Impact of cigarette smoking on recurrence of hyperlipidemic acute pancreatitis

Abstract

AIMTo investigate the impact of cigarette smoking on the recurrence rate and recurrence-free survival in patients with hyperlipidemic acute pancreatitis (HLAP).METHODSA total of 863 patients were admitted to our hospital for acute pancreatitis (AP) from January 2013 to March 2016, of whom 88 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 (RFS) was calculated using the Kaplan-Meier method, and the differences between groups were compared using the log-rank test.RESULTSNo significant differences were observed between the three groups in age or medical history of hyperlipidemia, fatty liver, diabetes mellitus, hypertension, or AP. The current smokers had a remarkably higher recurrence rate and a greater incidence of repeated episodes of AP (50.0% and 77.8%, respectively) than non-smokers (9.8% and 39.0%), 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 and HLAP recurred after hospital discharge in 23 (26.1%) patients. Multivariate analysis identified current smoking (HR = 6.3, P = 0.020) as an independent risk factor contributing to HLAP recurrence. Current smokers had significantly worse RFS than non-smokers (23 mo vs 42 mo), but no significant difference was documented between ex-smokers (34 mo) and non-smokers. The RFS was not significantly different between light and heavy smokers.CONCLUSIONSmoking is associated with worse RFS and an increased rate of HLAP recurrence. Continued smoking correlates with a compromised survival and smoking cessation should be recommended.

Assessment of Computed Tomography-Defined Muscle and Adipose Tissue Features in Relation to Length of Hospital Stay and Recurrence of Hypertriglyceridemic Pancreatitis

“… 27 The diagnosis of HTGP was confirmed if patients had AP with serum total triglyceride (TG) >11.3 mmol/L (1000 mg/dL), or a serum TG level of 5.65–11.3 mmol/L accompanied by chylous serum and the absence of other risk factors for AP. 5 The exclusion criteria were (1) indication of biliary, alcoholic, autoimmune, drug-induced or pancreatic tumor-related etiology of AP; (2) poor CT imaging of the abdomen; (3) pregnancy. This study was performed with approval from the ethics committee of the First Affiliated Hospital of Wenzhou Medical University (KY2019–011).…”

“… 2 Notably, hypertriglyceridemic pancreatitis (HTGP), which accounts for up to 10% of AP cases, occurs in the presence of hypertriglyceridemia with no signs of other causes. 5 Recent reports have indicated that the incidence of HTGP in Asia is increasing, 3 , 6 and is higher than that reported in Western countries, 7 which and ranked as the third leading cause for AP. 8 …”

<p>Individualized Prediction Of Stroke-Associated Pneumonia For Patients With Acute Ischemic Stroke</p>

“…Patients with SAP had a significantly higher NIHSS score on admission (9.0 vs 2.0), and higher fibrinogen (4.4 g/L vs 3.6 g/L), leukocyte counts (9.7×10 9 /L vs 7.3×10 9 /L). We selected 10.0×10 9 /L as the leukocyte cutoff point based on previous studies 21,22. The best cutoff value for fibrinogen in the training cohort, as revealed by ROC analysis, was 3.68 g/L.…”

Diabetes and Younger Age Are Vital and Independent Risk Factors for Acute Pancreatitis in Patients with Severe Hypertriglyceridemia

“…A recent comprehensive study analyzing 2810 patients demonstrated that cigarette smoking and drinking were associated with non-gallstone-related pancreatitis, including hypertriglyceridemia-induced acute pancreatitis [18]. Another study noted that cigarette smoking might contribute to hyperlipidemic acute pancreatitis recurrence [19]. Future studies are needed to clarify possible changes in the metabolic and molecular characteristics of HIAP related to tobacco use and drinking.…”