Nomogram for the Prediction of 30-Day Readmission in Acute Pancreatitis.

BACKGROUND: A prediction model for 30-day readmission in patients with acute pancreatitis (AP) was needed. AIMS: To develop a nomogram to predict 30-day readmission in patients with AP and validate the usefulness of serum indicators after discharge for the prediction of 30-day readmission. METHODS: This was a retrospective cohort study enrolling patients with the first attack of AP. Baseline characteristics, clinical profiles, and serum indicators after discharge were compared. Multivariate logistic regression analysis and a nomogram were employed to determine the independent risk factors for 30-day readmission. RESULTS: A total of 7.32% (121/1653) of the patients were readmitted within 30 days after discharge. Different etiologies (biliary pancreatitis (adjusted odds ratio (AdjOR), 9.63; 95% confidence interval (CI), 1.28-72.52; P = 0.028), other causes (AdjOR, 9.37; 95% CI, 1.15-76.12, P = 0.026), mixed causes (AdjOR, 10.76; 95% CI, 1.27-91.35; P = 0.03) compared with alcoholic pancreatitis)), infected pancreatitis necrosis (IPN) (AdjOR, 2.3; 95% CI, 1.2-4.42; P = 0.013), total bilirubin level ≥ 20.5 µmol/L (AdjOR, 2.42; 95% CI, 1.23-4.77; P = 0.01), glucose level ≥ 6.1 mmol/L (AdjOR, 1.93; 95% CI, 1.16-3.19; P = 0.011), and albumin level < 40 g/L (AdjOR, 4.25; 95% CI, 2.44-7.41; P < 0.001) were independently associated with 30-day readmission. A nomogram incorporating these factors demonstrated good discrimination, calibration, and clinical utility. Serum indicators after discharge added predictive value compared with clinical variables alone (AUC, 0.78 vs. 0.685; P = 0.0001). CONCLUSIONS: The nomogram combining etiology, IPN, and serum indicators after discharge has favorable predictive performance for 30-Day readmission. The close monitoring and reexamination of serum indicators are essential for AP patients at high risk.

Elevated CA125 levels are associated with adverse clinical outcomes in acute pancreatitis: A propensity score-matched study.

OBJECTIVES: Glycosylation alterations are indicative of tissue inflammation and neoplasia. However, there are no large-sample, real-world studies assessing the levels of serum carbohydrate antigen 125 (CA125) in patients with acute pancreatitis (AP). We aimed to identify the association between elevated CA125 levels and adverse clinical outcomes in AP. METHODS: This was a retrospective cohort study with an analysis of 3939 patients with AP who were admitted to the First Affiliated Hospital of Nanchang University between January 2015 and September 2019 that used data from a prospectively maintained database. Multivariate logistic regression analysis and a propensity score-matched analysis were conducted to reveal the relationship between elevated CA125 levels and poor prognosis. RESULTS: The overall prevalence of elevated CA125 (>35 U/mL) levels was 38.51% (1517/3939) in AP patients. Elevated CA125 levels were independently associated with higher risks of mortality (adjusted odds ratio (AdjOR), 1.82; 95% confidence interval (CI), 1.30-2.54; P < 0.001), severe acute pancreatitis (SAP) (AdjOR, 2.40; 95% CI, 2.00-2.88; P < 0.001), and infected pancreatic necrosis (IPN) (AdjOR, 3.54; 95% CI, 2.65-4.71; P < 0.001). The propensity score-matched cohort analysis also demonstrated that mortality (OR, 1.57; 95% CI, 1.06-2.23; P < 0.05), SAP (OR, 2.20; 95% CI, 1.77-2.73; P < 0.001), and IPN (OR, 2.79; 95% CI, 1.98-3.92; P < 0.001) were more common in the elevated CA125 group than in the normal CA125 group. CONCLUSIONS: Elevated CA125 levels (>35 U/mL) are independently associated with adverse clinical outcomes in AP patients. These observations justify ongoing efforts to understand the role of CA125 in the pathogenesis and prognosis of AP.

New Risk Factors for Infected Pancreatic Necrosis Secondary to Severe Acute Pancreatitis: The Role of Initial Contrast-Enhanced Computed Tomography.

BACKGROUND AND AIMS: Pancreatic necrosis is a risk factor for poor prognosis of acute pancreatitis (AP). However, the associations between the findings on initial contrast-enhanced computed tomography (CT) of the pancreas and infected pancreatic necrosis (IPN) are unclear. METHODS: This was a retrospective cohort study. Patients with severe AP (SAP) from January 2014 to December 2016 at the First Affiliated Hospital of Nanchang University were enrolled and assigned to an IPN group and a non-IPN group. Univariate and multivariate logistic regression analyses were sequentially performed to assess the associations between the variables and IPN development. A receiver operating characteristic (ROC) curve was generated for the qualified independent risk factor. RESULTS: Forty-two patients with IPN were compared with 100 patients without IPN. Contrast-enhanced CT was performed 7 (range 3-10) days after AP onset. Multivariate stepwise logistic regression analyses showed that the number of acute peripancreatic fluid collections (APFCs) (OR 1.328, P = 0.006), presence of peripancreatic and pancreatic parenchymal necrosis (OR 4.001, P = 0.001), and gastrointestinal wall thickening (OR 3.353, P = 0.006) were independent risk factors for IPN secondary to SAP. The area under an ROC curve for the number of APFCs was 0.714, the sensitivity was 78.60%, and the specificity was 57.30% at a cutoff value of 4.5. CONCLUSIONS: The number of APFCs, presence of peripancreatic and pancreatic parenchymal necrosis, and gastrointestinal wall thickening were independent risk factors associated with IPN. As initial contrast-enhanced CT (about 7 days from AP onset) plays an important role in predicting IPN, it is important for clinicians to consider initial imaging of the pancreas.

Double-catheter lavage combined with percutaneous flexible endoscopic debridement for infected pancreatic necrosis failed to percutaneous catheter drainage.

BACKGROUND: Infected pancreatic necrosis (IPN) is a serious local complication of acute pancreatitis, with high mortality. Minimally invasive therapy including percutaneous catheter drainage (PCD) has become the preferred method for IPN instead of traditional open necrosectomy. However, the efficacy of double-catheter lavage in combination with percutaneous flexible endoscopic debridement after PCD failure is unknown compared with surgical necrosectomy. METHODS: A total of 27 cases of IPN patients with failure PCD between Jan 2014 and Dec 2015 were enrolled in this retrospective cohort study. Fifteen patients received double-catheter lavage in combination with percutaneous flexible endoscopic debridement, and 12 patients underwent open necrosectomy. The primary endpoint was the composite end point of major complications or death. The secondary endpoint included mortality, major complication rate, ICU admission length of stay, and overall length of stay. RESULTS: The primary endpoint occurrence rate in double-catheter lavage in combination with percutaneous flexible endoscopic debridement group (8/15, 53%) was significantly lower than that in open necrosectomy group (11/12, 92%) (RR = 1.71, 95% CI = 1.04 - 2.84, P < 0.05). Though the mortality between two groups showed no statistical significance (0% vs. 17%, P = 0.19), the rate of new-onset multiple organ failure and ICU admission length of stay in the experimental group was significantly lower than that in open necrosectomy group (13% vs. 58%, P = 0.04; 0 vs. 17, P = 0.02, respectively). Only 40% of patients required ICU admission after percutaneous debridement, which was markedly lower than the patients who underwent surgery (83%; P < 0.05). CONCLUSIONS: Double-catheter lavage in combination with percutaneous flexible endoscopic debridement showed superior effectiveness, safety, and convenience in patients with IPN after PCD failure as compared to open necrosectomy.

Comparison of multifactor scoring systems and single serum markers for the early prediction of the severity of acute pancreatitis.

BACKGROUND: The purpose of this study was to clarify whether the current scoring systems and single serum markers used in pancreatitis remain applicable for the early prediction of infected pancreatic necrosis (IPN) and the severity and mortality of acute pancreatitis (AP) in accordance with the revised Atlanta and determinant-based classifications. METHODS: Demographic, clinical, and laboratory data from 708 consecutive patients with AP were prospectively collected between January 2011 and December 2012. The severity was classified using the revised Atlanta and determinant-based classification systems. The predictive accuracies for moderately severe AP (MSAP), severe AP (SAP), critically severe AP (CAP), IPN, and mortality were measured using area under the receiver operating characteristic curves. RESULTS: The receiver operating characteristic analysis showed that the multifactor scoring systems and single serum markers had a low predictive accuracy regarding moderately severe AP. The Acute Physiology and Chronic Health Evaluation (APACHE) II score had the highest accuracy in predicting SAP with area under the curve (AUC) values of 0.75 (95% CI = 0.71-0.79) and 0.77 (95% CI = 0.73-0.81) at 24 and 48 h after admission, respectively. Procalcitonin was the most accurate predictor for CAP and IPN, with respective AUCs of 0.86 (95% CI = 0.82-0.89) and 0.83 (95% CI = 0.78-0.87) at 48 h after admission. In predicting mortality, both the APACHE II score and blood urea nitrogen had the highest accuracy. CONCLUSIONS: The APACHE II score had the highest predictive accuracy for SAP and mortality as defined by the revised Atlanta classification, whereas procalcitonin was the most accurate predictor for CAP and IPN.

The outcomes of initial endoscopic transluminal drainage are superior to percutaneous drainage for patients with infected pancreatic necrosis: a prospective cohort study.

BACKGROUND AND STUDY AIM: The commonly used minimally invasive methods for patients with infected pancreatic necrosis (IPN) are initial endoscopic transluminal drainage (ETD) and percutaneous catheter drainage (PCD), which are followed, if necessary, by endoscopic or surgical necrosectomy. This study intends to explore which of the two minimally invasive treatments leads to a better prognosis. PATIENTS AND METHODS: Patients with IPN and an indication for intervention were prospectively enrolled and underwent either initial ETD or PCD followed, if necessary, by endoscopic or surgical necrosectomy. RESULTS: Initial treatment success occurred in 8 of 11 patients after ETD (72.7%) and in 3 of 13 patients after PCD (30.8%) (risk ratio [RR] with ETD, 2.36; 95% CI 0.97-5.77; P = 0.04). After 1 year of follow-up, 72.7% of patients survived with ETD, and 69.2% survived with PCD (RR 1.05; 95% CI 0.63-1.75; P = 0.85). Intestinal fistula seems to have occurred less in the patients who received initial ETD rather than PCD therapy (9.1 vs. 38.5%; RR 0.24; 95% CI 0.03-1.73; P = 0.098). Fewer patients who underwent an initial ETD were transferred to surgery (9.1 vs. 46.2%; RR 0.20; 95% CI 0.03-1.40; P = 0.047). A higher rate of new-onset diabetes (3 cases) or impaired glucose tolerance (1 case) occurred in initial PCD compared to ETD (40 vs. 0%, P = 0.042). CONCLUSION: The outcomes of initial endoscopic transluminal drainage are superior to percutaneous drainage for patients with infected pancreatic necrosis (ChiCTR-ONRC-13003653).

Emergent Triglyceride-lowering Therapy With Early High-volume Hemofiltration Against Low-Molecular-Weight Heparin Combined With Insulin in Hypertriglyceridemic Pancreatitis: A Prospective Randomized Controlled Trial.

OBJECTIVES: To compare the value of emergent triglyceride (TG)-lowering therapies between early high-volume hemofiltration (HVHF) and low-molecular-weight heparin (LMWH) combined with insulin (LMWH+insulin) as well as their effects on the outcomes of hypertriglyceridemic pancreatitis (HTGP) patients. METHODS: In this randomized controlled trial, 66 HTGP patients presenting within 3 days after the onset of symptoms from August 2011 to October 2013 were assigned randomly to receive either HVHF or LMWH+insulin as an emergent TG-lowering therapy. Thirty-three patients were included in each group, and the therapy was started as soon as possible after admission. TG levels, clinical outcomes, and inflammatory biomarkers were compared between the 2 groups. RESULTS: Thirty-two individuals in the HVHF group and 34 in the LMWH+insulin group were included in the final analysis. Characteristics of the patients in both groups were roughly comparable. HVHF could remove TG from the plasma and achieve its target (<500 mg/dL) in approximately 9 hours, whereas the target was not achieved within 48 hours in patients receiving the LMWH+insulin treatment (P<0.05). However, no differences were found in terms of the majority of the clinical outcomes, including local pancreatic complications (P>0.05), the requirement of surgical intervention (P=0.49), mortality (P=0.49), and the duration of hospitalization (P=0.144). Furthermore, an unexpectedly higher incidence of persistent organ failure was observed in the HVHF group compared with the LMWH+insulin group (risk ratio with HVHF, 2.42; 95% confidence interval, 1.15-5.11; P=0.01). Hospital charges for patients in the HVHF group were approximately 2-fold higher than those for patients in the LMWH+insulin group (5.20±4.90 vs. 2.92±3.21, P=0.03). We selected a systemic inflammatory response syndrome score of at least 2 at baseline as a predictor of SAP patients, and the subgroup analyses showed that HVHF cannot improve the prognosis of the predicted SAP patients compared with the LMWH+insulin group. CONCLUSIONS: HVHF can lower TG levels more efficiently than LMWH+insulin therapy, but it is not superior in terms of clinical outcomes and costs. Further multicenter studies with large samples are required to clarify the feasibility of administering the HVHF treatment to HTGP patients (ChiCTR-TRC-13003274).

[The comparison of different clinical scoring systems for predicting prognosis in acute pancreatitis based on the revised Atlanta classification].

OBJECTIVE: To compare the predictive value of BISAP (bedside index for severity in acute pancreatitis), APACHE II (acute physiology and chronic health evaluation II), and Ranson scoring system in persistent organ failure (POF) and mortality in patients diagnosed as acute pancreatitis (AP) based on the revised Atlanta classification. METHODS: Demographic, clinical and laboratory data of 350 consecutive AP patients admitted to the First Affiliated Hospital of Nanchang University were prospectively collected from November, 2009 to January, 2012. A retrospective analysis was performed and 310 patients finished the follow-up. The median age of whole population was (50.5 ± 16.4) years old. Patients were classified into early phase group ( ≤ 7 days) and late phase group ( > 7 days) based on the interval between onset of AP and admission. Demographics and clinical data were collected to calculate Ranson, APACHE II and BISAP scores during the first 3 days of hospitalization. Poor prognosis was defined as POF or death. RESULTS: The three scoring systems similarly demonstrated modest accuracy for predicting POF or death in early phase group [area under the receiver operating characteristic curve (AUCROC):0.68-0.84], but failed to predict the prognosis of AP patients in late phase group. Daily scoring of APACHE IIand BISAP on the first 3 days after admission demonstrated modest to high predictive accuracy to poor prognosis (AUCROC:0.69-0.95), but this was not statistically significant (P > 0.05) . CONCLUSIONS: These three clinical scoring systems show modest accuracy for predicting POF or death in AP patients on the early phase based on the revised Atlanta classification. The BISAP scoring system has similar prognostic value to APACHE II and Ranson. However, due to the simplicity and convenience, BISAP scoring system is more popular in clinical practice. Daily scoring on the first 3 days after admission fails to predict the prognosis accurately.

Elevated CK-MB levels are associated with adverse clinical outcomes in acute pancreatitis: a propensity score-matched study.

Aim: Cardiac injury, reflected by the measured concentrations of chemicals released from injured cardiac muscle, is common in acute pancreatitis (AP). However, there is no adequate evidence assessing the impact of cardiac injury on AP-related outcomes. Creatine kinase-myocardial band (CK-MB) mainly exists in the myocardium. Therefore, we sought to evaluate the relationship between the increase in CK-MB and the adverse clinical outcomes of AP. Methods: This propensity score-matched study analyzed AP patients admitted to the Department of Gastroenterology in the First Affiliated Hospital of Nanchang University from June 2017 to July 2022. Propensity score matching and multivariate logistic regression analysis were used to explore the relationship between CK-MB elevation and AP outcome variables. Results: A total of 5,944 patients were screened for eligibility, of whom 4,802 were ultimately enrolled. Overall, 896 (18.66%) of AP patients had elevated (>24 U/ml) CK-MB levels, and 895 (99.89%) were paired with controls using propensity score matching. The propensity score-matched cohort analysis demonstrated that mortality (OR, 5.87; 95% CI, 3.89-8.84; P < 0.001), severe acute pancreatitis (SAP) (OR, 2.74; 95% CI, 2.23-3.35; P < 0.001), and infected necrotizing pancreatitis (INP) (OR, 3.40; 95% CI, 2.34-4.94; P < 0.001) were more frequent in the elevated CK-MB (>24 U/ml) group than in the normal CK-MB (≤ 24 U/ml) group. Using the multivariate logistic regression analysis, elevated CK-MB levels were independently associated with increased mortality (OR, 2.753, 95% CI, 2.095-3.617, P < 0.001), SAP incidence (OR, 2.223, CI, 1.870-2.643, P < 0.001), and INP incidence (OR, 1.913, 95% CI, 1.467-2.494, P < 0.001). CK-MB elevation was an independent risk factor for adverse clinical outcomes in AP patients. Conclusion: CK-MB elevation was significantly related to adverse outcomes in AP patients, which makes it a potentially useful laboratory parameter for predicting adverse clinical outcomes of AP.

Association between morphological features of necrotizing pancreatitis on endoscopic ultrasound and outcomes of the endoscopic transmural step-up approach.

OBJECTIVE: To investigate the association between necrotic collections on endoscopic ultrasound (EUS) and outcomes of the endoscopic transmural step-up approach in necrotizing pancreatitis (NP). METHODS: Adult NP patients who had undergone endoscopic transmural step-up approach, endoscopic transmural drainage or endoscopic transmural necrosectomy, were retrospectively enrolled, and divided into groups 1, 2 and 3 based on the amount of solid necrotic debris (quantified as a percentage of the total collection size of <30%, 30%-50%, and >50%). RESULTS: A total of 134 patients were included, of whom 52, 59 and 23 patients were categorized into groups 1, 2 and 3. Patients with more solid necrotic debris required more necrosectomy sessions (group 3 vs group 2 vs group 1: 2.0 vs 1.0 vs 1.0, P < 0.001), were more likely to experience stent occlusion (group 3 vs group 2 vs group 1: 34.8% vs 16.9% vs 9.6%, P = 0.011), and had a longer hospitalization (group 3 vs group 2 vs group 1: 40.0 d vs 28.0 d vs 25.5 d, P = 0.015). High procalcitonin level (adjusted odds ratio [aOR] 6.14, 95% confidence interval [CI] 1.40-26.94, P = 0.016) and any organ failure (aOR 11.51, 95% CI 2.42-54.78, P = 0.002) were independently associated with clinical failure of endoscopic transmural step-up approach. CONCLUSIONS: More solid necrotic debris on EUS is related to more necrosectomy sessions, higher incidence of stent occlusion and longer hospitalization. A nomogram combining procalcitonin and any organ failure performs well in predicting clinical failure of endoscopic transmural step-up approach.

[The role and mechanism of NADPH oxidase in leptin-induced reactive oxygen species production in hepatic stellate cells].

OBJECTIVE: To investigate whether or not NADPH oxidase (NOX) participates in leptin-induced reactive oxygen species (ROS) production in hepatic stellate cells (HSC) and to explore the possible mechanism. METHODS: HSC-T6 cells (rat hepatic stellate cells line) were divided into nine groups: Group1: leptin (100 ng/ml) treated; Group2-6: leptin treated together with inhibitors that block different ROS-producing systems: diphenylene-iodonium (DPI) (20 micromol/L), Rotenone (20 micromol/L), Metyrapone (250 micromol/L), Allopurinol (100 micromol/L) and Indomethacin(100 micromol/L); Group7: leptin treated together with Janus kinase (JAK) inhibitor AG490 50 micromol/L; Group8: normal control group (treated DMEM with 0.1% DMSO); Group9: negative control group (untreated). Intracellular ROS levels were measured with dichlorodihydrofluorescein diacetate (DCFH-DA) dye assay by Fluorescence microscope and/or flow cytometry. NOX activity was analyzed by using spectrophotometer to calculate the absorbance of NADPH. The mRNA levels of Rac1 and p22Phox were evaluated by RT-PCR. RESULTS: (1) Leptin increased significantly the ROS production as compared to normal control group (92.91+/-4.19 vs.27.56+/-6.27, P<0.01) in HSC-T6 cells. Both the NADPH oxidase inhibitor DPI and AG490 (50 micromol/L) blocked the ROS production, inhibitors of other ROS producing systems had no significant effect on ROS production induced by lepin (P is more than 0.05). (2) Leptin treated HSC-T6 cells for 1 hour up-regulated the NOX activity significantly compared with that in normal control group [(1.90+/-0.22) pmol.min(-1).mg(-1) vs. (0.76+/-0.06) pmol.min(-1).mg(-1), P<0.05]. Furthermore, the NOX activity increased after being treated with leptin for 12 hours and 24 hours than being treated for 1 hour. Leptin-induced up-regulation of NOX activity was inhibited by pretreatment with DPI or AG490. (3) The RT-PCR results indicated that mRNA expressions of Rac1 and p22Phox in HSC-T6 cells with 12 hours of leptin stimulation increased significantly as compared with normal control group (0.41+/-0.13 vs 0.14+/-0.08, 0.45+/-0.12 vs 0.20+/-0.08, all P<0.05), while the DPI and AG490 had no effect on the mRNA expressions of Rac1 and p22Phox. CONCLUSION: NOX is the main cellular source of the reactive oxygen species (ROS) generated by HSCs in response to leptin stimulation. The mechanism is probably that leptin can directly activate NOX through JAK signal transduction and hence induce the expression of NOX subunit to promote the activity of NOX which generates considerable ROS in HSC.

Risk Factors for Acute Kidney Injury in Acute Pancreatitis: A 7-Year Retrospective Analysis of Patients in a Large Tertiary Hospital.

OBJECTIVE: The aim of our study was to investigate the risk factors for acute kidney injury (AKI) in patients with acute pancreatitis (AP). METHODS: Acute pancreatitis patients were retrospectively divided into 2 groups: AKI and non-AKI. We used logistic regression analysis to investigate the risk factors for AP patients with AKI. We also compared the incidence of complications and mortality between the non-AKI and AKI groups. RESULTS: A total of 1255 AP patients without AKI and 430 AP patients with AKI were included. The risk factors for AKI in AP were hypertriglyceridemia (P = 0.001), severity (P = 0.001), etiology (P = 0.001), and Acute Physiology and Chronic Health Evaluation II scores (P = 0.001). The incidences of organ failure (P = 0.001), pancreatic necrosis (P = 0.001), and mortality (P = 0.001) were greater in the AKI group than in the non-AKI group. CONCLUSIONS: Hypertriglyceridemia, severity, etiology, and Acute Physiology and Chronic Health Evaluation II scores are independent risk factors for AKI in AP patients. Those patients have serious outcomes such as high rate of organ failure, pancreatic necrosis, and debridement of necrosis.

Pancreatic necrosis and severity are independent risk factors for pancreatic endocrine insufficiency after acute pancreatitis: A long-term follow-up study.

BACKGROUND: Pancreatic endocrine insufficiency after acute pancreatitis (AP) has drawn increasing attention in recent years. AIM: To assess the impact of risk factors on the development of pancreatic endocrine insufficiency after AP. METHODS: This retrospective observational long-term follow-up study was conducted in a tertiary hospital. Endocrine function was evaluated by the oral glucose tolerance test. The data, including age, sex, body mass index, APACHE II score, history of smoking and drinking, organ failure, pancreatic necrosis, debridement of necrosis (minimally invasive and/or open surgery), and time interval, were collected from the record database. RESULTS: A total of 361 patients were included in the study from January 1, 2012 to December 30, 2018. A total of 150 (41.6%) patients were diagnosed with dysglycemia (including diabetes mellitus and impaired glucose tolerance), while 211 (58.4%) patients had normal endocrine function. The time intervals (mo) of the above two groups were 18.73 ± 19.10 mo and 31.53 ± 27.27 mo, respectively (P = 0.001). The morbidity rates of pancreatic endocrine insufficiency were 46.7%, 28.0%, and 25.3%, respectively, in the groups with different follow-up times. The risk factors for pancreatic endocrine insufficiency after AP were severity (odds ratio [OR] = 3.489; 95% confidence interval [CI]: 1.501-8.111; P = 0.004) and pancreatic necrosis (OR = 4.152; 95%CI: 2.580-6.684; P = 0.001). CONCLUSION: Pancreatic necrosis and severity are independent risk factors for pancreatic endocrine insufficiency after AP. The area of pancreatic necrosis can affect pancreatic endocrine function.

Severity of acute gastrointestinal injury grade is a good predictor of mortality in critically ill patients with acute pancreatitis.

BACKGROUND: Gastrointestinal (GI) dysfunction is a common and important complication of acute pancreatitis (AP), especially in patients with severe AP. Despite this, there is no consensus means of obtaining a precise assessment of GI function. AIM: To determine the association between acute gastrointestinal injury (AGI) grade and clinical outcomes in critically ill patients with AP. METHODS: Patients with AP admitted to our pancreatic intensive care unit from May 2017 to May 2019 were enrolled. GI function was assessed according to the AGI grade proposed by the European Society of Intensive Care Medicine in 2012, which is mainly based on GI symptoms, intra-abdominal pressure, and feeding intolerance in the first week of admission to the intensive care unit. Multivariate logistic regression analysis was performed to assess the association between AGI grade and clinical outcomes in critically ill patients with AP. RESULTS: Among the 286 patients included, the distribution of patients with various AGI grades was 34.62% with grade I, 22.03% with grade II, 32.52% with grade III, and 10.84% with grade IV. The distribution of mortality was 0% among those with grade I, 6.35% among those with grade II, 30.11% among those with grade III, and 61.29% among those with grade IV, and AGI grade was positively correlated with mortality (χ 2 = 31.511, P < 0.0001). Multivariate logistic regression analysis showed that age, serum calcium level, AGI grade, persistent renal failure, and persistent circulatory failure were independently associated with mortality. Compared with the Acute Physiology and Chronic Health Evaluation II score (area under the curve: 0.739 vs 0.854; P < 0.05) and Ranson score (area under the curve: 0.72 vs 0.854; P < 0.01), the AGI grade was more useful for predicting mortality. CONCLUSION: AGI grade is useful for identifying the severity of GI dysfunction and can be used as a predictor of mortality in critically ill patients with AP.

[Change of ROCK1 Gene Expression Level in Patients with Acute Lymphoblastic Leukemia and Its Clinical Significance].

OBJECTIVE: To investigate the expression change of ROCK1 gene in patients with acute lymphoblastic leukemia (ALL) and its prognostic significance. METHODS: Sixty patients with ALL were selected in our hospital from April 2017 to April 2018, and 60 healthy persons subjected to physical examination were selected as control. The venous blood was taken from the subjects, and then the mononuclear cells were separated. The ROCK1 gene expression level in the samples was detected by RT-PCR, and the expression level of ROCK1 protein was detected by Western blot. The correlation between ROCK1 gene expression and clinical characteristics of ALL patients was analyzed by using statistical methots. RESULTS: The RT-PCR showed that the relative expression level of ROCK1 gene in ALL patients was 1.37 (1.28-1.46), which was significantly higher than that in the control group (P<0.05). Western blot showed that the protein expression level of ROCK1 in ALL patients was higher than that in the control group (P<0.05). The expression level of ROCK1 gene correlated with age, WBC count, lactate dehydrogenase (LDH) level, peripheral blood immature cell count, and risk stratification of ALL patients (P<0.05). The expression level of ROCK1 gene did not correlate with sex, hemoglobin (Hb) level, platelet count and immunophenotype in ALL patients (P>0.05). The standard risk ratio of B-ALL and T-ALL patients with low ROCK1 expression was significantly higher than that in patients with high ROCK1 expression (P<0.05). The high risk ratio of B-ALL and T-ALL patients with low ROCK1 expression was significantly lower than those with high ROCK1 expression (P<0.05). The ratio of CR in the group with low ROCK1 expression patients was significantly higher than that in patients with high ROCK1 expression (P<0.05). The Relapse rate of the group with low ROCK1 expression was significantly lower than that of the group with high ROCK1 expression (P<0.05). Kaplan-Meier survival analysis showed that OS and DFS in ALL patients with low ROCK1 expression were superior to those in ALL patients with high ROCK1 expression (P<0.05). Multiple factor Cox regression analysis showed that age and ROCK1 gene were independent influencing factors for OS (P<0.05); leukocyte count and ROCK1 gene were independent influencing factors for DFS (P<0.05). CONCLUSION: The expression level of ROCK1 gene in ALL patients is high, which may stimulate the genesis of ALL, and the down-regulation of ROCK1 gene expression may help improve the therapeutic effect for ALL patients.

Hypertriglyceridemia-induced acute pancreatitis: progress on disease mechanisms and treatment modalities.

Acute pancreatitis (AP) is a common and destructive inflammatory condition of the pancreas. Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) has become the second major cause of AP. Although the association between HTG and AP is well established, HTG as a risk factor of AP in the general population is not well identified. In this review, we summarize recent progress in our understanding of the pathogenesis of HTG-AP and clinical management of this disease. The mechanism responsible for HTG-AP is related to high-level free fatty acid (FFA), microcirculatory disorder, oxidative stress, Ca2+ overload, and genetic polymorphism. Heparin and insulin therapy in diabetic patients with HTG can dramatically reduce triglyceride levels. Use of plasmapheresis is still experimental and better-designed studies are needed to evaluate the promise in the management of HTG-AP. Dietary intervention, lifestyle changes, and control of secondary causes are critical to the management and treatment of HTG-AP.

Blue laser magnifying endoscopy in the diagnosis of chronic gastritis.

The current study aimed to evaluate the clinical value of using blue laser imaging combined with magnifying endoscopy in the diagnosis of chronic gastritis (CG). The groups used were as follows: The white light group (WLI, control group), linked color imaging group (LCI, observation group 1), blue laser imaging (BLI)-bright (brt) group (BLI-brt; observation group 2), BLI + magnified imaging (ME) group (observation group 3). WLI mode initially allowed the observation of mucosal suspicious lesions on the gastric mucosa. These lesions were photographed and the mode was changed to LCI, BLI-brt and BLI + ME. Different observational patterns were compared between modes to diagnose various grades of chronic gastritis. No significant differences were observed in the baseline information of enrolled patients. The LCI mode diagnosis rate was higher for Helicobacter pylori (HP) infection than in any other mode. LCI exhibited a high diagnostic rate for HP, BLI-brt exhibited a high diagnostic rate for atrophy and BLI/BLI + ME exhibited a high diagnostic rate for intestinal metaplasia and intraepithelial neoplasia. All modes exhibited higher diagnostic rates compared with the WLI mode. The pathological HP diagnosis rate (consistency) of HP infection was the greatest in the LCI group (endoscopic findings and pathological consistency). The BLI-BRT mode exhibited the highest pathological diagnosis rate for atrophic gastritis and the BLI/BLI + ME mode exhibited the highest diagnostic rate for intestinal metaplasia and low-grade intraepithelial neoplasia.

Percutaneous Drainage Versus Peritoneal Lavage for Pancreatic Ascites in Severe Acute Pancreatitis: A Prospective Randomized Trial.

OBJECTIVES: This study aimed to compare the efficacy of percutaneous drainage (PCD) versus peritoneal lavage (PL) for the treatment for severe acute pancreatitis patients with pancreatic ascites (PAs). METHODS: Severe acute pancreatitis patients with PAs were randomly assigned within 3 days of onset of symptoms to receive either PL or PCD. The primary end point was a composite of mortality or major complications during hospitalization and within 1 month of discharge. Per-protocol analyses were performed. RESULTS: Between September 2011 and June 2014, 86 patients were randomly assigned to intervention with PL or PCD. Ultimately, 41 patients in the PCD group and 39 patients in the PL group completed the study. The primary end point occurred in 15 (36.6%) of 41 patients in the PCD group and in 17 (43.6%) of 39 patients in the PL group (risk ratio, 0.84; 95% confidence interval, 0.49-1.44; P = 0.27). Mortality or major complications did not differ between the groups. Percutaneous drainage reduced intra-abdominal hypertension; however, PL reduced the incidence of deep venous thrombosis and pancreatic encephalopathy and was associated with a reduced need for intervention. CONCLUSIONS: In our study, the PCD was not superior to the PL in reducing mortality or major complications in severe acute pancreatitis patients with PAs.

Portosplenomesenteric vein thrombosis in patients with early-stage severe acute pancreatitis.

AIM: To investigate the incidence and risk factors of portosplenomesenteric vein thrombosis (PSMVT) in the early stage of severe acute pancreatitis (SAP). METHODS: Patients with SAP in a tertiary care setting from January 2014 to December 2016 were retrospectively reviewed. All contrast-enhanced computed tomography (CT) studies were reassessed and reviewed. Clinical outcome measures were compared between SAP patients with and without PSMVT in the early stage of the disease. Univariate and multivariate logistic regression analyses were sequentially performed to assess potential risk factors for the development of PSMVT in SAP patients. A receiver operating characteristic (ROC) curve was generated for the qualifying independent risk factors. RESULTS: Twenty-five of the one hundred and forty (17.86%) SAP patients developed PSMVT 6.19 ± 2.43 d after acute pancreatitis (AP) onset. PSMVT was confirmed by contrast-enhanced CT. Multivariate stepwise logistic regression analyses showed that Balthazar's CT severity index (CTSI) scores [odds ratio (OR): 2.742; 95% confidence interval (CI): 1.664-4.519; P = 0.000], hypoalbuminemia (serum albumin level < 25 g/L) (OR: 32.573; 95%CI: 2.711-391.353; P = 0.006) and gastrointestinal wall thickening (OR: 4.367, 95%CI: 1.218-15.658; P = 0.024) were independent risk factors for PSMVT developed in patients with SAP. The area under the ROC curve for Balthazar's CTSI scores was 0.777 (P = 0.000), the sensitivity was 52%, and the specificity was 93% at a cut-off value of 5.5. CONCLUSION: High Balthazar's CTSI scores, hypoalbuminemia and gastrointestinal wall thickening are independent risk factors for PSMVT developed in the early stage of SAP.

Ursolic acid suppresses TGF-ß1-induced quiescent HSC activation and transformation by inhibiting NADPH oxidase expression and Hedgehog signaling.

Activation of quiescent hepatic stellate cells (q-HSCs) and their transformation to myofibroblasts (MFBs) is a key event in liver fibrosis. Hedgehog (Hh) signaling stimulates q-HSCs to differentiate into MFBs, and NADPH oxidase (NOX) may be involved in regulating Hh signaling. The author's preliminary study demonstrated that ursolic acid (UA) selectively induces apoptosis in activated HSCs and inhibits their proliferation in vitro via negative regulation of NOX activity and expression. However, the effect of UA on q-HSCs remains to be elucidated. The present study aimed to investigate the effect of UA on q-HSC activation and HSC transformation and to observe alterations in the NOX and Hh signaling pathways during q-HSC activation. q-HSC were isolated from adult male Sprague-Dawley rats. Following culture for 3 days, the cells were treated with or without transforming growth factor-ß1 (TGF-ß1; 5 µg/l); intervention groups were pretreated with UA (40 µM) or diphenyleneiodonium chloride (DPI; 10 µM) for 30 min prior to addition of TGF-ß1. mRNA and protein expression of NOX and Hh signaling components and markers of q-HSC activation were examined by western blotting and reverse transcription-polymerase chain reaction. TGF-ß1 induced activation of q-HSCs, with increased expression of α-smooth muscle actin (α-SMA) and type I collagen. In addition, expression of NOX subunits (gp91phox, p67phox, p22phox, and Rac1) and Hh signaling components, including sonic Hh, sterol-4-alpha-methyl oxidase, and Gli family zinc finger 2, were upregulated in activated HSCs. Pretreatment of q-HSCs with UA or DPI prior to TGF-ß1 significantly downregulated expression of NOX subunits and Hh signaling components and additionally inhibited expression of α-SMA and type I collagen, thereby preventing transformation to MFBs. UA inhibited TGF-ß1-induced activation of q-HSCs and their transformation by inhibiting expression of NOX subunits and the downstream Hh pathway.