Acute Pancreatitis Research Articles

Sex differences in cardiovascular outcomes in patients with acute pancreatitis.

The risk of cardiovascular disease increases in patients with acute pancreatitis. However, it remains unknown whether this increase varies between males and females. To assess sex differences in cardiovascular outcomes among acute pancreatitis patients during long-term follow-up. Participants were recruited from the UK-biobank, which is a population-based cohort study consisting of 502 368 individuals aged 40-69 years old. Cardiovascular outcomes were defined as major cardiovascular and cerebrovascular adverse events (MACCE), encompassing all-cause death, myocardial infarction, and stroke. We compared sex difference in MACCE incidence using incidence rate per 1,000 person-years. The association between sex and MACCE risk was assessed using Cox proportional hazards models and win-ratio method, adjusted for demographic, lifestyle, metabolic factors and medication use. A total of 1371 participants with acute pancreatitis were included, 42.5% were male. Over a median follow-up of 13.9 years, 226 MACCE cases occurred. The incidence rate of MACCE for male was 16.44, compared to 9.80 in female. Multivariate Cox regression analysis indicated a higher risk of MACCE in male compared to female (HR 1.80 [95% CI 1.36-2.38]). Adjusted HR for all-cause mortality, myocardial infarction, and stroke were 1.49, 2.75, and 1.67, respectively. The adjusted win ratio by inverse probability of treatment weighting was 0.55 (P <0.001), suggesting a worse outcome in male acute pancreatitis patients. Male experienced more adverse cardiovascular outcomes than female in the long follow-up after acute pancreatitis, suggesting a need for sex-specific management strategies in acute pancreatitis patients.

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.

Efficacy of integrated traditional Chinese and western medicine in managing mild-moderate acute pancreatitis: a real-world clinical perspective analysis

BackgroundGiven the prevalent utilization of integrated traditional Chinese and western medicine (ITCWM) in the management of acute pancreatitis, the majority of studies have concentrated on severe cases, lacking robust evidence-based medical research. Real-world investigations can provide an objective assessment of the clinical effectiveness of combining traditional Chinese medicine with western medicine. Consequently, relying on real-world research, we intend to evaluate the clinical efficacy and safety of the combined approach in treating mild to moderate acute pancreatitis.MethodsA total of 563 AP patients from Henan Central Hospital were collected from January 2019 to October 2023. A propensity score matching (PSM) analysis was conducted to evaluate the clinical efficacy of traditional Chinese medicine (TCM) in treating mild to moderate acute pancreatitis. Patients were divided into a control group (61 cases) and an integrated traditional Chinese and Western medicine (ITCWM) group (120 cases). To further assess the clinical efficacy of TCM enema in the treatment of mild to moderate acute pancreatitis, PSM analysis was conducted across three groups. The patients were categorized into a control group (n = 49), an oral TCM treatment group (OCM group, n = 274), and an oral TCM plus enema treatment group (OCM+E group, n = 131). Logistic regression was used to analyze factors after treatment in each group, and the Kaplan-Meier method compared symptom duration in each group.ResultsCompared with the control group, the ITCWM group significantly decreased C-reactive protein (CRP, mg/L) (17.8 [1.2–59.5] vs. 8.0 [3.3–33.5], P = 0.022), shortened the duration of abdominal distension, abdominal pain, nausea and bitter taste symptoms (P &amp;lt; 0.05), and shortened the length of hospital stay (median 19.0 and 11.5 days, respectively, P = 0.001); Compared with the other two groups, the neutrophil percentage (NEUT%) was lower (74.1 vs. 61.9 vs. 59.5, P &amp;lt; 0.05) and serum prealbumin (PA, mg/L) was higher (116.0 vs. 184.4 vs. 220.0, P &amp;lt; 0.05), the length of hospitalization (days) was shortened (19.0 vs.12.0 vs.10.0, P &amp;lt; 0.05) in the OCM+E group.ConclusionThe combination of traditional Chinese medicine and modern medicine has been shown to effectively decrease inflammatory indicators in patients with mild to moderate acute pancreatitis, leading to a reduction in symptom duration and hospitalization period, as well as promoting disease recovery. Notably, the use of traditional Chinese medicine in conjunction with enema therapy yields more pronounced benefits.

MiR-103–3p attenuates liver injury with severe acute pancreatitis by inhibiting pyroptosis through miR-103–3p/NLRP1 axis

BackgroundSevere acute pancreatitis (SAP) is a common digestive system disorder in clinical practice, and it is often associated with liver damage in patients with severe acute pancreatitis. Several studies have indicated that pyroptosis plays a role in liver damage following severe acute pancreatitis (SAP). However, the precise mechanisms remain unclear. This study aims to elucidate the association and specific mechanisms between liver injury following SAP and pyroptosis, providing theoretical support for research on SAP-induced liver injury. MethodsA rat model of SAP with concomitant liver injury was successfully established. The expression levels of miR-103–3p across different liver tissue groups were quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Bioinformatic analyses and dual-luciferase reporter assays confirmed that NLRP1 is a direct target of miR-103–3p. In vivo assessments of miR-103–3p levels were performed, and the extent of cell pyroptosis during liver injury post-SAP was evaluated through western blotting, qRT-PCR, scanning electron microscopy, histopathology, immunofluorescence, and immunohistochemistry. The role of miR-103–3p in regulating NLRP1-mediated pyroptosis and its impact on SAP-induced liver injury were validated. ResultsThis study reports that following SAP-induced liver injury, the expression of miR-103–3p in liver tissue was significantly decreased, and cell pyroptosis was involved in the process of liver injury. Experimental validation indicated that NLRP1 was a downstream target of miR-103–3p. Overexpression of miR-103–3p in vitro significantly alleviated the severity of liver injury following SAP, while simultaneously inhibiting cell pyroptosis. ConclusionThese findings indicate that pyroptosis may be linked to SAP-induced liver injury and that miR-103–3p mitigates hepatocyte pyroptosis by reducing liver injury through the suppression of NLRP1 expression.

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.

For adult patients hospitalized with mild-to-moderate acute pancreatitis, does early oral feeding lead to decreased length of stay compared with delayed oral feeding?

For adult patients hospitalized with mild-to-moderate acute pancreatitis, does early oral feeding lead to decreased length of stay compared with delayed oral feeding?

Retracted] Ginsenoside Rg3 ameliorates acute pancreatitis by activating the NRF2/HO‑1‑mediated ferroptosis pathway.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 1D, DCFH‑DA‑stained cellular data in Fig. 2A, and western blotting data in Figs. 2G and 5B were strikingly similar to data that had either already appeared in previously published articles written by different authors at different research institutes (one of which has since been retracted), or were featured in an article that was submitted for publication to a different journal at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 50: 89, 2022; DOI: 10.3892/ijmm.2022.5144].

Rationale and design of the SHASTA-3 and SHASTA-4 studies: randomized, double-blind, placebo-controlled, phase 3 studies of plozasiran in patients with severe hypertriglyceridemia

Abstract Severe hypertriglyceridemia (sHTG) confers an increased risk of atherosclerotic cardiovascular disease (ASCVD) and acute pancreatitis (AP). sHTG-associated AP is a substantial source of morbidity, mortality, reduced quality of life and financial burden to health care systems. Currently available therapeutic approaches for sHTG are often insufficient to reduce triglyceride (TG) levels and prevent AP. Plozasiran, an investigational siRNA therapeutic, inhibits hepatic production of apolipoprotein C3 (APOC3), a key regulator of lipoprotein lipase-mediated TG metabolism and clearance. In a phase 2 study of sHTG patients [TG ≥500 mg/dL (≥5.65 mmol/L)], plozasiran demonstrated durable reductions in TG levels of up to -80%, 12 weeks after the last dose, and decreased TG below 500 mg/dL (5.65 mmol/L), a threshold of increased risk for AP in most participants. The SHASTA-3 and SHASTA-4 trials will evaluate safety and efficacy of plozasiran, including AP rates, in patients with sHTG. SHASTA-3 and SHASTA-4 are phase 3, randomized, double-blind, placebo-controlled, multi-center trials. Key inclusion criteria are prior sHTG and fasting TG ≥500 mg/dL (≥5.65 mmol/L), at screening. Key exclusion criteria include use of any hepatocyte targeted siRNA treatments that target lipids and/or TGs within 1 year (except inclisiran at least 4 weeks prior to enrollment), siRNA or ASO within 60 days, known FCS diagnosis, and AP within 4 weeks of screening. 700 adults with sHTG will be enrolled in these two trials in several sites across multiple countries. Patients will be randomized 2:1 to receive 4 quarterly subcutaneous injections of plozasiran 25 mg or matching placebo over a 1-year double-blinded period, followed by post-treatment evaluation or entry into the open-label extension study. The randomization will be stratified based on TG levels (≥880 mg/dL vs &amp;lt;880 mg/dL [≥ vs &amp;lt;10 mmol/L]) and prior history of AP, within 5 years of screening. The primary efficacy endpoint of the studies is placebo-adjusted percent change in fasting TG from baseline to month 12 with plozasiran. Secondary endpoints include percent change in fasting TG from baseline to month 10 compared to placebo, percent of patients achieving fasting TGs of &amp;lt;500 mg/dL (&amp;lt;5.65 mmol/L) and TGs of &amp;lt;150 mg/dL (&amp;lt;1.69 mmol/L) at month 10 and 12 compared to placebo, and event rate of adjudicated abdominal clinical events including ER visits and hospitalization for abdominal pain attributed to HTG and events of documented pancreatitis. The effect of plozasiran on other lipids and lipoproteins, inflammatory biomarkers, and liver fat content using magnetic resonance imaging-proton density fat fraction will be assessed. Adjudicated major adverse cardiovascular event rates, safety and tolerability will be assessed. SHASTA-3 and SHASTA-4 are designed to determine whether the quarterly-dosed APOC3 siRNA plozasiran, added to standard of care, safely reduces TG levels and the rate of AP in patients with sHTG.

Transition of patients with familial chylomicronaemia syndrome from volanesorsen to olezarsen: safety and pharmacokinetic results

Abstract Background Familial chylomicronaemia syndrome (FCS) is a rare genetic disorder of lipoprotein lipase deficiency resulting in severe hypertriglyceridaemia and pancreatitis risk. Volanesorsen is a weekly-injected antisense oligonucleotide (ASO) designed to degrade APOC3 mRNA that is approved as an adjunct to diet to treat FCS in the EU, UK, and Brazil. Olezarsen is an investigational monthly-injected ASO-GalNAC3 conjugate also designed to degrade APOC3 mRNA, but directed to hepatocytes, resulting in more potency and less systemic exposure and making it a potential alternative to volanesorsen for FCS. Purpose This interim analysis of an open-label phase 3 trial evaluated olezarsen safety and pharmacokinetics in patients (pts) with FCS previously treated with volanesorsen. Methods Adults with FCS with prior volanesorsen treatment, or actively participating in an expanded access programme (US and Canada), started olezarsen 80 mg by subcutaneous injection every 4 weeks after a minimum washout of 6 weeks. Historical volanesorsen laboratory and safety data were unavailable. The primary objective was to assess safety from changes vs baseline in platelet count, liver enzymes, and renal function; bleeding events; and adverse events. Pharmacokinetic measurements included plasma volanesorsen and olezarsen concentrations. Immunogenicity was assessed by measuring anti-drug antibodies (Abs). Results Of 24 pts enrolled, the majority were female (n=13; 54.2%) and White (n=21; 87.5%), with mean age of 49.1 years; 20 (83.3%) had genetically and 4 (16.7%) clinically validated FCS, all had history of acute pancreatitis (or symptoms suggestive of pancreatitis requiring hospitalisation or emergency room/urgent care visit; mean, 3.4 episodes within 5 years) and 5 (20.8%) of thrombocytopaenia. Time since last volanesorsen dose was 42—1118 days. Baseline fasting triglyceride (median [interquartile range (IQR)], 18.6 [9.6,34.0] mmol/L [1648 (852,3007) mg/dL]; mean [standard deviation (SD)], 25.5 [20.5] mmol/L [2256 (1812) mg/dL]) and apolipoprotein C-III (median [IQR], 0.2 [0.1,0.4] g/L [16.1 (12.4,39.0) mg/dL]; mean [SD], 0.3 [0.2] g/L [25.9 (19.5) mg/dL]) levels were elevated. During a mean (SD) of 329 (95) days of olezarsen 80 mg treatment, no pts experienced hepatic failure, renal impairment, major bleeding events, or platelet count below the prespecified threshold of 50,000 mm³ (Table 1). Olezarsen levels at trough were elevated during the first 3 months, mainly due to residual volanesorsen levels in pts with washout &amp;lt;90 days (Figure 1). Eleven (45.8%) pts had treatment-emergent anti-olezarsen Abs, of whom 5 (20.8%) had anti-volanesorsen Abs, with no impact on safety or efficacy; pts with vs without anti-drug Abs had higher olezarsen trough levels (mean, 4.4–7.8 ng/mL vs 1.1 ng/mL). Conclusions In this interim analysis, olezarsen was safe and well tolerated in pts with FCS previously treated with volanesorsen after a minimum washout of 6 weeks.

Endoscopic diagnosis and treatment of recurrent acute pancreatitis after pancreaticojejunostomy: A case report

Endoscopic diagnosis and treatment of recurrent acute pancreatitis after pancreaticojejunostomy: A case report

Minocycline-Induced Acute Pancreatitis With Cyst Formation in a Young Man

Minocycline-Induced Acute Pancreatitis With Cyst Formation in a Young Man

The molecular mechanism of PLD2-mediated regulation of apoptosis and cell edema in pancreatic cells via the Nrf2/NF-κB pathway

This study aimed to elucidate the molecular mechanisms by which PLD2 controls apoptosis and edema in pancreatic cells via the Nrf2/NF-κB pathway. AR42J rat pancreatic cells were treated with 10 nM mitomycin to create an in vitro pancreatitis model (model group), with a control group receiving phosphate-buffered saline. Cells were transfected with a PLD2 overexpression plasmid using Lipofectamine 3000, forming the PLD2 overexpression group. PLD2 protein expression was assessed by Western blotting, and TNF-α, IL-6, and IL-10 levels were measured by RT-qPCR. Nrf2/NF-κB protein expressions were also analyzed. Apoptosis and necrosis were evaluated using Annexin V-FITC/PI staining and the LDH release test. Cell edema was assessed by cell volume, ion content, and membrane damage. Western blotting was used to analyze pan-apoptosis-related proteins. PLD2 expression was lower in the model group compared to controls (P < 0.05) but higher in the PLD2 overexpression group (P < 0.05). TNF-α, IL-6, and IL-10 levels were elevated in the model group (P < 0.05) and reduced in the PLD2 overexpression group (P < 0.05). Nrf2 expression decreased in the model group but increased with PLD2 overexpression (P < 0.05). NF-κB expression increased in the model group but decreased with PLD2 overexpression (P < 0.05). Apoptosis and necrosis rates were higher in the model group (P < 0.05) but lower in the PLD2 overexpression group (P < 0.05). Cell volume, Na + content, and LDH release increased in the model group (P < 0.05) but decreased with PLD2 overexpression (P < 0.05). RIPK1 expression decreased in the model group (P < 0.05) but increased with PLD2 overexpression (P < 0.05). CASP8, FADD, and ZBP1 levels were higher in the model group (P < 0.05) and reduced with PLD2 overexpression (P < 0.05). PLD2 exerts a protective effect in acute pancreatitis by activating Nrf2 and inhibiting NF-κB, reducing apoptosis, cell swelling, and membrane damage. This highlights potential therapeutic targets for pancreatic inflammation.

Angiotensin-(1-7) improves intestinal microbiota disturbances and modulates fecal metabolic aberrations in acute pancreatitis.

Acute pancreatitis (AP) is a serious health problem that dysregulates intestinal microbiota. Angiotensin (Ang)-(1-7) plays a protective role in the intestinal barrier in AP, but its effect on intestinal microbiota remains clear. To investigate the impact of Ang-(1-7) on AP-induced intestinal microbiota disorder and metabolites. We collected blood and fecal samples from 31 AP patients within 48 h after admission to the hospital, including 11 with mild AP (MAP), 14 with moderately severe AP (MSAP), six with severe AP (SAP). Mice were divided into four groups: control, AP, AP + Ang-(1-7) via tail vein injection, and AP + Ang-(1-7) via oral administration. The samples of mice were collected 12 h after AP. Pancreatic and intestinal histopathology scores were analyzed using the Schmidt and Chiu scores. Fecal microbiota and metabolites analysis was performed via 16S rDNA sequencing and nontargeted metabolomics analysis, respectively. In patients, the abundance of beneficial bacteria (Negativicutes) decreased and pathogenic bacteria (Clostridium bolteae and Ruminococcus gnavus) increased in SAP compared with MAP. Ang-(1-7) levels were associated with changes in the microbiota. There were differences in the intestinal microbiota between control and AP mice. Ang-(1-7) attenuated intestinal microbiota dysbiosis in AP mice, reflecting in the increase in beneficial bacteria (Odoribacter and Butyricimonas) than AP, as well as pancreatic and intestinal injuries. Oral administration of Ang-(1-7) reversing AP-induced decreases in metabolisms: secondary bile acids, emodin, and naringenin. Ang-(1-7) may improve intestinal microbiota dysbiosis and modulate fecal metabolites in AP, thereby reducing the damage of AP.

Systematic review of treatments for the gastrointestinal manifestations of systemic lupus erythematosus

ObjectivesTo comprehensively assess and present the evidence for treatments used in the management of the gastrointestinal manifestations of SLE. MethodsA systematic search of the literature from January 1990 to June 2022 was performed using the following databases: MEDLINE, EMBASE, PubMed and Cochrane. Key words relating to the gastrointestinal system, SLE, and treatment were used. Where there was sufficient evidence for the treatment of a manifestation, we excluded case series with <10 cases and case reports. However, for rarer manifestations with insufficient higher-level evidence, smaller case series and case reports were included. ResultsA total of 29 studies including 767 patients were included in the review; six cohort studies, 11 case-control studies, and 11 case series. Specific gastrointestinal manifestations included enteritis (5 studies), mesenteric vasculitis (3 studies), acute pancreatitis (5 studies), chronic pancreatitis (1 study), intestinal pseudo-obstruction (IPO) (2 studies), hepatitis (4 studies), protein-losing enteropathy (PLE) (6 studies), acute acalculous cholecystitis (2 studies), and Budd-Chiari Syndrome (1 study). Evidence for the treatment of Ascites (13 case reports), peritonitis (3 case reports), and miscellaneous GI manifestations (11 case reports) are included as a supplemental file. Most studies demonstrated a benefit from pulsed intravenous methylprednisolone (IVMP) in severe or life-threatening manifestations, and oral prednisolone for less severe manifestations. However, the quality of evidence was low, with a high risk of bias in all studies. ConclusionThis review highlights the need for standardised disease definitions and terminology, as well as consideration of including gastrointestinal manifestations in disease scoring systems. There is a significant need for high-quality clinical trials in the treatment of the gastrointestinal manifestations of SLE, which will likely need to be multi-centre. We hope that this review will promote awareness of the gastrointestinal manifestations of SLE, and serve as a practical guide for evidence-based treatment.

Anlotinib plus TQB2450, a PD-L1 Antibody, in Patients with Advanced Alveolar Soft Part Sarcoma: a single-arm, phase 2 trial.

Alveolar soft part sarcoma (ASPS) is an ultra-rare soft-tissue sarcoma with a high rate of metastasis and no established treatment. This study aimed to explore the efficacy and safety of anlotinib (a tyrosine-kinase inhibitor) and TQB2450 (a PD-L1 inhibitor) in ASPS patients. This single-arm, phase 2 study evaluated the efficacy of TQB2450, an anti-programmed death ligand 1 (PD-L1) agent, combined with anlotinib, a TKI, in adults with advanced ASPS. TQB2450 was given intravenously (1,200 mg) on day 1, and anlotinib (12 mg/day) was taken orally from day 1 to day 14 every 3 weeks. The primary endpoint was overall response rate, with secondary endpoints including duration of response (DOR), progression-free survival (PFS), and overall survival (OS). Lymphocyte infiltration and tertiary lymphoid structure (TLS) were also analyzed as potential prognostic biomarkers. The study enrolled 29 patients, with 28 evaluable (one withdrew due to acute pancreatitis). An objective response was achieved in 82.1% of patients, including 4 complete and 19 partial responses. The median time to response was 2.8 months, and the DOR was not reached, with an estimated median PFS of 35.2 months. Grade 3-4 treatment-related adverse events occurred in 44.8% of patients, with no study-related deaths. Responders had a higher proportion of TLS area, density, and CD20-positive immune cells. The combination of anlotinib and TQB2450 is effective and tolerable in ASPS patients. TLS may serve as a prognostic biomarker, meriting further investigation.

Role of Sphingosine-1-Phosphate Signaling Pathway in Pancreatic Diseases.

Sphingosine-1-phosphate (S1P) is a sphingolipid metabolic product produced via the phosphorylation of sphingosine by sphingosine kinases (SPHKs), serving as a powerful modulator of various cellular processes through its interaction with S1P receptors (S1PRs). Currently, this incompletely understood mechanism in pancreatic diseases including pancreatitis and pancreatic cancer, largely limits therapeutic options for these disorders. Recent evidence indicates that S1P significantly contributes to pancreatic diseases by modulating inflammation, promoting pyroptosis in pancreatic acinar cells, regulating the activation of pancreatic stellate cells, and affecting organelle functions in pancreatic cancer cells. Nevertheless, no review has encapsulated these advancements. Thus, this review compiles information about the involvement of S1P signaling in exocrine pancreatic disorders, including acute pancreatitis, chronic pancreatitis, and pancreatic cancer, as well as prospective treatment strategies to target S1P signaling for these conditions. The insights presented here possess the potential to offer valuable guidance for the implementation of therapies targeting S1P signaling in various pancreatic diseases.

Feeding Intolerance-A Key Factor in the Management of Acute Pancreatitis: A Review.

Acute pancreatitis (AP) is one of the most common diseases of the gastrointestinal tract, which in 20% of cases can turn into a severe form, with mortality reaching up to 30%. One of the cornerstones of AP treatment is early nutritional treatment. Feeding intolerance (FI) occurs in up to 25% of patients with AP and is associated with a more severe disease course and poorer clinical outcome. Feeding intolerance can have a multifaceted clinical presentation. The early identification of FI risk factors and appropriately conducted nutritional treatment are critical to the course of the disease. In this review, we summarize the current knowledge of feeding intolerance in AP, its pathomechanisms and risk factors, and its impact on disease progression. We also present suggestions for the management of feeding intolerance.

Relationship of Crohn’s disease and acute pancreatitis in pediatric practice: literature review

Inflammatory bowel diseases (IBD) are a certain group of pathologic conditions of the gastrointestinal tract (GIT), including Crohn’s disease (CD) and ulcerative colitis (UC). In the modern world, vigilance for these diseases is growing, because their characteristic feature is the involvement of other organs in the pathological inflammatory process, as well as the development of local and systemic complications. As a rule, in children CCD occurs mainly at the age of 12-16 years. Recently, the attention of the medical world has been drawn to the issue of extraintestinal manifestations of CD. Pathological manifestations associated with lesions of the skin and mucous membranes, eyes, bone and joint system, pancreas, negatively affect both physical and psychological health of the child. Such pathology associated with pancreatic malfunction, such as acute pancreatitis (AP) often occurs in patients with inflammatory bowel disease and is one of the main causes of hospitalization for diseases of the digestive system. According to statistics, the incidence ranges from 15 to 40 cases per 100,000 per year in European countries. According to the Gastroenterological Society, there are different variations in the course of acute pancreatitis, whether occurring in patients with IBS due to the disease itself or as a side effect of drug therapy. However, IBD patients are at increased risk of developing both acute and chronic pancreatitis. In this review, we consider the relationship and mutual influence of these two pathologies.

Association Between Body Composition Measured by Artificial Intelligence and Long-Term Sequelae After Acute Pancreatitis.

The clinical utility of body composition in the development of complications of acute pancreatitis (AP) remains unclear. We aimed to describe the associations between body composition and the recurrence of AP. We performed a retrospective study of patients hospitalized with AP at three tertiary care centers. Patients with computer tomography (CT) imaging of the abdomen at admission were included. A previously validated and fully automated abdominal segmentation algorithm was used for body composition analysis. Hospitalization for a recurrent episode of AP was the primary endpoint. Secondary endpoints included the development of chronic pancreatitis (CP) or diabetes mellitus (DM) in patients who were evaluated. Cox Proportional Hazards regression was used. From a total of 347 patients, 89 (25.6%) were hospitalized for recurrent AP (median time: 219days). Thirty-four of 112 patients (30.4%) developed CP (median time: 311days) and 22 of 88 (25.0%) developed DM (median time: 1104days). After adjusting for age, male sex, first episode of AP, BUN, and severity of AP, we found that obesity, body mass index, alcohol pancreatitis, and gallstone pancreatitis were significantly associated with a recurrent episode of AP. Body composition was not associated with recurrent AP. In unadjusted analysis, subcutaneous adipose tissue (SAT) (HR 0.87 per 10 cm2, p = 0.002) was associated with CP. Skeletal muscle (SM) mass approached significance for CP (p = 0.0546). Intermuscular adipose tissue (IMAT) (HR 1.45 per 5 cm2, p = 0.0264) was associated with DM. Body composition was not associated with having a recurrent AP. At follow-up, 30% and 25% of evaluated patients developed CP and DM, respectively. A higher SAT and IMAT were associated with a lower incidence of CP and higher incidence of DM, respectively.

Psoas Muscle Index and Density as Prognostic Predictors in Patients Hospitalized with Acute Pancreatitis.

Background: Early prognostication of acute pancreatitis (AP) patients for those at high risk of complications during hospitalization can facilitate clinical decision-making. Sarcopenia has been proven to be a risk factor for poor prognosis in patients with AP. We aimed to evaluate the association between the muscle parameters measured in computed tomography (CT) and the clinical outcomes of hospitalized patients with AP. Methods: A total of 132 consecutive patients hospitalized between 1 January 2015 and 31 December 2021 for AP with a valid CT scan were analyzed. The first CT conducted during hospitalization was analyzed for psoas muscle area (PMA), index (PMI), and density (PMD) at the L3 vertebral level. The main adverse outcomes indicating a worse prognosis were the development of extrapancreatic complications, infections, ICU transfer, in-hospital mortality, and hospitalization length. Results: The lowest tertile of PMI, as a surrogate for sarcopenia, was significantly correlated with increased rates of extrapancreatic complications, infections, and longer hospitalizations. It was additionally correlated with a worse CT severity index. The results for PMA and PMD also showed worse outcomes, largely mirroring the results for PMI. Although in-hospital mortality was relatively low, none of the patients died in the highest tertile of PMI. A clear cutoff with sufficient predictive capability could not be found. Conclusions: A low psoas muscle index can serve as an additional potential predictive marker for more severe disease and worse outcomes in hospitalized acute pancreatitis patients. More studies are needed to determine its combination with existing prediction tools.