Published online Dec 21, 2017. doi: 10.3748/wjg.v23.i47.8387
Peer-review started: October 18, 2017
First decision: November 8, 2017
Revised: November 11, 2017
Accepted: November 27, 2017
Article in press: November 27, 2017
Published online: December 21, 2017
Processing time: 62 Days and 23.9 Hours
Hyperlipidemic acute pancreatitis (HLAP) is a form of AP occurring in the presence of severe hypertriglyceridemia and in the absence of other causes. The exact pathophysiology of HLAP is not entirely certain. It is believed that HLAP is related to pancreatic tissue injury and microcirculation disturbance caused by free fatty acids. Some recent studies identified that smoking was significantly associated with non-biliary AP instead of biliary AP, but whether cigarette smoking has any long-term impact on HLAP recurrence has not yet been investigated. This is the first study evaluating the influence of cigarette smoking on HLAP recurrence.
Authors performed this study to better understand the relationship between cigarette smoking and HLAP recurrence, as well as the pathophysiologic mechanism of recurrent HLAP.
The main objective of this study was to investigate the impact of cigarette smoking on the recurrence rate and recurrence-free survival in HLAP. The authors found that cigarette smoking was associated with worse RFS and an increased recurrence rate of HLAP. These findings provide references for further clarifying the mechanism of HLAP.
A total of 88 patients diagnosed with HLAP were enrolled in this retrospective study. Demographic data, medical history, previous episodes of pancreatitis, consumption of alcohol and cigarettes, as well as biochemical and hematological data were carefully recorded for univariate and multivariate analyses. During follow-up, the information on current smoking status and recurrent AP was gathered. Recurrence-free survival was calculated using the Kaplan-Meier method, and the differences between groups were compared using the log-rank test.
Current smokers had a remarkably higher recurrence rate and a greater incidence of repeated episodes of AP than non-smokers, and these two percentages were reduced to 9.1% and 36.4% for patients who gave up smoking. The median follow-up time was 13.5 mo. Multivariate analysis identified current smoking as an independent risk factor contributing to HLAP recurrence. Current smokers had significantly worse RFS than non-smokers, but no significant difference was documented between ex-smokers and non-smokers.
In the present study, the authors found that cigarette smoking was associated with worse RFS and an increased recurrence rate of HLAP. For smokers, continued smoking might be strongly correlated with HLAP recurrence and compromised survival. Smoking cessation for at least 6 mo would lead to a significant advantage in recurrence rate and RFS compared to current smokers.
The study revealed that smoking is associated with worse RFS and higher recurrence rate of HLAP. Besides, smoking cessation for at least 6 mo would lead to a significant advantage in recurrence rate and RFS compared to current smokers. For the future research, more detailed classification is needed to clarify the potential dose- and duration-dependent correlation between cigarette smoking and HLAP. Besides, expanding the number of cases and long-term follow-up are needed.