To evaluate temporal trends in gender, etiology, severity, outcomes, cost and median length of stay (MLS) in patients with acute pancreatitis (AP) in a third-tier Chinese city.

Patients with AP admitted to a university hospital between January 2013 and December 2021. Relationships between etiology, prevalence of severe acute pancreatitis (SAP) and survey years were investigated by joinpoint regression analysis.

A total of 5459 (male 62.3%) patients with AP were included. Between January 2013 and December 2021, we observed: (a) the prevalence of biliary diseases-related AP was stable, while the prevalence of hypertriglyceridemia (HTG)-associated AP (Ptrend = 0.04) and alcohol-associated AP (Ptrend < 0.0001) both increased; (b) there was an increase in crude prevalence of SAP from 4.97% to 12.2% between 2013 and 2021 (Ptrend < 0.0001); (c) compared to female populations, male gender had a higher prevalence of AP; (d) there was a decrease in MLS from 11 days to 8 days (Ptrend < 0.0001) and in median cost of hospitalization (MCH) for all patients (from 20,166 to 12,845 YUAN) (Ptrend < 0.0001); (e) the overall in-hospital mortality rate was 1.28% (70/5459) for patients with AP. There was no statistically significant in the time trend of mortality during the study period (Ptrend = 0.5873). At multivariate analysis, survey year was associated with prevalence of SAP after adjustment by age and biliary diseases (OR: 1.07; 95% CI: 1.03-1.12). Based on the stratification by severity of disease, the decrease of MLS and MCH was more significant in non-SAP vs. SAP patients.

Over the observational period, the proportion of male patients with AP, prevalence of age-adjusted rate of HTG and alcohol-associated AP and SAP increased, while MLS and MCH for all patients decreased, and the time trend of mortality of AP was stable.

This systematic review aims to comprehensively assess the epidemiology and identify risk factors associated with the severity and recurrence of hypertriglyceridemia-induced acute pancreatitis (HTG-AP). A search of PubMed, Web of Science, and Cochrane databases was conducted to identify all relevant randomized controlled trials (RCTs), prospective, or retrospective cohort studies on HTG-AP. Data related to epidemiology and risk factors for severity and recurrence of HTG-AP were extracted and analyzed. Seventy-seven studies met the inclusion criteria, comprising 1 RCT, 21 prospective studies, and 55 retrospective studies. A total of 56,617 acute pancreatitis (AP) patients were included, of which 19.99% were diagnosed with HTG-AP (n = 11,315). Compared to non-HTG-AP patients, HTG-AP patients were more likely to be male (68.7% vs. 57.3%) and younger (mean age 41.47 ± 4.32 vs. 50.25 ± 7.70 years). HTG-AP patients exhibited higher mortality rates (up to 20% vs. 15.2%), increased severity (8.3% to 100% vs. 3.8% to 47.2%), and higher recurrence rates (up to 64.8% vs. 23.3%). Analysis of temporal trends from 2002 to 2023 showed a range of HTG-AP prevalence in overall AP patients from 1.6% to 47.6%, with a slight upward trend that was not statistically significant (P = 0.1081). Regional analysis indicated relatively stable prevalence in North America (P = 0.5787), Europe (P = 0.0881), other regions (P = 0.738), while prevalence in China showed a significant increase (P = 0.0119). Thirteen studies investigated risk factors affecting HTG-AP severity, with elevated serum triglyceride (TG) levels associated with increased risk of complications such as pancreatic necrosis, systemic inflammatory response syndrome (SIRS), shock, and multi-organ failure. Additional factors including high neutrophil-to-lymphocyte ratio (NLR), elevated levels of amylase and C-reactive protein (CRP), hypocalcemia, and hypoalbuminemia were also implicated in HTG-AP severity. Smoking history, poor lipid control (TG > 3.1 mmol/L), or recurrent hypertriglyceridemia during follow-up were identified as potential predictors of HTG-AP recurrence. Our findings indicate a stable global prevalence of HTG-AP within AP patients, but a notable increase in China, possibly attributed to socio-economic and dietary factors.

Background: Alcohol use and hypertriglyceridemia are the second and third common causes of acute pancreatitis after choledocholithiasis. Still, few studies directly compare the severity and outcomes of these two groups, which share pathophysiology pathways. Methods: In our study, we compared the biologic profile, severity according to the Atlanta classification and Balthazar index, intensive care unit admissions, and mortality between patients with hypertriglyceridemia-induced pancreatitis (HTGP) and alcohol-induced acute pancreatitis (AAP). A total of 78 patients were included in this study, 37.17% of which had HTGP, and 62.82% had AAP. Results: HTGP was more severe in terms of the Atlanta revised classification severity assessment (82.76% vs. 46%, p = 0.014), led to more extended hospitalizations (p = 0.024), and resulted in similar serum CRP levels among patients, with a significant difference regarding median serum fibrinogen values (739 vs. 563 mg/dL, p = 0.030) and necrotizing forms (24.13% vs. 10.20%). Hyponatremia was more significant in HTGP patients compared with AAP patients (130 vs. 137 mmol/L, p < 0.000). No differences were found in other inflammation indexes such as NLR (neutrophil count/lymphocyte count), PLR (platelet count/lymphocyte count), MLR (monocyte/lymphocyte count), SII (systemic immune-inflammation index), or SIRI (systemic inflammation response index). Conclusions: The pattern of acute pancreatitis is related to its etiology and may have different grades of severity. In our study, we found that hypertriglyceridemia-induced pancreatitis required twice as many admissions to the intensive care unit and was associated with lower serum sodium levels, and almost twice as many patients with HTGP had moderate or severe forms of acute pancreatitis compared to alcohol-induced pancreatitis cases.

The incidence of hypertriglyceridemia (HTG)-induced acute pancreatitis (AP) is steadily increasing in China, becoming the second leading cause of AP. Clinical complications and outcomes associated with HTG-AP are generally more severe than those seen in AP caused by other etiologies. HTG-AP is closely linked to metabolic dysfunction and frequently coexists with metabolic syndrome or its components. However, the impact of metabolic syndrome components on HTG-AP clinical outcomes remains unclear.

To investigate the impact of metabolic syndrome component burden on clinical outcomes in HTG-AP.

In this retrospective study of 255 patients diagnosed with HTG-AP at the First Affiliated Hospital of Guangxi Medical University, we collected data on patient demographics, clinical scores, complications, and clinical outcomes. Subsequently, we analyzed the influence of the presence and number of individual metabolic syndrome components, including obesity, hyperglycemia, hypertension, and low high-density lipoprotein cholesterol (HDL-C), on the aforementioned parameters in HTG-AP patients.

This study found that metabolic syndrome components were associated with an increased risk of various complications in HTG-AP, with low HDL-C being the most significant risk factor for clinical outcomes. The risk of complications increased with the number of metabolic syndrome components. Adjusted for age and sex, patients with high-component metabolic syndrome had significantly higher risks of renal failure [odds ratio (OR) = 3.02, 95%CI: 1.12-8.11)], SAP (OR = 5.05, 95%CI: 2.04-12.49), and intensive care unit admission (OR = 6.41, 95%CI: 2.42-16.97) compared to those without metabolic syndrome.

The coexistence of multiple metabolic syndrome components can synergistically worsen the clinical course of HTG-AP, making it crucial to monitor these components for effective disease management.

Acute pancreatitis (AP) is a complex and unpredictable condition, of which hypertriglyceridemia (HTG) is the third most prevalent cause. This study aimed to conduct a retrospective analysis of clinical data from hospitalized AP patients to uncover a potential correlation between triglyceride (TG) levels and the necessity for intensive care unit (ICU) admission. This retrospective cohort study utilized the Medical Information Mart for Intensive Care IV 2.2 (MIMIC-IV) critical care dataset, incorporating data from 698 patients with hypertriglyceridemic acute pancreatitis (HTG-AP). The analysis employed the RCS model along with univariate and multivariate logistic regression methods to affirm the association between triglyceride levels and ICU admission. Subgroup analysis was performed to investigate specific populations. The study included 698 patients with AP, 42.41% of whom experienced HTG during hospitalization. RCS analysis revealed a linear association between TG levels and risk of ICU admission (p for nonlinear = .219, p for overall = .009). Multivariate logistic regression analysis indicated an increased risk of ICU admission in the TG range of 1.7-5.65 mmol/L (aOR = 1.83, 95% CI 1.12-2.99, P = .015) and TG >11.3 mmol/L (aOR = 5.69, 95% CI 2.36-13.74, P < .001) compared to the normal group. Similar results were observed across the various subgroups. As triglyceride levels increased, there was a corresponding increase in ICU admissions. Patients within the 1.7 to 5.65 mmol/L and > 11.3 mmol/L triglyceride groups exhibited higher rates of ICU admissions. Moreover, we observed a higher risk of ICU hospitalization even with mild TG elevation.

Severe acute pancreatitis (SAP) is a dangerous condition with a high mortality rate. Many studies have found an association between adipokines and the development of SAP, but the results are controversial. Therefore, we performed a meta-analysis of the association of inflammatory adipokines with SAP.

We screened PubMed, EMBASE, Web of Science and Cochrane Library for articles on adipokines and SAP published before July 20, 2023. The quality of the literature was assessed using QUADAS criteria. Standardized mean differences (SMD) with 95% confidence intervals (CI) were calculated to assess the combined effect. Subgroup analysis, sensitivity analysis and publication bias tests were also performed on the information obtained.

Fifteen eligible studies included 1332 patients with acute pancreatitis (AP). Pooled analysis showed that patients with SAP had significantly higher serum levels of resistin (SMD = 0.78, 95% CI:0.37 to 1.19, z = 3.75, P = 0.000). The difference in leptin and adiponectin levels between SAP and mild acute pancreatitis (MAP) patients were not significant (SMD = 0.30, 95% CI: -0.08 to 0.68, z = 1.53, P = 0.127 and SMD = 0.11, 95% CI: -0.17 to 0.40, z = 0.80, P = 0.425, respectively). In patients with SAP, visfatin levels were not significantly different from that in patients with MAP (SMD = 1.20, 95% CI: -0.48 to 2.88, z = 1.40, P = 0.162).

Elevated levels of resistin are associated with the development of SAP. Resistin may serve as biomarker for SAP and has promise as therapeutic target.

Acute pancreatitis (AP) is an unpredictable and potentially fatal disorder. A derailed or unbalanced immune response may be the root of the disease's severe course. Disorders of lipid metabolism are highly correlated with the occurrence and severity of AP. We aimed to characterize the contribution and immunological characteristics of lipid metabolism-related genes (LMRGs) in non-mild acute pancreatitis (NMAP) and identify a robust subtype and biomarker for NMAP.

The expression mode of LMRGs and immune characteristics in NMAP were examined. Then LMRG-derived subtypes were identified using consensus clustering. The weighted gene co-expression network analysis (WGCNA) was utilized to determine hub genes and perform functional enrichment analyses. Multiple machine learning methods were used to build the diagnostic model for NMAP patients. To validate the predictive effectiveness, nomograms, receiver operating characteristic (ROC), calibration, and decision curve analysis (DCA) were used. Using gene set variation analysis (GSVA) and single-cell analysis to study the biological roles of model genes.

Dysregulated LMRGs and immunological responses were identified between NMAP and normal individuals. NMAP individuals were divided into two LMRG-related subtypes with significant differences in biological function. The cluster-specific genes are primarily engaged in the regulation of defense response, T cell activation, and positive regulation of cytokine production. Moreover, we constructed a two-gene prediction model with good performance. The expression of CARD16 and MSGT1 was significantly increased in NMAP samples and positively correlated with neutrophil and mast cell infiltration. GSVA results showed that they are mainly upregulated in the T cell receptor complex, immunoglobulin complex circulating, and some immune-related routes. Single-cell analysis indicated that CARD16 was mainly distributed in mixed immune cells and macrophages, and MGST1 was mainly distributed in exocrine glandular cells.

This study presents a novel approach to categorizing NMAP into different clusters based on LMRGs and developing a reliable two-gene biomarker for NMAP.

Acute pancreatitis is a frequent inflammatory gastrointestinal disorder with high mortality rates in severe forms. An early evaluation of its severity is key to identify high-risk patients. This study assessed the influence of waist circumference together with hypertriglyceridemia on the severity of acute pancreatitis.

A retrospective study was performed, which included patients admitted with acute pancreatitis from March 2014 to March 2021. Patients were classified into four phenotype groups according to their waist circumference and triglyceride levels: normal waist circumference and normal triglycerides; normal waist circumference and elevated triglycerides; enlarged waist circumference and normal triglycerides; and enlarged waist circumference and triglycerides, namely hypertriglyceridemic waist (HTGW) phenotype. Clinical outcomes were compared among the groups.

407 patients were included. Systemic inflammatory response syndrome (SIRS) and intensive care unit admission were most frequent among patients in the HTGW phenotype group, at 44.9% and 8.2%, respectively. The incidence of local complications was higher in the normal waist circumference with elevated triglycerides group (27%). On multivariable analysis, an enlarged waist circumference was related to an increase of 4% and 2% in the likelihood of developing organ failure and SIRS, respectively. Hypertriglyceridemia was an independent risk factor for both organ failure and local complications.

HTGW phenotype was significant related to developing of SIRS. It seems that an enlarged waist circumference has a greater role than hypertriglyceridemia in the development of SIRS. Obesity and hypertriglyceridemia were both independent risk factors for organ failure. Patients with hypertriglyceridemia were more likely to develop local complications.

Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is characterized by a violent cytokine storm-driven inflammation and is associated with a predisposition to severe disease. The treatment strategy for HTG-AP consists mainly of conventional symptomatic and lipid-lowering treatments. For early-stage HTG-AP, blood purification (BP) can rapidly and effectively reduce serum triglyceride and inflammatory cytokine levels, block the development of systemic inflammatory response syndrome, and improve patient outcomes. Currently, the primary modalities for BP in patients with HTG-AP include plasma exchange, hemoperfusion, and hemofiltration. When using BP to treat patients with HTG-AP, a comprehensive analysis incorporating the elevated lipid levels and severity of the patient's condition contributes to the selection of different treatment modes. Moreover, the timing of the treatment is also imperative. Early intervention is associated with a better prognosis for patients with HTG-AP requiring lipid-lowering treatment.

Obese people with acute pancreatitis (AP) have an increased risk of developing severe acute pancreatitis (SAP), which prolongs the length of hospital stay and increases mortality. Thus, elucidation of the mechanisms through which SAP occurs in obese individuals will provide clues for possible treatment targets. Differences in early events in obese or lean patients with AP have not been conclusively reported. We selected C57BL/6 mice as lean mice models, ob/ob mice or diet induced obese (DIO) mice as obese mice models and then induced experimental AP in mice via injections of caerulein. There were suppressed p-AMPK expressions in the pancreas of obese mice, compared with same-age lean C57BL/6 mice, which were further reduced in AP mice models. Obese AP mice were treated using AICAR, a direct AMPK agonist, which prevented pancreatic damage and cell death, suppressed pancreatic enzyme levels in serum, reduced the areas of fat saponification in the peritoneal cavity, prevented injury in other organs and decreased mice mortality rate. Further assays showed that AICAR activates p-AMPK to stabilize pro-caspase-8. Pro-caspase-8 enhances RIPK3 degradation, inhibits pancreatic acinar cell necroptosis, and downregulates the release of pancreatic enzymes. Thus, activation of AMPK by AICAR alleviates pancreatic acinar cell necroptosis and converts SAP to mild acute pancreatitis in obese mice.

Hypertriglyceridemia (HTG) is a major cause of acute pancreatitis (AP). We aimed to determine whether HTG is an independent risk factor for AP complications and construct a prediction model for non-mild AP.

We conducted a multi-center cohort study including 872 patients with AP and divided them into HTG-AP and non-HTG-AP groups. Multivariate logistic regression was performed, and a prediction model for non-mild HTG-AP was developed.

HTG-AP patients had a higher risk of systemic complications, including systemic inflammatory response syndrome [odds ratio (OR): 1.718; 95% confidence interval (CI): 1.286-2.295], shock (OR: 2.103; 95%CI: 1.236-3.578), acute respiratory distress syndrome (OR: 2.231; 95%CI: 1.555-3.200), acute renal failure (OR: 1.593; 95%CI: 1.036-2.450), and local complications such as acute peripancreatic fluid collection (OR: 2.072; 95%CI: 1.550-2.771), acute necrotic collection (OR: 1.996; 95%CI: 1.394-2.856), and walled-off necrosis (OR: 2.157; 95%CI: 1.202-3.870). The area under curve of our prediction model was 0.898 (95%CI: 0.857-0.940) and 0.875 (95%CI: 0.804-0.946) in the derivation and validation datasets respectively.

HTG is an independent risk factor for AP complications. We constructed a simple and accurate prediction model for progression of non-mild AP.

The hypertriglyceridaemic waist (HTGW) phenotype, an indicator to assess metabolic syndrome, could be a useful predictive marker for the risk of acute pancreatitis. This study aimed to evaluate the association between the HTGW phenotype and the risk of acute pancreatitis with a nationwide population-based cohort.

A retrospective, nationwide cohort study.

Registry of health check-up result from Korean National Health Insurance Service.

A total of 3 912 551 adults who underwent health checkups under the National Health Insurance Service in 2009 were enrolled in this study.

Subjects with both increased waist circumference (WC) and elevated blood triglyceride concentrations were defined as the HTGW phenotype. The participants were divided into four groups, classified as NWNT (normal WC-normal triglycerides), EWNT (elevated WC-normal triglycerides), NWET (normal WC-elevated triglycerides) and HTGW. The WC triglyceride index (WTI) is a quantitative indicator of the HTGW phenotype which is calculated by multiplying WC (cm) by triglyceride levels (mmol/L).

The subjects were followed until 31 December 2018. The adjusted HRs of acute pancreatitis in each group were estimated.

During the follow-up, there were a total of 8933 of acute pancreatitis occurrences. The incidence of acute pancreatitis in all subjects was 0.278 per 1000 person-year. The HTGW group had the highest incidence (0.444), followed by the NWET (0.381), and EWNT (0.316) groups. The HTGW group had a significant higher incidence of acute pancreatitis than the NWNT groups (HR 1.364 (95% CI 1.279 to 1.454)). The risk of acute pancreatitis steadily increased as the WTI increased (HR 1.847 (95% CI 1.657 to 2.058) in 10th decile).

The HTGW phenotype is confirmed to be an independent risk factor that increases the risk of acute pancreatitis.

Twenty-three percent of patients are diagnosed with diabetes mellitus after the first episode of acute pancreatitis. The incidence of post-acute pancreatitis diabetes mellitus is significantly higher than that of type 1 diabetes mellitus. Some studies have concluded that the all-cause mortality and worse prognosis of diabetes after pancreatitis are higher. We predicted that number of recurrences of pancreatitis would be significantly associated with the incidences of metabolic syndrome, abdominal obesity, and post-acute pancreatitis diabetes mellitus.

Patients admitted to our hospital for hypertriglyceridemic acute pancreatitis from 2013-2021 were selected for a cross-sectional study. Statistical analysis methods were used to analyze the effect of recurrences on the long-term prognosis of patients with hypertriglyceridemic acute pancreatitis.

In this study, 101 patients with hypertriglyceridemic acute pancreatitis were included: 60 (59.41%) in the recurrent acute pancreatitis group and 41 (40.59%) in the only one episode of acute pancreatitis group. Among all hypertriglyceridemic acute pancreatitis patients, approximately 61.4% were diagnosed with abdominal obesity, 33.7% of patients are diagnosed with metabolic syndrome, 34.7% of patients are diagnosed with diabetes mellitus, and 21.8% of patients are diagnosed with post-acute pancreatitis diabetes mellitus. Recurrent acute pancreatitis were independent risk factors for post-acute pancreatitis diabetes mellitus in patients with hypertriglyceridemic acute pancreatitis (odds ratio [OR] = 3.964, 95% confidence interval [CI] = 1.230-12.774) and the risk of post-acute pancreatitis diabetes mellitus in patients with three or more recurrent episodes was 6.607 times higher than that in patients without recurrent episodes (OR = 6.607, 95% CI = 1.412-30.916).

Recurrence is an independent risk factor for the development of post-acute pancreatitis diabetes mellitus and is significantly associated with the number of recurrences.

Hypertriglyceridemia (HTG) is a metabolic disorder, defined when serum or plasma triglyceride concentration (seTG) is >1.7 mM. HTG can be categorized as mild to very severe groups based on the seTG value. The risk of acute pancreatitis (AP), a serious disease with high mortality and without specific therapy, increases with the degree of HTG. Furthermore, even mild or moderate HTG aggravates AP initiated by other important etiological factors, including alcohol or bile stone. This review briefly summarizes the pathophysiology of HTG, the epidemiology of HTG-induced AP and the clinically observed effects of HTG on the outcomes of AP. Our main focus is to discuss the pathophysiological mechanisms linking HTG to AP. HTG is accompanied by an increased serum fatty acid (FA) concentration, and experimental results have demonstrated that these FAs have the most prominent role in causing the consequences of HTG during AP. FAs inhibit mitochondrial complexes in pancreatic acinar cells, induce pathological elevation of intracellular Ca²⁺ concentration, cytokine release and tissue injury, and reduce the function of pancreatic ducts. Furthermore, high FA concentrations can induce respiratory, kidney, and cardiovascular failure in AP. All these effects may contribute to the observed increased AP severity and frequent organ failure in patients. Importantly, experimental results suggest that the reduction of FA production by lipase inhibitors can open up new therapeutic options of AP. Overall, investigating the pathophysiology of HTG-induced AP or AP in the presence of HTG and determining possible treatments are needed.

Resistin is a small secretory adipokine which is implicated to obesity and associated diseases. Recently, plenty of research papers have been conducted to explore the association between peripheral resistin and the severity of acute pancreatitis (AP). However, the results were controversial. In this study, we aimed to confirm the effect of peripheral resistin and the development of acute pancreatitis.

A comprehensive online search was performed using the PubMed, Embase, Web of Science, CNKI, and Wanfang databases up through January 20, 2022. The retrieved records and their references were screened to identify additional studies. Data were extracted to calculate the pooled Hedges' g and its 95% CI, which were selected to assess peripheral resistin levels and the severity of acute pancreatitis. Subgroup analyses, sensitivity analyses, meta-regression, and publication bias tests were also undertaken based on obtained information.

A total of eleven studies with 892 acute pancreatitis patients were enrolled in the study. Peripheral resistin levels were significantly increased in severe acute pancreatitis compared with mild acute pancreatitis (Hedges' g = 2.092, 95% CI: 0.994-3.190, P < 0.001). Subgroup analyses based on sample types and ethnicity also showed similar results. A single study did not affect our results, which was verified by sensitivity analysis. Meta-regression analyses revealed that age, gender of the included subjects, sample size, and publication year did not moderate effects on the present results.

In our study, peripheral resistin levels were significantly elevated in patients with severe AP compared with patients with mild AP. Abnormal resistin levels may provide us some new insights in predicting the severity of AP.