Acute Failure Research Articles

Global use of angiotensin receptor neprilysin inhibitor in heart failure and reduced, below normal and supranormal ejection fraction.

The global use of angiotensin receptor neprilysin inhibitor (ARNI) in clinical practice, especially in patients with heart failure and below-normal ejection fraction (HFbnEF), has not been thoroughly evaluated. We aimed to investigate the characteristics, outcomes, and adverse events in patients treated with ARNI for HF with reduced (HFrEF), below-normal (HFbnEF), and supranormal left ventricular EF (HFsnEF). This observational study analyzed data from the electronic healthcare records (EHR) of patients with HF treated with ARNI between 2015 and 2022 in North and South America, Europe, the Middle East, Africa, and Asia-Pacific. Based on the left ventricular EF, patients were categorized as HFrEF (< 40%), HFbnEF (40-60%), and HFsnEF (> 60%). Mortality and the incidence of adverse events were investigated. Of the 11,141 patients analyzed, HFrEF, HFbnEF and HFsnEF accounted for 74%, 22%, and 4%, respectively. Patients with a higher EF were more likely to be older, female, and obese. Hypertension and atrial fibrillation were the most common in HFsnEF. Systolic blood pressure was lower and natriuretic peptide levels were higher in the lower EF groups. Mortality was lowest in HFbnEF (7.7 per 100 patient-years follow-up in HFrEF, 5.8 in HFmrEF, and 6.0 in HFsnEF). Similarly, hypotension and acute kidney injury were the least frequent in HFbnEF. Incidence of elevated serum potassium levels was similar between the groups. In this analysis of large-scale EHR, ARNI was mainly used in HFrEF and HFbnEF, consistent with previous randomized trials and pooled analyses. Adverse events were less common in HFbnEF.

Latent space representation of electronic health records for clustering dialysis-associated kidney failure subtypes

ObjectiveKidney failure manifests in various forms, from sudden occurrences such as Acute Kidney Injury (AKI) to progressive like Chronic Kidney Disease (CKD). Given its intricate nature, marked by overlapping comorbidities and clinical similarities—including treatment modalities like dialysis—we sought to design and validate an end-to-end framework for clustering kidney failure subtypes. Materials and methodsOur emphasis was on dialysis, utilizing a comprehensive dataset from the UK Biobank (UKB). We transformed raw Electronic Health Record (EHR) data into standardized matrices that incorporate patient demographics, clinical visit data, and the innovative feature of visit time-gaps. This matrix structure was achieved using a unique data cutting method. Latent space transformation was facilitated using a convolution autoencoder (ConvAE) model, which was then subjected to clustering using Principal Component Analysis (PCA) and K-means algorithms. ResultsOur transformation model effectively reduced data dimensionality, thereby accelerating computational processes. The derived latent space demonstrated remarkable clustering capacities. Through cluster analysis, two distinct groups were identified: CKD-majority (cluster 1) and a mixed group of non-CKD and some CKD subtypes (cluster 0). Cluster 1 exhibited notably low survival probability, suggesting it predominantly represented severe CKD. In contrast, cluster 0, with substantially higher survival probability, likely to include milder CKD forms and severe AKI. Our end-to-end framework effectively differentiates kidney failure subtypes using the UKB dataset, offering potential for nuanced therapeutic interventions. ConclusionsThis innovative approach integrates diverse data sources, providing a holistic understanding of kidney failure, which is imperative for patient management and targeted therapeutic interventions.

7335 Myxedema Coma in an Adolescent Patient: A rare, lethal manifestation of profound hypothyroidism

Abstract Disclosure: C. Rodriguez: None. E.M. Mejias: None. L.R. Berrios: None. C. Currais: None. Myxedema coma is a rare, life-threatening condition that represents the most severe manifestation of profound hypothyroidism. It is characterized by extensive end-organ dysfunction. Therefore, it is crucial to have a high index of suspicion in order to identify it promptly and initiate treatment. We report a case of an adolescent patient with past medical history of Type 1 Diabetes Mellitus and hypothyroidism who was initially admitted to pediatric wards due to hypertension, constipation and acute kidney injury (AKI). The patient was transferred to the pediatric intensive care unit (PICU) after he developed multi-organ failure secondary to myxedema coma. His laboratory work up was remarkable for severe hypothyroidism with a thyroid-stimulating hormone (TSH) &amp;gt; 679, uncontrolled diabetes mellitus (Glycosylated Hemoglobin 13.1%) and chronic kidney disease (Creatinine 2.56). During his hospital course, he required long term hemodialysis, mechanical ventilation and underwent cardiorespiratory resuscitation multiple times. Since myxedema coma is an uncommon manifestation of pediatric hypothyroidism, pediatric guidelines are not available. We aim to reinforce the awareness of myxedema coma and encourage physicians to have a high index of suspicion as the widespread availability of TSH assays and its use can aid in the diagnosis and treatment of these patients. Furthermore, we emphasize an interdisciplinary approach to avoid mortality and long-term complications. Presentation: 6/1/2024

7648 Bilateral Adrenal Hemorrhage After Laminectomy: A Rare Complication

Abstract Disclosure: M. Rizk: None. S. Sharma: None. H. Qadeer: None. R. Paudel: None. C. Sherpa: None. Introduction: Bilateral Adrenal Hemorrhage (BAH) is an exceedingly uncommon complication of laminectomy, with few cases reported in the literature. In patients with history of any surgical procedure who present with unexplained symptoms of abdominal pain, back pain, hypotension, fever, confusion, or electrolyte abnormalities especially hyponatremia, acute adrenal insufficiency (AI) should be highly suspected. We herein describe a case of BAH following laminectomy. Clinical Case: 63-year-old male with past medical history of hypertriglyceridemia was admitted for post traumatic L1 burst fracture and was treated with T11-L3 fusion and T12-L3 laminectomy. The patient had normal bilateral adrenal glands after the fall on CT thoracic/lumbar spine imaging. The course was complicated by thrombocytopenia initially thought to be induced by therapeutic heparin since heparin antibody was positive. Serotonin-release assay returned negative weeks later ruling out heparin induced thrombocytopenia. Two weeks later, he developed unexplained tachycardia and CT angiogram was done which showed segmental pulmonary embolism and bilateral adrenal nodules measuring at least 3.9 cm on right side and 3.3 cm on left side. He was treated with Eliquis and was discharged home. Two weeks later, he was readmitted with weight loss of 30 lbs, weakness and altered mental status. His vital signs were significant for hypotension and tachycardia. Initial work up showed profound hyponatremia (sodium 121 mEq/L), hyperkalemia (potassium 6.1 mEq/L), hypoglycemia (Glucose 58 mg/dL), hypercalcemia (calcium 11.7 mg/dL) and acute kidney injury (creatinine 2.58 mg/dL). Repeat CT scan of chest/abdomen/pelvis without contrast showed bilateral hyperdense 4 cm adrenal mass/hematoma. Since initial CT of thorax/spine done after the fall showed normal adrenal glands, the new bilateral hyperdense adrenal masses noted post procedure is suggestive of adrenal hemorrhage/hematoma. Undetectable cortisol and high ACTH confirmed AI. Patient was treated with stress dose hydrocortisone followed by slow taper. MRI of pituitary gland showed partial empty Sella however since ACTH was high, empty sella was only an incidental finding and not the cause of AI. He is maintained on hydrocortisone 15 mg in the morning and 5 mg in the evening plus fludrocortisone 0.1 mg daily. His fatigue has improved, he is gaining weight and electrolytes are normal. Conclusions: This case report emphasizes the significance of timely diagnosis and management of BAH, which leads to primary AI. BAH is a rare complication following laminectomy. Clinicians should be aware of this possibility and consider it in the differential diagnosis of postoperative abdominal pain and electrolyte abnormalities, especially hyponatremia. Timely recognition and high index of suspicion should prompt empiric glucocorticoid replacement to decrease mortality. Presentation: 6/1/2024

8290 Hypervitaminosis A Induced Severe Hypercalcemia In A Patient With Cirrhosis

Abstract Disclosure: N. Vennelaganti: None. S. Vennelaganti: None. R.L. Fitzgerald: None. K.C. McCowen: None. Introduction The liver stores vitamin A in hepatic stellate cells and regulates its absorption through bile production and distribution via retinol-binding protein 4 and transthyretin synthesis. Cirrhosis compromises these functions, resulting in vitamin A deficiency, which is inversely linked to the severity of nonalcoholic steatohepatitis. Addressing this deficiency in chronic liver diseases, particularly cirrhosis, is challenging due to the risk of vitamin A toxicity. This case describes a cirrhotic patient who developed hypervitaminosis A, leading to severe hypercalcemia. Clinical Case A 54-year-old male with alcoholic cirrhosis was diagnosed with hypovitaminosis A. He was prescribed 10,000 IU of vitamin A due to a low serum retinol level of less than 0.06 mg/L (reference range: 0.3-1.2 mg/L ). Two months later, he presented to the hospital with an erythematous patchy, scaling facial rash. His serum calcium corrected for albumin was high at 15.6 mg/dL. The rash and hypercalcemia, alongside vitamin A supplementation, raised suspicion of vitamin A toxicity. The patient, however, exhibited no hypercalcemia symptoms. He also had an acute kidney injury. His lab results revealed a PTH level of 10 pg/mL (normal range 15-65 pg/ml) and a normal myeloma screen, as well as normal vitamin D and TSH levels. An elevated PTHrP level of 5.2 pmol/l (normal range 0-2.3) was noted, which was attributed to the kidney injury(Cr 2.55 mg/l, eGFR 23 ml/min). Malignancy was excluded after a pan scan. Hypervitaminosis A is a clinical diagnosis, as serum vitamin A levels correlate poorly with toxicity. His serum retinol was normal at 0.83 mg/l, but his retinyl palmitate was high at 0.38 mg/L(reference range 0-0.10 mg/l), which supported our diagnosis. He received continuous IV 0.9% saline and subcutaneous calcitonin at 4 units/kg twice, and had a reduction in corrected calcium to 11 mg/dL over a week. The vitamin A-induced contact dermatitis improved with topical steroids. He was discharged; two months later, he remained asymptomatic with a corrected calcium of 11.1 mg/dL. He was not interested in further management as he was asymptomatic and serum calcium levels were improving. Labs were, however, notable for worsening renal function of unclear etiology. We will be trending his labs for improvement in serum calcium as the Vitamin A clears from his system. Clinical Lesson Vitamin A supplementation in cirrhotic patients is necessary in those with deficiency but carries a risk of toxicity. There are no definitive hepatology guidelines on the replacement of Vitamin A in patients with cirrhosis. This case emphasizes the importance of awareness of hypervitaminosis A-induced hypercalcemia in this population. Clinicians must carefully monitor and manage Vitamin A levels to avoid toxicity. Further research is essential for the management of this condition in cirrhotic patients. Presentation: 6/2/2024

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

8533 Salt on the Kidneys A case of DDAVP induced arginine vasopressin resistance

Abstract Disclosure: M.M. Jordan: None. J.R. Islam: None. R. Hassan: None. A 63-year old female with a history of head trauma complicated by polyuria and excessive fatigue diagnosed with central DI and started on treatment with oral Desmopressin. She had no other known pertinent medical history. Patient was lost to follow-up with an eventual visit to the emergency department with complaints of bilateral leg cramps, nausea and persistent headaches. She was noted to have been initiated intranasal desmopressin in addition to oral DDAVP. On initial lab work, Sodium was 114 along with acute kidney injury. She was admitted to ICU and treated with hypertonic saline. DDAVP was withheld until sodium normalized and stabilization of renal functions. GFR still remained impaired on discharge at 40 mL/min/1.73m*2. She was then discharged on DDAVP with reestablished follow up in the endocrinology clinic with complaints of persistent polyuria. Once more, she was sent to the emergency room and was admitted for acute renal injury secondary to dehydration in the setting of polyuria and altered mentation. Upon review of her medications, the patient continued both oral and inhaled DDAVP. No other medications or supplements were reported. During this subsequent hospitalization, sodium remained between 131-135 with urine output 4.5L/ day despite increasing doses of oral DDAVP and oral sodium supplementation. At which point, suspicion for mixed DI was hypothesized (central DI and arginine vasopressin resistance). Other causes of polyuria were ruled out. Labs for persistent AKI revealed gross proteinuria. Renal biopsy was performed during hospitalization which showed acute to chronic vascular thrombotic microangiopathy and focal segmental glomerulosclerosis with collapsing features. Extensive workup for chronic infections, autoimmune conditions and hematological malignancies were negative. This showed concerns for possible DDAVP induced renal injury. Presentation: 6/2/2024

7915 A Case of Severe Hypothyroidism in a Patient with Nephrotic Syndrome presenting with Rhabdomyolysis requiring Levothyroxine and Liothyronine combination therapy

Abstract Disclosure: S.S. Mohammed: None. E.T. Ngo: None. S. Tadisina: None. B.M. Drees: None. Background: Nephrotic syndrome is known to worsen hypothyroidism via urinary loss of thyroid binding globulin, transthyretin, albumin and other proteins, often requiring escalating levothyroxine doses. Severe uncontrolled hypothyroidism can result in rhabdomyolysis, although this presentation is quite rare. Clinical case: We present a case of a 50-year-old male with long-standing Hashimoto’s hypothyroidism, biopsy-proven minimal change disease with nephrotic syndrome, dyslipidemia, and hypertension, who was admitted for generalized myalgia, weakness, and progressive swelling of bilateral hands and feet for one month. He had been off levothyroxine 3 months prior to presentation. He previously required large doses of oral levothyroxine, as high as 350mcg daily, but never achieved a euthyroid state despite reported adherence to therapy with the high levothyroxine doses.Laboratory workup showed severe hypothyroidism (free thyroxine &amp;lt;0.25ng/dL [0.6-1.6ng/dL] with markedly elevated thyroid stimulating hormone 282.03 mIU/mL [0.3-5.6mIU/mL]), along with acute kidney injury and rhabdomyolysis (Creatine kinase 4882 U/L[38-234U/L]). He was hemodynamically stable with intact mentation and was not deemed to be in myxedema coma. Physical examination was consistent with hypothyroidism with periorbital swelling, dry skin, deep hoarse voice, bilateral hand and feet edema, and delayed deep tendon reflexes. Thyroid function tests and clinical symptoms failed to improve after 8 days, despite high doses of levothyroxine IV (200mcg). Creatine kinase remained high at 4994 U/L [38-234U/L] despite adequate fluid hydration. Liothyronine 5mcg orally was started in addition to levothyroxine 200mcg IV. Repeat thyroid function tests after 2 days of combined IV levothyroxine and oral liothyronine therapy showed significant downtrend in TSH to 154.12 uIU/ml [0.3-5.6mIU/mL] and increase in free thyroxine to 0.44ng/dl [0.6-1.6ng/dL]. Creatine kinase also down trended to 3181U/L[38-234U/L] on D4 of IV levothyroxine 200mcg IV with liothyronine 5mcg daily. He was discharged stable and clinically improved on oral levothyroxine and liothyronine. Laboratory evaluation 10 days later showed further improvement in TFTs (TSH 66.0[0.3-5.6mIU/mL]), free thyroxine 0.6 [0.6-1.6ng/dL] Conclusion: This case presents a unique and unusual clinical course in symptomatic primary hypothyroidism with rhabdomyolysis and AKI. Rhabdomyolysis due to hypothyroidism, without an obvious precipitating factor, has been previously reported, but is very rare. There is limited evidence regarding combination treatment with levothyroxine and liothyronine in primary hypothyroidism; however, as demonstrated in this patient, combination therapy resulted in clinical and biochemical improvement of thyroid function. Presentation: 6/2/2024

9185 Pembrolizumab-Induced New-Onset Type 1 Diabetes Mellitus: A Case Report

Abstract Disclosure: D. Teng: None. T.L. Connelly: None. M. Ahmad: None. R. Saeed: None. Introduction: Immune checkpoint inhibitors are becoming essential in the treatment of various cancers. Pembrolizumab is a monoclonal antibody that binds PD-1 receptors, thereby enabling an anti-tumor response by preventing T-cell suppression. Common side effects associated with pembrolizumab include thyroid disorders, hepatitis, pneumonitis, and acute kidney injury, among others. We describe an interesting case of a woman presenting with diabetic ketoacidosis (DKA) in the setting of pembrolizumab-associated new-onset type 1 diabetes mellitus, which was reported at 0.1% during initial clinical trials but is now being increasingly recognized as a complication of immune checkpoint therapy. Case Description: The patient is a 70-year-old female with past medical history notable for stage IIIA vulvar squamous cell carcinoma initially diagnosed and treated in 2017, with recurrence in 2022 and in 2023, at which point pembrolizumab therapy was initiated. Approximately one month after her first dose, the patient presented to the emergency department with palpitations, nausea, non-bloody vomiting, polydipsia, and non-bloody diarrhea. On arrival, the patient’s vital signs were as follows: 97.2 °F, BP 128/74 mmHg, heart rate 80 bpm, respiratory rate 18 per minute, and SpO2 100% on room air. No acute findings were noted on physical exam. Initial blood work was notable for: pH 7.146, lactate 2.4 mmol/L, bicarbonate 8 mmol/L, anion gap 37 mmol/L, creatinine 1.59 mg/dL, glucose 563 mg/dL, C-peptide 0.16 ng/mL, HbA1c 6.9%, and WBC 18.8 B/L with neutrophilic predominance. Urinalysis was notable for 4+ glucose and 4+ ketones. The patient was admitted to the progressive care unit and DKA protocol was initiated including the administration of IV fluids, insulin infusion, and electrolyte replacement. Additional blood work was unrevealing, including insulin autoantibodies &amp;lt;0.4 U/mL, negative islet cell IgG cytoplasmic autoantibodies, and negative anti-GAD65 antibodies. The patient was eventually discharged with outpatient Endocrinology follow-up. Discussion: Immunotherapy is quickly redefining the standard of care in the treatment of several types of malignancies through the leveraging of the body’s immune defense apparatus. Pembrolizumab prevents the deactivation of T-cells via the PD-1/PD-L1 pathway. Unfortunately, this also predisposes non-cancerous cells to autoimmune destruction by these T-cells. It is proposed that such is the mechanism by which pancreatic beta islet cells are destroyed in the setting of pembrolizumab use, thereby resulting in a rapid reduction in insulin production capability. New-onset type 1 diabetes complicated by DKA is potentially life-threatening, and so we believe this case highlights the need for both pre-treatment counseling as well as follow-up screening following initiation of pembrolizumab therapy. Presentation: 6/2/2024

8270 A Rare Case Of PTHrP Induced Severe Hypercalcemia Secondary To Squamous Cell Carcinoma Of Tongue

Abstract Disclosure: N. Vennelaganti: None. S. Vennelaganti: None. K. McCowen: None. Background: PTHrP-mediated hypercalcemia is often associated with solid organ malignancies and indicates a poor prognosis. The occurrence of this condition due to SCC of the head and neck, particularly of the tongue, is uncommon. This case report aims to shed light on this rare clinical presentation. Clinical Case: A 70-year-old woman with a history of tobacco use disorder, alcoholic liver cirrhosis, and a chronic fungal prosthetic joint infection presented with altered mental status and acute kidney injury. Laboratory tests revealed a corrected calcium level of 15.4 mg/dL and suppressed PTH of 3 pg/mL, indicating non-PTH-dependent hypercalcemia. Differentials considered included malignancy, multiple myeloma, 1,25 OH Vit D mediated hypercalcemia via fungal granuloma formation, and immobilization. Diagnostic evaluation revealed normal levels of 25 hydroxy Vitamin D ie: 54 ng/mL, normal kappa to lambda ratio suggestive of negative myeloma screen, normal TSH of 2.81 uIU/mL, and a low 1,25 OH Vit D level ie: 11.4 pg/mL (Ref range: 19.9-79.3 pg/mL). An elevated PTHrP concentration of 9.7 pmol/L (ref range 0-3.4 pmol/L) was noted. CT angiography performed for stroke evaluation incidentally discovered a base of tongue mass, which was difficult to appreciate on exam due to obtundation. A biopsy confirmed SCC of the tongue, and she was determined to be Stage IVA. The patient's hypercalcemia was determined to be secondary to PTHrP production from the tongue SCC compounded by immobilization. She was treated with IV fluids and subcutaneous calcitonin, normalizing her calcium levels over 20 days. IV Bisphosphonates were held inpatient due to poor renal function. She was seen by oncology and determined to not be fit for surgical management or chemotherapy. Radiation therapy was advised for management and patient was discharged. While awaiting her outpatient radiation treatment, the patient had another episode of altered mental status and was found to have a serum calcium of 16.4 mg/dL. She was managed with IV fluids, calcitonin and IV Zoledronate which improved her serum calcium. She has since been receiving monthly IV Zometa with oncology for hypercalcemia of malignancy. She was recently readmitted with severe oropharyngeal and pharyngeal dysphagia and has received a PEG tube for feeding. She is still pending radiation therapy for SCC tongue. Conclusion: Initially, during the workup of this case, we believed her hypercalcemia was likely immobilization-induced, but thorough investigation and the elevated PTHrP levels steered us towards malignancy as a potential etiology. This case is an example of an occult malignancy which lead to severe hypercalcemia. It also contributes to the understanding of hypercalcemia in cancer patients and highlights the rare association of SCC of the tongue with PTHrP-mediated hypercalcemia . PTHrP secreting SCC of head and neck are typically associated with a poor prognosis. Presentation: 6/2/2024

7315 Does Protein Energy Malnutrition Impact Outcomes in Hypothyroidism? A National Inpatient Sample Analysis

Abstract Disclosure: S. Karki: None. B. Neupane: None. S. Neupane: None. A. Bhandari: None. U. Farooq: None. K. Rajamani: None. Introduction: Hypothyroidism poses a significant public health burden in the United States, affecting approximately 4.6 % of the population. Various nutritional deficiencies can adversely affect thyroid function, potentially leading to thyroid disorders. Despite this, there is limited literature exploring the influence of Protein Energy Malnutrition (PEM) on outcomes in hypothyroidism. Objective of our study:This investigation aims to assess the impact of PEM on the healthcare burden and costs associated with hospitalizations in patients with and without hypothyroidism. Methods: A retrospective study was conducted using the National Inpatient Sample (NIS) data from 2017 to 2020. Among the 14,418,310 patients aged 18 and above with a primary diagnosis of hypothyroidism, two groups were formed based on the presence or absence of PEM, determined by International Classification of Diseases (ICD-10) codes. Statistical analysis was performed using STATA, employing the student’s t-test and Fischer’s exact test for continuous variables and proportions, respectively. Adjusted odds ratio was calculated through multivariate regression analysis. The primary outcome was mortality, with secondary outcomes encompassing mean length of stay (LOS), total cost, and various medical complications. Trends in mortality, LOS and total cost were compared for both groups. Results: Out of 14,418,310 hypothyroid patients, 7.06% (1,1018,310) were diagnosed with PEM. Patients with PEM exhibited higher mortality (6.80 % vs. 2.39 %, p&amp;lt;0.001), extended mean length of hospital stay (8.88 days vs. 4.85 days, p&amp;lt;0.001), and higher increased total hospitalization costs ($96,443 vs. $58,262, p&amp;lt;0.001). Furthermore, patients with PEM had elevated rates of various complications, including acute coronary syndrome, septic shock, pulmonary edema, mechanical ventilation, acute respiratory failure, acute respiratory distress syndrome, acute kidney injury, and cerebrovascular accident. Increasing trends in mortality, length of stay, and total cost of hospitalization were observed in hypothyroid patients with PEM. A similar upward trend was noted in hypothyroid patients without PEM. Conclusion: Our study underscores that the presence of PEM in hypothyroid patients substantially increases the healthcare burden, which is reflected in elevated mortality rates, prolonged hospital stays, higher total costs, and a range of adverse outcomes. Screening of PEM in hypothyroid patients is recommended, and early nutritional interventions, possibly involving dieticians, may mitigate these adverse effects. Further research is warranted to explore the association between PEM and hypothyroidism, as well as strategies for early identification and intervention. Presentation: 6/1/2024

6608 Racial Disparities In Outcomes of Hyperosmolar Hyperglycemic State- A National Inpatient Sample Analysis

Abstract Disclosure: S. Karki: None. S. Neupane: None. B. Neupane: None. L.F. Chavez: None. Introduction: Numerous studies have explored variations in access to healthcare among racial and ethnic groups, revealing disparate challenges in insurance coverage and other healthcare services. Hyperosmolar Hyperglycemic State (HHS) or Hyperosmotic Hyperglycemic Nonketotic State (HHNK) represents a severe complication associated with type 2 diabetes mellitus. Objective of the study:To investigate if there are any racial disparities between white and black populations with the diagnosis of HHS, focusing on outcomes such as mortality rates, length of stay (LOS), hospital costs, and other outcomes. Methods: Retrospective data encompassing adult patients (age &amp;gt;18) with HHS between 2017 and 2020 were extracted from the National Inpatient Sample (NIS). Employing STATA as the data analysis tool, the International Classification of Diseases (ICD-10) was utilized to select disease and outcome codes. Multivariate regression analysis adjusted for relevant variables determining the adjusted odds ratio (aOR). Proportions were compared using the Fisher exact test, while continuous variables were assessed via the student t-test. The study's primary outcome was mortality, with secondary outcomes including LOS, total hospitalization costs, Acute Coronary Syndrome (ACS), septic shock, pulmonary edema, Acute Respiratory Failure (ARF), mechanical ventilation, Acute Respiratory Distress Syndrome (ARDS), Acute Kidney Injury (AKI), and Cerebrovascular Accident (CVA). Results: Among 181,720 HHS-diagnosed patients, 84,140 were white, and 58,645 were black. White patients exhibited a $2,741 higher total hospital expenses compared to their black counterparts. Rates of septic shock (aOR=0.78, 5.26% vs. 4.1%, p&amp;lt;0.001) and ARF (aOR=0.83%, 10.54 vs. 9%, p&amp;lt;0.001) were elevated in whites compared to blacks. Conversely, rates of AKI were higher in blacks (aOR=1.48, 58.29% vs. 50.58%, p&amp;lt;0.001) compared to whites. No statistically significant differences in mortality rates, mean LOS, ACS, pulmonary edema, mechanical ventilation, ARDS, and CVA were observed. Conclusion: Whites demonstrated increased rates of total hospital expenses, septic shock, and ARF compared to blacks, while blacks exhibited higher rates of AKI. No significant differences were observed in mortality rates, LOS, ACS, pulmonary edema, mechanical ventilation, ARDS, and CVA. Presentation: 6/2/2024

7668 Rhabdomyolysis Associated with Severe Hypothyroidism

Abstract Disclosure: H. Soe: None. P. Mikkilineni: None. Background: Over 70% of the patients with newly diagnosed hypothyroidism can present with muscle complaints such as weakness, fatigability, cramps, myalgia. However, rhabdomyolysis, which is the rapid breakdown of skeletal muscle cells, is the rare presentation. Clinical Case: A 70-year old male patient with history of rheumatoid arthritis, hyperlipidemia, prior CVA (left hemispheric subcortical stroke) 6 months ago without residual deficit presented to the hospital with poor oral intake and generalized muscle weakness for 3 weeks. He was unable to get out of bed without assistance and also needed adult diapers. Found to have new-onset severe hypothyroidism with TSH 228 uIU/ml (Ref: 0.350-4.940) and FT4 &amp;lt;0.40 ng/dL (Ref: 0.70-1.50), positive TPO antibody 197 IU/ml (Ref: 0-34). No prior thyroid labs were available and no known history of thyroid disorder was recorded. He has never been on Amiodarone or Lithium before. On physical exam, he was alert and oriented. There was no goiter or palpable thyroid nodule. There was no focal neurological deficit and no peripheral edema. There were no other signs and symptoms pertinent to hypothyroidism except mild bradycardia (HR 56-60) and borderline low blood pressure. AM cortisol was 10.1 ug/dL (Ref: 3.7-19.4). EKG showed low-voltage sinus bradycardia. Echocardiogram was normal. Urinalysis was positive for large blood but only 3 RBCs were present which raised the suspicion of rhabdomyolysis. Creatinine kinase (CK) was 15,584 IU/L (Ref: 30-200). Other laboratory studies were significant for acute renal failure with mild hyperkalemia and mild hypocalcemia, also transaminitis; BUN 130 mg/dl (Ref: 8-26), Creatinine 9.51 mg/dl (Ref: 0.72-1.25), eGFR 5 ml/min/1.73 m2 (Ref: &amp;gt;59), AST 435 IU/L (Ref: 5-34), ALT 269 IU/L (Ref: &amp;lt;55), ALP 171 IU/L (Ref: 40-150). On medication review, he was started on Atorvastatin 80 mg daily during prior admission for CVA 6 months ago. He received IV fluids, s/p 1 dose of Hydrocortisone 100 mg IV, Levothyroxine IV 200 mcg, followed by Levothyroxine IV 50 mcg daily x 3 days and switched to Levothyroxine PO 100 mcg daily (weight-based dose). Atorvastatin was on hold. He became anuric during the hospital course and received 2-3 sessions of hemodialysis. 3-4 days later, CK was trending down to 3000 IU/L, FT4 improved to 0.54 ng/dl and there was also significant improvement in kidney and liver functions. The patient was diagnosed with acute renal failure secondary to rhabdomyolysis associated with severe hypothyroidism caused by Hashimoto's thyroiditis, in the setting of high dose statin use. Conclusion: Clinicians should raise the suspicion of rhabdomyolysis in a patient with severe hypothyroidism, especially in patients with recent high dose statin use as rhabdomyolysis can be a rare and fatal complication of severe hypothyroidism, in the presence of precipitating factors. Presentation: 6/2/2024

12620 Developing Hospital Protocols For Managing Patients With Hypertriglyceridemia-induced Acute Pancreatitis In Diabetic Ketoacidosis Hospitalizations

Abstract Disclosure: U. Agbedia-ejughemre: None. Methods: We queried the combined 2017-2020 nationwide inpatient sample database for all adult hospitalizations for DKA with and without HTG-AP using the ICD-10 revision codes. Baseline characteristics were compared between DKA hospitalizations with and without HTG-AP using Pearson’s χ2 tests and Student’s t-test for categorical and continuous variables. Study endpoints were the incidence, predictors, and outcomes of HTG-AP, including mortality, hospitalization duration, mean hospital costs, and acute in-hospital complications (sepsis, ARDS, and acute renal failure). Predictors of HTG-AP were assessed using stepwise multivariable logistic regression analysis. Illness severity, baseline risk of mortality, and comorbidity burden were adjusted using APR-DRG metrics and CCI. Prolonged hospitalization was defined as the length of hospital stay in the top decile of hospital stay for all hospitalizations in the study. Results: We analyzed 630,435 hospitalizations for DKA. The study cohort was 51.4% male, 57.6% white Americans and 26.1% Blacks, with a mean age of 40 (SD, 16.2) years. Incidence of HTG-AP was 2.1% (13,445). Hospitalizations with HTG-AP were older (mean age: 44 vs. 40 years; P&amp;lt;0.001) and had greater comorbidity (CCI score of 2: 38.7 vs. 33.8; P&amp;lt;0.001) compared with DKA hospitalizations without HTG-AP. While DKA hospitalizations showed an uptrend, increasing from 105,769 to 199,429 hospitalizations (Average annual percent change [AAPC]: 27.04%; P=0.029), the incidence of HTG-AP showed a downtrend from 2650 (2.5%) to 4085 (2.0%) (P=0.006). Predictors of HTG-AP included Hispanic (aOR: 2.45; 95% CI: 1.95-3.07; P&amp;lt;0.001) or Asian race (aOR: 2.48; 95% CI: 1.37-4.48; P=0.003), private insurance (aOR: 1.57; 95% CI: 1.10-2.25; P=0.013), self-pay (aOR: 2.2; 95% CI: 1.49-3.27; P&amp;lt;0.001), APR-DRG moderate risk of mortality (aOR: 1.52; 1.21-1.92; P&amp;lt;0.001), APR-DRG major loss of function (aOR: 1.46; 95% CI: 1.31-1.69; P&amp;lt;0.001), dyslipidemia (aOR: 1.87; 95% CI: 1.47-2.38; P&amp;lt;0.001), hypertension (aOR: 1.39; 95% CI: 1.13-1.72; P=0.002), obesity (aOR: 3.09; 95% CI: 2.42-3.96; P&amp;lt;0.001), obstructive sleep apnea (aOR: 2.05; 95% CI: 1.35-3.10; P=0.001), chronic liver disease (aOR: 9.44; 95% CI: 6.61-13.48; P&amp;lt;0.001), old MI (aOR: 2.11; 95% CI: 1.02-4.38; P=0.045), and COPD (aOR: 2.31; 95% CI: 1.47-3.64; P&amp;lt;0.001). DKA hospitalizations with HTG-AP were correlated with higher risk of septicemia (aOR: 1.20; 95% CI: 1.05-1.69; P=0.029), ARDS (aOR: 1.24; 95% CI; 1.04-2.07; P=0.004), and resource use, including prolonged hospitalization (26.3% vs. 11.1%; P&amp;lt;0.001), and higher mean hospital costs ($57,773 vs. $32,692; P&amp;lt;0.001). Conclusion: HTG-AP was linked to worse outcomes, excluding mortality, in hospital admissions for DKA. There is a need for enhanced diagnostic guidelines and protocols targeting this subgroup of patients could improve outcomes. Presentation: 6/2/2024

6980 A Case Report Of Severe Hypercalcemia In Acute Decompensated Liver Cirrhosis

Abstract Disclosure: M.M. Eid: None. R.M. Sargis: None. Introduction: Hypercalcemia in advanced liver disease in the absence of malignancy is a rare condition. Case: A 26 year old female with history of liver cirrhosis secondary to alcohol use disorder, presented with hematemesis and ascites. She was diagnosed with acute decompensated liver cell failure and transferred to our facility for liver transplantation. On Day 10 of her hospital course, she had an acute rise in serum calcium (Ca) to 10.8 mg/dl (N 8.7-10.5),albumin (Alb) 2.6 g/dl, corrected calcium (CCa) 11.9mg/dl. On day 13 Ca peaked to 13.5 mg/dl, CCa 14 mg/dl, ionized Ca 6.5mg/dl (N 4.2-5.4 mg/dl). Serum Ca was normal on day 9, Ca 8.7mg/dl, Alb 2.5 g/dl and CCa 9.9 mg/dl. She was not taking lithium, vitamin A or antacid. No personal or family history of bone disorder, fracture or kidney stone. On exam, blood pressure 85/45, heart rate 110 bpm, jaundiced with abdominal distension and respiratory distress. Labs: hemoglobin 8.1 g/dl, WBC 32.5K/Ul, platelet 136 K/Ul, serum creatinine 1.82 mg/dl, Na 133 mmol/l, K 3.5 mmol/l, Total/Direct bilirubin 29.9/18.1 mg/dl, alkaline phosphatase 166 U/L, AST/ALT 60/42U/l, Mag 2.3 mg/dl, Phos 5 mg/dl, INR 3, PTT 50 sec, parathyroid hormone (PTH) 12 pg/ml (N12-88), TSH 1.02 mciu/ml (N 0.34-4), 25 hydroxy vitamin D 17 ng/ml (N 20-80), parathyroid related peptide (PTHrP) 3.9 pmol/l (N&amp;lt;3.4), 1,25 di-hydroxy vitamin D 9.8 pg/ml (N 19.9-79.3), alpha fetoprotein 9.1 ng/ml (N &amp;lt;9). Normal anti smooth muscle and anti mitochondrial antibodies. Negative viral hepatitis serology. CT abdomen did not reveal hepatobiliary mass or tumor nor kidney stone. She was intubated and mechanically ventilated. Vasopressor support was initiated. One dose of calcitonin 4 units/kg and zoledronic acid 4 mg were given. Serum Ca decreased to 12 mg/dl, CCa 12.6 mg/dL then to 10.2 mg/dl, CCa 11mg/dl within hrs. Calcium normalized to 8.4mg/dl, CCa 9.2 mg/dl, ionized Ca 4.3 mg/dl within 24 hrs. Her condition deteriorated and withdrawal of care was decided. Conclusion: Our case demonstrates non PTH and non vitamin D mediated severe hypercalcemia in setting of acute decompensated cirrhosis and absence of malignancy. Previous literature has noted poor prognosis of hypercalcemia with acute decompensated cirrhosis. While hypercalcemia in cirrhosis may arise from paraneoplastic processes, in absence of malignancy it is speculated that acute hypercalcemia may arise from the inflammatory mediators inducing osteoclastic bone resorption as osteoclast activating factor, prostaglandin and immobilization. Some reports found an association between hypercalcemia and elevations in bilirubin and creatinine(1). Further research is needed to understand the pathophysiology and the management of hypercalcemia in acute decompensated cirrhosis.

8192 A Two-Cycle Clinical Audit Testing Inpatient Management Of Hypophosphatemia In A UK District Hospital

Abstract Disclosure: J. Porto: None. E. Ssemmondo: None. N. Obike: None. A. Abobaker: None. R. March: None. N. Tun: None. T. Pawlak: None. Objective: A clinical audit was conducted to assess if there was any improvement in management of hypophosphatemia among patients admitted to the medical wards using the local Trust protocol, following structured edcational sessions to the junior doctors covering medical wards. Design and methodology: The 2 cycles of the audit were conducted between March 2020 and September 2021 in Scarborough district Hospital. The clinical notes of 52 patients (20 in the first cycle and 32 in the re-audit) with hypophosphatemia were reviewed. These were identified using the electronic laboratory results of patients within the study period. The aspects of the trust protocol for management of hypophosphatemia that were audited; documentation of symptoms associated with low phosphate levels, cardiac monitoring in severe hypophosphatemia, identification of the likely cause of hypophosphatemia, the presence or absence of associated acute kidney injury (AKI) and initiation of phosphate replacement. The results of the first audit were presented at the local hospital clinical governance meeting (August 2020). Following this, 2 teaching sessions and 2-case based discussion on hypophosphatemia were organised for all the doctors in the department of medicine. The re-audit was subsequently conducted after the fourth teaching session. The proportions of each audited item were compared between the first audit and the re-audit using Fisher exact probability test. Results:25% of patients in the first audit had severe hypophosphatemia compared to 28% in the re-audit. In patients with severe hypophosphataemia, only 33.3% had cardiac monitoring during the re-audit cycle compared to 60% in the first cycle, and the difference was not statistically significant (p=0.58). There was significant improvement in the documentation of symptoms of hypophosphataemia amongst inpatients during the re-audit cycle compared with the initial cycle; 62.5% vs only 10% (P 0.002). Most patients had an underlying cause of the hypophosphatemia identified (80% and 62.5%-first and second cycle respectively). AKI was associated with hypophosphataemia in 15% &amp; 34.4% (P 0.2) in the first and second cycles respectively. Despite low phosphate levels, 25% and 28.1% at the initial audit and the second cycle respectively did not receive any form of phosphate replacement. Conclusion: The two-cycle clinical audit showed that the teaching sessions on management of hypophosphatemia increased the awareness of the importance to document whether the patients were symptomatic or asymptomatic following the drop in their phosphate levels, which can help to identify patients at risk of developing complications, such as cardiac arrythmias. However, these sessions were not sufficient to improve overall management of patients with low phosphate levels. Presentation: 6/1/2024

8472 A Little Too Much Of Tums: A Unique Presentation Of Milk Alkali Syndrome

Abstract Disclosure: Z. Al-Hiti: None. A. Misbah: None. Milk-Alkali Syndrome is characterized by a triad of hypercalcemia, metabolic alkalosis, and renal dysfunction. Historically associated with the excessive consumption of milk and alkali-containing antacids, it has re-emerged in recent years due to the widespread use of calcium and vitamin D supplements. It primarily results from an imbalance between calcium intake and renal excretion, leading to elevated calcium levels in the bloodstream. We present a case of milk-alkali syndrome with persistent renal dysfunction after normalizing calcium levels. We present the case of a 65-year-old male who presented to the emergency department with generalized weakness, poor oral intake, and confusion for 3 days. He was noted to have been more adherent with taking his prescribed medications over the last 2 weeks, which include calcitriol 0.5 mcg BID, calcium acetate 667 mg TID, and calcium carbonate 800 mg TID. On admission, he was afebrile and hemodynamically stable. . On examination, he had dry mucous membranes. He had no focal neurological deficits but he was confused and lethargic, and was only oriented to self. Other examination was noncontributory. Complete blood count and urinalysis were largely unremarkable. Chemistry demonstrated an elevated calcium level of 16.0 (8.3-10.6 mg/dL), ionized calcium of 7.3 (4.6-5.3 mg/dL), sodium of 134 (135-145 mmol/L), potassium of 5.4 (3.5-5.1 mmol/L), high phosphorus of 5.3 (2.4-5.1 mg/dL), and bicarbonate of 36 (20-31 mEq/L). Creatinine was elevated at 2.9 (0.6-1.1 mg/dL) from baseline of 1.3 to 1.4 mg/dL, and he had a BUN of 40(9-23 mg/dL). Venous blood gas showed a pH of 7.54( 7.32-7.42), pCO2 of 56 (40-52 mm Hg), and bicarbonate of 38 (23-28 mEq/L), indicating metabolic alkalosis. TSH was elevated at 36.15 (0.55- 4.78 uIU/mL) with a level of 140 two weeks back. Chest X-ray, renal ultrasound and CT head all showed no acute disease. Further work-up revealed a low PTH level of 6.3 (18.4-80 pg/mL), normal PTHrP level and 25-OH Vitamin D. There was no monoclonal gammopathy. Management included aggressive IV fluid resuscitation and IV calcitonin. However, no zoledronic acid was given due to a history of parathyroidectomy and risk of hypocalcemia. His serum calcium improved and eventually normalized. His confusion resolved. However, his creatinine and BUN increased to 3.4 mg/dL and 77, respectively, and did not improve to his baseline. This case highlights the importance of recognizing Milk-Alkali Syndrome as a potential consequence of over-the-counter calcium supplementation and highlights the potential for acute kidney injury which could be irreversible. Healthcare providers should be vigilant in identifying patients at risk, which includes older patients and patients with chronic kidney disease. Early recognition and appropriate management are crucial to prevent further renal deterioration and improve outcomes in individuals with Milk-Alkali Syndrome. Presentation: 6/2/2024

6702 Management And Complications Of Metastatic Adrenocortical Carcinoma Presenting With Severe Cushing Syndrome

Abstract Disclosure: S. Rodrigues: None. A.K. Sumal: None. Background: Metastatic adrenocortical carcinoma (ACC) presenting with Cushing syndrome (CS) is a complicated, aggressive disease that commonly requires multiple adrenal steroidogenesis inhibitors and chemotherapy to achieve hormonal and tumor control. Clinical Case: A 66-year-old man with a history of prostate cancer and hypertension presented with right flank and back pain, worsening type 2 diabetes, profound proximal muscle weakness, and 3+ lower extremity edema to his thighs. CT and PET-CT revealed a 10.9 cm right adrenal mass with pericaval lymphadenopathy and metastatic disease at the L2 vertebral body. Laboratory testing demonstrated evidence of hypercortisolism with elevated 24-hour urinary cortisol excretion (449 mcg/24h; n&amp;lt;45 mcg/24h), and abnormal 1 mg dexamethasone suppression test (cortisol 15 mcg/dL; n&amp;lt; 1.8 mcg/dL) with suppressed ACTH (&amp;lt;6 pg/mL; n=7-63 pg/mL). Surgical resection of the primary tumor was aborted intraoperatively given the discovery of new peritoneal metastases, which were confirmed by biopsy to be metastatic ACC. He was started on mitotane and osilodrostat to manage his severe CS. He was also started on dexamethasone, both to prevent adrenal insufficiency and to avoid influencing serum cortisol measurements used to assess disease control. However, given his significant peripheral edema and weakness, he was functionally unable to receive chemotherapy. Despite rapid uptitration of mitotane and osilodrostat over three weeks, his CS remained uncontrolled, and he was ultimately hospitalized for lower extremity paralysis and septic shock due to pyelonephritis. Repeat imaging revealed severe spinal canal stenosis from an L2 pathologic fracture, as well as worsening hepatic, osseous, peritoneal, and retroperitoneal metastases. After recovery from his septic shock, he was started on chemotherapy with carboplatin and etoposide while hospitalized, but his mitotane was intermittently held due to elevated transaminases. His hospital course was complicated by hypotension requiring pressor support, atrial fibrillation, hemoperitoneum, worsening anasarca, and acute kidney injury requiring continuous renal replacement therapy. Given his worsening condition that precluded him from further chemotherapy or palliative radiation, he elected to pursue comfort care measures and expired shortly thereafter. Conclusion: This case highlights the therapeutic challenges of metastatic ACC presenting with life-threatening CS. Simultaneous use of multiple adrenal steroidogenesis inhibitors is often required for control of hypercortisolism, and chemotherapy is equally necessary to manage tumor burden. However, as in this case, disease-related complications can limit treatment management and result in rapid deterioration. Thus, early diagnosis and prompt treatment of metastatic ACC presenting with CS is critical to prevent morbidity and mortality. Presentation: 6/3/2024

8418 Association of GLP-1 Receptor Agonists and SGLT-2 Inhibitors with Major Adverse Cardiovascular Events and Serious Liver Events among Patients with Type 2 Diabetes and MASLD

Abstract Disclosure: A. Kutz: None. D.J. Wexler: None. J. Liu: None. J.M. Paik: None. E. Patorno: None. Introduction and study question Little is known about the cardiovascular (CV) and hepatic effectiveness of glucagon-like peptide 1 receptor agonists (GLP-1 RA) and sodium–glucose cotransporter 2 inhibitors (SGLT-2i) in people with type 2 diabetes (T2D) and known metabolic dysfunction-associated steatotic liver disease (MASLD) in clinical practice. We assessed the comparative CV and hepatic effectiveness and the safety of GLP-1 RA and SGLT-2i in people with T2D and prevalent MASLD. Methodology Using pooled data from Medicare fee-for-service (2013–2020) and a large U.S. health insurance database (2013-June 2022), we conducted two propensity-score fine stratification weighted cohort studies including adults with T2D and a diagnosis of MASLD who initiated GLP-1RA, SGLT-2i, or dipeptidyl peptidase 4 inhibitors (DPP-4i, reference). Using Cox proportional hazards models, we assessed the primary CV effectiveness composite outcome of acute myocardial infarction, ischemic stroke, hospitalization for heart failure, or all-cause mortality. The primary hepatic effectiveness outcome was a composite of serious liver events (hospitalization for ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, bleeding esophageal varices, hepatic encephalopathy, or liver transplantation). The safety outcome was a composite of severe adverse events (lower limb amputation, non-vertebral fracture, emergency admission for hypoglycemia, or hospitalization for acute kidney injury, diabetic ketoacidosis [DKA], severe genital or urinary tract infection, acute pancreatitis, or biliary event). Major results Compared with DPP-4i (n=17,084 initiators), the hazard ratio (HR) for the primary CV outcome associated with GLP-1 RA (n=13,666 initiators) was 0.67 (95% CI, 0.56 to 0.81), corresponding to an incidence rate difference (IRD) per 1,000 person-years of -21.6 (95% CI, -26.7 to -16.6). The HR for the primary hepatic outcome was 0.47 (95% CI, 0.25 to 0.90), the IRD -2.1 (95% CI -3.4 to -0.9). Similar CV benefits were observed for SGLT-2i (n=11,108) vs DPP-4i (n=16,979), with a HR for the primary CV outcome of 0.82 (95% CI 0.70–0.96) and an IRD of -11.0 (95% CI -16.2 to -5.8). For the primary hepatic outcome, the HR was 0.81 (95% CI 0.45 to 1.44) and the IRD -1.1 (95% CI -2.4 to 0.3). Severe adverse events were not more frequent with GLP-1RA or SGLT-2i compared with DPP-4i. Interpretation and conclusion Among people with T2D and MASLD, the use of GLP-1 RA or SGLT-2i was associated with fewer CV events, vs DPP-4i, while GLP-1 RA also reduced serious liver events. Compared with DPP-4i, GLP-1RA or SGLT-2i were not associated with higher safety adverse event rates. Presentation: 6/2/2024

6769 Rhabdomyolysis In Diabetic Emergencies Highlighting The Necessity Of Prompt Creatine Kinase Monitoring

Abstract Disclosure: A. Tiwari: None. M. Corsten: None. W. salari: None. N. Malik: None. A. Dabaja: None. C. Saad: None. Rhabdomyolysis results from skeletal muscle necrosis, causing the release of intracellular contents into the bloodstream. While its association with life-threatening diabetic emergencies is rare, it remains a significant complication. We detail the case of a 37-year-old male admitted with acute pancreatitis who subsequently developed a hyperosmolar hyperglycemic state accompanied by significant electrolyte imbalances. Upon arrival at our emergency department, he displayed severe dehydration, stupor, a blood glucose level surpassing 2,000 mg/dl, and high anion gap metabolic acidosis. His condition worsened when his creatine kinase levels surged from 210 U/L to 39,000 U/L, leading to oliguric renal failure and the need for hemodialysis. His thyroid profile was unremarkable and was not on any medication. Comprehensive treatment included crystalloids, parenteral insulin, and rigorous ICU monitoring with mechanical ventilation. Following this, the patient showed rapid improvement and was discharged without requiring further dialysis. A thorough history and observation established a rare but strong link between rhabdomyolysis and hyperosmolar hyperglycemic states. These situations can intensify nephrotoxic events, especially in patients already facing severe dehydration and prerenal factors. This case emphasizes the critical need for consistent monitoring of creatine kinase levels in diabetic emergencies. Such monitoring ensures early detection and facilitates effective management of rhabdomyolysis-induced acute kidney injury, reducing potential complications and improving patient outcomes. Presentation: 6/3/2024