Background: To systematically assess and compare the predictive value of the Ranson and Bedside Index of Severity in Acute Pancreatitis (BISAP) scoring systems for the severity and prognosis of acute pancreatitis (AP). Methods: PubMed, Embase, Cochrane Library, and Web of Science were systematically searched until February 15, 2023. Outcomes in this analysis included severity and prognosis [mortality, organ failure, pancreatic necrosis, and intensive care unit (ICU) admission]. The revised Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool was used to evaluate the quality of diagnostic accuracy studies. The threshold effect was evaluated for each outcome. The sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under the summary receiver operating characteristic (SROC) curve (AUC) as well as 95% confidence intervals (CI) were calculated. The DeLong test was used for AUC comparisons. For the outcome evaluated by over 9 studies, publication bias was assessed using the Deeks’ funnel plot asymmetry test. Results: Totally 17 studies of 5476 AP patients were included. For severity, the pooled sensitivity of the Ranson and BISAP was 0.95 (95%CI: 0.87, 0.98) and 0.67 (95%CI: 0.27, 0.92); the pooled specificity of the Ranson and BISAP was 0.74 (0.52, 0.88) and 0.95 (95%CI: 0.85, 0.98); the pooled AUC of the Ranson and BISAP was 0.95 (95%CI: 0.93, 0.97) and 0.94 (95%CI: 0.92, 0.96) (P = 0.480). For mortality, the pooled sensitivity of the Ranson and BISAP was 0.89 (95%CI: 0.73, 0.96) and 0.77 (95%CI: 0.58, 0.89); the pooled specificity of the Ranson and BISAP was 0.79 (95%CI: 0.68, 0.87) and 0.90 (95%CI: 0.86, 0.93); the pooled AUC of the Ranson and BISAP was 0.91 (95%CI: 0.88, 0.93) and 0.92 (95%CI: 0.90, 0.94) (P = 0.480). For organ failure, the pooled sensitivity of the Ranson and BISAP was 0.84 (95%CI: 0.76, 0.90) and 0.78 (95%CI: 0.60, 0.90); the pooled specificity of the Ranson and BISAP was 0.84 (95%CI: 0.63, 0.94) and 0.90 (95%CI: 0.72, 0.97); the pooled AUC of the Ranson and BISAP was 0.86 (95%CI: 0.82, 0.88) and 0.90 (95%CI: 0.87, 0.93) (P = 0.110). For pancreatic necrosis, the pooled sensitivity of the Ranson and BISAP was 0.63 (95%CI: 0.35, 0.84) and 0.63 (95%CI: 0.23, 0.90); the pooled specificity of the Ranson and BISAP was 0.90 (95%CI: 0.77, 0.96) and 0.93 (95%CI: 0.89, 0.96); the pooled AUC of the Ranson and BISAP was 0.87 (95%CI: 0.84, 0.90) and 0.93 (95%CI: 0.91, 0.95) (P = 0.001). For ICU admission, the pooled sensitivity of the Ranson and BISAP was 0.86 (95%CI: 0.77, 0.92) and 0.63 (95%CI: 0.52, 0.73); the pooled specificity of the Ranson and BISAP was 0.58 (95%CI: 0.55, 0.61) and 0.84 (95%CI: 0.81, 0.86); the pooled AUC of the Ranson and BISAP was 0.92 (95%CI: 0.81, 1.00) and 0.86 (95%CI: 0.67, 1.00) (P = 0.592). Conclusion: The Ranson score was an applicable tool for predicting severity and prognosis of AP patients with reliable diagnostic accuracy in resource and time-limited settings. Future large-scale studies are needed to verify the findings.

INTRODUCTION: Although the 9-minute mean withdrawal time (m-WT) is often reported to be associated with the optimal adenoma detection rate (ADR), no randomized trials of screening colonoscopy have confirmed the impact of a 9-minute m-WT on adenoma miss rate (AMR) and ADR. METHODS: A multicenter tandem trial was conducted in 11 centers. Seven hundred thirty-three asymptomatic participants were randomized to receive segmental tandem screening colonoscopy with a 9-minute withdrawal, followed by a 6-minute withdrawal (9-minute-first group, 9MF, n = 366) or vice versa (6-minute-first group, 6MF, n = 367). The primary outcome was the lesion-level AMR. RESULTS: The intention-to-treat analysis revealed that 9MF significantly reduced the lesion-level (14.5% vs 36.6%, P < 0.001) and participant-level AMR (10.9% vs 25.9%, P < 0.001), advanced adenoma miss rate (AAMR, 5.3% vs 46.9%, P = 0.002), multiple adenomas miss rate (20.7% vs 56.5%, P = 0.01), and high-risk adenomas miss rate (14.6% vs 39.5%, P = 0.01) of 6MF without compromising detection efficiency ( P = 0.79). In addition, a lower false-negative rate for adenomas ( P = 0.002) and high-risk adenomas ( P < 0.05), and a lower rate of shortening surveillance schedule ( P < 0.001) were also found in 9MF, accompanying with an improved ADR in the 9-minute vs 6-minute m-WT (42.3% vs 33.5%, P = 0.02). The independent inverse association between m-WT and AMR remained significant even after adjusting ADR, and meanwhile, 9-minute m-WT was identified as an independent protector for AMR and AAMR. DISCUSSION: In addition to increasing ADR, 9-minute m-WT also significantly reduces the AMR and AAMR of screening colonoscopy without compromising detection efficiency.

Objective. To evaluate the diagnostic value of gastrin-17 (G-17) and pepsinogen (PG) in gastric cancer (GC) screening in China, especially eastern China, and to determine the best diagnostic combination and threshold (cutoff values) to screen out patients who need gastroscopy. Methods. The serum concentrations of G-17 and pepsinogen I and II (PGI and PGII) in 834 patients were analyzed, and the PGI/PGII ratio (PGR) was calculated. According to pathological results, patients can be divided into chronic nonatrophic gastritis (NAG)/chronic atrophic gastritis (CAG)/intraepithelial neoplasia (IN)/GC groups. The differences in G-17, PG, and PGR in each group were analyzed, and their values in GC diagnosis were evaluated separately and in combination. Results. There were differences in serum G-17, PGII, and PGR among the four groups (NAG/CAG/IN/GC) ( ). In total, 54 GC cases were diagnosed, of which 50% were early GC. There was no significant difference in the PGI levels among the four groups ( ). NAG and CAG composed the chronic gastritis (CG) group. The G-17 and PGII levels in the IN and GC groups were higher than those in the CG group (both ), while the PGR levels were lower ( ). When distinguishing NAG from CAG, the best cutoff value for G-17 was 9.25 pmol/L, PGII was 7.06 μg/L, and PGR was 12.07. When distinguishing CG from IN, the best cutoff value for G-17 was 3.86 pmol/L, PGII was 11.92 μg/L, and PGR was 8.26. When distinguishing CG from GC, the best cutoff value for G-17 was 3.89 pmol/L, PGII was 9.16 μg/L, and PGR was 14.14. The sensitivity, specificity, accuracy, and positive and negative predictive values of G-17/PGII/PGR for GC diagnosis were 83.3%/70.4%/79.6%, 51.8%/56.3%/47.8%, 53.8%/57.2%/49.9%, 10.7%/10.9%/9.6%, and 97.8%/96.5%/97.1%, respectively. The sensitivity, specificity, accuracy, and positive predictive and negative predictive values of PGII/G-17 vs. PGR/G-17 vs. PGR/PGII in the diagnosis of GC were 63.0% vs. 70.4% vs. 64.8%, 70.5% vs. 70.1% vs. 60.4%, 70.0% vs. 70.1% vs. 60.7%, 12.9% vs. 14.0% vs. 10.2%, and 96.5% vs. 97.2% vs. 96.1%, respectively. Conclusion. The PGII and G-17 levels in patients with gastric IN and GC were significantly increased, while the serum PGR level was significantly decreased. Serological detection is effective for screening GC. The combination of different markers can improve the diagnostic efficiency. The highest diagnostic accuracy was G-17 combined with PGR, and the best cutoff values were and .

Acute pancreatitis (AP) is characterized by autodigestion of the pancreas, and some patients may rapidly progress to systemic inflammation, pancreatic necrosis, and multi-organ failure. Numerous studies have detailed the bidirectional communication networks between the pancreas and the intestinal microbiota, as well as its metabolites. Such crosstalk affects the progression of AP and recovery through intestinal barrier disruption. Furthermore, advances in experimental research and clinical studies have indicated that gut microorganisms exhibit distinct alterations in response to different levels of severity and etiologies of AP. This information has greatly expanded our knowledge of the role of the gut microflora and microbial metabolites in the pathology of disease and has reinforced the basis of therapeutic approaches that target candidate intestinal microbiota. In this review, we aim to provide an overview of the composition and diversity of the gut microbial community, to highlight the candidate bacteria and microbiota-derived metabolites responsible for AP, and to elucidate their interactions with and regulation of immune-relevant receptors in intestinal epithelial cells (IECs) in the host. Future research should focus on identifying and characterizing AP-associated bacterial strains, elucidating their distinct pathogenic mechanisms across different etiologies and stages of AP, and leveraging these insights to develop preventive and therapeutic strategies.

Introduction: Acute pancreatitis (AP) is an inflammatory disease with very poor outcomes. However, the order of induction and coordinated interactions of systemic inflammatory response syndrome (SIRS) and compensatory anti-inflammatory response syndrome (CARS) and the potential mechanisms in AP are still unclear.Methods: An integrative analysis was performed based on transcripts of blood from patients with different severity levels of AP (GSE194331), as well as impaired lung (GSE151572), liver (GSE151927) and pancreas (GSE65146) samples from an AP experimental model to identify inflammatory signals and immune response-associated susceptibility genes. An AP animal model was established in wild-type (WT) mice and Tlr2-deficient mice by repeated intraperitoneal injection of cerulein. Serum lipase and amylase, pancreas impairment and neutrophil infiltration were evaluated to assess the effects of Tlr2 in vivo.Results: The numbers of anti-inflammatory response-related cells, such as M2 macrophages (P = 3.2 × 10^–3), were increased with worsening AP progression, while the numbers of pro-inflammatory response-related cells, such as neutrophils (P = 3.0 × 10^–8), also increased. Then, 10 immune-related AP susceptibility genes (SOSC3, ITGAM, CAMP, FPR1, IL1R1, TLR2, S100A8/9, HK3 and MMP9) were identified. Finally, compared with WT mice, Tlr2-deficient mice exhibited not only significantly reduced serum lipase and amylase levels after cerulein induction but also alleviated pancreatic inflammation and neutrophil accumulation.Discussion: In summary, we discovered SIRS and CARS were stimulated in parallel, not activated consecutively. In addition, among the novel susceptibility genes, TLR2might be a novel therapeutic target that mediates dysregulation of inflammatory responses during AP progression.