Heterozygous Spink1 c.194+2T>C mutation promotes chronic pancreatitis after acute attack in mice.

BACKGROUND & AIMS: Mutations in genes, including serine protease inhibitor Kazal-type 1 (SPINK1), influence disease progression following sentinel acute pancreatitis event (SAPE) attacks. SPINK1 c.194+2T > C intron mutation is one of the main mutants of SPINK1，which leads to the impairment of SPINK1 function by causing skipping of exon 3. Research on the pathogenesis of SAPE attacks would contribute to the understanding of the outcomes of acute pancreatitis. Therefore, the aim of the study was to clarify the role of SPINK1 c.194+2T > C mutation in the CP progression after an AP attack. METHODS: SAPE attacks were induced in wildtype and SPINK mutant (Spink1 c.194+2T > C) mice by cerulein injection. The mice were sacrificed at 24 h, 14 d, 28 d, and 42 d post-SAPE. Data-independent acquisition (DIA) proteomic analysis was performed for the identification of differentially expressed protein in the pancreatic tissues. Functional analyses were performed using THP-1 and HPSCs. RESULTS: Following SAPE attack, the Spink1 c.194+2T > C mutant mice exhibited a more severe acute pancreatitis phenotype within 24 h. In the chronic phase, the chronic pancreatitis phenotype was more severe in the Spink1 c.194+2T > C mutant mice after SAPE. Proteomic analysis revealed elevated IL-33 level in Spink1 c.194+2T > C mutant mice. Further in vitro analyses revealed that IL-33 induced M2 polarization of macrophages and activation of pancreatic stellate cells. CONCLUSION: Spink1 c.194+2T > C mutation plays an important role in the prognosis of patients following SAPE. Heterozygous Spink1 c.194+2T > C mutation promotes the development of chronic pancreatitis after an acute attack in mice through elevated IL-33 level and the induction of M2 polarization in coordination with pancreatic stellate cell activation.

Role of imaging in evaluating the complications of endoscopic management of pancreatic fluid collections in acute pancreatitis.

Acute pancreatitis is associated with local and systemic complications. Pancreatic fluid collection (PFC) is the most common local complication. Infected or symptomatic PFCs need drainage. Endoscopic drainage (ED) is the first-line procedure for accessible PFCs adjacent to the stomach and duodenum. ED is performed under endoscopic ultrasound (EUS) guidance. The technical and clinical success rates of EUS-guided ED in well-encapsulated PFCs are high. ED of poorly encapsulated PFCs is associated with complications. Bleeding and perforation are the most common complications. Contrast-enhanced computed tomography is critical in planning ED and early detection and management of complications. With the increasing utilization of ED for PFC, the radiologist must be familiar with the ED techniques, types of stents, and the complications related to ED. In this review, we discuss the technical aspects of the ED as well as the imaging findings of ED-related complications.

Involvement of circ_0029407 in Caerulein-Evoked Cytotoxicity in Human Pancreatic Cells via the miR-579-3p/TLR4/NF-κB Pathway.

Acute pancreatitis (AP) is the most prevalent gastrointestinal inflammatory disease. Circular RNAs (circRNAs) are implicated in the development of AP. Here, we identified the precise action of circ_0029407 in AP development. Human pancreatic epithelial cells (HPECs) were stimulated with caerulein. Cell viability, proliferation, and apoptosis were gauged by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays, respectively. Circ_0029407, microRNA (miR)-579-3p, and toll-like receptor 4 (TLR4) were quantified by a qRT-PCR or western blot assay. Dual-luciferase reporter and RNA pull-down assays were performed to evaluate the direct relationship between miR-579-3p and circ_0029407 or TLR4. Our results indicated that circ_0029407 was markedly overexpressed in AP serum samples and caerulein-stimulated HPECs. Reduction of circ_0029407 attenuated caerulein-imposed HPEC damage by promoting cell proliferation and repressing cell apoptosis and inflammation. Mechanistically, circ_0029407 contained a miR-579-3p binding site, and miR-579-3p downregulation reversed the effect of circ_0029407 reduction on caerulein-imposed HPEC damage. TLR4 was identified as a direct and functional target of miR-579-3p, and TLR4 overexpression reversed the impact of miR-579-3p upregulation on attenuating caerulein-imposed HPEC damage. Moreover, circ_0029407 regulated the TLR4/nuclear factor NF-kappaB (NF-κB) signaling by acting as a competing endogenous RNA (ceRNA) for miR-579-3p. Our study suggests that circ_0029407 regulates caerulein-imposed cell injury in human pancreatic cells at least in part via the TLR4/NF-κB signaling pathway by functioning as a ceRNA for miR-579-3p.

Assessment of triglyceride clearance of haemoperfusion from three cases of hypertriglyceridaemia-induced acute pancreatitis: a case series.

Rapid reduction of plasma triglycerides (TG) is believed to improve the outcome of pancreatitis in the context of hypertriglyceridaemia (HTG)-induced acute pancreatitis (HTG-AP). Previous studies have suggested that haemoperfusion (HP) with the Jafron cartridge series could be effective for reducing TG concentrations in patients with HTG-AP. However, the clearance capacity (CC) for TG removal has not been reported. This case series reports on data from three patients with HTG-AP who underwent HP with HA230 or HA330 cartridges. Blood samples were collected from both before and after the cartridge circuit every 30 min and the CC was calculated. Twelve pairs of blood samples were collected for each type of HP cartridge. The mean ± SD CC of the HA230 cartridge for TG removal in this case series was 0.009781 ± 1.117235 ml/min (95% confidence interval [CI], -0.7000762, 0.7196384 ml). The mean ± SD CC of the HA330 cartridge for TG removal in this case series was 0.344914 ± 1.412183 ml/min (95% CI, -0.5523448, 1.2421721 ml). Based on the findings of this small case series, special caution is advised when considering the use of the HA230 and HA330 cartridges for reducing blood TG concentration pending further conclusive evidence from larger studies.

Glycyrrhizin Ameliorates Cardiac Injury in Rats with Severe Acute Pancreatitis by Inhibiting Ferroptosis via the Keap1/Nrf2/HO-1 Pathway.

BACKGROUND: Severe acute pancreatitis (SAP) is a potential fatal gastrointestinal disease that is usually complicated by myocardial injury and dysfunction. Due to the lack of understanding of the mechanism of SAP-associated cardiac injury (SACI), there is still no complete treatment. AIMS: To explore the alleviative effect and anti-ferroptosis mechanism against SACI of glycyrrhizin (GL), an inhibitor of oxidative stress. METHODS: The SAP model was established by perfusing 5% sodium taurocholate into biliopancreatic duct in rats. H&E staining and serum assays were used to assess the injury changes of pancreas and heart. Echocardiography was used to evaluate the cardiac function. Transmission electron microscopy (TEM) and oxidative stress assays were used to investigate the ferroptosis-related morphological and biochemical changes. Western blot and immunofluorescence were performed to analyzed the expression of ferroptosis-related proteins. RESULTS: Significant myocardial impairment was found in SAP rats according to increased histopathological scores, serum creatine kinase-MB (CK-MB) and cardiac troponin-I (cTnI) levels, and a decreased fractional shortening and ejection fraction. The decreased mitochondrial cristae and significant expression changes of ferroptosis-related proteins confirmed the presence of ferroptosis in SACI. GL treatment attenuated above-mentioned cardiac tissues damage by inhibiting ferroptosis via restoring the expression of Nrf2 and HO-1 in vivo and in vitro. Treating with ML385 (a Nrf2 inhibitor) or transfecting with siRNA-Nrf2 reversed the protective effect of GL. CONCLUSIONS: Our findings demonstrate the involvement of ferroptosis in SACI and suggest a potential role for GL in the treatment of SACI by supressing ferroptosis via Keap1/Nrf2/HO-1 pathway.

Identification and analysis of chemokine-related and NETosis-related genes in acute pancreatitis to develop a predictive model.

Background: Chemokines and NETosis are significant contributors to the inflammatory response, yet there still needs to be a more comprehensive understanding regarding the specific molecular characteristics and interactions of NETosis and chemokines in the context of acute pancreatitis (AP) and severe AP (SAP). Methods: To address this gap, the mRNA expression profile dataset GSE194331 was utilized for analysis, comprising 87 AP samples (77 non-SAP and 10 SAP) and 32 healthy control samples. Enrichment analyses were conducted for differentially expressed chemokine-related genes (DECRGs) and NETosis-related genes (DENRGs). Three machine-learning algorithms were used for the identification of signature genes, which were subsequently utilized in the development and validation of nomogram diagnostic models for the prediction of AP and SAP. Furthermore, single-gene Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) were performed. Lastly, an interaction network for the identified signature genes was constructed. Results: We identified 12 DECRGs and 7 DENRGs, and enrichment analyses indicated they were primarily enriched in cytokine-cytokine receptor interaction, chemokine signaling pathway, TNF signaling pathway, and T cell receptor signaling pathway. Moreover, these machine learning algorithms finally recognized three signature genes (S100A8, AIF1, and IL18). Utilizing the identified signature genes, we developed nomogram models with high predictive accuracy for AP and differentiation of SAP from non-SAP, as demonstrated by area under the curve (AUC) values of 0.968 (95% CI 0.937-0.990) and 0.862 (95% CI 0.742-0.955), respectively, in receiver operating characteristic (ROC) curve analysis. Subsequent single-gene GESA and GSVA indicated a significant positive correlation between these signature genes and the proteasome complex. At the same time, a negative association was observed with the Th1 and Th2 cell differentiation signaling pathways. Conclusion: We have identified three genes (S100A8, AIF1, and IL18) related to chemokines and NETosis, and have developed accurate diagnostic models that might provide a novel method for diagnosing AP and differentiating between severe and non-severe cases.

Hidden Dangers of Frailty: Higher Mortality, Complications and Costs in Acute Pancreatitis.

BACKGROUND: Frailty is a clinically recognizable state of increased vulnerability due to age-related decline in reserve and function across multiple physiologic systems that compromises the ability to cope with acute stress. As frailty is being identified as an important risk factor in outcomes of gastrointestinal pathologies, we aimed to assess outcomes in patients with acute pancreatitis within this cohort. METHOD: We conducted a retrospective study using the Nationwide Inpatient Sample (NIS) database. ICD-10 codes were used to inquire for patients admitted with acute pancreatitis between September 2015 through 2017. ICD-10 codes corresponding to the Hospital Frailty Risk Score (HFRS) were used to divide the study sample into 2 cohorts: low risk (< 5 points) and intermediate or high risk (> 5 points). To calculate the points, we fitted a logistic regression model that included membership of the frail group as the binary dependent variable (frail vs. non-frail) and the set of ICD-10 codes as binary predictor variables (1 = present, 0 = absent for each code). To simplify the calculation and interpretation, we multiplied regression coefficients by five to create a points system, so that a certain number of points are awarded for each ICD-10 code and added together to create the final frailty risk score. Multivariate regression analysis was performed to find adjusted mortality. RESULTS: Out of a total of 1,267,744 patients admitted with acute pancreatitis, 728,953 (57.5%) were identified as intermediate and high risk (> 5 points) (study cohort) and 538,781 (42.5%) as low risk (< 5 points). The mean age in the study cohort was 64.8 ± 12.6 and that in the low-risk group was 58.6 ± 9.5. Most of the patients in both groups were males and Caucasians; Medicare was the predominant insurance provider. A majority of the admissions in both groups were in an urban teaching hospital and were emergency. (Table 1). The primary outcome was in-hospital mortality which was significantly higher in the study cohort as compared to the low-risk group (4.3% vs. 2.5%, p < 0.0001). The age-adjusted Odds ratio of mortality was 1.72(95% CI (Confidence Interval) 1.65-1.80, p < 0.05). When compared between the two groups; median length of stay (6 vs. 4); hospitalization cost ($14,412 vs. $10,193), disposition to a skilled nursing facility (SNF) (17.1% vs. 8.6%) and need for home health care (HHC) was significantly higher in the study cohort. Complications like septicemia, septic shock, and acute kidney injury were also higher in the study group (Table 2). Table 1 Baseline demographics of the cohort Characteristics Acute pancreatitis with High HES Frailty score (> 5, intermediate + high) Acute pancreatitis with low HES Frailty score (< 5) P-value N = 1,267,744 N = 728,953 (57.5%) N = 538,781 (42.5%) Age  Mean years (Mean ± SD) 64.8 ± 12.6 58.6 ± 9.5 < 0.001 Gender < 0.001  Male 59.1% 52.3%  Female 40.9% 47.7% *Missing-475 Age groups < 0.001  18-44 3.7% 14.3%  45-64 48% 52.9%  65-84 32.2% 28.7%  ≥ 85 16.1% 4.1% Race < 0.001  Caucasians 67.4% 61.9%  African Americans 9.6% 16.8%  Others 23% 21.3% *Missing-10 Insurance type < 0.001  Medicare 40.9% 36.3%  Medicaid 17.2% 24.3%  Private 31.8% 27.9%  Other 9.9% 11.4% *Missing-75 Active smoking 32.7% 37.9% 0.005 Biliary Stone 36.2% 16.7% < 0.001 Admission Type < 0.001  Emergent 93.7% 94.3%  Elective 6.3% 5.7% *Missing-2880 Hospital ownership/control < 0.001  Rural 7.8% 10%  Urban nonteaching 26.3% 26.6%  Urban teaching 65.9% 63.4% Table 2 Outcomes Outcomes Acute pancreatitis with High HES Frailty score (> 5, intermediate + high) Acute pancreatitis with low HES Frailty score (< 5) P-value In-hospital mortality *Missing-920 4.3% 2.5% < .0001 1.72(1.65-1.80) < .0001 Length of stay, days (Median,IQR) 6(3-8) 4(2-6) < .0001 Total hospitalization cost, $ (Median,IQR) 14,412(8843-20,216) 10,193(6840-13,842) < .0001 In-Hospital Complications  ARDS 0.4% 0.3% 0.08  Ventilator dependence respiratory failure 0.23% 0.29% 0.25  Septicemia 15.2% 9.6% < .0001  Septic Shock 6.1% 2.9% < .0001  AKI 24.8% 14.9% < .0001 Disposition < .0001  Discharge to home 58.9% 74.9%  Transfer other: includes  Skilled Nursing Facility (SNF), Intermediate Care Facility (ICF), and another type of facility 17.1% 8.6%  Home health care 11.5% 8.1%  Against medical advice (AMA) 1.6% 3.4% *Missing-920 CONCLUSION: Using frailty as a construct to identify those who are at greater risk for adverse outcomes, can help formulate interventions to target individualized reversible factors to improve outcomes in patients with acute pancreatitis. Future large-scale prospective studies are warranted to understand the dynamic and longitudinal relationship between pancreatitis and frailty.

A Rare Case of Acute Pancreatitis as an Initial Presentation of Acute Myeloid Leukemia.

Acute pancreatitis is a rare manifestation of acute myeloid leukemia which can be a presentation at the initial diagnosis or during or after the onset of the disease. Acute myeloid leukemia occurs due to the abnormal proliferation of undifferentiated hematopoietic stem cells in the bone marrow which alter the normal hematopoiesis. We report the case of a 32-year-old male admitted with a one-month history of fever and backache, followed by 15 days of blackish stool discoloration and two days of abdominal pain and reduced urine output. On clinical examination, he was hypoxic with respiratory distress with epigastric tenderness. Blood investigations and imaging were consistent with acute pancreatitis. A complete blood count with peripheral smear showed severe normocytic normochromic anemia and an increased myeloid series containing 50% myeloblasts and 30% monoblasts. Additionally, some cells displayed cytoplasmic vacuolations, with a reticulocyte count of 2%. These findings were suggestive of acute myeloid leukemia M5. Due to the poor Glasgow Coma Scale (GCS), he was intubated and placed on mechanical ventilation. Unfortunately, he did not improve despite treatment and succumbed to the illness.

The role of Interleukin-22 in severe acute pancreatitis.

Severe acute pancreatitis (SAP) begins with premature activation of enzymes, promoted by the immune system, triggering a potential systemic inflammatory response that leads to organ failure with increased mortality and a bleak prognosis. Interleukin-22 (IL-22) is a cytokine that may have a significant role in SAP. IL-22, a member of the IL-10 cytokine family, has garnered growing interest owing to its potential tissue-protective properties. Recently, emerging research has revealed its specific effects on pancreatic diseases, particularly SAP. This paper provides a review of the latest knowledge on the role of IL-22 and its viability as a therapeutic target in SAP.

Acute pancreatitis: A narrative review.

Acute pancreatitis is a common cause of acute abdominal pain and can range from mild oedema to severe necrosis of the pancreas. It has a significant impact on morbidity, mortality and financial burden. The global prevalence of pancreatitis is substantial, with the highest rates observed in central and eastern Europe. Diagnosing acute pancreatitis involves considering clinical symptoms, elevated serum amylase and/or lipase levels, and characteristic imaging findings. The causes of acute pancreatitis include obstructive disorders, such as gallstones and biliary sludge, alcohol consumption, smoking, drug-induced pancreatitis, metabolic disorders, trauma, medical procedures, infections, vascular diseases and autoimmune pancreatitis. Appropriate management of acute pancreatitis involves determining the severity of the condition, providing supportive care, addressing the underlying cause, and preventing complications. Advances in classifying the severity of acute pancreatitis and implementing goal-directed therapy have contributed to a decrease in mortality rates. Understanding its prevalence, aetiology and management principles is crucial for clinicians to appropriately diagnose and manage patients with acute pancreatitis.

Urolithin A's Role in Alleviating Severe Acute Pancreatitis via Endoplasmic Reticulum-Mitochondrial Calcium Channel Modulation.

Severe acute pancreatitis (SAP), characterized by pancreatic acinar cell death, currently lacks effective targeted therapies. Ellagic acid (EA), rich in pomegranate, shows promising anti-inflammatory and antioxidant effects in SAP treatment. However, the roles of other forms of EA, such as plant extracellular vesicles (EVs) extracted from pomegranate, and Urolithin A (UA), converted from EA through gut microbiota metabolism in vivo, have not been definitively elucidated. Our research aimed to compare the effects of pomegranate-derived EVs (P-EVs) and UA in the treatment of SAP to screen an effective formulation and to explore its mechanisms in protecting acinar cells in SAP. By comparing the protective effects of P-EVs and UA on injured acinar cells, UA showed superior therapeutic effects than P-EVs. Subsequently, we further discussed the mechanism of UA in alleviating SAP inflammation. In vivo animal experiments found that UA could not only improve the inflammatory environment of pancreatic tissue and peripheral blood circulation in SAP mice but also revealed that the mechanism of UA in improving SAP might be related to mitochondria and endoplasmic reticulum (ER) through the results including pancreatic tissue transcriptomics and transmission electron microscopy. Further research found that UA could regulate ER-mitochondrial calcium channels and reduce pancreatic tissue necroptosis. In vitro experiments of mouse pancreatic organoids and acinar cells also confirmed that UA could improve pancreatic inflammation by regulating the ER-mitochondrial calcium channel and necroptosis pathway proteins. This study not only explored the therapeutic effect of plant EVs on SAP but also revealed that UA could alleviate SAP by regulating ER-mitochondrial calcium channel and reducing acinar cell necroptosis, providing insights into the pathogenesis and potential treatment of SAP.

Clostridium butyricum upregulates GPR109A/AMPK/PGC-1α and ameliorates acute pancreatitis-associated intestinal barrier injury in mice.

Acute pancreatitis frequently causes intestinal barrier damage, which aggravates pancreatitis. Although Clostridium butyricum exerts anti-inflammatory and protective effects on the intestinal barrier during acute pancreatitis, the underlying mechanism is unclear. The G protein-coupled receptors 109 A (GPR109A) and adenosine monophosphate-activated protein kinase (AMPK)/ peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) signaling pathways can potentially influence the integrity of the intestinal barrier. Our study generated acute pancreatitis mouse models via intraperitoneal injection of cerulein and lipopolysaccharides. After intervention with Clostridium butyricum, the model mice showed reduced small intestinal and colonic intestinal barrier damage, dysbiosis amelioration, and increased GPR109A/AMPK/PGC-1α expression. In conclusion, Clostridium butyricum could improve pancreatic and intestinal inflammation and pancreatic injury, and relieve acute pancreatitis-induced intestinal barrier damage in the small intestine and colon, which may be associated with GPR109A/AMPK/PGC-1α.

Melatonin ameliorates multiorgan injuries induced by severe acute pancreatitis in mice by regulating the Nrf2 signaling pathway.

Severe acute pancreatitis (SAP) is a complicated inflammatory reaction that impacts the pancreas, often resulting in damage to numerous organs. This disorder encompasses a range of processes such as inflammation, oxidative stress, and pancreatitis. The hormone melatonin (MT) is primarily secreted by the pineal gland and plays a crucial role in mitigating inflammation, countering the harmful effects of free radicals, and regulating oxidative stress. The aim of this research was to investigate the potential protective impact and the underlying mechanism of melatonin in mice afflicted with SAP. The biochemical and histological assessments unequivocally demonstrated that melatonin effectively inhibited necrosis, infiltration, edema and cell death in pancreatic tissues, thereby suppressing acute pancreatitis. Notably, melatonin also alleviated the consequent harm to distant organs, notably the lungs, liver, and kidneys. Furthermore, both preventive and therapeutic administration of melatonin prompted nuclear factor E2-related factor 2 (Nrf2) activation followed by Nrf2 target gene expression. Nrf2 initiates the activation of antioxidant genes, thereby providing defense against oxidative stress. Conversely, Nrf2 reduction may contribute to impaired antioxidant protection in SAP. The beneficial impact of Nrf2 on antioxidants was absent in Nrf2-knockout mice, leading to the accumulation of LDH and exacerbation of cell death. This deterioration in both pancreatitis and injuries in distant organs intensified significantly. The results indicate that melatonin has an enhanced ability to protect against multiorgan damage caused by SAP, which is accomplished through the increase in Nrf2 expression. Additionally, Nrf2 initiates the activation of antioxidant genes that offer defense against cell death.

Case report: GLP1RA for the treatment of diabetes in liver transplanted people. Do they increase the risk of pancreatitis?

The incidence of acute pancreatitis (AP) in liver transplanted people is reported to be 1.5-8%. On the other hand, the evidence for a causal relationship between glucagon-like peptide 1 receptor agonists (GLP1RAs) and pancreatitis in people with type 2 diabetes is still weak. In addition, there are currently no data on a possible increased risk of AP in liver-transplanted individuals with diabetes treated with GLP1RAs. In a population of liver-transplanted individuals with diabetes receiving GLP1RA-based therapy, we reported an incidence of AP of 3.0% (two subjects). No cases were reported in liver-transplanted individuals with diabetes receiving SGLT2 inhibitors, insulin or metformin, neither in kidney or lung-transplanted patients treated with GLP1RAs. In both patients with AP, the only additional risk factor for its development was a history of re-transplantation (liver or combined kidney/liver). For this reason, we suggest particular caution when considering GLP1RAs-based therapies in liver transplanted patients with multiple risk factors for AP, such as a history of repeated and complex abdominal surgery.

Algal Oil Mitigates Sodium Taurocholate-Induced Pancreatitis by Alleviating Calcium Overload, Oxidative Stress, and NF-κB Activation in Pancreatic Acinar Cells.

Acute pancreatitis (AP) is characterized by elevated intracellular Ca2+ concentrations, mitochondrial dysfunction, and oxidative stress in pancreatic acinar cells. Algal oil (AO) has demonstrated antioxidant and anti-inflammatory properties. This study aims to explore the effects of algal oil on the microenvironment of AP. Rat pancreatic acinar AR42J cells were pretreated with AO containing 0, 50, 100, or 150 µM of docosahexaenoic acid (DHA) 2 h prior to AP induction using sodium taurocholate (STC). After 1 h of STC treatment, AR42J cells exhibited a significant increase in intracellular Ca2+ concentration and the production of amylase, lipase, reactive oxygen species, and pro-inflammatory mediators, including tumor necrosis factor-α and interleukin-6. These STC-induced increases were markedly reduced in cells pretreated with AO. In comparison to cells without AO, those treated with a high dose of AO before STC exposure demonstrated a significant increase in mitochondrial membrane potential and a decrease in lipid peroxidation. Furthermore, STC-activated nuclear factor kappa-B (NF-κB) was attenuated in AO-pretreated cells, as evidenced by a significant decrease in activated NF-κB. In conclusion, AO may prevent damage to pancreatic acinar cells by alleviating intracellular Ca2+ overload, mitigating mitochondrial dysfunction, reducing oxidative stress, and attenuating NF-κB-targeted inflammation.

Penoscrotal Edema as a Rare Complication of Acute Pancreatitis: A Case Report.

Background and Objectives: Scrotal swelling or hydrocele is a rare complication of acute pancreatitis described in the literature. We present a case of penoscrotal swelling caused by the first attack of acute interstitial edematous alcohol-induced pancreatitis in a young male patient. Case report: A 22-year-old man was admitted to the emergency unit due to diarrhea and vomiting since morning which was followed by severe abdominal pain. Urgent abdominal multislice CT scan showed steatosis, pancreatic swelling and acute peripancreatic fluid collection (interstitial edematous pancreatitis). Also, scan showed fluid between small bowel loops and along the anterior renal fascia, while there was minimal amount of fluid in the Douglas space. There was no sign of penoscrotal swelling. On the second day of admission, the patient developed left scrotal swelling and mild pain without erythema. On the fourth day, a control CT scan showed progression to moderately severe pancreatitis (CT severity index 4). Dilated scrotal veins of the pampiniform venous plexus with an increased caliber of the testicular veins were present on both sides, from the scrotum to the level of the inguinal canal. Penoscrotal swelling was significantly reduced on discharge. Conclusions: Penoscrotal swelling is a rare complication or manifestation of acute inflammation of the pancreas. It is important to identify scrotal swelling caused by pancreatitis because in severe cases it can be related to possible infertility in the future.

Opportunistic screening for long-term muscle wasting in critically ill patients: insights from an acute pancreatitis cohort.

OBJECTIVES: To assess the feasibility of long-term muscle monitoring, we implemented an AI-guided segmentation approach on clinically indicated Computed Tomography (CT) examinations conducted throughout the hospitalization period of patients admitted to the intensive care unit (ICU) with acute pancreatitis (AP). In addition, we aimed to investigate the potential of muscle monitoring for early detection of patients at nutritional risk and those experiencing adverse outcomes. This cohort served as a model for potential integration into clinical practice. MATERIALS: Retrospective cohort study including 100 patients suffering from AP that underwent a minimum of three CT scans during hospitalization, totaling 749 assessments. Sequential segmentation of psoas muscle area (PMA) was performed and was relative muscle loss per day for the entire monitoring period, as well as for the interval between each consecutive scan was calculated. Subgroup and outcome analyses were performed including ANOVA. Discriminatory power of muscle decay rates was evaluated using ROC analysis. RESULTS: Monitoring PMA decay revealed significant long-term losses of 48.20% throughout the hospitalization period, with an average daily decline of 0.98%. Loss rates diverged significantly between survival groups, with 1.34% PMA decay per day among non-survivors vs. 0.74% in survivors. Overweight patients exhibited significantly higher total PMA losses (52.53 vs. 42.91%; p = 0.02) and average PMA loss per day (of 1.13 vs. 0.80%; p = 0.039). The first and the maximum decay rate, in average available after 6.16 and 17.03 days after ICU admission, showed convincing discriminatory power for survival in ROC analysis (AUC 0.607 and 0.718). Both thresholds for maximum loss (at 3.23% decay per day) and for the initial loss rate (at 1.98% per day) proved to be significant predictors of mortality. CONCLUSIONS: The innovative AI-based PMA segmentation method proved robust and effortless, enabling the first comprehensive assessment of muscle wasting in a large cohort of intensive care pancreatitis patients. Findings revealed significant muscle wasting (48.20% on average), particularly notable in overweight individuals. Higher rates of initial and maximum muscle loss, detectable early, correlated strongly with survival. Integrating this tool into routine clinical practice will enable continuous muscle status tracking and early identification of those at risk for unfavorable outcomes.

Step-Up Management in Acute Pancreatitis: A Tertiary Care Center's Experience From Southern India.

Background The clinical spectrum of acute pancreatitis (AP) ranges from mild disease to severe form associated with multiorgan failure, prolonged hospital stay, high morbidity, and mortality. Acute necrotizing pancreatitis (ANP) is a severe form of AP. This study evaluates AP's outcomes after applying principles of the step-up approach in a tertiary healthcare center in south India. Methodology This prospective observational study was carried out from January 2021 to December 2022. The study population includes patients admitted to our department with AP. Results Ninety patients were included in the study, most of them were middle-aged males with ethanol ingestion as the common etiology. Thirty-seven (41.1%) patients had mild AP, 25 (27.7%) had moderately severe AP, and 28 (31.1%) had severe AP. Organ failure at admission was noted in 36 (40%) patients. Twenty-three (25.5%) patients developed ANP. Infected necrosis was noted in 3 (3.33%) patients. Eighteen (20%) patients needed image-guided percutaneous drainage. Seven (38.8%) needed necrosectomy following percutaneous drainage. Mortality was observed in 8 (8.8%) patients. Specifically, mortality was noted in 6 (6.6%) patients who presented later in their disease course. Conclusions Percutaneous catheter drainage is a safe and effective therapy to tide over the initial phase of AP. It also serves as a bridging therapy till the patient is clinically fit for a necrosectomy. Severe AP cases presenting late in their course are associated with significant mortality even after step-up management. Standardized protocols for referral and management are essential to obtain a good clinical outcome.

Development and Validation of a Nomogram for Predicting the Severity of the First Episode of Hyperlipidemic Acute Pancreatitis.

Purpose: Early detection of hyperlipidemic acute pancreatitis (HLAP) with exacerbation tendency is crucial for clinical decision-making and improving prognosis. The aim of this study was to establish a reliable model for the early prediction of HLAP severity. Patients and Methods: A total of 225 patients with first-episode HLAP who were admitted to Fujian Medical University Union Hospital from June 2012 to June 2023 were included. Patients were divided into mild acute pancreatitis (MAP) or moderate-severe acute pancreatitis and severe acute pancreatitis (MSAP+SAP) groups. Independent predictors for progression to MSAP or SAP were identified through univariate analysis and least absolute shrinkage and selection operator regression. A nomogram was established through multivariate logistic regression analysis to predict this progression. The calibration, receiver operating characteristic(ROC), and clinical decision curves were employed to evaluate the model's consistency, differentiation, and clinical applicability. Clinical data of 93 patients with first-episode HLAP who were admitted to the First Affiliated Hospital of Fujian Medical University from October 2015 to October 2022 were collected for external validation. Results: White blood cell count, lactate dehydrogenase, albumin, serum creatinine, serum calcium, D-Dimer were identified as independent predictors for progression to MSAP or SAP in patients with HLAP and used to establish a predictive nomogram. The internally verified Harrell consistency index (C-index) was 0.908 (95% CI 0.867-0.948) and the externally verified C-index was 0.950 (95% CI 0.910-0.990). The calibration, ROC, and clinical decision curves showed this nomogram's good predictive ability. Conclusion: We have established a nomogram that can help identify HLAP patients who are likely to develop MSAP or SAP at an early stage, with high discrimination and accuracy.