Diabetic ketoacidosis-induced hypertriglyceridemic acute pan
Diabetic ketoacidosis (DKA)-induced hypertriglyceridemia causing pancreatitis is an interesting phenomenon that has rarely been reported in the literature. Plasmapharesis is a well known treatment modality for hypertriglyceridemia-induced pancreatitis. Published in the Clin Med Insights Gastroenterol, the authors report a patient with DKA-induced hypertriglyceridemic acute pancreatitis treated successfully with plasmapharesis.

The authors present the case of a male in his 40’s with extensive past medical and surgical history. This included hypertension, dyslipidemia (never worked up in the past, previous reported TG level of 315 mg/dL, managed with 20 mg daily pravastatin), alcohol abuse (≥1 L of hard liquor/day), and recurrent episodes of acute on chronic alcoholic pancreatitis. The patient underwent distal pancreatectomy and splenectomy secondary to splenic subcapsular liquefactive hematomas and a benign cystic lesion in the tail of pancreas, in the setting of an attack of acute pancreatitis (presumably involving trauma) following an alcohol binge, seven months ago.

He developed diabetes mellitus post distal pancreatectomy and was being managed with subcutaneous NPH insulin therapy, 40 units in the morning and 36 units in the evening. HbA1c was 14.4 three months prior to current admission.
He presented to the emergency room with worsening abdominal pain, nausea, and vomiting for 1 day. He reported insulin rationing for a week and therefore had been taking less than the prescribed doses.

Physical exam revealed stable vital signs with a BMI of 25.85. Examination of the abdomen revealed diffuse tenderness to palpation, no distension with normal bowel sounds. Initial lab work revealed a milky plasma, blood glucose of 665 mg/dL, CO2 of 6 mmol/L, anion gap of 31, a white count of 14,610/mm3, lipase of 8223 U/L, TG of 4,854 mg/dL, sodium of 126 mg/dL, potassium of 5.3 mg/dL, calcium of 8.3 mg/dL, and albumin of 3.3 g/dL.

The patient was found to be in DKA and was admitted to the medical intensive care unit. CT scan revealed severe acute inflammatory changes and edema of the residual pancreas. DKA was treated with intravenous hydration using normal saline, potassium supplementation, and intravenous regular insulin—initial bolus of 0.1 units (u)/kg body weight followed by an infusion at the rate of 0.1 u/kg/hour. When blood glucose was lowered <200 mg/dL, rate of infusion was halved to 0.05 u/kg/hour.

Once the anion gap normalized and the patient was able to eat, subcutaneous insulin was overlapped with intravenous infusion for two hours. This was followed by discontinuation of infusion. With DKA being treated, the patient underwent one cycle of plasmapheresis for four hours, following which TG levels decreased from 4,854 to 537 U/L.

The patient’s symptoms resolved after plasmapheresis and treatment of DKA. He was then transferred to a regular medicine floor. The subsequent stay in the hospital was uneventful and the patient was discharged on the 5th day. TG on discharge was 629 IU/L. Discharge medications included gemfibrozil (600 mg three times daily) for hypertriglyceridemia.

Learning Points:-
• In DKA, insulin deficiency leads to lipolysis and inhibition of lipoprotein lipase in peripheral tissues that leads to elevated triglycerides (TG).

• A toxic role of accumulated free fatty acids in the pancreatic tissues, post-pancreatic lipase mediated hydrolysis of TG has been suggested. TG levels greater than 1,000 U/L have been implicated as a cause of acute pancreatitis.

• Types I, IV, and V dyslipidemias have also been associated with acute pancreatitis.

• Types I and V dyslipidemias can cause acute pancreatitis without a predisposing factor, whereas Type IV can do so in the presence of an underlying condition that may increase serum TG levels.

• Infusions of insulin, heparin, and plasmapheresis have been used to lower TG levels in different subsets of patients.

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