Hypertriglyceridemia is the third most common cause of acute pancreatitis, accounting for about 10% of cases. It is thought that the hydrolysis of triglycerides by pancreatic enzymes leads to the production of free fatty acids in the pancreatic capillaries, which produces pancreatic ischemia, acidosis, trypsinogen activation, and acute pancreatitis. The management of hypertriglyceridemia-induced acute pancreatitis is not standardized. It consists of continuous insulin infusions (CII) or plasmapheresis with the goal of therapy being a triglyceride (TG) level less than 1,000 mg/dL.

The purpose of this retrospective study was to investigate the rate of hypertriglyceride response to CII in patients with acute pancreatitis due to elevated triglyceride levels and to identify the predictive factors associated with this response.

Patients were included in this study if they were aged 18 years or older, were admitted to the ICU with a diagnosis of acute pancreatitis, had an admission triglyceride level of greater than 1,000 mg/dL, and had received a CII. Pregnant patients, those who underwent therapeutic plasma exchange, and those who did not receive a bolus prior to CII were excluded from analysis.

The primary outcome was the achievement of the triglyceride goal, which was a triglyceride level of 1,000 mg/dL or less. Secondary outcomes were time duration to achieve TG 50% (half of the respective initial triglyceride level) and TG goal.

Investigators examined age, gender, race, BMI, excess alcohol use, history of gallbladder disease, diabetes mellitus, and hypothyroidism as possible contributing factors to acute pancreatitis.

Seventy-seven patients were included in the final analysis. Their average age was 39.3 years, and almost three-quarters of the patients (74.0%) had diabetes. Most patients were male (66.2%) and Hispanic (58.4%) with a BMI greater than 30 kg/m2, which indicated obesity. Additionally, half of the patients used alcohol in excess.

Overall, 95% (N = 73) of patients reached the TG goal and were considered responders. Four patients did not reach the TG goal and were subsequently treated with either therapeutic plasma exchange or oral fibrates.

The time to reach TG 50% ranged from 8 to 24.5 hours, and the time to reach TG goal ranged from 16 to 52 hours. The responders were further subdivided into rapid responders (i.e., those who reached TG goal in fewer than 36 hours), which accounted for 53.4% of responders, and slow responders (i.e., those who reached TG goal in 36 hours or more), who accounted for the remaining 46.6% of patients.

Factors that were significantly associated with a slow response included obesity, diabetes, a higher initial serum triglyceride level, and taking longer to reach TG 50%. Patients with diabetes took longer to reach TG 50%, and TG goal and required higher daily insulin doses (1.7 U/kg vs. 1.1 U/kg, P = .041).

The absence of diabetes was associated with an 18.9-fold chance of a faster triglyceride response (odds ratio [OR] = 18.9, CI 3.02-119.2, P = .002), whereas a higher daily insulin dose/kg was associated with a 3.11-fold chance of a quicker triglyceride response (OR = 3.11, CI 1.19-8.15, P = .02). Higher total daily insulin use was also predictive of a more rapid response in patients with diabetes.

Once the CII was completed, 70.1% were converted to subcutaneous insulin and over 90% were given fibrates. For the rapid responders, initiating a fibrate fewer than 36 hours or at 36 hours or later after the start of the CII did not affect TG goal. The authors concluded that CII is effective in reaching TG goal in 95% of patients with hypertriglyceridemia-induced acute pancreatitis.

This study helps to provide additional clarity for the ICU pharmacist who assists in the management of patients with acute pancreatitis secondary to hypertriglyceridemia.

The content contained in this article is for informational purposes only. The content is not intended to be a substitute for professional advice. Reliance on any information provided in this article is solely at your own risk.

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