremarkable for an insulin-producing tumor. Two months off metformin, she had no further episodes of hypoglycemia, but her weight loss continued. Fasting labs were repeated: BG 129 mg/dL, C-peptide 5.15 ng/mL, insulin 18.2 uIU/mL, proinsulin 40.5 pmol/L, and BHB 0.27 mmol/L. Review of her medications identified apremilast as a potential culprit contributing to both her hypoglycemia and weight loss, as her symptoms started 1 month after starting apremilast. Over 9 months using apremilast, her A1c decreased by 1% and weight decreased by 27%. Hypoglycemia resolved off all glucose-lowering agents. Conclusion: Significant weight loss with apremilast may be explained by PDE-4 inhibition increasing cyclic AMP, which triggers the release of GLP-1 with subsequent effects on pancreatic beta cells. Apremilast has also been shown to significantly increase fasting insulin levels in patients without insulin resistance, as seen in our patient (1). Given these effects, patients may be at higher risk of hypoglycemia with concurrent glucose-lowering agents, particularly secretagogues. BG and weight need careful monitoring for patients with T2DM using PDE-4 inhibitors. Reference: 1. Ikumi K, et al. J Dermatol. 2022;49(4):e125-e126. Presentation: 6/3/2024

7375 Severe Hypoglycemia In Graves’ Hyperthyroidism: A Rare Consequence Of Methimazole Induced Insulin Autoimmune Syndrome

Abstract Disclosure: J. Ratnasingam: None. N. Ismail: None. Y. Ng: None. T. Sarvanandan: None. N. Hee: None. Q. Lim: None. L. Lim: None. S. Paramasivam: None. P. Sthaneshwar: None. S. Vethakkan: None. Background: Islet autoimmune syndrome (IAS) is a rare disease characterized by elevated insulin autoantibodies (IAA), triggered by genetic, environmental or drug (sulfhydryl containing) factors. We describe a case of Graves’ hyperthyroidism who developed IAS with methimazole. Clinical Case: A 28-year-old Malaysian-Chinese woman presented with tremors and palpitations. She weighed 56 kg, had no palpable goiter or thyroid eye signs. The diagnosis of Graves’ disease was confirmed with ft4 66.5 (11.5-22.7)pmol/L and TSH <0.01 (0.55-4.78)mIU/L with elevated thyroid stimulating immunoglobulin of 5.4 (< 0.55)IU/L. She was treated with methimazole 20mg BID and Propranolol 20mg TID. After 5 weeks of methimazole, she experienced recurrent episodes of sweating and presented with a generalized tonic-clonic seizure with capillary blood glucose of 27mg/dL. Seizures aborted after resuscitation with dextrose. There was no history of fever, exposure to insulin or other drugs, weight gain, family history of diabetes or alcohol use. CT brain and other parameters were normal and she had no other apparent cause of seizures. During the hypoglycemic episode; with the plasma glucose of 32 mg/dL, she had disproportionately high insulin: 9309 (3-25)mIU/L relative to C-peptide: 18.6 (0.9-7.1)ng/mL, with appropriate cortisol levels of 958 nmol/L. Sulphonylurea screen and pancreatic imaging was negative. Low insulin recovery was documented following PEG precipitation suggesting the presence of anti-insulin antibody. Elevated serum IAA levels at >20 (<2.4)U/mL with positive HLA-DRB1*04:06, confirmed the diagnosis of IAS. Multiple small, low carbohydrate and frequent meals were prescribed to prevent hypoglycemia and methimazole was discontinued as she had mild hyperthyroidism at this point (ft4 20.6 pmol/L, TSH <0.01mIU/L). Three days after discontinuation of methimazole, hypoglycemia completely resolved without need for dextrose infusion or corticosteroids. She received immediate 131-iodine therapy and developed hypothyroidism within two months, requiring levothyroxine replacement. She had not reported any hypoglycemia since and repeated IAA titre significantly diminished to 3.2 U/mL two months after discontinuation of methimazole. Conclusion: Methimazole-induced IAS is a rare cause of insulin mediated hypoglycemia, caused by cleaving of the disulphide bonds of insulin by the drug, leading to a cascade of autoimmune response in susceptible individuals. This is the first reported Malaysian case of methimazole- induced IAS. To date, this condition have almost always been reported in East- Asians in whom the DRB1*0406 genotype is relatively common. Unprovoked hypoglycaemia in a patient on anti-thyroid medications should prompt clinicians to consider methimazole-induced IAS. Presentation: 6/1/2024

9267 Targeting IGF-I to Growth Plate Cartilage Augments Therapeutic Effects on Skeletal Growth and Reduces Hypoglycemic Effects in Mice

Abstract Disclosure: K. Tailor: None. T. Stowe: None. J. Ree: None. B. Ventura: None. J. Deursen: None. R. O'Brien: None. J. Baron: None. J. Lui: None. Recombinant human growth hormone (GH) is commonly used to treat short stature in children but has limited efficacy in severe, non-GH-deficient conditions, such as skeletal dysplasias, and has adverse off-target effects. Because short stature is the result of reduced growth plate chondrogenesis, we hypothesized that targeting chondrogenic growth factors specifically to the growth plate might augment the therapeutic skeletal effect while diminishing adverse effects on non-target tissues. Toward this end, we previously developed fusion proteins conjugating insulin-like growth factor-1 (IGF-1) with a single-chain human monoclonal antibody fragment (ScFv) targeting matrillin-3 (1), a protein specifically expressed in cartilage matrix, and demonstrated increased on-target therapeutic efficacy at the growth plate and decreased off-target effects in a GH-deficient (lit) mouse model (2). In the current study, we established a second GH-deficiency model by administration of a GH antagonist, pegvisomant (PEG), in C57BL/6 wild-type male mice. Alternate-day injection of pegvisomant at 40 mg/kg for 7 days reduced body weight, serum IGF-1 levels, and growth plate height in mice. Using this model, we found that once-daily SQ administration of cartilage-targeted IGF-I (named CV1574-1) for five days increased body weight and growth plate height greater than an equimolar dose of IGF-I itself administered twice daily. Hypoglycemia is an adverse effect of recombinant IGF-1 treatment. Therefore, we also monitored blood glucose levels after a single SQ injection of CV1574-1 and found that this fusion protein showed a reduced hypoglycemic effect compared to injection of IGF-I itself. Lastly, to gain mechanistic insight into the role of matrillin-3 targeting on therapeutic efficacy, we assessed the ability of CV1574-1 to induce pAKT signaling in vitro. Transient exposure to CV1574-1 caused more prolonged induction of pAKT signal in wild-type rat chondrosarcoma (RCS) cells compared to matrillin-3-knockout RCS cells, suggesting that matrillin-3 targeting extends the duration of IGF-1 receptor activation. To summarize, the current findings demonstrate that CV1574-1, a fusion protein that targets IGF-1 to cartilage, improves efficacy at the growth plate, reduces hypoglycemic effects, and, in vitro, prolongs receptor activation. Our study provides further evidence that cartilage-targeted therapy has the potential to provide new pharmacological approaches for the treatment of childhood linear growth disorders, including skeletal dysplasias and growth failure due to systemic disease. Reference:(1) Cheung et al. Pharma Res 2015, 32(7):2439-49.(2) Lui et al. Molecular Therapy 2019, 27(3):673-680 Presentation: 6/3/2024

7237 Targeting IGF-I to Growth Plate Cartilage Augments Therapeutic Effects on Skeletal Growth and Reduces Hypoglycemic Effects in Mice

Abstract Disclosure: K. Tailor: None. T. Stowe: None. J. Ree: None. B. Ventura: None. J. Deursen: None. R. O'Brien: None. J. Baron: None. J. Lui: None. Recombinant human growth hormone (GH) is commonly used to treat short stature in children but has limited efficacy in severe, non-GH-deficient conditions, such as skeletal dysplasias, and has adverse off-target effects. Because short stature is the result of reduced growth plate chondrogenesis, we hypothesized that targeting chondrogenic growth factors specifically to the growth plate might augment the therapeutic skeletal effect while diminishing adverse effects on non-target tissues. Toward this end, we previously developed fusion proteins conjugating insulin-like growth factor-1 (IGF-1) with a single-chain human monoclonal antibody fragment (ScFv) targeting matrillin-3 (1), a protein specifically expressed in cartilage matrix, and demonstrated increased on-target therapeutic efficacy at the growth plate and decreased off-target effects in a GH-deficient (lit) mouse model (2). In the current study, we established a second GH-deficiency model by administration of a GH antagonist, pegvisomant (PEG), in C57BL/6 wild-type male mice. Alternate-day injection of pegvisomant at 40 mg/kg for 7 days reduced body weight, serum IGF-1 levels, and growth plate height in mice. Using this model, we found that once-daily SQ administration of cartilage-targeted IGF-I (named CV1574-1) for five days increased body weight and growth plate height greater than an equimolar dose of IGF-I itself administered twice daily. Hypoglycemia is an adverse effect of recombinant IGF-1 treatment. Therefore, we also monitored blood glucose levels after a single SQ injection of CV1574-1 and found that this fusion protein showed a reduced hypoglycemic effect compared to injection of IGF-I itself. Lastly, to gain mechanistic insight into the role of matrillin-3 targeting on therapeutic efficacy, we assessed the ability of CV1574-1 to induce pAKT signaling in vitro. Transient exposure to CV1574-1 caused more prolonged induction of pAKT signal in wild-type rat chondrosarcoma (RCS) cells compared to matrillin-3-knockout RCS cells, suggesting that matrillin-3 targeting extends the duration of IGF-1 receptor activation. To summarize, the current findings demonstrate that CV1574-1, a fusion protein that targets IGF-1 to cartilage, improves efficacy at the growth plate, reduces hypoglycemic effects, and, in vitro, prolongs receptor activation. Our study provides further evidence that cartilage-targeted therapy has the potential to provide new pharmacological approaches for the treatment of childhood linear growth disorders, including skeletal dysplasias and growth failure due to systemic disease. Reference:(1) Cheung et al. Pharma Res 2015, 32(7):2439-49.(2) Lui et al. Molecular Therapy 2019, 27(3):673-680 Presentation: 6/3/2024

9391 Clinical Accuracy Of Continuous Glucose Monitoring In Post-kidney Transplant Patients With Type 2 Diabetes

Abstract Disclosure: Q. Aziz: None. K. Batra: None. S. Fatima: None. J. Splinter: None. A.L. Champion: None. A.M. Kumar: None. K.E. Izuora: Research Investigator; Self; Novo Nordisk. Background: Continuous glucose monitoring (CGM) devices provide real time blood glucose data to guide therapy in patients with diabetes mellitus. Diabetic nephropathy is a major complication of diabetes which can eventually lead to End Stage Renal Disease (ESRD). Kidney transplant is a treatment option for ESRD and patients who undergo kidney transplant are exposed to anti-rejection therapy, including high-dose steroids, resulting in significant fluctuations in blood glucose. Having a reliable system for monitoring blood glucose continuously, such as a CGM, can provide valuable information to guide optimal diabetes management. Objective This study aims to compare the clinical accuracy of the CGM data with the Point of Care Testing (POCT) glucose values as a reference among post kidney transplant patients with Type 2 diabetes mellitus (T2DM). Methodology This study was conducted at an academic medical center from September 2023 to January 2024, enrolling subjects ≥ 18 years, diagnosed with T2DM , admitted for kidney transplant. Following informed consent, a blinded CGM (Freestyle Libre Pro®) was applied. We collected all POCT and serum glucose values and downloaded corresponding CGM glucose data. Using matched pairs between CGM and POCT glucose values, bias and absolute relative differences (ARD) were calculated. Based on the ARD, the Clarke error grid (CEG) analysis was conducted to quantify the clinical accuracy of CGM and POCT by assigning glucose data points into 5 zones A, B, C, D, and E. Summary statistics for numeric variables included mean and standard deviation, whereas categorical variables were described as counts and proportions. All analyses were performed using SAS, 9.4 version. Results: A total of 22 subjects were analyzed after excluding one patient due to CGM malfunction. Subjects were 58±9.69 years old, and 82% were males. The mean body mass index was 30±6.41 kg/m2 and mean HbA1c was 6.7 ± 1.07%, at baseline. The mean duration of diabetes and ESRD were 19±10.6 years and 3±2.27 years respectively. Average CGM wear time was 76±24.5 hours. The CEG comparing CGM values with POCT values showed 83.79% values in zone A, 15.29% in zone B (combined =99.08%) with the Mean Absolute Relative Difference (MARD) of 13.24%. The CEG comparing CGM values with serum glucose showed 83.1% values in zone A, 16.9% in zone B (combined =100%) with the MARD of 13.10%. Conclusion: Our results indicate that CGM values are comparable to the POCT and serum glucose values in post kidney transplant patients with T2DM receiving high dose steroids. Therefore, use of CGMs should be considered as a useful tool, providing timely information to guide prompt interventions and improve outcomes in this patient population. Presentation: 6/3/2024

8469 Endocrinologists Underutilize Virtual Care Services Resulting in Suboptimal Clinical and Financial Outcomes

Abstract Disclosure: D. Terry: Employee; Self; Valendo Health. Less than 150,000 Medicare patients with diabetes (PWD) receive billable telehealth and remote monitoring services, even though over 12 million PWDs are eligible for these services. This is a missed quality opportunity, as studies show that PWDs who receive these services experience reductions in A1C levels and improvements in TIR. It is also a missed financial opportunity for Endocrinologists, who are among the lowest paid specialists in the US. The economics of Endocrinology are important, because inadequate compensation is leading to access constraints when the diabetes population is growing, and care complexity is increasing. We analyzed billed virtual health claims for every Medicare PWD in 2022. The types of services we examined included: Chronic Care Management (CCM & PCM), Continuous Glucose Monitoring (CGM & RPM), Medical Nutrition Therapy (MNT), and Diabetes Self-Management Training (DSMT). When we looked by Endocrinologist by virtual care service type, we found the following levels of service delivery for Endocrinologists at the median levels of utilization:4.8% of eligible PWDs received remote Continuous Glucose Monitoring support.4.2% received virtual Chronic Care Management services.6.2% received virtual Diabetes Self-Management Support.<1% received Medical Nutrition Therapy This is clearly a missed clinical quality opportunity as a study published in JAMA in October 2023, Comprehensive Telehealth Model to Support Diabetes Self-Management, reported the following improvements for PWDs who received virtual care for 6 months:Mean change in A1C levels: Type 1: -0.6%; Type 2: -1.0%Mean TIR Improvement: Type 1: 16%; Type 2: 18% It is also a missed financial opportunity for Endocrinology practices. Each patient with diabetes is potentially eligible for $100 or more of virtual care services per month. We’ve looked at every Endocrinology practice in the US and many are missing out on over a million dollars of annual revenue opportunity. This is important as Endocrinology organizations everywhere, independent and hospital based, are struggling to retain the doctors & staff necessary to provide adequate access to care - leading to months of wait time to see an Endocrinologist. The prevalence of diabetes is growing significantly, while Endocrinologist capacity is shrinking. Value added and billable virtual care services create new opportunities for Endocrinologist to generate the revenue necessary to increase clinical capacity and improve access by creating diverse clinical teams led by Endocrinologists and supported by Diabetes Educators, Dietitians, and others with expertise in diabetes who can care for many more PWDs. Creating virtual care capabilities is also an early step in moving Endocrinology into Value-Based Care arrangements that reward providers for improving care and reducing costs rather than for generating more visits. Presentation: 6/1/2024