AP is a common disease of the abdomen necessitating emergency department visits [3, 24, 25]. Biliary tract stones and alcoholism are the most common etiologies of AP [2]. Recent reports have indicated an increasing prevalence of HTGP in Asia [3, 6]. Jin et al. showed that from 2001 to 2016, the prevalence of HTGP increased from 14.0–34.0% [3]. These changes may be related to caloric intake and an increasing incidence of diabetes [26].
A plethora of clinical and experimental data have identified obesity as a risk factor for AP [4, 8–13]. Hansen et al. studied 118,000 patients with AP, and confirmed that BMI is an independent factor of AP [9]. Blaszczak et al. reported that class III obesity seems to have an adverse mortality effect in patients with AP [11]. A recent study by Thavamani et al. suggested that morbid obesity is an independent risk factor for clinical outcomes in pediatric AP [12]. The mechanism by which obesity aggravates pancreatitis has been investigated. Pérez et al. revealed that obesity may result in reduced pancreatic peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) levels by decreasing the binding of PGC-1α to the p65 subunit of nuclear factor-κB, and potentiating oxidative and interleukin-6-mediated inflammatory damage during AP attacks [13]. Ye et al. demonstrated that obesity may aggravate AP through damaging the intestinal mucosal barrier by decreasing the binding of intestinal leptin and its receptor (ObR-b), increasing intestinal inflammatory injury, and resulting in insufficient intestinal epithelial cell proliferation in rats [27]. However, most studies did not distinguish between VAT and SAT depots. The study of fat distribution is crucial to understanding the metabolic implications of excess adiposity. More and more researchers have realized that the study of fat distribution is important in obesity research [14–17]. CT imaging is a reliable method for the analysis of fat distribution and the measurement of adipose tissues [18]. The axial CT image at L3 is known to represent muscle tissues and fat distribution [18, 28]. Blaszczak et al. conducted a study in 68,158 individuals, among whom 424 developed AP, and demonstrated that greater abdominal adiposity is associated with a higher severity of AP [29]. O’Leary et al. showed a similar finding in 214 patients with AP [30]. However, many studies have suggested that VAT is not significantly associated with AP [31–33]. Duarte-Rojo et al. have shown that both SAT and VAT independently predict a severe outcome of AP [34]. The differences in results across different studies may be explained by several factors. First, the studies involved a heterogeneous population of patients, including those from Southeast Asia, Europe, and North America. Second, different software programs were used to analyze body composition, which may be an additional confounding factor. Third, most studies did not classify the etiological patterns of AP, which may be mainly because of the different proportions of the etiological patterns in previous studies. Therefore, studies on the etiologies of AP are needed. To our knowledge, this is the first study on the impact of body composition on the outcomes of HTGP.
In this study, we investigated the impact of body composition on LOS and recurrence in patients with HTGP. Our results revealed that SAT and HDL-C were independent predictors of LOS, and there was no significant association between body composition and the recurrence of HTGP. Patients in the long LOS group (> 14 days), based on the median LOS of the entire sample, had higher SAT than patients in the short LOS group (≤ 14 days). Previous studies have also determined that patients with LOS > 14 days have more severe pancreatitis [29]. Szentesi et al. studied 1,257 individuals with AP, and reported that obese patients had longer LOS than non-obese patients [35]. Murata et al. showed a similar finding in pediatric AP [36]. However, they did not conduct further analysis on fat distribution and etiological classification. Fujisawa et al. suggested that SAT may be an especially important factor related to the incidence of post-endoscopic retrograde cholangiopancreatography pancreatitis; however, they did not investigate its relationship with LOS [37]. Few studies have been conducted on the correlation between obesity and the recurrence of pancreatitis. Shimonov et al. found that higher amounts of VAT and TAMA were significantly associated with a lower recurrence rate of AP in 158 patients; however, no significance was identified in our study [38]. HTGP may be different from other etiologies of pancreatitis in terms of the effect of body composition. The doctor’s medical advice for TG control after discharge may be another reason because the body composition of the patients after 1 year may be different from that at the first hospitalization. Dynamic changes in body composition may be the direction of future research. In addition, many studies have shown that alcoholism, cigarette smoking, hypertriglyceridemia, and local complications are risk factors for recurrent pancreatitis [39, 40]. Our study showed no significant association between hypertriglyceridemia and recurrence of HTGP.
This study had some limitations. First, the number of patients with HTGP within categories by pancreatitis type was small; thus, studies with larger sample sizes are required. Second, as our study results were derived from a retrospective single-center analysis, further prospective and multicenter studies should be conducted in the future. Finally, the outcome of recurrence was assessed within 1 year after discharge, which may not reflect the long-term outcome of patients.