Diagnostic accuracy of endoscopic ultrasonographic shear wave elastography for assessing early chronic pancreatitis using the Japanese diagnostic criteria 2019.

Background and Aim: Endoscopic ultrasound shear wave elastography (EUS-SWE) can facilitate an objective evaluation of pancreatic fibrosis. Although it is primarily applied in evaluating chronic pancreatitis, its efficacy in assessing early chronic pancreatitis (ECP) remains underinvestigated. This study evaluated the diagnostic accuracy of EUS-SWE for assessing ECP diagnosed using the Japanese diagnostic criteria 2019. Methods: In total, 657 patients underwent EUS-SWE. Propensity score matching was used, and the participants were classified into the ECP and normal groups. ECP was diagnosed using the Japanese diagnostic criteria 2019. Pancreatic stiffness was assessed based on velocity (Vs) on EUS-SWE, and the optimal Vs cutoff value for ECP diagnosis was determined. A practical shear wave Vs value of ≥50% was considered significant. Results: Each group included 22 patients. The ECP group had higher pancreatic stiffness than the normal group (2.31 ± 0.67 m/s vs. 1.59 ± 0.40 m/s, p < 0.001). The Vs cutoff value for the diagnostic accuracy of ECP, as determined using the receiver operating characteristic curve, was 2.24m/s, with an area under the curve of 0.82 (95% confidence interval: 0.69-0.94). A high Vs was strongly correlated with the number of EUS findings (rs = 0.626, p < 0.001). Multiple regression analysis revealed that a history of acute pancreatitis and ≥2 EUS findings were independent predictors of a high Vs. Conclusions: There is a strong correlation between EUS-SWE findings and the Japanese diagnostic criteria 2019 for ECP. Hence, EUS-SWE can be an objective and invaluable diagnostic tool for ECP diagnosis.

Antioxidative effect of astragalosides on acute pancreatitis in mice.

Introduction: The research examined the antioxidative impact of astragalosides (AST) on experimental acute pancreatitis (AP) in mice. This study aims to assess the correlation between varying doses of astragalosides and superoxide dismutase (SOD) activity in an acute pancreatitis mouse model. By examining the interplay between astragaloside's protective effects and its antioxidant properties, we aim to deepen our understanding of its therapeutic potential in acute pancreatitis. Methods: The AP model in mice was induced by retrograde injection of sodium deoxycholate into the biliary and pancreatic ducts. Serum amylase activity was monitored at various time points following induction. Furthermore, 24 hours post-induction, levels of serum nitric oxide (NO), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content in pancreatic tissue were assessed. Results: The findings of this study illustrated that AST, while exhibiting a protective effect in experimental AP, could effectively lower the elevated serum NO levels, reduce MDA production, and enhance SOD activity in model mice. AST notably reduced MDA levels in the pancreatic tissue of AP mice, underscoring its ability to inhibit membrane peroxidation induced by oxygen free radicals. Furthermore, AST was observed to elevate SOD activity in scavenging oxygen free radicals in pancreatic tissue. Conclusion: These findings suggest that AST enhances recovery in an experimental acute pancreatitis mouse model by exerting antioxidative effects.

Incidence and risk factors for deep vein thrombosis (DVT) and pulmonary embolism (PE) in acute necrotizing pancreatitis (ANP) - A single center experience.

INTRODUCTION: Inflammation-induced dysregulation of the coagulation cascade and vascular stasis in hospitalized patients with acute necrotizing pancreatitis (ANP) serve as a milieu for venous thromboembolism (VTE). Deep vein thrombosis (DVT) and pulmonary embolism (PE) are often underrecognized. We evaluated the incidence and risk factors for VTE in a cohort of patients with ANP. METHODS: All adult patients with ANP at our center between 2009 and 2022 were followed for three months after index hospitalization and categorized into cases and controls based on development of VTE. Demographic, clinical, and radiologic characteristics during admission were compared. A multivariable analysis was done to identify independent predictors for VTE. A p value of <0.05 was taken as significant. RESULTS: Among 643 ANP patients, 512 [males-350, median age-52 years] were eligible for inclusion. VTE developed in 64 (12.5 %) patients - 28 DVT (5 %), 22 PE (4 %) and both in 14 (3 %) after a median 16 days from the diagnosis of ANP. Significant independent predictors for VTE on multivariable analysis were age ≥60 years (OR 1.91; 95 % CI 1.04-3.53), peri-pancreatic extent of necrosis (OR 7.61; 95 % CI 3.94-14.70), infected necrosis (OR 2.26; 95 % CI 1.13-4.50) and total length of stay ≥14 days (OR 4.08; 95 % CI 1.75-9.50). CONCLUSIONS: The overall incidence of VTE in our cohort of patients with ANP was 12.5 %, which was usually diagnosed within one month of hospitalization. High-risk patients can be stratified based on clinical and imaging characteristics and may benefit from intensive DVT screening and prophylaxis during hospitalization and following discharge.

Spontaneous total regression of post-acute pancreatitis splenic artery pseudoaneurysm: A case report and review of the literature.

INTRODUCTION: Splenic artery pseudoaneurysms (SAP) are uncommon but significant vascular complications frequently associated with pancreatitis. These lesions carry a substantial risk of rupture and subsequent life-threatening hemorrhage. Standard treatment typically involves surgical or endovascular intervention to prevent such catastrophic outcomes. However, this case report documents a rare instance of spontaneous regression of a SAP following severe pancreatitis, challenging the established treatment protocols and highlighting the potential for conservative management under specific conditions. CASE PRESENTATION: A 65-year-old male with a past history of acute biliary pancreatitis secondary to gallstones, which was treated with laparoscopic cholecystectomy, presented with severe abdominal pain and a significant drop in hemoglobin levels. Imaging revealed acute pancreatitis with multiple pseudocysts and a newly identified 10 mm splenic artery pseudoaneurysm exhibiting recent bleeding. Although arterial embolization was recommended, the patient opted for non-invasive management. Intensive monitoring and conservative treatment were initiated. Over several days, his symptoms improved, and follow-up imaging showed spontaneous thrombosis of the SAP. One month later, a CT scan confirmed the complete resolution of the pseudoaneurysm. DISCUSSION: SAPs are serious complications of pancreatitis, often necessitating urgent intervention due to high rupture risk. This case of spontaneous regression underscores the importance of individualized management strategies. It suggests that conservative treatment may be a viable option for stable patients with resolving pancreatitis, although such cases are rare and require careful monitoring. CONCLUSION: While the primary approach to managing SAP remains interventional due to the high risk of rupture, this case highlights the potential for spontaneous regression in select circumstances. It underscores the need for personalized treatment plans.

Autophagy-mediated ferroptosis is involved in development of severe acute pancreatitis.

BACKGROUND: Ferroptosis is a newly recognized form of regulatory cell death characterized by severe lipid peroxidation triggered by iron overload and the production of reactive oxygen species (ROS). However, the role of ferroptosis in severe acute pancreatitis(SAP) has not been fully elucidated. METHODS: We established four severe acute pancreatitis models of rats including the sham control group, the SAP group, the Fer -1-treated SAP (SAP + Fer-1) group, the 3-MA-treated SAP (SAP + 3-MA) group. The SAP group was induced by retrograde injection of sodium taurocholate into the pancreatic duct. The other two groups were intraperitoneally injected with ferroptosis inhibitor (Fer-1) and autophagy inhibitor (3-MA), respectively. The model of severe acute pancreatitis with amylase crest-related inflammatory factors was successfully established. Then we detected ferroptosis (GPX4, SLC7A1 etc.) and autophagy-related factors (LC3II, p62 ect.) to further clarify the relationship between ferroptosis and autophagy. RESULTS: Our study found that ferroptosis occurs during the development of SAP, such as iron and lipid peroxidation in pancreatic tissues, decreased levels of reduced glutathione peroxidase 4 (GPX 4) and glutathione (GSH), and increased malondialdehyde(MDA) and significant mitochondrial damage. In addition, ferroptosis related proteins such as GPX4, solute carrier family 7 member 11(SLC7A11) and ferritin heavy chain 1(FTH1) were significantly decreased. Next, the pathogenesis of ferroptosis in SAP was studied. First, treatment with the ferroptosis inhibitor ferrostatin-1(Fer-1) significantly alleviated ferroptosis in SAP. Interestingly, autophagy occurs during the pathogenesis of SAP, and autophagy promotes the occurrence of ferroptosis in SAP. Moreover, 3-methyladenine (3-MA) inhibition of autophagy can significantly reduce iron overload and ferroptosis in SAP. CONCLUSIONS: Our results suggest that ferroptosis is a novel pathogenesis of SAP and is dependent on autophagy. This study provides a new theoretical basis for the study of SAP.

Using Acidosis as a Surrogate for or Supplement to the Bedside Index of Severity in Acute Pancreatitis Scoring Prediction System Has a Nonsignificant Effect.

Currently, risk stratification calculators for acute pancreatitis (AP) can at best predict acute pancreatitis mortality at 12 hours from the presentation. Given the severe morbidity associated with AP, the identification of additional prognostic indicators, which may afford earlier prediction in length of stay (LOS) and mortality, is desired. Metabolic acidosis can be a prognostic marker for the severity of AP, and venous bicarbonate can reliably and accurately be substituted for arterial base deficit to detect metabolic acidosis. Since serum bicarbonate, anion gap (AG), and corrected AG (CAG) are routinely obtained upon presentation to the emergency department and often daily in the hospital, we conducted a retrospective analysis of 443 patients, evaluating if venous bicarbonate could predict the severity of pancreatitis as well as mortality, admission to the ICU, ICU LOS, and hospital LOS. The inclusion of venous bicarbonate, AG, and CAG in the first 12 hours only slightly improved the predictive capabilities of the Bedside Index for Severity in Acute Pancreatitis (BISAP) score for these secondary outcomes. None of our incorporations of acidemia improved severity predictions more than the BISAP alone. Adding CAG to BISAP scoring had the largest effect on predicting ICU admission and hospital LOS (area under the curve (AUC): 1.12 (confidence interval (CI) 95%: 1.06-1.19), p <.001 and AUC 1.02 (CI 95% 1.01-1.04), p <.001; respectively). ICU LOS was not impacted by the addition of AG, CAG, or venous bicarbonate. In-hospital death (n=12) was too small to be determined.

Comparing prognostic scoring systems in acute pancreatitis: Bedside Index of Severity in Acute Pancreatitis, WL, and Chinese Simple Scoring System Scores.

OBJECTIVES: Several scoring systems are used to predict prognosis in acute pancreatitis (AP), but their predictive success varies. This study compares the validity of the commonly used Bedside Index of Severity in AP (BISAP) score with the newly developed WL score and the Chinese Simple Scoring System (CSSS) score in predicting mortality and unfavorable prognostic outcomes in AP patients. METHODS: This retrospective descriptive study included all AP patients presenting to the emergency department from June 2, 2019, to June 2, 2022. Patient demographics, vital signs, laboratory values, and imaging findings were recorded, and WL, CSSS, and BISAP scores were calculated. The effectiveness of these scores in predicting adverse outcomes and mortality was compared. RESULTS: Among 357 patients, 53.2% were male, with a median age of 62 years (interquartile range: 48-75). Area under the curve (AUC) values for 7-day outcomes were 0.956 for WL, 0.759 for CSSS, and 0.871 for BISAP; for 30-day outcomes, AUC values were 0.941 for WL, 0.823 for CSSS, and 0.901 for BISAP; and for poor prognostic outcomes, AUC values were 0.792 for WL, 0.769 for CSSS, and 0.731 for BISAP. CONCLUSION: In AP patients, WL, CSSS, and BISAP scores are effective predictors of unfavorable prognosis and mortality. WL score outperforms the CSSS and BISAP scores in predicting 7-day and 30-day mortality and poor prognosis. After WL, BISAP is the second-best system for predicting mortality. For predicting unfavorable prognoses, CSSS is the second-best system after WL. The simplicity of calculating the WL score based on four laboratory parameters makes it a preferable choice.

Global trends in opioid use for pain management in acute pancreatitis: A multicentre prospective observational study.

BACKGROUND: Since there is no current international consensus on the optimal approach for pain management in acute pancreatitis (AP), analgesic practices may vary across different healthcare settings. OBJECTIVE: This study explored global disparities in analgesic use, in particular opioids, during admission and at discharge in hospitalised AP patients. METHODS: This was a post hoc analysis of the prospective PAINAP database, which included all admissions for AP between April and June 2022 with a 1-month follow-up. Demographic details, analgesic use, and clinical outcomes were recorded during admission and at discharge. Odds ratios (ORs) for opioid use during admission and at discharge were identified using multivariable regression analyses. RESULTS: Amongst the 1864 patients (52% males, median age 56 (interquartile range, 41-71)) across three different continents, simple analgesics were predominantly used as the primary analgesic (70%). Opioid use during admission was lowest in European centres (67%). Admission in Asian (OR, 2.53 (95% confidence interval (CI), 1.59-4.04), p < 0.001), and Australian (OR, 5.81 (95% CI, 3.19-10.56), p < 0.001) centres was associated with opioid administration during admission compared with European centres. Increased pain severity, longer pre-admission pain duration, organ failure, and longer length of admission increased opioid use during admission. At discharge, Asian (OR, 2.01 (95% CI, 1.40-2.88), p < 0.001) and Australian (OR, 1.91 (95% CI, 1.28-2.85), p = 0.002) centres were associated with opioid prescription compared with European centres. Increased pain severity, longer pre-admission pain duration, acute necrotic collections, and walled-off necrosis also increased the likelihood of opioid prescription at discharge. CONCLUSION: There are substantial intercontinental differences in opioid use for AP pain. Accordingly, there is a need for international guidelines on pain management in AP.

Less Aggressive Hydration May Be More in Acute Pancreatitis?

Consider a more conservative approach to fluid resuscitation in mild acute pancreatitis to avoid fluid overload without sacrificing patient-oriented clinical outcomes.

Natural history of spontaneous pancreatic portal vein fistulae: A systematic review of the literature.

BACKGROUND: Spontaneous pancreatic portal vein fistula (PPVF) - a rare complication of pancreatic inflammation - varies widely in presentation and means of diagnosis but has been previously associated with bleeding complications and mortality. A systematic review of published literature was performed to assess the frequency of outcomes. METHODS: A search of electronic databases (PubMed, Ovid MEDLINE, Scopus, EMBASE, gray literature) resulted in 1667 relevant unique manuscripts; 52 met inclusion criteria. RESULTS: A total of 74 unique (male n = 47, 63.5 %) patients were included. Mean age was 53.5 (±11.9) years. History of alcohol use was reported in 55 (74.3 %). Underlying chronic pancreatitis (CP) was present in 49 (66.2 %). In cases where presenting symptoms were reported (n = 57, 77.4 %), the most frequent were abdominal pain (63.5 %), weight loss (14.9 %), rash (12.2 %), nausea/vomiting (12.2 %), and polyarthritis (9.5 %). Computed tomography was the most common imaging modality used to confirm the diagnosis (n = 20, 27.0 %), followed by magnetic resonance cholangiopancreatography (n = 14, 18.9 %). Portal vein thrombosis was reported in 57 (77.0 %), and bleeding events (luminal, variceal, or intra-pseudocyst) were reported in 13(17.6 %) patients. Younger age was associated with higher risk of bleeding events. Mortality was reported in 12 (16.2 %) patients at any time during follow up. Older age and polyarthritis at presentation were associated with mortality. CONCLUSIONS: PPVF is a rare and potentially fatal condition, though rates of bleeding complication and death were relatively low in this population. High-quality observational studies are needed to better understand the pathophysiology and natural history of this diagnosis.

Severity and outcome of a first episode of idiopathic acute pancreatitis is not more severe than pancreatitis of other etiologies.

BACKGROUND: With respect to severity and outcome of an index episode of idiopathic acute pancreatitis the current literature reports conflicting retrospective results. One reason might be the retrospective study design precluding in depth analysis resulting in mixed etiologies and combination of index episode versus recurrent idiopathic acute pancreatitis. METHODS: In this retrospective monocentric cohort study, we retrieved all patients with a first acute pancreatitis episode treated between 2005 and 2021 at the LMU University Hospital from our clinical information system based on the respective ICD-10 codes. In an initial sample of 1390 presumed idiopathic pancreatitis patients we identified 68 confirmed idiopathic acute pancreatitis patients and compared those to 75 first-time alcohol-induced acute pancreatitis patients and 390 first-time biliary-induced acute pancreatitis patients. Clinical outcome (severity, SIRS, mortality, and re-admission rate) was set as outcome measures. Multinomial logistic regression analysis was performed. RESULTS: In alcohol-induced acute pancreatitis moderate and severe courses occur significantly more often when compared to idiopathic acute pancreatitis (17.33 % vs. 10.29 %; multinomial logistic regression p = 0.0021). There were no significant differences in mortality between first-time alcoholic, idiopathic and biliary pancreatitis (p = 0.6328). Patients with idiopathic acute pancreatitis had significantly more hospital readmissions (within 30 days) compared to alcohol-induced pancreatitis patients (p = 0.0284). CONCLUSION: In the context of a first episode of acute pancreatitis, idiopathic acute pancreatitis remains a challenging diagnosis posing an increased risk of recurrence, but not an increased risk for a more severe disease course.

Exploring the gut microbiota's crucial role in acute pancreatitis and the novel therapeutic potential of derived extracellular vesicles.

During acute pancreatitis, intestinal permeability increases due to intestinal motility dysfunction, microcirculatory disorders, and ischemia-reperfusion injury, and disturbances in the intestinal flora make bacterial translocation easier, which consequently leads to local or systemic complications such as pancreatic and peripancreatic necrotic infections, acute lung injury, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Therefore, adjusting intestinal ecosystem balance may be a promising approach to control local and systemic complications of acute pancreatitis. In this paper, we reviewed the causes and manifestations of intestinal flora disorders during acute pancreatitis and their complications, focused on the reduction of acute pancreatitis and its complications by adjusting the intestinal microbial balance, and innovatively proposed the treatment of acute pancreatitis and its complications by gut microbiota-derived extracellular vesicles.

A dose-response correlation between smoking and severity of acute pancreatitis: a propensity score-matched study.

Background: Acute pancreatitis, among the most prevalent gastrointestinal disorders, exhibits a continual rise in its incidence recent years. This study endeavor to explore the correlation between smoking exposure and the severity of acute pancreatitis (AP). Methods: Five hundred and eight patients diagnosed as acute pancreatitis (AP) were included in our data analysis. Patients were categorized based on their smoking pack-years into four groups: light, moderate, heavy, and non-smokers. Outcomes were classified as two: "mild acute pancreatitis (MAP)" and "moderately severe acute pancreatitis (MSAP) or severe acute pancreatitis (SAP)". We conducted propensity score matching (PSM) to adjust confounding factors and multivariable logistic regression analysis to determine adjusted odds ratios and 95% confidence intervals. Additionally, a dose-dependent association analysis between smoking exposure and the incidence rate of "MSAP or SAP" was performed. Results: Smokers exhibited a higher risk of "MSAP or SAP" compared to non-smokers, both before (17.1 vs. 54.9%, p < 0.001) and after (9.4 vs. 24.7%, p < 0.001) PSM. With an area under the ROC curve of 0.708, smoking showed a moderate level of predictive ability. Furthermore, propensity score matching analysis showed that patients who smoked compared to non-smokers had significantly higher risks of "MSAP or SAP" for light smoking (OR 3.76, 95% CI 1.40-10.07, p = 0.008), moderate smoking (OR 4.94, 95% CI 2.23-10.92, p < 0.001), and heavy smoking (OR 8.08, 95% CI 3.39-19.25, p < 0.001). Conclusion: Smoking is an independent risk factor that can raise the severity of pancreatitis. Moreover, the severity of acute pancreatitis escalates in tandem with the accumulation of pack-years of smoking.

Timing, initiation and function: An in-depth exploration of the interaction network among neutrophil extracellular traps related genes in acute pancreatitis.

BACKGROUND: Exogenous inhibition of neutrophil extracellular traps (NETs) was believed to alleviate acute pancreatitis (AP). This study aimed to comprehensively explore the key biological behavior of NETs including timing and pathogenesis in AP by integrating of single cell RNA sequencing(scRNA-seq) and bulk RNA-seq. METHODS: Differentially expressed NETs-related genes and the hub genes of NETs were screened by bulk RNA-seq. ScRNA-seq was used to identify the cell types in pancreas of AP mice and to depict the transcriptomic maps in neutrophils. The mouse AP models were build to verify the timing of initiation of NETs and underlying pathogenesis of damage on pancreas acinar cells. RESULTS: Tlr4 and Ccl3 were screened for hub genes by bulk RNA-seq. The trajectory analysis of neutrophils showed that high expression of Ccl3, Cybb and Padi4 can be observed in the middle stage during AP. Macrophages might be essential in the biological behavior of neutrophils and NETs. Through animal models, we presented that extensive NETs structures were formed at mid-stage of inflammation, accompanied by more serious pancreas and lung damage. NETs might promote necroptosis and macrophage infiltration in AP, and the damage on pancreatic injury could be regulated by Tlr4 pathway. Ccl3 was considered to recruit neutrophils and promote NETs formation. CONCLUSION: The findings explored the underlying timing and pathogenesis of NETs in AP for the first time, which provided gene targets for further studies.

Case Report: Acute Pancreatitis in an Uncontrolled Diabetic Patient Presenting With a Skin Rash Later Found to Be Eruptive Xanthoma, a Dermatological Manifestation and Diagnostic Clue to Recognizing Hypertriglyceridemia as the Cause of Disease.

Acute pancreatitis results from any insult that leads to inflammation of the organ. Hypertriglyceridemia is one of the risk factors associated with acute pancreatitis. The typical presentation is abdominal pain, nausea, and vomiting. We present a unique case in which the patient's condition was further complicated by diabetic ketoacidosis. Consequently, he presented somnolent to the emergency room, providing a limited history only pertaining to generalized weakness and a skin rash. The patient was found to have hypertriglyceridemia-induced pancreatitis, which was appropriately managed in the intensive care unit. The skin lesions were diagnosed as xanthomas, which are associated with hypertriglyceridemia and acute pancreatitis secondary to hypertriglyceridemia. The patient was discharged on fibrate therapy, dietary counseling, and strict monitoring by his primary care physician. This unique case highlights the importance of recognizing dermatological conditions and their associated diseases to allow for prompt diagnosis and treatment in the face of limited history.

Beyond the Splanchnic Area: Extra-splanchnic Thrombosis in Acute Pancreatitis.

Acute pancreatitis (AP) is an inflammatory condition with varied clinical presentations. Local complications include peripancreatic fluid collection, acute necrotic collection, walled-off necrosis, and pancreatic pseudocyst, but vascular complications like pseudoaneurysm and venous thrombosis are also reported. Patients often experience splanchnic venous thrombosis, which can affect the splenic vein, portal vein, and superior mesenteric vein individually or in combination. Rarely, extra-splanchnic venous thrombosis, including renal vein, superior vena cava, and inferior vena cava thrombosis, has been reported in cases of chronic pancreatitis. The formation of a venous thrombus in acute pancreatitis is multifaceted, with pancreatic inflammation and the immune response mounted by the patient playing a significant role. There is a dearth of medical literature regarding extra-splanchnic venous thrombosis and the use of therapeutic anticoagulation in the successful treatment of the above-mentioned complication. This case report highlights the rare complications that can be seen in cases of acute pancreatitis.

Hypertriglyceridemia-Induced Acute Pancreatitis Exacerbated by Combined Oral Contraceptive Use: A Case Report.

Acute pancreatitis can be induced by a vast variety of etiologies including its more common causes such as cholelithiasis and alcohol abuse, but in certain cases it can also be secondary to hypertriglyceridemia. Additionally, combined oral contraceptive use can enhance the severity of hypertriglyceridemia-induced acute pancreatitis (HTG-AP). The data between this association is much more limited than the more common causes of acute pancreatitis. In this case, we aim to highlight the onset of hypertriglyceridemia-induced acute pancreatitis due to recent combined oral contraceptive use in a 34-year-old Hispanic female patient with a family history of hypertriglyceridemia. With the initiation of a low-fat diet, insulin regimen, and lipid-lowering medications, she was able to significantly improve her elevated triglyceride levels from 3772 to 440 throughout the duration of her six-day hospital stay. Due to the less commonly known relationship between combined oral contraceptive use and HTG-AP, this case serves to enhance understanding of the pathophysiology of this condition, the appropriate diagnostic evaluation, and the associated treatment options to optimize patient care and create efficacious management plans. By increasing awareness of this association, patients with familial hypertriglyceridemia can be made aware of the risks of combined oral contraceptive use to accordingly prevent complications and improve clinical outcomes.

Serum uric acid concentration in acute pancreatitis is significantly higher than healthy population.

Acute pancreatitis (AP) is a common disease caused by a variety of causes. Is uric acid associated with the onset of AP? The objective of this study was to assess whether uric acid concentration in AP patients was higher than that in healthy population, and whether there were associations between uric acid concentration and serological indicators related to AP. A total of 205 AP patients were included in this study. Two hundred and five people who underwent physical examination in our hospital were randomly selected as controls. We analyzed whether there was difference in uric acid concentrations between the two groups. If the difference was statistically significant, the correlations between uric acid concentration and serological indicators in AP patients was further analyzed. There was significant difference in uric acid concentration (P < 0.001) between AP patients and healthy population. Serum uric acid concentration in AP group was significantly higher than that in control group. Two hundred and five AP patients were divided into mild AP group and non-mild AP group. There was no statistically significant difference in uric acid concentration between the two groups (P = 0.176). There was a low linear correlation between serum uric acid concentration and triglyceride level (r = 0.316, P < 0.001). But there was no linear correlation between serum uric acid concentration and hypersensitive C-reactive protein (r = 0.126, P = 0.072), white blood cell (r = 0.192, P = 0.006), albumin (r = 0.183, P = 0.009), total cholesterol concentration (r = 0.133, P = 0.058), fasting blood-glucose (r = 0.133, P = 0.058) and blood calcium (r = 0.155, P = 0.026). Uric acid concentration in patients with AP was significantly higher than healthy population. There was correlation between uric acid concentration and triglyceride in AP patients.