Current literature on temporal trends reveals that the incidence of acute pancreatitis has been increasing globally over the past 20 years, with average annual per cent changes of 3.67 and 2.77% across North America and Europe, respectively[12].Acute pancreatitis (AP) is among the most common clinical digestive system diseases. It is an inflammatory disease caused by the abnormal activation of pancreatic enzymes, leading to the digestion of pancreatic tissues. AP has a rapid onset and progression and can develop into moderately severe acute pancreatitis (MSAP) or severe acute pancreatitis (SAP), which has many complications,dangerous conditions,and high mortality[13].
Mortality for pancreatitis is approximately 1% overall,however, among hospitalized patients with pancreatitis and organ failure or pancreatic necrosis, mortality may be as high as 30–40%[14].
Thus, active research into the microscopic mechanisms of immune imbalance and inflammatory amplification in SAP is essential for improving its prognosis[15].Pathology of AP begins with the early conversion of pancreatic enzymes from inactive to active forms inside the acinar cells which leads to autodigestion of the pancreatic tissue[16].On a molecular level, the triggers of acute pancreatitis induce injury of pancreatic acinar and ductal cells by disrupting normal intracellular calcium signalling that maintains stimulus-secretion coupling[17].Due to the limited understanding of AP pathophysiology, the treatment of this disease remains not specific. Hence, it is vitally important to investigate the mechanism underlying AP to find novel therapeutic strategy[18].
The main causes of acute pancreatitis in high-income countries are gallstones (45%), alcohol use (20%), and hypertriglyceridemia (10%)[19].In this study, the three major causes of binge-eating, biliary and pancreatic duct obstruction, and hyperlipidemia were basically consistent with the above studies.AP is a common clinical acute abdominal disease with pancreatic inflammation, including pancreatic edema, bleeding, and even necrosis. The clinical features of AP are acute epigastric pain, nausea, vomiting, fever, and even slipping into shock[20]. The mean age of participants was 45.3 ± 8.7 years, and 82.7% were male. Abdominal pain was the most frequent clinical sign (100%), followed by dyspepsia(87.7%), nausea or vomiting (72.8%), and a bloated stomach (61.7%)[21]. Our statistical analysis of the general clinical symptoms of acute pancreatitis, including nausea, vomiting, abdominal pain, abdominal distension and fever, it was found that the severe group was significantly higher than the non-severe group (P < 0.05). Meanwhile, the history of hypertension, diabetes, cerebrovascular disease, liver disease and kidney disease in the severe group was higher than that in the non-severe group (P < 0.05). This indicates that those with underlying diseases are more likely to develop acute severe pancreatitis than previously healthy ones.
Because of the relative inaccessibility of pancreatic tissue and the rapid course of AP, obtaining blood samples seems advantageous for establishing early diagnosis. At present, there is no gold standard laboratory test for diagnosing AP, and serum lipase activity at least three times greater than the upper limit is often adopted to assess pancreatic inflammation. However, these biomarkers have not been incorporated into clinical use for various reasons, such as their low diagnostic accuracy and availability[22]. In our laboratory analysis of acute pancreatitis, we found that: Serum amylase, lipase, fasting blood glucose, calcium, total cholesterol, triglyceride, activated coagulation time, D-dimer, fibrinogen, fibrin degradation products, erythrocyte sedimentation rate, lactic acid, lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, etc., were significantly increased in severe group compared with non-severe group (P < 0.05).D-dimer is a specific product of degradation of crosslinked fibrin, which indirectly reflects the coagulation disorder. Some studies have found that D-dimer is related to the severity and complications of acute pancreatitis, and patients with acute pancreatitis may develop coagulation and microcirculation disorders in the acute phase[23]. In the present study, the plasma levels of D-dimer in patients with AP, recurrent acute pancreatitis (RAP)and chronic pancreatitis(CP)were measured. Subsequently, correlations between D-dimer levels and diferent types of pancreatitis were assessed.In diferent types of pancreatitis, D-dimer levels in AP patients and RAP patients were signifcantly higher than those in control group (p < 0.05), and there was no signifcant diference in D-dimer levels between CP group and control group[24]. Clinical studies revealed that the levels of plasma fibrinogen degradation products (FDP) are significantly higher in AP patients compared to healthy individuals, and higher levels of FDP are related to severity,and portosplenomesenteric venous thrombosis occurs in about 17.86% of patients with early-stage SAP.These phenomena indicated that the hypercoagulable state during AP and the therapeutic strategies aimed at enhancing microcirculation by anticoagulant therapy might improve the outcomes in AP[25]. Acute pancreatitis is a procoagulant state. The leakage of activated digestive enzymes from damaged pancreatic acinar cells results in injury to the adjacent vascular epithelial cells, leading to the exposure of tissue factor, activation of platelets, and the initiation of the coagulation cascade[26].
Clinical study found that AP patients with complications, such as pseudocyst, acute respiratory failure, sepsis, infectious pancreatic necrosis, and acute renal failure had significantly increased inflammatory indicators, such as WBC, neutrophils, CRP, and ESR, while RBC, Hb decreased significantly, indicating that the pathological basis of AP complications is an inflammatory response, and malnutrition and ischemia and hypoxia may further aggravate this inflammatory response[27]. Animal studies have shown that cells of the innate immune response, such as neutrophils and macrophages rapidly migrate into the pancreas after the onset of the disease[28]. Understanding the precise roles of these immune cells in AP will help develop targeted therapeutic strategies to modulate the immune response and improve patient outcomes. Further research is needed to elucidate the roles of these immune cells in the development of AP and to evaluate the potential of targeting specific immune cell populations for treating this complex and severe inflammatory disorder[29]. Neutrophils can not only produce a large number of reactive oxygen species and reactive nitrogen, leading to worsening inflammation, but can also activate various immune cells and stromal cells to secrete inflammatory cytokines, leading to aggravation of inflammation[30]. The CRP can also be applied as both an inflammatory mediator and a nonspecific sensitive indicator of the immune inflammation[31]. Several biological markers have been proposed for the prediction of the severity and mortality of acute pancreatitis. These results suggest that CRP can be used to select mild cases of acute pancreatitis which can be discharged early and managed in an ambulatory setting. Other proposed markers were the white blood cell count, neutrophil number, erythrocyte sedimentation rate, and Hb level[32]. C-reactive protein (CRP) levels above 150 mg/dL predict severe acute necrotizing pancreatitis (ANP) on admission. Procalcitonin (PCT) above 0.5 ng/mL is a predictor of ANP from the first twenty-four hours. Serial assessment of changes in PCT reflects the course of the disease. Levels above 1.8 ng/mL are an indication of infected ANP. Lactate levels greater than 2 mmol/L (> 18 mg/dL) indicate severe sepsis[33]. Both IL-6 and CRP are known as inflammatory markers that predict severe AP and are useful in the early phase of AP[34]. IL-6 is a prototypical cytokine that has redundant and pleiotropic activity, the synthesis of which is promptly induced to aid in host defense when tissue damage or inflammation because of infections or injuries occurs. Several studies have demonstrated an association between IL-6 and AP and found that IL-6 is a useful marker for the assessment of the severity of AP in its early stages[35]. In the analysis of laboratory inflammation indicators of acute pancreatitis, we found that the leukocyte count, neutrophil count, hypersensitive C-reactive protein, interleukin-6, procalcitonin, etc., were significantly higher in the severe group than in the non-severe group (P < 0.05).ROC curves can be used to improve clinical care by determining both cut of points and the best performing diagnostic tests[36]. In this study, ROC curve analysis was performed on the inflammatory indexes: WBC, NEUT, hs-CRP, IL-6 and PCT, and the CUT-OFF values of each inflammatory indicator were 8.170, 9.455, 45.400, 8.530 and 1.000, respectively. The area under the curve (AUC) was 0.629, 0.606, 0.602, 0.611 and 0.598, and the largest area under the curve was WBC. The AUC is a measure of the overall performance of a diagnostic test and can be interpreted as the average value of sensitivities for all possible specificities. The AUC has a value between 0 and 1, but is meaningful as a diagnostic test only when it is > 0.5. The larger the value, the better the overall performance of the test[37].
In summary, through the analysis of clinical characteristics and inflammatory indicators of 116 patients with acute pancreatitis in this paper, it is concluded that patients in the severe and non-severe groups have significant differences in age, underlying diseases, biochemistry, inflammatory indicators and clinical manifestations, which is conducive to early clinical detection, diagnosis, treatment and prevention in the future, and to reduce mortality to a certain extent. Improve the quality of life and prognosis of patients, and play a positive role in further standardizing the clinical diagnosis and treatment of AP.
In addition, this study is limited to retrospective studies, and there are still some limitations in evaluating the severity and prognosis of AP patients. First of all, this study is a single-center, small-sample study, which may cause statistical deviation due to sample size. Secondly, the course of acute pancreatitis is extremely complicated, and the peripheral blood indexes change significantly at different time points, and the results of a single blood collection have a certain chance. In the future, multi-source, multi-center, prospective and reproducible clinical data are still needed to verify its reliability.