8093 The Interplay Between Hypertriglyceridemia And Pancreatogenic Diabetes Mellitus

Abstract Disclosure: T. Tselovalnikova: None. R.K. Bhattacharya: None. B.M. Drees: None. E.T. Ngo: None. Severe hypertriglyceridemia may induce acute pancreatitis with subsequent development of ketosis-prone pancreatogenic diabetes. This presentation is rare. We present a case of a 36-year-old female referred to our clinic for management of diabetes mellitus. At the age of 12 years, her menarche coincided with an episode of acute pancreatitis (AP) in the setting of severe hypertriglyceridemia, as well as diabetic ketoacidosis (DKA). No other causes of AP were identified - no cholecystitis, no alcohol use, no illicit substance abuse. Family history of dyslipidemia or diabetes is unclear. She was managed with insulin for hypertriglyceridemia-induced pancreatitis as well as DKA. She developed significant insulin resistance, along with elevated BMI (30.25 kg/m2), and was subsequently diagnosed with polycystic ovary syndrome, requiring metformin. Autoimmune antibodies for type 1 diabetes mellitus were all negative. Sequence analysis of the HNF1A, HNF4A, and GCK genes did not identify any sequence variants associated with maturity-onset diabetes in the young. Her diabetes has been poorly controlled with HgbA1c as high as 14.4%. Management has been complicated by non-adherence. She subsequently developed diabetic proliferative retinopathy with vitreal hemorrhages, diabetic nephropathy, and diabetic neuropathy complicated by osteomyelitis with right toe amputation. She continued to have severe hypertriglyceridemia up to 8,216 mg/dL (reference range: 0-150) associated with numerous episodes of AP with concomitant DKA, prompting frequent hospitalizations. She does not have any xanthomas or lipodystrophy on examination. No genetic testing to confirm familial causes of hypertriglyceridemia was performed as yet. There is no pre-existing cardiac conditions. She is being managed with insulin glargine, insulin aspart, metformin, pancrelipase, fenofibrate, atorvastatin, and omega-3 polyunsaturated fatty acid; however, her triglyceride level remains high at 5,353 mg/dL and diabetes remains uncontrolled with most recent HbA1c of 9%. Given the timeline of presentation in this patient, a physiological increase in estrogen level may aggravate pre-existing common or familial forms of severe hypertriglyceridemia, causing chylomicron buildup, eventually leading to recurrent pancreatitis. The manifestation of diabetes with DKA along with severe hypertriglyceridemia-induced pancreatitis is rare. Uncontrolled hypertriglyceridemia leads to frequent pancreatitis exacerbations, resulting in chronic pancreatitis and eventual overlap of pancreatogenic (Type 3c) diabetes and insulin resistance. Presentation: 6/1/2024