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High Triglyceride Variability Increases the Risk of First Attack of Acute Pancreatitis
Ying-Chang Tung1,2, Fu-Chih Hsiao1, Chia-Pin Lin1
1Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Introduction:
Hypertriglyceridemia is the third most common etiology of acute pancreatitis. Whether triglyceride variability, independent of absolute triglyceride levels, is a predictor of acute pancreatitis is unknown.
Methods:
We identified 98,819 patients who were diagnosed with hyperlipidemia between January 1, 2007, and December 31, 2013, and had at least 1 triglyceride measurement annually for 4 consecutive years from the Chang Gung Research Database in Taiwan. Triglyceride variability, defined as variability independent of the mean, was calculated in the 4-year run-in period. The patients were stratified according to the quartiles of triglyceride variability and were followed until December 31, 2019, for first attack of acute pancreatitis.
Results:
During a mean follow-up of 5.9 years, 825 (0.83%) patients were newly diagnosed with acute pancreatitis (14.1 events per 10,000 person-years; 95% confidence interval 13.2-15.1). Triglyceride variability was significantly associated with an increased risk of acute pancreatitis, independent of baseline triglyceride and mean triglyceride levels (hazard ratio, 1.28 [95% confidence interval 1.05-1.57] for the highest vs the lowest quartiles of triglyceride variability; P for trend = 0.006 over the quartiles of triglyceride variability). Subgroup analysis showed that this association was more pronounced among the patients with a higher neutrophil-to-lymphocyte ratio ( P for trend = 0.022).
Discussion:
In this multi-institutional cohort study, high triglyceride variability was associated with an increased risk of first attack of acute pancreatitis, independent of baseline and mean triglyceride levels. The association between triglyceride variability and acute pancreatitis may be partly mediated by subclinical inflammation.
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