Necrosis In Acute Pancreatitis Research Articles

Intestinal microflora and metabolites affect the progression of acute pancreatitis (AP)

Specific intestinal metabolites are closely associated with the classification, severity, and necrosis of acute pancreatitis (AP) and provide novel insights for in-depth clinical investigations. In this study, the gut microbiota and metabolites of 49 AP patients at different treatment stages and severities were analysed via 16S rDNA sequencing and untargeted metabolomics to investigate the trends in gut microbiota composition and metabolome profiles observed in patients with severe AP. These findings revealed an imbalance in intestinal flora homeostasis among AP patients characterized by a decrease in probiotics and an increase in opportunistic pathogens, which leads to damage to the intestinal mucosal barrier through reduced short-chain fatty acid (SCFA) secretion and disruption of the intestinal epithelium. This dysbiosis influences energy metabolism, anti-inflammatory responses, and immune regulation, and these results highlight significant differences in energy metabolism pathways. These findings suggest that the differential composition of intestinal flora, along with alterations in intestinal metabolites and metabolic pathways, contribute to the compromised integrity of the intestinal mucosal barrier and disturbances in energy metabolism in patients with severe AP.

Pharmacological Inhibition of Phosphoglycerate Kinase 1 Reduces OxiDative Stress and Restores Impaired Autophagy in Experimental Acute Pancreatitis.

Damage to pancreatic acinar cells (PAC) and intracellular metabolic disturbances play crucial roles in pancreatic necrosis during acute pancreatitis (AP). Phosphoglycerate kinase 1 (PGK1) is a crucial catalytic enzyme in glycolysis. However, the impact of PGK1-involving glycolysis in regulating metabolic necrosis in AP is unclear. Transcriptome analysis of pancreatic tissues revealed significant changes in the glycolysis pathway and PGK1 which positively correlated with the inflammatory response and oxidative stress injury in AP mice. Furthermore, we observed a substantial increase in PGK1 expression in damaged PAC, positively correlating with PAC necrosis. Treatment with NG52, a specific PGK1 inhibitor, ameliorated pancreatic necrosis, inflammatory damage, and oxidative stress. Transcriptomic data before and after NG52 treatment along with the Programmed Cell Death database confirmed that NG52 protected against PAC damage by rescuing impaired autophagy in AP. Additionally, the protective effect of NG52 was validated following pancreatic duct ligation. These findings underscore the involvement of PGK1 in AP pathogenesis, highlighting that PGK1 inhibition can mitigate AP-induced pancreatic necrosis, attenuate inflammatory and oxidative stress injury, and rescue impaired autophagy. Thus, the study findings suggest a promising interventional target for pancreatic necrosis, offering novel strategies for therapeutic approaches to clinical AP.

ПЕРФУЗИОННАЯ КОМПЬЮТЕРНАЯ ТОМОГРАФИЯ – НОВЫЕ ГОРИЗОНТЫ В ДИАГНОСТИКЕ ЗАБОЛЕВАНИЙ ПОДЖЕЛУДОЧНОЙ ЖЕЛЕЗЫ

Abstract. Introduction. According to the World Health Organization, the most common disease of the pancreas is acute pancreatitis, which can lead to the development of pancreatic necrosis. In this regard, early diagnosis and assessment of the pancreatic necrosis risk development are of paramount importance for choosing adequate treatment approaches and improving outcomes for patients. Radiological research methods have become the “gold” standard in clinical practice for the primary diagnosis of pancreatic diseases. Contrast-enhanced computed tomography has traditionally been used to visualize the pancreas and assess the extent of inflammation and necrotic changes. However, standard computed tomography has limitations in assessing tissue perfusion, which is an important aspect of the pathophysiology of acute pancreatitis. Perfusion computed tomography of the pancreas has become a colossal breakthrough in radiation imaging, has become widespread as a method that allows the quantitative assessment of blood supply to the pancreas, including information about microcirculation, and it can be used for the early detection of ischemic changes that precede tissue necrosis in the pancreas. Aim. To study the capabilities of perfusion computed tomography and computed tomography angiography of the pancreas for evaluating the area of pancreatic necrosis in acute pancreatitis, with the aim of improving diagnosis and planning treatment measures to minimize the consequences and increase patient survival. Materials and Methods. A single-center examination was carried out on 42 patients (18 women, 24 men, mean age 38±2 years) with suspected acute pancreatitis. All patients underwent perfusion computed tomography within the first 3 days; over the next 3-5 days, computed tomography angiography of the pancreas was performed with bolus intravenous contrast to confirm the development of necrotic changes. Results and Discussion. After performing perfusion computed tomography within the first 3 days from the onset of symptoms, areas of ischemic damage to the pancreas tissue were identified in 16 (38.1%) out of 42 patients. After computed tomography angiography, the development of necrotic changes was confirmed in 7 patients (16.7%). The localization of the necrosis zone detected in computed tomography coincided with the ischemic zones on the color hemodynamic maps of perfusion computed tomography.

Peak Serum Creatinine as a Biomarker of Pancreatic Necrosis in Acute Pancreatitis: A Cross-Sectional Study

Pancreatitis is the inflammation of the pancreas. Pancreatitis can result in pancreatic necrosis which may lead to significant morbidity and mortality. It is possible to predict pancreatic necrosis and organ dysfunction using many biochemical indicators and markers. Peak serum creatinine has been identified as one of such useful markers to predict pancreatic necrosis. Objective: To find the diagnostic accuracy of elevated peak serum creatinine as a predictor of pancreatic necrosis in patients with acute pancreatitis taking the contrast-enhanced computed tomogram scan (CECT) as the gold standard and to establish the degree of agreement between the two clinical tests. Methods: A cross-sectional, analytical study that was carried out at the Department of Surgery, Benazir Bhutto Hospital, Rawalpindi from January 2020 to January 2023. 150 patients diagnosed as having pancreatitis were enrolled in the study. Peak serum creatinine at 48 hours > 1.8 mg/dl was labeled as a predictor of pancreatic necrosis. Contrast-enhanced computed tomogram scan was done within 96 hours of admission. The pancreatic necrosis suggested by raised serum creatinine was confirmed by CECT. The diagnostic accuracy of peak serum creatinine and the degree of agreement between the two modalities was calculated. The Kappa coefficient was used to calculate the strength of agreement. Results: The results show that Peak serum creatinine has a sensitivity of 45.5%, specificity of 97.35%, PPV of 85.0 %, NPV of 93.8 %, and accuracy of 84.6%. This study found that the degree of agreement between raised peak serum creatinine levels and CECT to predict pancreatic necrosis was 84.7% with a “Kappa coefficient” of 0.51. Consequently, the null hypothesis was rejected in light of these findings. Conclusions: It was concluded that elevated serum creatinine (SCr >1.8 mg/dl) at 48 h of admission can be used as a predictor of pancreatic necrosis in patients with acute pancreatitis.

The TRIM28/miR133a/CD47 axis acts as a potential therapeutic target in pancreatic necrosis by impairing efferocytosis

Efferocytosis, the clearance of apoptotic cells by macrophages, plays a crucial role in inflammatory responses and effectively prevents secondary necrosis. However, the mechanisms underlying efferocytosis in acute pancreatitis (AP) remain unclear. In this study, we demonstrated the presence of efferocytosis in injured human and mouse pancreatic tissues. We also observed significant upregulation of CD47, an efferocytosis-related the "do not eat me" molecule in injured acinar cells. Subsequently, we used CRISPR-Cas9 gene editing, anti-adeno-associated virus (AAV) gene modification, and anti-CD47 antibody to investigate the potential therapeutic role of AP. CD47 expression was negatively regulated by upstream miR133a, which is controlled by the transcription factor TRIM28. To further investigate the regulation of efferocytosis and reduction of pancreatic necrosis in AP, we used miR-133a-agomir and pancreas-specific AAV-shTRIM28 to modulate CD47 expression. Our findings confirmed that CD47-mediated efferocytosis is critical for preventing pancreatic necrosis and suggest that targeting the TRIM28-miR133a-CD47 axis is clinically relevant for the treatment of AP.

Neutrophil CD64 index as a new early predictive biomarker for infected pancreatic necrosis in acute pancreatitis

ObjectiveInfectious pancreatic necrosis (IPN) is a serious complication of acute pancreatitis, and early recognition and timely intervention are the keys to improving clinical outcomes. The purpose of this study was to investigate the predictive capacity of the neutrophil CD64 index (nCD64 index) on IPN in patients with acute pancreatitisMethodsThis study comprises two independent cohorts: the training cohort consisted of 202 patients from Hunan Provincial People's Hospital, and the validation cohort consisted of 100 patients from Changsha Central Hospital. Peripheral blood samples were collected on the day of admission and on the 3rd, 5th, 7th, and 10th days of hospitalization, and the nCD64 index was detected by flow cytometry. Additionally, relevant clinical characteristics and laboratory biomarkers were collected and analyzed.ResultsWe observed that nCD64 index on admission was significantly higher in the IPN group than Non-IPN group (p < 0.001). In the training cohort, a higher occurrence rate of IPN was observed in the high nCD64 index group compared to the moderate and low nCD64 index group (p < 0.001). Further analysis showed that nCD64 index was significant positive correlated with the incidence rate of IPN (p < 0.001, correlation coefficient = 0.972). Furthermore, logistic regression analysis showed that high expression of the nCD64 index on admission was a risk factor for the occurrence of IPN (OR = 2.971, p = 0.038). We further found that the nCD64 index of IPN patients was significantly higher than the Non-IPN patients on the days 1, 3, and 5 after admission, and the nCD64 index of IPN patients before and after the onset (p < 0.05). At the same time, this study revealed that the nCD64 index on admission showed good predictive efficacy for IPN (AUC = 0.859, sensitivity = 80.8%, specificity = 87.5%), which was comparable to APACHE II score. And this finding was further validated in an independent cohort of 100 participants (AUC = 0.919, Sensitivity = 100.0%, Specificity = 76.6%).ConclusionThis study demonstrated the clinical value of nCD64 index in patients with IPN patients for the first time through two independent cohort studies. The nCD64 index can be used as an early prediction and risk assessment tool for the occurrence of IPN, contributing to the improvement of patient outcomes and efficiency of medical resource allocation.

Prognostic significance of organ failure and infected pancreatic necrosis in acute pancreatitis: An updated systematic review and meta-analysis.

In patients with acute pancreatitis (AP), minimally invasive treatment and the step-up approach have been widely used to deal with infected pancreatic necrosis (IPN) in the last decade. It is unclear whether IPN has become a less important determinant of mortality relative to organ failure (OF). We aimed to statistically aggregate recent evidence from published studies to determine the relative importance of IPN and OF as determinants of mortality in patients with AP (PROSPERO: CRD42020176989). Relevant studies were sourced from MEDLINE and EMBASE databases. Relative risk (RR) or weighted mean difference (WMD)was analyzed as outcomes. A two-sided P value of less than 0.05 was regarded as statistical significance. Forty-three studies comprising 11 601 patients with AP were included. The mortality was 28% for OF patients and 24% for those with IPN. Patients with OF without IPN had a significantly higher risk of mortality compared to those with IPN but without OF (RR 3.72, P < 0.0001). However, patients with both OF and IPN faced the highest risk of mortality. Additionally, IPN increased length of stay in hospital for OF patients (WMD 28.75, P = 0.032). Though IPN remains a significant concern, which leads to increased morbidity and longer hospital stay, it is a less critical mortality determinant compared to OF in AP.

Risk factors for pancreatic necrosis in acute pancreatitis in obese patients

Background. Acute pancreatitis is an aseptic inflammation of the pancreas with diverse complications and further development of necrosis of the gland, parapancreatic tissue and possible addition of secondary infection. A significant number of biochemical markers that can be predictors of pancreatitis complications are still being researched. However, most of them are expensive and their indicators are increased only in the first 24–48 hours after the onset of the disease, so they are not used in daily clinical routine. The purpose of this study is to evaluate the factors that indicate an elevated risk of necrosis in acute severe pancreatitis. Materials and methods. A retrospective analysis of 80 patients with acute pancreatitis was performed via creation of a multivariate logistic regression model. Results. The dependence of the risk of pancreatic necrosis on the following factor signs was found: lipase at the onset of the disease (cut-off value = 599.6 U/l, area under the receiver operating characteristic curve (АUС) = 0.72 (95% confidence interval (СІ) 0.57–0.88)), severity of the disease, fibrinogen on day 3 of the disease (cut-off value = 9.7, АUС = 0.65 (95% СІ 0.48–0.81)), C-reactive protein (cut-off value = 175.7 mg/L, AUC = 0.70 (95% CI 0.54–0.86)), and intra-abdominal mean capillary perfusion pressure on the first day of the disease (cut-off value ≤ 63.3 mm Hg, АUС = 0.88 (95% СІ 0.77–0.99)). The autopsy results revealed the presence of necrosis and microthrombosis of the pancreas. Conclusions. Factors that may indicate an increased risk of pancreatic necrosis were high levels of lipase, fibrinogen on the third day of the disease, C-reactive protein, decreased intra-abdominal mean capillary perfusion pressure, severity of the disease, and the presence of portosplenomesentric thrombosis.

Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis

Bile acids are altered and associated with prognosis in patients with acute pancreatitis (AP). Here, we conduct targeted metabolomic analyses to detect bile acids changes in patients during the acute (n= 326) and the recovery (n= 133) phases of AP, as well as in healthy controls (n= 60). Chenodeoxycholic acid (CDCA) decreases in the acute phase, increases in the recovery phase, and is associated with pancreatic necrosis. CDCA and its derivative obeticholic acid exhibit a protective effect against acinar cell injury invitro and pancreatic necrosis in murine models, and RNA sequencing reveals that the oxidative phosphorylation pathway is mainly involved. Moreover, we find that overexpression of farnesoid X receptor (FXR, CDCA receptor) inhibits pancreatic necrosis, and interfering expression of FXR exhibits an opposite phenotype in mice. Our results possibly suggest that targeting CDCA is a potential strategy for the treatment of acinar cell necrosis in AP, but further verification is needed.

HDL inhibits pancreatic acinar cell NLRP3 inflammasome activation and protect against acinar cell pyroptosis in acute pancreatitis

Background and PurposeRecent clinical studies have shown that serum high-density lipoprotein (HDL) levels are correlated with acute pancreatitis (AP) severity. We aimed to investigate the role of HDL in pancreatic necrosis in AP. Experimental approachApoA-I is the main constitution and function component of HDL. The roles of healthy human-derived HDL and apoA-I mimic peptide D4F were demonstrated in AP models in vivo and in vitro. Constitutive Apoa1 genetic inhibition on AP severity, especially pancreatic necrosis was assessed in both caerulein and sodium taurocholate induced mouse AP models. In addition, constitutive (Casp1-/-) and acinar cell conditional (Pdx1CreNlrp3Δ/Δ and Pdx1CreGsdmdΔ/Δ) mice were used to explore the effects of HDL on acinar cell pyroptosis in AP. Key resultsApoa1 knockout dramatically aggravated pancreatic necrosis. Human-derived HDL protected against acinar cell death in vivo and in vitro. We found that mimic peptide D4F also protected against AP very well. Constitutive Casp1 or acinar cell-conditional Nlrp3 and Gsdmd genetic inhibition could counteract the protective effects of HDL, implying HDL may exert beneficial effects on AP through inhibiting acinar cell pyroptosis. Conclusion and implicationsThis work demonstrates the protective role of HDL and apoA-I in AP pathology, potentially driven by the inhibition of NLRP3 inflammasome signaling and acinar cell pyroptosis. Mimic peptides have promise as specific therapies for AP.

Acute Esophageal Necrosis in Acute Pancreatitis-Report of a Case and Endoscopic and Clinical Perspective.

Esophageal stroke, also known as acute esophageal necrosis or Gurvits syndrome, is an entity that has gained more and more recognition in the last two decades. It is also named "black esophagus" because of striking black discoloration of the esophageal mucosa, with an abrupt transition to normal mucosa at the gastroesophageal junction. Its most common clinical presentation is represented by upper gastrointestinal bleeding and esophagogastroduodenoscopy is the main diagnostic tool. Among the etiopathogenetic and multiple predisposing factors described are hypovolemia, shock state, ischemia, congestive heart failure, acute renal failure, infections, trauma, and diabetes mellitus. Current management of this condition consists of treating the underlying pathology, nil per os, and antacid administration in uncomplicated cases. Although most of the cases have favorable prognosis, complications such as pneumomediastinum or esophageal stricture may occur and fatal cases are a consequence of underlying comorbidities.

Identification of early predictors for infected necrosis in acute pancreatitis

BackgroundIn acute pancreatitis, secondary infection of pancreatic necrosis is a complication that mostly necessitates interventional therapy. A reliable prediction of infected necrotizing pancreatitis would enable an early identification of patients at risk, which however, is not possible yet.MethodsThis study aims to identify parameters that are useful for the prediction of infected necrosis and to develop a prediction model for early detection. We conducted a retrospective analysis from the hospital information and reimbursement data system and screened 705 patients hospitalized with diagnosis of acute pancreatitis who underwent contrast-enhanced computed tomography and additional diagnostic puncture or drainage of necrotic collections. Both clinical and laboratory parameters were analyzed for an association with a microbiologically confirmed infected pancreatic necrosis. A prediction model was developed using a logistic regression analysis with stepwise inclusion of significant variables. The model quality was tested by receiver operating characteristics analysis and compared to single parameters and APACHE II score.ResultsWe identified a total of 89 patients with necrotizing pancreatitis, diagnosed by computed tomography, who additionally received biopsy or drainage. Out of these, 59 individuals had an infected necrosis. Eleven parameters showed a significant association with an infection including C-reactive protein, albumin, creatinine, and alcoholic etiology, which were independent variables in a predictive model. This model showed an area under the curve of 0.819, a sensitivity of 0.692 (95%-CI [0.547–0.809]), and a specificity of 0.840 (95%-CI [0.631–0.947]), outperforming single laboratory markers and APACHE II score. Even in cases of missing values predictability was reliable.ConclusionA model consisting of a few single blood parameters and etiology of pancreatitis might help for differentiation between infected and non-infected pancreatic necrosis and assist medical therapy in acute necrotizing pancreatitis.

Preexisting diabetes, serum calcium and D-dimer levels as predictable risk factors for pancreatic necrosis of patients with acute pancreatitis: a retrospective study

ABSTRACT Background Some individuals with acute pancreatitis (AP) suffer from pancreatic necrosis. Diabetes affects the severity of AP, but whether diabetes influences pancreatic necrosis is unclear. This study aims to investigate the clinical characteristics of AP patients with and without diabetes as well as analyze the risk factors of pancreatic necrosis. Research design and methods A total of 625 AP patients participated in the study. Clinical and laboratory data were retrieved. Multivariate logistic regression analysis was used to identify the risk factors for pancreatic necrosis. ROC curves assess the accuracy of indicators for predicting pancreatic necrosis in AP. Results AP patients with diabetes had high BMI, CTSI scores, pancreatitis severity, WBC, neutrophil, CRP, triacylglycerols and glucose levels. Diabetes, serum calcium and D-dimer were independent risk factors for pancreatic necrosis. Pancreatic necrosis in diabetes patients is also associated with sex and age. D-dimer is a better predictor of pancreatic necrosis in AP patients than serum calcium. Conclusions Diabetic patients are more likely to suffer severe AP. Serum calcium and D-dimer are independent predictors for pancreatic necrosis. Furthermore, low serum calcium, high D-dimer levels, younger age and female sex are independent risk factors for pancreatic necrosis in AP patients with diabetes.

Radiomics and Its Applications and Progress in Pancreatitis: A Current State of the Art Review

Radiomics involves high-throughput extraction and analysis of quantitative information from medical images. Since it was proposed in 2012, there are some publications on the application of radiomics for (1) predicting recurrent acute pancreatitis (RAP), clinical severity of acute pancreatitis (AP), and extrapancreatic necrosis in AP; (2) differentiating mass-forming chronic pancreatitis (MFCP) from pancreatic ductal adenocarcinoma (PDAC), focal autoimmune pancreatitis (AIP) from PDAC, and functional abdominal pain (functional gastrointestinal diseases) from RAP and chronic pancreatitis (CP); and (3) identifying CP and normal pancreas, and CP risk factors and complications. In this review, we aim to systematically summarize the applications and progress of radiomics in pancreatitis and it associated situations, so as to provide reference for related research.

The Role of Perfusion Computed Tomography as a Predictor of Pancreatic Necrosis in Acute Pancreatitis

The article analyzes the data obtained as a result of the use of imaging methods in 35 patients with a new coronavirus infection who were treated in the infectious diseases department of the Surgut Regional Clinical Hospital. In the course of treatment in this group of patients, the appearance of symptoms of acute pancreatitis was noted. The criteria for inclusion in the study, in addition to the presence of a coronavirus infection confirmed by PCR, were a laboratory-detected increase in blood amylase and lipase. In the infectious diseases hospital, patients underwent perfusion computed tomography (PCT) when the first symptoms of acute pancreatitis appeared. Subsequently, in accordance with national recommendations, the entire group of patients underwent multislice computed tomography (MSCT) with bolus intravenous contrast on days 3–5. As a result of the complex of imaging research methods, 40 % (14 patients out of 35) showed a decrease in perfusion parameters characterizing the development of ischemic lesions of the pancreatic parenchyma. Later, in 11.4 % (in 4 patients out of 14), this was confirmed by MSCT with bolus intravenous contrast enhancement and was expressed as the formation of a site of destruction of the pancreatic parenchyma. In 60 % of cases (35 in 21 patients), there was no decrease in perfusion parameters during PCT, which was also later confirmed by contrast-enhanced computed tomography. Thus, we can conclude that perfusion computed tomography can play the role of an effective predictor of the development of necrotic changes in the pancreatic parenchyma in patients with acute pancreatitis that developed against the background of a new coronavirus infection.

MiR-325-3p Alleviates Acute Pancreatitis via Targeting RIPK3

Acute pancreatitis (AP) is an acute inflammatory disease that can lead to death. Mir-325-3p is strongly and abnormally expressed in many diseases, necessitating exploration of its function and mechanism in AP. Blood samples from AP patients and mice were analyzed. The expression levels of miR-325-3p in AP patients and mouse were detected. Whether miR-325-3p targets RIPK3 gene was predicted by TargetScan online database and dual luciferase reporter assay. In vitro experiments verified the effect of miR-325-3p overexpression on caerulein-induced MPC83 pancreatic acinar cancer cell line. In vivo experiments verified the effect of overexpression of miR-325-3p on the disease degree of pancreatic tissues in AP mice. Analysis of blood samples from AP patients and experiments in mice demonstrated that expression of miR-325-3p was significantly reduced during the process of AP in humans and mice. Predicted using the TargetScan online database and through dual luciferase reporter assay detection, miR-325-3p directly targets the RIPK3 gene. In vitro experiments revealed that overexpression of miR-325-3p reversed caerulein-induced apoptosis and necroptosis in MPC83 pancreatic acinar cancer cell line. We used Z-VAD-FMK to assess necroptosis and demonstrated that miR-325-3p targets necroptosis to reduce cell damage. In subsequent experiments in mice, we verified that overexpression of miR-325-3p reduces inflammation, edema, hemorrhage, and necrosis in acute pancreatitis. Characteristic western blot, immunohistochemistry, and transmission electron microscopy results revealed that overexpression of miR-325-3p reduces the severity of acute pancreatitis by inhibiting pancreatic necroptosis in AP mice. The current research results indicate that miR-325-3p directly targets RIPK3 and exerts a protective role in mouse AP. Necroptosis is still the primary mechanism of RIPK3 regulation. MiR-325-3p inhibits acute pancreatitis by targeting RIPK3-dependent necroptosis, which may represent a novel treatment method for acute pancreatitis.

Accuracy of a CT density threshold enhancement to identify pancreatic parenchyma necrosis in acute pancreatitis during the first week

PurposeThe purpose of this study was to identify attenuation threshold value on computed tomography (CT) that allowed discriminating between interstitial edematous pancreatitis (IEP) and necrotizing pancreatitis (NP) in patients with acute pancreatitis during the first week of the disease and evaluate interobserver reproducibility for the diagnosis of acute pancreatitis category. Materials and methodsPatients with acute pancreatitis who underwent CT examination of the abdomen between March 2015 and December 2019 were retrospectively included. Actual diagnosis of IEP or NP was based on final clinical report, follow-up evaluation, and complications. Six regions of interest were manually placed in the pancreatic gland and peripancreatic fat, and differences in CT attenuation values before contrast injection and during the portal venous phase of enhancement were computed. Performance in the diagnosis of AP category was evaluated using receiver operating characteristic analysis. Interobserver agreement was estimated by the intraclass correlation coefficient (ICC) and Bland Altman analysis was used to estimate reproducibility between pairs of observers. ResultsSixty-six patients with NP (46 men, 20 women; mean age, 55 ± 17 [SD] years; age range: 20-89 years) and 70 patients with IEP (39 men, 31 women; mean age, 54 ± 18 [SD] years; age range: 21–87 years) were included. An enhancement value less than 30 Hounsfield units (HU) in the pancreatic gland during the portal phase compared to non-contrast phase, yielded 90.9% sensitivity (60/66; 95% CI: 81.3–96.6), 94.3% specificity (66/70; 95% CI: 86.0–98.4) and an area under curve of 0.958 (95% CI: 0.919–0.996) for the diagnosis of NP versus IEP. Interobserver reproducibility for pancreas enhancement was good using Bland Altman plot and ICC was excellent for pancreatic gland analysis (ICC 0.978; 95% CI: 0.961–0.988) but poor or moderate (ICC ≤0.634) regarding peripancreatic fat necrosis. ConclusionBy using a pancreas enhancement threshold value of 30 HU, CT is accurate and reproducible for the diagnosis of NP during the first week of the disease.

C-reactive protein/albumin and ferritin as predictive markers for severity and mortality in patients with acute pancreatitis.

Acute pancreatitis (AP) is a life-threatening gastrointestinal disease with high mortality and morbidity. However, scoring systems or prognostic indicators for assessing AP are cumbersome and expensive, and have not proved accurately to predict outcomes. We conducted a study with the aim of evaluating the predictive accuracy of C-reactive protein (CRP)/albumin and ferritin regarding outcomes in patients with AP. A prospective study was conducted in a tertiary care referral centre in Odisha from March 2020 to April 2021. A total of 116 consecutive patients of AP were enrolled in the study. CTSI, APACHE II, ferritin, and the CRP/albumin ratio were calculated. The mean age of patients was 40.63 ±5.49 years with a male predominance (73%). Alcohol was most common aetiology (46.6%), and the overall mortality was 18%. Mean ferritin and the CRP/albumin ratio were also significantly higher in severe AP as compared to moderately severe AP and mild AP (p < 0.001). The CRP/albumin ratio (AOR = 1.26, 95% CI: 1.02-1.56, p = 0.02) was found to be independent predictor of mortality in Cox regression multivariate analysis and had the highest AUC for predicting the severity of acute pancreatitis. Serum ferritin had higher AUC (0.89, 0.83-0.91, p < 0.001) for the development of necrosis in acute pancreatitis, but it failed to be proven as an independent predictor of mortality. CRP/albumin is a simple, cheap, and easily available biomarker predicting the development of severe pancreatitis, and it was found to be an independent predictor of mortality in AP.

Magnetic Resonance Imaging-Based Radiomics Models to Predict Early Extrapancreatic Necrosis in Acute Pancreatitis.

The aim of the study was to investigate radiomics models based on magnetic resonance imaging (MRI) for predicting early extrapancreatic necrosis (EXPN) in acute pancreatitis. Radiomics features were extracted from T2-weighted images of extrapancreatic collections and late arterial-phase images of the pancreatic parenchyma for 135 enrolled patients (94 in the primary cohort, including 47 EXPN patients and 41 in the validation cohort, including 20 EXPN patients). The optimal features after dimension reduction were used for radiomics modeling through a support vector machine. A clinical model, the MR severity index score, and extrapancreatic inflammation on MRI were evaluated. Twelve optimal features from the extrapancreatic collection images and 10 from the pancreatic parenchyma images were selected for modeling. The pancreatic parenchyma-based and extrapancreatic collection-based radiomics models showed good predictive accuracy in both the training and validation cohorts. The areas under the curve of the extrapancreatic collection-based radiomics model (0.969 and 0.976) were consistent with those of the pancreatic parenchyma-based model (0.931 and 0.921) for both cohorts and better than those of the clinical model and imaging scores for both cohorts. The MRI-based radiomics models of both the extrapancreatic collections and the pancreatic parenchyma had excellent predictive performance for early EXPN.

Blood sugar level as an indicator of necrosis in patients of gallstone induced acute pancreatitis

Acute necrotizing pancreatitis is a severe disease with more mortality as compared to interstitial pancreatitis. A screening test which is readily available for the detection of pancreatic necrosis would aid a lot in the early management of gallstone induced acute necrotizing pancreatitis. This study was conducted in patients of gallstone induced acute pancreatitis presenting to the emergency department of Indira Gandhi medical college, Shimla, Himachal Pradesh. 61 patients were included in this study. Initial blood sugar levels were compared to the occurrence of pancreatic necrosis. We concluded that normal or low blood sugar level reflects absence of necrosis in acute pancreatitis. Therefore, it may be used to rule out the possibility of acute necrotizing pancreatitis. This will help a lot in management of such patients in areas where resources are limited and scarce.