Hypertriglyceridemia is a highly prevalent metabolic disorder which arises as a result of secondary conditions such as high fat diet or definite inherited basis such as lipoprotein lipase gene deficiency [6]. Severe cases of hypertriglyceridemia, that is sHTG, are presented in approximately 1.7% of these adult population and about 15–20% of this group develop sHTGP [5]. It is widely accepted that the increase in serum TG levels has a positive correlation with disease severity and AP recurrence [12]. As regards disease severity, 23.4% sHTGP patients developed SAP in our study and the proportion was only 9.6% in whole HTG-induced pancreatitis cohort as reported previously [16]. The current reported recurrence rate of HTG-induced pancreatitis was about 25–30%, while the recurrence of sHTGP was about 50% in our study [16, 17]. A longitudinal cohort study of patients with HTG-induced pancreatitis demonstrated that even moderate elevation in subsequent TG levels was associated with increased risk of recurrence compared to patients that achieved normalization (RR 5.47 [1.80, 16.65]) [18]. It is generally considered that patients with HTG are often complicated with metabolic abnormalities such as diabetes [6]. 36.1% sHTGP patients in our cohort were complicated with diabetes and the proportion was higher in the recurrence group. A multivariate analysis had illustrated that presence of diabetes was an independent risk factor for AP recurrence [19].
In our study, we found that the lipid profile of sHTGP changed obviously after DFPP in the first day and the level of parameters maintained stability except for serum TG. Compared with other parameters of the lipid profile, TG was the most intense and variable parameter during the explosion of sHTGP. All the patients resumed oral feeding at discharge and the level of parameters at this point may serve as the normal reference. Interestingly, the levels of lipid profile at disease onset exhibited significant difference from the normal level of patients, indicating the burst of sHTGP may be concerned with an acute and dramatic fluctuation of the lipid metabolism. The results conform to the prevalent speculations for the pathogenesis of sHTGP [8].
It is generally accepted that rapid decrease in TG levels is critical to the successful management of HTG-induced pancreatitis [20]. However, the pharmacologic dyslipidemia therapy such as insulin and heparin was insufficient to lowering TG rapidly [21]. In contrast, apheresis can rapidly reduce serum chylomicron and TG levels. According to a systemic review published in 2017, apheresis can reduce the pre-treatment serum TG (mean: 42.0 mmol/L) by 72%. As a therapeutic plasmapheresis which can remove macromolecules selectively, DFPP has been applied for sHTGP management in recent years. Our results showed similar efficiency of TG lowering effect with previous studies (pretreatment TG: 42.68 mmol/L by 71.2%). There were few studies exploring the effect of DFPP on sHTGP management. Chang et al. investigated the effectiveness of DFPP in twelve sHTGP patients and found that DFPP could shorten hospitalization duration and minimizes AP recurrence. In our study, we found that sHTGP patients in which TG level reached below 5.6 mmol/L after DFPP had shorter hospitalization duration [22].
Lipids and lipoproteins undergo changes during systemic inflammatory response syndrome (SIRS) and may act as potential biomarkers (especially HDL) [23]. It was observed that critically ill patients showed low concentrations of HDL and Apo A1 upon ICU admission which correlated with increased severity, ICU duration and mortality [24, 25]. Similar to findings in previous studies, we found that decreased HDL appears to be indicative of the extension of sHTGP hospitalization [11, 26]. HDL is the complex of lipoprotein species which contain approximately 25% of the cholesterol and < 5% of the triglyceride in human blood [27]. They play a major role in TG transport and removal after lipase action. It is generally considered that HDL has potent anti-inflammatory properties which may be critical for protection against AP and other inflammatory disease through modulating macrophages reprogramming [11, 28]. Lower levels of HDL were elucidated to be associated with increased cardiovascular events and poor outcomes [29, 30]. Bugdaci et al. reported that the levels of HDL were negatively associated with the Ranson score of AP [26]. Khan et al. found that levels of serum HDL was significantly lower in SAP patients and was associated with longer hospitalization [11].
There were several limitations of this study. First, this was a retrospective analysis and we included relatively small number of patients due to the single center design. Second, this study lacks the control group for comparison with the DFPP group. In the real-world practice, all the sHTGP patients received DFPP on admission in our center and consequently the study lacks untreated sHTGP cohort. Further large scale and multicenter studies are needed.