Different Clinical Presentations of Hyperlipidemic Acute Pancreatitis

Guo, Yin; Cang, Xiaofeng; Yu, Ge; Hu, Guoyong; Ni, Jiahua; Xiong, Jie; Hu, Yanling; Xing, Miao; Chen, Congying; Huang, Yinshi; Tang, Maochun; Zhao, Yan; Cheng, Guangfeng; Wan, Rong; Wang, Shaofeng; Wang, Xingpeng

doi:10.1097/mpa.0000000000000403

Cited by 58 publications

(50 citation statements)

References 12 publications

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“…In the present study, patients with HTGAP accounted for 12.2% (40/329) of all patients with AP. We found that younger age, diabetes mellitus, fatty liver, a high recurrence rate and a more severe prognosis were more commonly observed in HTGAP, a finding similar to that reported in recent studies …”

Section: Discussionsupporting

confidence: 92%

Hypertriglyceridemic acute pancreatitis in emergency department: Typical clinical features and genetic variants

Chen

Sun

Zhang

et al. 2017

J of Digest Diseases

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OBJECTIVE:To investigate the clinical characteristics of patients with hypertriglyceridemic acute pancreatitis (HTGAP), and the molecular foundation contributing to hypertriglyceridemia in such patients. METHODS:Clinical data from 329 patients with acute pancreatitis (AP) were analyzed. The patients were divided into the HTGAP group, with fasting serum triglyceride (TG) levels ≥500 mg/dL (5.65 mmol/L), and the non-HTGAP (NHTGAP) group. Targeted next-generation sequencing was applied to 11 HTGAP patients to identify the genetic mutations associated with hypertriglyceridemia, including apolipoprotein A-V (APOA5), APOC2, APOC3 and APOE, BLK, LPL, GPIHBP1 and LMF1. RESULTS:Patients in the HTGAP group, compared with those in the NHTGAP group, had a higher mortality rate (7.5% vs 0.7%, P = 0.001), more commonly seen severe AP (17.5% vs 5.2%, P = 0.004) as well as a higher recurrence rate (32.4% vs 19.9%, P = 0.070). DNA sequencing showed that two patients carried the same compound of p.G185C and p.V153M heterozygous mutations located in the APOA5 gene. Two patients carried a homozygous variation of p.C14F, in the GPIHBP1 gene. One patient had a homozygous variation of p.R176C in the APOE gene. And a rare heterozygous LMF1 gene mutation of p.P562R was detected in two patients.CONCLUSIONS: HTGAP was significantly severe than NHTGAP, with a high recurrence rate. Genetic information may be useful in the clinical setting for the investigation of the pathogenesis of HTGAP and its interventions.

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Section: Discussionsupporting

confidence: 92%

Hypertriglyceridemic acute pancreatitis in emergency department: Typical clinical features and genetic variants

Chen

Sun

Zhang

et al. 2017

J of Digest Diseases

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“…Hypertriglyceridemiainduced acute pancreatitis (HTG-AP) is defined by serum triglyceride (TG) level exceeding 11.3 mmol/L (1000 mg/ dL) or between 5.6 to 11.3 mmol/L (500~1000 mg/dL) together with lipemic serum [5,6]. As compared to other etiologies, HTG-AP is usually more severe and has higher recurrence rate [7,8].…”

Section: Introductionmentioning

confidence: 99%

Identification of a novel LPL nonsense variant and further insights into the complex etiology and expression of hypertriglyceridemia-induced acute pancreatitis

Chen

et al. 2020

Lipids Health Dis

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Background: Hypertriglyceridemia (HTG) is a leading cause of acute pancreatitis. HTG can be caused by either primary (genetic) or secondary etiological factors, and there is increasing appreciation of the interplay between the two kinds of factors in causing severe HTG. Objectives: The main aim of this study was to identify the genetic basis of hypertriglyceridemia-induced acute pancreatitis (HTG-AP) in a Chinese family with three affected members (the proband, his mother and older sister). Methods: The entire coding and flanking sequences of LPL, APOC2, APOA5, GPIHBP1 and LMF1 genes were analyzed by Sanger sequencing. The newly identified LPL nonsense variant was subjected to functional analysis by means of transfection into HEK-293 T cells followed by Western blot and activity assays. Previously reported pathogenic LPL nonsense variants were collated and compared with respect to genotype and phenotype relationship. Results: We identified a novel nonsense variant, p.Gln118* (c.351C > T), in the LPL gene, which co-segregated with HTG-AP in the Chinese family. We provided in vitro evidence that this variant resulted in a complete functional loss of the affected LPL allele. We highlighted a role of alcohol abuse in modifying the clinical expression of the disease in the proband. Additionally, our survey of 12 previously reported pathogenic LPL nonsense variants (in 20 carriers) revealed that neither serum triglyceride levels nor occurrence of HTG-AP was distinguishable among the three carrier groups, namely, simple homozygotes, compound heterozygotes and simple heterozygotes. Conclusions: Our findings, taken together, generated new insights into the complex etiology and expression of HTG-AP.

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“…It is widely believed that the most common etiologies of AP are gallstone disease and alcohol abuse. Currently, 12%-20% of patients with AP have previous hypertriglyceridemia, which has become a well-recognized etiology[ 2 - 4 ]. Hyperlipidemic acute pancreatitis (HLAP) is a form of AP occurring in the presence of severe hypertriglyceridemia and in the absence of other causes[ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of cigarette smoking on recurrence of hyperlipidemic acute pancreatitis

Xiang¹,

Hu²,

Liu³

et al. 2017

WJG

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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.

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Different Clinical Presentations of Hyperlipidemic Acute Pancreatitis

Abstract: Different clinical presentations of HLAP should be applied to be distinguished from non-HLAP in the clinic.

Cited by 58 publications

References 12 publications

Hypertriglyceridemic acute pancreatitis in emergency department: Typical clinical features and genetic variants

Hypertriglyceridemic acute pancreatitis in emergency department: Typical clinical features and genetic variants

Identification of a novel LPL nonsense variant and further insights into the complex etiology and expression of hypertriglyceridemia-induced acute pancreatitis

Impact of cigarette smoking on recurrence of hyperlipidemic acute pancreatitis

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