Hypertriglyceridemia-induced Pancreatitis Research Articles

The use of subcutaneous instead of intravenous insulin in a hypothyroid and diabetic patient with hypertriglyceridemia-induced pancreatitis - a case report

The use of subcutaneous instead of intravenous insulin in a hypothyroid and diabetic patient with hypertriglyceridemia-induced pancreatitis - a case report

Management of hypertriglyceridemia-induced pancreatitis - case series

Management of hypertriglyceridemia-induced pancreatitis - case series

Variants APOA5 p.G185C and p.S19W associated with early-onset severe hypertriglyceridemia-induced pancreatitis and diabetes complications in a Vietnamese girl

An imbalance of glucose and severely high triglyceride are the key characteristics driving hypertriglyceridemia and hyperlipidemic pancreatitis. Hereditary factors considerably promote the increase of triglyceride levels and secondary complications. This study explored the clinical characteristics and genetic causes of a young girl with recurrent severe hypertriglyceridemia-developed pancreatitis at 9-year-olds and diabetes mellitus appearance at 14-year-olds. At 20 years old, she was admitted to the hospital in critical condition and had pancreatitis pain with triglyceride level at 26.22 mmol/L, HbA1c 15%, and glucose at 21.3 mmol/L. Whole exome sequencing analysis showed that she had two heterozygous variants of the APOA5 gene, (p.G185C and p.S19W), one homozygous variant of the APOE gene (p.C156R), which were previously reported to cause critical hypertriglyceridemia condition of patients. The results and analysis propose these variations were the underlying causes of a heightened of patient's plasma triglycerides and lead metabolic complication onset at a young age. These findings shed light on the molecular mechanism of her elevated plasma triglyceride and the early onset of diabetes following hyperlipidemic pancreatitis.

The Case Files

The Case Files

Abstract #1406325: The Complexities of Managing Hypertriglyceridemia-Induced Pancreatitis in a Critically-Ill COVID-19 Patient

Hypertriglyceridemia-induced pancreatitis (HTP) is a variant of pancreatitis requiring unique management. The complications of COVID-19 and its treatments can make HTP therapy more nuanced. This case describes a patient who presented in diabetic ketoacidosis (DKA) with HTP, and COVID-19. The patient developed renal and respiratory failure, necessitating hemodialysis (HD) and extracorporeal membrane oxygenation (ECMO), complicating an otherwise straightforward medical management plan. A morbidly obese (BMI 38.9 kg/m2) 43-year-old male presented to an outside hospital with abdominal pain, and vomiting, and was found to have HTP with triglycerides (TG) >2000 mg/dL (<149 mg/dL) and presumed new-onset type 2 Diabetes (HbA1c 10.9%) with DKA. Treatment with fluids, intravenous (IV) insulin infusion and plasmapheresis were initiated. He developed hypoxia after receiving over 17 liters of fluids and was intubated, subsequently developing renal failure and was transferred to our tertiary center for HD and ECMO. On admission, he tested positive for COVID-19, rhabdomyolysis [creatinine kinase 5600 U/L (30-200 U/L)], HTP [TG 783 mg/dL (<149 mg/dL), lipase 461 U/l (7-60 U/L)], glucose 269 mg/dL (not in DKA), transaminitis [AST 184 U/L (4-40 U/L), ALT 61 U/L (4-41 U/L)] and renal failure (GFR 10 ml/min/1.73m2). IV insulin infusion was initiated for hyperglycemia worsened by COVID-19 dexamethasone treatment. Plasmapheresis was performed twice with minimal effect at maintaining a low TG. Fenofibrate was not initiated due to renal failure; Lovaza could not be given via oral gastric tube; Atorvastatin was attempted once rhabdomyolysis resolved, with subsequent worsening of liver function tests. Heparin infusion was initiated for deep vein thrombosis treatment and HTP but was stopped after development of heparin induced thrombocytopenia. The patient developed worsening hypoglycemia requiring cessation of IV insulin, hypotension requiring maximum pressor support, and worsening sepsis leading to his death. This case illustrates the challenges of managing a patient with HTP and COVID-19. It demonstrates how a normally straightforward treatment algorithm can become increasingly complex when factoring the patient’s comorbid conditions. The case highlights the importance of knowing both treatment indications and contraindications for HTP. In this case, HTP may have been the initial diagnosis, straightforward for most endocrinologists, but its treatments and comorbid conditions ultimately made the landscape more challenging, limiting effective management and ultimately leading to this patient’s demise.

Diabetic Ketoacidosis Related to Hypertriglyceridemia-Induced Pancreatitis: A Case Report.

Both diabetic ketoacidosis and acute pancreatitis can result in critical illness. Although not the most common cause of acute pancreatitis, hypertriglyceridemia can account for up to 10% of cases. One source of hypertriglyceridemia is unrecognized diabetes and resultant hyperglycemia. Identifying the underlying cause of acute pancreatitis can guide the most appropriate therapy to resolve this critical illness. This case report addresses the use of insulin infusions to treat hypertriglyceridemia-induced pancreatitis in the setting of concomitant diabetic ketoacidosis.

Therapeutic Plasma Exchange in ICU Patients with Acute Hypertriglyceridemia-Induced Pancreatitis Improves Patient Outcomes

Background: Acute severe pancreatitis is associated with high morbidity and mortality. Hypertriglyceridemia is the third most common cause of acute pancreatitis and higher triglyceride levels increase the risk for severe acute pancreatitis. Plasma exchange is an effective treatment method to lower triglycerides. Our study aimed to investigate the efficiency of plasma exchange as a treatment option for acute hypertriglyceridemia-induced pancreatitis (HTGP), the impact on mortality assessed by the SOFA, SAPS II, BISAP Score, Ranson’s, and Glasgow-Imrie Criteria, as well as the overall length of stay in hospital and ICU. Methods: In this retrospective single-center cohort study, triglycerides before and after plasma exchange were compared. SOFA and SAPS II were taken on ICU admission and at discharge. To further characterize the patient cohort, BISAP Score (on admission), Ranson’s Criteria (on admission and after 48 h), and the Glasgow-Imrie Criteria (48 h after admission) were calculated. Results: The study included 11 patients (91% male; median age 45 years). Triglycerides were reduced from 4,266 ± 3,560.6 to 842 ± 575.9 mg/dL during plasmapheresis (p < 0.001). The median ICU length of stay was 3 ± 4.2 days. In-hospital mortality was 0%. The SOFA score was significantly reduced from 4 ± 3.4 points on admission to 2 ± 2.1 points at discharge (p = 0.017). Triglycerides and cholesterol decreased from 3,126 ± 3,665 to 531 ± 273 mg/dL (p = 0.003) and from 438 ± 137.9 to 222 ± 59.5 mg/dL (p = 0.028), respectively. The BISAP Score on admission was 3 ± 0.5 points, Ranson’s Criteria were 3 ± 1.5 points (48 h after admission, cumulative), and Glasgow-Imrie Criteria 3 ± 1.3 points (48 h after admission). Conclusion: Plasmapheresis is an efficient and safe treatment method for ICU patients with acute HTGP and significantly reduces triglycerides. Furthermore, plasmapheresis significantly improves the clinical outcomes of patients with HTGP.

Pregnancy-induced severe hypertriglyceridemia effectively treated with therapeutic plasmapheresis

IntroductionHypertriglyceridemia is associated with significant morbidity during pregnancy. Hypertriglyceridemia-induced pancreatitis (HTGP) is associated with genetically determined dyslipidemia or a secondary condition such as diabetes, alcohol, pregnancy, or medication use. The lack of data on the safety of drugs to be used to decrease triglyceride levels during pregnancy dictates that other strategies must be chosen. Patient and methodsWe describe a case of a pregnant woman with severe hypertriglyceridemia treated with two different techniques of plasmapheresis (Dual Filtration apheresis and Centrifugal Plasma Separation). ResultsThe patient could be treated throughout the pregnancy, with good control of the triglycerides, and a healthy baby was born. ConclusionHypertriglyceridemia is a major issue during pregnancy. The use of plasmapheresis is a safe and efficient tool in that clinical scenario.

ODP135 A New Life-Saving Treatment not yet Included in Guidelines for Recurrent Severe Hypertriglyceridemia-Induced Pancreatitis

Abstract Severe hypertriglyceridemia is a rare cause of acute pancreatitis especially in non-alcoholic, non- gallstones, non-obese, non-diabetic patients and has a few options for its management. Hypertriglyceridemia-induced pancreatitis causes 1 to 14 percent of all cases of acute pancreatitis. The risk of developing acute pancreatitis is approximately 5 percent with serum triglycerides &amp;gt;1000 mg/dL and 10 to 20 percent with triglycerides &amp;gt;2000 mg/dL. This is the case of a 63-year-old female who came to the Emergency Department with acute onset of abdominal pain, located at the mid-epigastric region, radiating to back, 10/10 in a scale of severity, no alleviating or aggravating factor, accompanied by nausea, 5 episodes of bilious emesis. Past medical history includes recurrent acute pancreatitis induced by hypertriglyceridemia (3 episodes last year), arterial hypertension, and dyslipidemia treated with Fenofibrate and Atorvastatin. Denies toxic habits. Physical examination showed abdominal tenderness with positive bowel sounds. Laboratories report cholesterol: 44mg/dl, triglycerides: 5,831mg/dl, LDL: -735 mg/dl, and HDL: 13 mg/dl. The patient condition warranted admission to the intensive care unit with the diagnosis of severe hypertriglyceridemia induced pancreatitis. Initially managed with insulin drip, bowel rest, and conservative management, which did not result in any improvement in her symptoms. A successful method of treatment relies on plasmapheresis for the lowering of triglyceride levels. This was first reported in 1978 by Betteridge and can result in a rapid decrease in triglyceride levels over a short period of time compared to the other treatment options. In this case, vascular surgery was consulted for apheresis catheter placement, with triglyceride improvement from 5,831mg/dl to 973 mg/dl after initial and single apheresis intervention, as the patient's symptoms resolved. Triglyceride levels decreased to 113 mg/dl after a week of therapy with plasmapheresis. The patient continues evaluation at the outpatient clinic and currently has been without recurrence of pancreatitis for the last year. Finally, the use of insulin infusion in conjunction with plasmapheresis has been demonstrated to be a viable option for rapid improvement in symptoms associated with acute pancreatitis associated with elevated triglycerides. Plasmapheresis rapidly removes triglycerides from the circulation removing the inciting factor, decreasing inflammation, and damage to the pancreas. The patient's triglyceride level decreased to 973 mg/dl the next day from 5,831mg/dl initially and the patient's symptoms resolved. Plasmapheresis is not an established guideline for the management of hypertriglyceridemia -induced pancreatitis. Plasmapheresis lowers the lipid levels drastically within hours compared to conservative therapy that usually takes several days to achieve the same reduction in triglycerides levels. Presentation: No date and time listed

ODP153 Recurrent hypertriglyceridemia-induced pancreatitis due to multifactorial chylomicronemia syndrome in a patient with ketosis-prone diabetes mellitus

Abstract Background Hypertriglyceridemia-induced pancreatitis is associated with significant morbidity and mortality. The triad of diabetic ketoacidosis (DKA), severe hypertriglyceridemia, and acute pancreatitis have been occasionally described in severely obese patients with type 2 diabetes mellitus (T2DM). However, the occurrence of this triad in newly diagnosed ketosis-prone diabetes mellitus (KPDM) is rarely reported. Herein, we report a long-term follow-up of a Thai man with KPDM complicated with recurrent pancreatitis due to multifactorial chylomicronemia syndrome. Case Description A 33-year-old Thai male patient with a history of insulin-independent diabetes mellitus, recurrent hypertriglyceridemic pancreatitis, and recurrent DKA (three times within the past 5 years) came to our hospital in 2020 for the management of plasma triglyceride levels. At the age of 29 years (BMI 31.2 kg/m2), he experienced the first hypertriglyceridemia-induced pancreatitis (plasma triglyceride 8,189 mg/dL) in association with DKA. After resolution of DKA, insulin therapy was successfully discontinued for 3 years. Then, recurrent hypertriglyceridemic pancreatitis in association with multiple organ failures was developed during travelling to India. After treatment with plasmapheresis and continuous intravenous insulin infusion, he was able to extubate but pulmonary embolism at right pulmonary artery was discovered. Subcutaneous low molecular weight heparin was given for 6 months and then discontinued. The last hypertriglyceridemia-induced pancreatitis attack in association with DKA was aggravated by a high fat buffet meal 1 month prior to our hospital visit. He denied any tobacco, alcohol, or substance use. The patient had no known family medical history of lipid disorders. Further investigations revealed preserved beta-cell function by mixed meal stimulation test and negative pancreatic autoantibodies. Genetic testing showed no mutation in lipoprotein lipase (LPL) and its co-factors. Therefore, multifactorial chylomicronemia syndrome with KPDM was diagnosed. The patient was referred to multidisciplinary team for lifelong weight loss, limiting intake of fat and simple carbohydrates, and adherence to lipid-lowering medications. Subsequent follow-up 2 years later showed no recurrent pancreatitis. Conclusion The triad of acute pancreatitis, severe hypertriglyceridemia and DKA constitutes a unique subgroup of patients which insulin deficiency state is the core defect in association with underlying genetic predisposition. Molecular diagnosis of underlying genetic defect should be pursued to exclude familial chylomicronemia syndrome. In patients with multifactorial chylomicronemia syndrome, long-term management with dietary modifications together with pharmacotherapy remains the cornerstone of successful treatment. Presentation: No date and time listed

ODP150 Hypertriglyceridemic Induced Acute Pancreatitis with Diabetic Ketoacidosis Treated with Insulin: A Case Report

Abstract Introduction Acute pancreatitis due to hypertriglyceridemia with DKA is a unique entity. The diagnosis of acute pancreatitis in DKA is challenging as most patients present with abdominal pain, and elevated amylase, and lipase are quite common in DKA. Hypertriglyceridemia-induced pancreatitis (HTGP) accounts for 1 to 35 percent of all cases of acute pancreatitis. Pancreatitis may occur in DKA with high anion gap metabolic acidosis. Lack of insulin results in lipolysis with release of free fatty acids. Increased free fatty acids presented to the liver, causes increased VLDL, which inhibits lipoprotein lipase in peripheral tissues and results in elevated triglycerides. Case presentation A 29-year-old morbidly obese male with Asperger's syndrome, prediabetes, and hyperlipidemia presented with a 3-day history of sharp, non-radiating, and progressively worsening right upper abdominal pain, associated with nausea, non-bilious vomiting, and shortness of breath. His past medical history was notable for a prior bout of gallstone pancreatitis, for which he underwent a laparoscopic cholecystectomy. On his arrival in the emergency department, he was afebrile, but tachycardic (HR 139), mildly hypertensive (BP 149/98) with a Kussmaul breathing saturating 98% on room air. His lung sounds were clear but diminished and his abdomen was soft but diffusely tender, without peritoneal signs. Initial laboratory tests showed a neutrophilic leukocytosis of 12K, glucose of 867 mg/dL, hyponatremia (corrected 131), ketonuria, with elevated lipase 1,164 U/L. Venous blood gas showed a pH of 7.18 and PCO2 24 mmHg. He also had severe hypertriglyceridemia with a total triglyceride level of &amp;gt; 9,000 mg/dL. His CT abdomen showed peripancreatic inflammation consistent with acute pancreatitis. He was admitted to the ICU, and initially managed with aggressive intravenous fluids and pain control, then was started on an insulin drip for diabetic ketoacidosis and hypertriglyceridemia. His hospital course was notable for the development of acute kidney injury requiring hemodialysis. His triglyceride level gradually decreased and was 396 U/L on hospital day #9. He was discharged on fenofibrate, Lantus 20 units daily and insulin lispro 10 units with meals. Conclusion Hypertriglyceridemia is an uncommon but a well-established cause of acute pancreatitis leading to significant morbidity and mortality. In this case, a prediabetic patient presented with DKA and further investigation revealed HTGP. There is currently a paucity of data to support an optimal treatment for this condition; however, both insulin and plasmapheresis have been successfully employed. Plasmapheresis helps remove plasma lipoproteins and reduces triglyceride more rapidly than insulin and has been recommended for severe cases. In our case, insulin infusion alone significantly reduced the triglyceride level. Presentation: No date and time listed

ODP197 Familial Hypertriglyceridemia Initially Presenting with Hypertriglyceridemia-induced Pancreatitis: A Case Report

Abstract Case Presentation A 28 year old male with a past medical history of diabetes mellitus type 2 (T2DM) and hypertension presented to the emergency room with acute onset, progressive epigastric pain associated with nausea. The pain suddenly started earlier that day after a large meal. He denied alcohol use. He was previously on insulin Glargine 55 units nightly but was not using it for several months. Vitals signs were within normal limits, BMI was 38.5 kg/m 2 . Physical examination revealed marked epigastric tenderness and multiple yellow papules on the abdomen and extensor surfaces of extremities. Lab findings revealed WBC 14.3 k/mm cu, lipase 437 IU/L, triglycerides greater than 3000 mg/dl with VLDL greater than 3000 mg/dl. Computerized tomography of the abdomen was consistent with acute pancreatitis. He was diagnosed with familial hypertriglyceridemia presenting with hypertriglyceridemia-induced pancreatitis and was admitted to the intensive care unit (ICU). Treatment with regular insulin infusion was started. On day 3, triglyceride levels decreased to 543 mg/dl and insulin infusion was stopped. He reported symptomatic improvement and was able to tolerate oral diet. He was counseled on significance of lifestyle modifications and medication compliance and was discharged on Niacin, Omega 3, Fenofibrate, Ezetimibe, and Pravastatin with plans to follow up with an Endocrinologist. Discussion This case of a young male presenting with hypertriglyceridemia-induced pancreatitis due to underlying familial hypertriglyceridemia emphasizes the significance of comprehensive history taking and work up for patients initially presenting to the clinic with risk factors such as obesity and insulin resistance. Our patient classically had a history of T2DM, and as cardiovascular complications are the leading cause of mortality in diabetic patients, screening for and managing dyslipidemia is pivotal. Eruptive xanthomas are erythematous-yellow papules typically located on extensor surfaces which appear when triglyceride levels exceed 1500-2000 mg/dl. This characteristic skin finding led to a prompt suspicion for familial hypertriglyceridemia in our patient. Our patient was stabilized in the ICU and subsequently discharged on multiple oral agents. The current consensus is that single statin therapy is not recommended; however, further research is indicated to specify the optimal combination of triglyceride lowering agents based on the severity of hypertriglyceridemia. Presentation: No date and time listed

RF32 | PSUN67 Recurrent Acute Pancreatitis Secondary to Hypertriglyceridemia in an Adolescent With Type 2 Diabetes, Symptomatic Hypocalcemia, and COVID-19 Infection

Abstract Introduction Hypertriglyceridemia is the third most common cause of acute pancreatitis, leading to increased morbidity and mortality. Hypocalcemia is a frequent complication of pancreatitis, attributed to saponification of calcium by the release of pancreatic lipase. Free fatty acids are released by the breakdown of triglycerides, then react with extracellular calcium, forming fatty acid salts that deposit in the retroperitoneum and reduce calcium availability.1 We present a case of an adolescent female with recurrent episodes of acute pancreatitis, hypertriglyceridemia, and hypocalcemia. Her first presentation of pancreatitis coincided with new-onset type 2 diabetes, while this third episode with COVID-19. Case An 18-year-old morbidly obese female with type 2 diabetes, hypertriglyceridemia, hepatomegaly, and recurrent acute pancreatitis was admitted for a third episode of pancreatitis secondary to severe hypertriglyceridemia. On admission, triglycerides were 3213 mg/dL (reference 35-134mg/dL), lipase 12,721 units/L (145-226u/L), amylase 323 units/L (&amp;lt;106u/L), AST 90 units/L (10-26u/L), and ALT 109 units/L (19-49u/L). A1C was 7.5%, blood glucose 301 mg/dL, bicarbonate 25 mmol/L, and large urine ketones. Initial calcium was 8.7 mg/dL (9.0-10.7mg/dL) and albumin 4.0 gm/dL (3.8-5.6gm/dL). The next day, she developed hypocalcemia with numbness and tingling. Serum calcium was 5.3mg/dL, ionized calcium 0.74 mmol/L (1.12-1.37mmol/L), and albumin &amp;lt;0.6 gm/dL. 25-hydroxy vitamin D level was 16.5 ng/mL (30-100). QTc was 470 ms (350-440ms). She was transferred to pediatric intensive care and initiated on an insulin drip at 0.1 units/kg/hour for hypertriglyceridemia. She received four IV calcium gluconate boluses (1000-2000 mg each). Symptoms improved within one day. Triglycerides decreased to 642 mg/dL, calcium and albumin normalized, and subcutaneous insulin regimen was resumed. She started vitamin D 3000 IU daily and elemental calcium carbonate 26 mg/kg/day. During her hospitalization, she was found to be COVID-19 positive and had become hypoxemic requiring 2.5 liters of oxygen. Upon resolution, she was discharged with outpatient follow-up. Of note, there is a strong maternal family history of type 2 diabetes and hypertriglyceridemia. The mother had three strokes in her forties. The patient has not previously undergone pancreatitis genetic testing. Discussion To conclude, this case affirms the importance of detecting hypertriglyceridemia-induced pancreatitis early on and improved outcomes with insulin drips. It is important to determine triggers for recurrent pancreatitis in those with underlying genetic etiologies of hypertriglyceridemia. Additionally, it is crucial to monitor for secondary hypocalcemia, particularly given the risk for prolonged QT interval and ventricular arrhythmias. Lastly, the COVID-19 pandemic may be associated with more severe presentations of pancreatitis. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:30 p.m. - 12:35 p.m.

S1834 Spontaneous Bacterial Peritonitis in a Postpartum Female Secondary to Necrotizing Pancreatitis

Introduction: SBP is an infection of the fluid that accumulates in the abdomen caused by translocation of bacteria without an obvious source, such as bowel perforation. Typically, this translocation represents a failure in defensive factors to contain pathogens to the bowel and can lead to seeding other extra-intestinal sites. Our patient is unique in that her SBP was characterized in the setting of a recent pregnancy. Her course was complicated by pre-eclampsia resulting in emergent c-section, further complicated by hypertriglyceridemia-induced pancreatitis. After significant intervention, necrotizing pancreatitis leading to retroperitoneal fat saponification and abscess formation was the likely etiology for SBP. Case Description/Methods: A 27-year-old female presented with diffuse abdominal pain, nausea, vomiting, and diarrhea. Past medical history is significant for recent emergency c-section due to pre-eclampsia complicated by hypertriglyceridemia-induced pancreatitis. On admission, she was hypotensive, tachycardic, tachypneic and febrile, with significant bilious emesis. CT revealed large volume ascites, peri-pancreatic fluid, small volume fluid and gas within the endometrial cavity. Peritoneal fluid analysis presented an SBP picture. Abdominal drains were placed to mitigate peritoneal fluid collection, which settled in the retro-peritoneal space. Cultures resulted in pan-sensitive E.coli growth and the patient was started on appropriate therapy. However, the patient continued to have persistent fevers and severe abdominal pain while on medical management. At this point, exploratory abdominal surgery was indicated revealing significant amounts of retroperitoneal saponified fat secondary to necrotizing pancreatitis, and extensive communicating abscesses which were subsequently drained. Discussion: SBP is an infection of fluid that accumulates within the abdomen, typically seen in patient's with chronic liver disease and can be managed with medical therapy. In our patient's case, there was no know history of liver disease. Our patient presented febrile, with diffuse abdominal pain. Imaging revealed significant ascites and cultures resulted in pan-sensitive E.coli. Multiple differentials were assessed including recurrent pancreatitis, C.difficile infection leading to bowel perforation and/or protein-losing enteropathy, endometritis given recent c-section amongst others. After surgical assessment, our likely diagnosis was necrotizing pancreatitis seeding pancreatic enzymes into the retroperitoneal cavity.

S2327 Gurvits Syndrome in Setting of Uncontrolled Diabetes and Acute Gastrointestinal Bleeding Successfully Treated with Extended Duration PPI Despite Continuing DOAC

Introduction: A young male with past medical history (PMH) of severely uncontrolled non-insulin dependent diabetes mellitus (NIDDM) with recurrent admissions for diabetic ketoacidosis (DKA) and hypertriglyceridemia-induced pancreatitis, both secondary to medication non-adherence, presented via emergency medical services (EMS) after being found unresponsive at home and subsequently developed acute esophageal necrosis (AEN) during a prolonged stay in the intensive care unit (ICU) for acute respiratory failure. He was successfully treated with extended duration of proton pump inhibitor (PPI) therapy and control of underlying risk factors despite being continued on anticoagulation. Case Description/Methods: A 39-year-old male with PMH of uncontrolled NIDDM presented was admitted for acute respiratory failure secondary to DKA and pneumonia. He was intubated and admitted to ICU, while continued on DKA protocol including antibiotics. GI was consulted for hematemesis and melena 2 weeks into hospitalization. EGD revealed circumferential black esophageal mucosa in the distal esophagus abruptly ending at the gastroesophageal junction (GEJ) and hiatal hernia. Recommendations included Intravenous (IV) proton pump inhibitor (PPI) and strict avoidance of naso/orgastric (NG/OG) tube. Follow up EGD few months after discharge showed remarkable improvement of mucosa as noted in Figures A and B, despite continuation of DOAC as per patient wishes for DVT developed during the stay. Discussion: AEN is a rare syndrome disproportionately reported in men which is characterized by circumferential black esophageal mucosa in the distal 2 thirds of the esophagus, abruptly ceasing at the GEJ. Ischemia is postulated to be an inciting event. Conditions associated with AEN are antibiotics, sepsis, gastric volvulus, hernia, DKA, malignancy, and prolonged vomiting. Symptoms of upper gastrointestinal bleeding (UGIB) and shock are common presentations. Although biopsy establishes diagnosis and rules out other causes, EGD finding is generally sufficient. Initial management consists of IV fluids and treatment of the underlying cause. IV PPI and nil per os (NPO) is recommended. NG/OG tubes are avoided unless vomiting or obstruction is present. Mortality is largely due to underlying disease rather than directly from AEN, hence supportive care results in resolution in most cases, as seen in our patient. Our case demonstrates the importance of addressing underlying causes, as well as PPI therapy, which can overcome continued anticoagulation.Figure 1.: A. Acute esophageal necrosis discovered on endoscopy while undergoing EGD for acute GI bleeding during ICU admission for DKA and acute respiratory failure requiring mechanical ventilation B. Resolution of acute esophageal necrosis with grossly normal mucosa on follow up endoscopy conducted after extended duration PPI therapy and relatively controlled diabetes.

S1847 The Enigmatic Triangle of Hypertriglyceridemia-Induced Pancreatitis and Its Association With Diabetic Ketoacidosis and Resulting Pancreatic Pseudocyst: A Case Report

S1847 The Enigmatic Triangle of Hypertriglyceridemia-Induced Pancreatitis and Its Association With Diabetic Ketoacidosis and Resulting Pancreatic Pseudocyst: A Case Report

S1749 Hypertriglyceridemia-Induced Pancreatitis in the Setting of Acute COVID-19 Infection

Introduction: Profound hypertriglyceridemia has been documented in cases of acute and prior COVID-19 infections. A common cause of acute pancreatitis is hypertriglyceridemia. In some cases, this can require intensive care unit (ICU) admission for management. Case Description/Methods: The patient is a 49-year-old male with a history of recent COVID-19 infection who initially presented for epigastric pain with intractable nausea and vomiting. He was found to have acute pancreatitis on imaging and lab work. Incidentally, he was found to be COVID-19 positive. He had no respiratory or infectious symptoms from this infection. The patient was initially admitted to ICU for his triglyceride level reading greater than 5680. He was managed with an insulin drip for resolution of his hypertriglyceridemia. The patient required an extended ICU stay as his triglyceride level remained difficult to decrease while on the insulin drip. Eventually, he was able to be downgraded to the hospital floor after a 6-day ICU stay requiring an insulin drip to decrease his profound hypertriglyceridemia. Discussion: Interestingly, the patient’s refractory hypertriglyceridemia remained difficult to treat. It has been previously documented that COVID-19 infections can lead to hypertriglyceridemia. This can lead to an increase of acute pancreatitis admissions secondary to COVID-19 infections. In conclusion, more research is warranted into the association between hypertriglyceride-induced pancreatitis and COVID-19 infection.

The modified computed tomography severity index combined with low skeletal muscle mass can better predict the severity of hypertriglyceridemia-induced pancreatitis.

Body composition parameters are associated with hypertriglyceridemia-induced pancreatitis (HTGP). This study investigated the association between the quantity of muscle assessed using computed tomography (CT) and the severity of HTGP. The modified CT severity index (MCTSI) was calculated from admission examination data. Patients' characteristics and body composition parameters were collected. Univariate and multivariate logistic regression analyses were also performed. The receiver operating characteristic curves and corresponding area under the curves (AUC) were calculated to test the efficiency of the model. A nomogram was then constructed. Of the 175 included patients, 138 were male, of which 85 had moderately severe to severe HTGP. Patients with low skeletal muscle mass (LSMM) and high MCTSI were significantly more likely to have moderately severe to severe HTGP. Patients with LSMM had lower body mass index, lower HDL-C level, higher amylase level, prevalence of surgery, shorter umbilical waist circumference, and longer length of hospital stay. Univariate and multivariate logistic regression analyses confirmed that female sex, lipase, total cholesterol, LSMM-MCTSI (P= .004, odds ratio=23.105), and albumin were risk factors. The TOTAL model that combined LSMM-MCTSI and clinical risk parameters performed best (AUCs=0.875), followed by other models (LSMM-MCTSI: AUCs=0.762, MCTSI: AUCs=0.728). The Delong test revealed significant difference. Finally, a nomogram was developed to predict the severity of HTGP. The performance of MCTSI in predicting severity can be improved by considering LSMM, which is a promising strategy for the treatment of HTGP.

Apheresis Technique for Acute Hyperlipidemic Pancreatitis: A Systemic Review and Meta-Analysis.

The apheresis technique is increasingly used in patients with hypertriglyceridemia-induced pancreatitis (HTGP), while its role in this context is still not well established. Thus, we aimed to evaluate the clinical outcomes of an apheresis therapy compared to usual care in such a patient population. We searched PubMed, Embase, and Cochrane library databases up to July 10, 2021. Studies were included if they focused on HTGP treated with or without apheresis technique. We used the Newcastle-Ottawa Scale to assess the quality of the included studies. The primary outcome was the mortality rate. We also explored the heterogeneity, sensitivity analysis, subgroup analysis, and publication bias. Sixteen observational studies with 1476 adults were included. The overall quality of included studies was moderate. Despite better TG level reduction with apheresis therapy (mean difference [MD], 12.27mmol/L, 95% CI, 3.74 to 20.81; I2 = 78%; P = 0.005), use of apheresis did not reduce the mortality (odds ratio [OR], 1.01; 95% CI, 0.65 to 1.59; P = 0.95) compared with usual care. This result was further confirmed by sensitivity analysis, subgroup analysis. The length of stay in hospital (MD, 0.96days; 95% CI, - 1.22 to 3.14; I2 = 70%; P = 0.39) and most complications were similar between the groups, while hospital cost was significantly higher in the apheresis group. The apheresis technique did not decrease the mortality in HTGP patients compared with usual care. Until the results of high-quality RCTs are known, these findings do not support the routine use of the apheresis technique in such a patient population.

Management of hypertriglyceridemia-induced pancreatitis – A review of updates from the past decade

Hypertriglyceridemia-induced acute-pancreatitis (HTG-AP) is an important etiology of acute pancreatitis (AP). The treatment includes general management of AP with bowel rest, analgesia, and venous thromboembolism prophylaxis. Specific treatment of HTG-AP focuses on reducing serum triglyceride (TG) levels. Various modalities have been used, including heparin infusion, insulin infusion, plasmapheresis, and double filtration plasmapheresis (DFPP). However, the extent to which TG reduction translates into a clinical response remains unclear. This review highlights the emerging evidence on the management of HTG-AP. Insulin therapy and plasmapheresis remain treatment options to reduce TG. DFPP is an emerging treatment modality to reduce TG levels in patients with AP. However, to what extent this translates into a better clinical response is yet to be answered in large and prospective study designs.