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BACKGROUND: Despite identifying numerous risk factors for postoperative Hirschsprung-associated enterocolitis (HAEC), predicting individual risk remains challenging. This study aimed to develop a clinical prediction model for predicting the probability of postoperative HAEC within 5 years after surgery in Hirschsprung individuals. METHODS: The study included all children with Hirschsprung disease who underwent definitive surgery at Chiang Mai University Hospital from 2006 to 2021. Concomitant anorectal abnormalities and incomplete data were excluded. A multivariable logistic regression analysis, adjusted for correlated data, was utilized to develop the prediction model. RESULTS: Of the included 274 patients, 75 patients (27.4%) experienced postoperative HAEC within 5 years, totaling 121 episodes. Based on statistical and theoretical significance, eight parameters were utilized as predictors, which included male (OR1.23,95%CI:0.53-2.86), trisomy21(OR1.34,95%CI:0.21-8.45), weight at the time of surgery (OR0.86,95%CI:0.73-1.02), absence of exclusive breastfeeding (OR1.51,95%CI:0.65-3.51), length of the aganglionic segment (rectosigmoid (OR1.32,95%CI:0.48-3.62), long segment (OR41.39,95%CI:3.00-570.37), and total colonic aganglionosis (OR710.20,95%CI:23.55-21420.72)), preoperative stoma (OR1.72,95%CI:0.34-8.58), surgical approach (Duhamel (OR0.06,95%CI:0.01-0.81) and abdominal assisted trans anal endorectal pull-through (OR0.04,95%CI:0.002-0.65)), and early HAEC before two weeks following surgery (OR1.98,95%CI:0.67-5.82). The derived predictive model exhibited acceptable discriminative performance (AuROC:0.749,95%CI:0.679-0.816). Risk groups were categorized into low and high-risk, with positive likelihood ratios of 0.65 and 10.70, respectively. Recommendations for management and follow-up were generated based on these risk groups. An online application has been developed for calculating individual risk of postoperative HAEC and offering management suggestions with follow-up schedule: [https://w1.med.cmu.ac.th/surgery/personnel/pedsurgerycmu/#HAEC-Calculator]. CONCLUSIONS: This risk predictive model accurately estimates the probability of postoperative HAEC within 5 years after surgery in Hirschsprung patients. It facilitates risk stratification and provides personalized recommendations to parents for the prevention and early detection of postoperative HAEC. LEVELS OF EVIDENCE: Level II Retrospective cohort study (Prognosis study).

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BACKGROUND: To construct a nomogram for predicting necrotizing enterocolitis (NEC) in preterm infants. METHODS: A total of 4,724 preterm infants who were admitted into 8 hospitals between April 2019 and September 2020 were initially enrolled this retrospective multicenter cohort study. Finally, 1,092 eligible cases were divided into training set and test set based on a 7:3 ratio. A univariate logistic regression analysis was performed to compare the variables between the two groups. Stepwise backward regression, LASSO regression, and Boruta feature selection were utilized in the multivariate analysis to identify independent risk factors. Then a nomogram model was constructed based on the identified risk factors. RESULTS: Risk factors for NEC included gestational diabetes mellitus, gestational age, small for gestational age, patent ductus arteriosus, septicemia, red blood cell transfusion, intravenous immunoglobulin, severe feeding intolerance, and absence of breastfeeding. The nomogram model developed based on these factors showed well discriminative ability. Calibration and decision curve analysis curves confirmed the good consistency and clinical utility of the model. CONCLUSIONS: We developed a nomogram model with strong discriminative ability, consistency, and clinical utility for predicting NEC. This model could be valuable for the early prediction of preterm infants at risk of developing NEC.

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BACKGROUND: Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease characterized by intestinal inflammation and injury, with high mortality risk. Extracellular cold-inducible RNA-binding protein (eCIRP) is a recently discovered damage-associated molecular pattern that propagates inflammation and tissue injury; however, the role of eCIRP in NEC remains unknown. We hypothesize that eCIRP exacerbates NEC pathogenesis and the novel eCIRP-scavenging peptide, milk fat globule-epidermal growth factor-factor VIII (MFG-E8)-derived oligopeptide 3 (MOP3), attenuates NEC severity, serving as a new therapeutic strategy to treat NEC. METHODS: Stool samples from premature neonates were collected prospectively and eCIRP levels were measured. Wild-type (WT) and CIRP-/- mouse pups were subjected to NEC utilizing a combination of hypoxia and hypercaloric formula orogastric gavage with lipopolysaccharide supplementation. In parallel, WT pups were treated with MOP3 or vehicle. Endpoints including NEC severity, intestinal injury, barrier dysfunction, lung injury, and overall survival were determined. RESULTS: Stool samples from NEC neonates had elevated eCIRP levels compared to healthy age-matched controls (p < 0.05). CIRP-/- pups were significantly protected from NEC severity, intestinal injury, bowel inflammation, intestinal barrier dysfunction, lung injury, and systemic inflammation. NEC survival was 100% for CIRP-/- pups compared to 65% for WT (p < 0.05). MOP3 treatment recapitulated the benefits afforded by CIRP-knockdown, preventing NEC severity, improving inflammatory profiles, and attenuating organ injury. MOP3 treatment improved NEC survival to 80% compared to 50% for vehicle treatment (p < 0.05). CONCLUSIONS: eCIRP exacerbates NEC evidenced by protection with CIRP-deficiency and administration of MOP3, a CIRP-directed therapeutic, in a murine model. Thus, eCIRP is a novel target with human relevance, and MOP3 is a promising treatment for lethal NEC.

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Hirschsprung disease (HD) is a congenital disorder characterized by the absence of ganglion cells in the distal colon and rectum, leading to functional obstruction and severe constipation. Over the past decades, the surgical management of HD has significantly evolved, with minimally invasive surgery (MIS) techniques revolutionizing treatment approaches. This review explores recent innovations in MIS for HD, focusing on laparoscopic, transanal endorectal pull-through (TERPT), and robotic-assisted techniques. These approaches offer numerous advantages over traditional open procedures, including reduced surgical trauma, improved cosmesis, faster recovery times, and potentially lower complication rates. Laparoscopic surgery has become widely adopted, providing excellent visualization and precise dissection. TERPT has gained popularity for short-segment disease, offering a completely transanal approach with minimal scarring. Robotic-assisted surgery represents the cutting edge, enhancing surgical precision and dexterity. The review also examines emerging technologies and future directions, such as advanced imaging techniques, artificial intelligence applications, and potential developments in tissue engineering. While MIS techniques have shown promising outcomes, challenges remain in standardizing approaches, addressing long-segment disease, and optimizing long-term functional results. The future of HD surgery lies in personalized approaches that integrate genetic and molecular profiling with advanced surgical technologies. As the field continues to evolve, comprehensive long-term studies and efforts to improve access to specialized care will be crucial to further enhancing outcomes for patients with HD.

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Background: Food allergic (FA) conditions have been classified as immunoglobulin E (IgE) and non-IgE-mediated reactions that affect as many as 8% of young children and 2% of adults in Western countries, and their prevalence seems to be rising. Although the immunologic basis of IgE-mediated FA is well established, the mechanisms that govern non-IgE-mediated FA are not well understood and are marked by a paucity of comprehensive insights. Objective: The purpose of the present report is to examine the current classification and epidemiology of non-IgE-mediated FA, the latest immunologic mechanisms that underlie the three most commonly cited non-IgE FA conditions, viz., eosinophilic esophagitis, food protein-induced enterocolitis, and food protein-induced allergic proctocolitis, and explore what allergist/immunologists in practice should be aware of with regard to the condition. Methods: An extensive research was conducted in medical literature data bases by applying terms such as FA, non-IgE allergy, tolerance, unresponsiveness, cytokines, CD4+ T helper cell pathways, and key cytokine pathways involved in FA. Results: Current evidence now supports the view that immune dysregulation and cytokine-induced inflammation are the fundamental bases for both IgE- and non-IgE-mediated FA. The existing non-IgE-related FA literature is mostly characterized by a relative dearth of mechanistic information in contrast to IgE-mediated FA, in which the immunologic underpinnings as a T helper type 2 directed entity are well established. Although the need for future methodologic research and adherence to rigorous scientific protocols is essential, it is also necessary to acknowledge past contributions that have given much to our understanding of the condition. In the present report, a novel signature cytokine-based classification of IgE-mediated and non-IgE-mediated allergy is proposed that may offer a novel template for future research in the field of non-IgE-mediated FA. Conclusion: The present report provides an overview of the current classification and frequency of IgE- and non-IgE-mediated FAs, and offers insights and potential solutions to address lingering questions, particularly when concerning the latest immunologic mechanisms that underlie the pathogenesis of non-IgE-mediated FA. Although some progress has been made in recent years toward making diagnostic and treatment options available for these conditions, there still remain many lingering questions and concerns to be addressed, which can be fully understood by future research.

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Microbiota and feeding modes influence the susceptibility of premature newborns to necrotizing enterocolitis (NEC) through mechanisms that remain unknown. Here, we show that microbiota colonization facilitated by breastmilk feeding promotes NOD-like receptor family CARD domain containing 5 (Nlrc5) gene expression in mouse intestinal epithelial cells (IECs). Notably, inducible knockout of the Nlrc5 gene in IECs predisposes neonatal mice to NEC-like injury in the small intestine upon viral inflammation in an NK1.1+ cell-dependent manner. By contrast, formula feeding enhances neonatal gut colonization with environment-derived tilivalline-producing Klebsiella spp. Remarkably, tilivalline disrupts microbiota-activated STAT1 signaling that controls Nlrc5 gene expression in IECs through a PPAR-γ-mediated mechanism. Consequently, this dysregulation hinders the resistance of neonatal intestinal epithelium to self-NK1.1+ cell cytotoxicity upon virus infection/colonization, promoting NEC development. Together, we discover the underappreciated role of intestinal microbiota colonization in shaping a disease tolerance program to viral inflammation and elucidate the mechanisms impacting NEC development in neonates.

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Background: Necrotizing enterocolitis (NEC) is a condition characterized by acquired damage to the mucosal lining, predominantly affecting premature infants. Bioinformatics assessments uncovered a notable rise in miR-155-5p expression in the intestinal tissues of infants suffering from NEC. Nevertheless, the development of NEC's underlying mechanisms and the role of miR-155-5p are still not well understood. This research aimed to explore the role of miR-155-5p in NEC and to elucidate its underlying mechanisms. Methods: To replicate NEC in vitro, lipopolysaccharide (LPS) was employed, whereas an in vivo rat model of NEC was established using formula feeding and exposure to hypoxia. Subsequently, levels of inflammatory cytokines, cell survival, and apoptosis rates were assessed. Various biochemical indicators such as glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) were measured utilizing a purchased diagnostic kit. For the assessment of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) within FHC cells, analysis by flow cytometry was conducted. Additionally, the technique of Western blotting was utilized to analyze the levels of ferroptosis-associated proteins. Moreover, hematoxylin and eosin (H&E) staining was carried out to observe the histopathological alterations in the intestinal tissue samples from rats with necrotizing enterocolitis (NEC). Results: Reducing miR-155-5p improved the survival of FHC cells exposed to LPS, decreased cell apoptosis, inflammation, and ferroptosis, and mitigated intestinal damage in NEC rats. Furthermore, SLC7A11 was found to be a direct target of miR-155-5p. The inhibition of miR-155-5p decreased LPS-induced inflammation and ferroptosis in both FHC cells and NEC rats by promoting SLC7A11 expression. This effect was evidenced by increased levels of ferroptosis-related proteins FTH1 and GPX4, decreased COX-2 and ACSL4 levels, lower lipid peroxidation marker MDA, reduced antioxidant markers GSH, SOD, and CAT, fewer IL-6 and TNF-α, and suppression of the IκBα/NF-κB p65 signaling pathway. Conclusions: In conclusion, reducing miR-155-5p could improve intestinal damage in NEC by inhibiting inflammation and ferroptosis. These findings may provide theoretical insights for the development of new therapies for NEC.

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Background: Immune checkpoint inhibitors (ICIs) have greatly improved the survival in several cancers. Immune-related adverse events (irAEs) are common in patients on ICI therapy, as inhibition of cytotoxic T-lymphocyte antigen 4 (CTLA-4) or programmed cell death protein 1 (PD-1) leads to non-selective activation of the immune system. ICI-induced enterocolitis is highly prevalent and corticosteroid administration is the first-line treatment. Selective immunosuppressive therapy was employed for steroid-refractory patients. The monoclonal antibody vedolizumab exhibits gut-specific immunosuppressive effects by targeting the α4ß7 integrin. Case Description: We report a case of corticosteroid-dependent camrelizumab-induced enterocolitis in a 58-year-old man with hepatocellular carcinoma (HCC) who was treated with vedolizumab. The patient's diarrhea resolved following the administration of two doses of vedolizumab (300 mg), and he was able to stop using corticosteroids. He later underwent surgery and HCC treatment, including appropriate management of ICI-induced enterocolitis, and achieved a complete pathological response. Conclusions: This report illustrates the valuable role of vedolizumab in treating ICI-induced enterocolitis that is refractory to corticosteroid treatment.

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Necrotizing enterocolitis (NEC) is a microbiota- and feeding-related gut inflammatory disease in preterm infants. The standard of care (SOC) treatment for suspected NEC is antibiotic treatment and reduced enteral feeding, but how SOC treatment mitigates NEC remains unclear. We explored whether SOC treatment alone or combined with an anti-inflammatory protein (inter-alpha inhibitor protein, IAIP) supplementation improves outcomes in a preterm piglet model of formula-induced NEC. Seventy-one cesarean-delivered preterm piglets were initially fed formula, developing NEC symptoms by day 3, and then randomized into CON (continued feeding) or SOC groups (feeding cessation and antibiotics), each with or without human IAIP (2×2 factorial design). By day 5, IAIP treatment did not significantly influence outcomes, whereas SOC treatment effectively reduced NEC lesions, diarrhea, and bloody stools. Notably, SOC treatment improved gut morphology and function, dampened gut inflammatory responses, altered the colonic microbiota composition, and modulated systemic immune responses. Plasma proteomic analysis revealed the effects of SOC treatment on organ development and systemic inflammatory responses. Collectively, these findings suggest that SOC treatment significantly prevents NEC progression in preterm piglets via effects on gut structure, function, and microbiota, as well as systemic immune and inflammatory responses. Timely feeding cessation and antibiotics are critical factors in preventing NEC progression in preterm infants, while the benefits of additional human IAIP treatment remain to be established.

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Necrotizing enterocolitis (NEC) is one of the most devasting diseases affecting preterm neonates. However, despite a lot of research, NEC's pathogenesis remains unclear. It is known that the pathogenesis is a multifactorial process, including (1) a pathological microbiome with abnormal bacterial colonization, (2) an immature immune system, (3) enteral feeding, (3) an impairment of microcirculation, and (4) possibly ischemia-reperfusion damage to the intestine. Overall, the immaturity of the mucosal barrier and the increased expression of Toll-like receptor 4 (TLR4) within the intestinal epithelium result in an intestinal hyperinflammation reaction. Concurrently, a deficiency in counter-regulatory mediators can be seen. The sum of these processes can ultimately result in intestinal necrosis leading to very high mortality rates of the affected neonates. In the last decade no substantial advances in the treatment of NEC have been made. Thus, NEC animal models as well as in vitro models have been employed to better understand NEC's pathogenesis on a cellular and molecular level. This review will highlight the different models currently in use to study immunological aspects of NEC.

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Food protein-induced enterocolitis syndrome (FPIES) caused by fish and others is prevalent in the Mediterranean regions but is less frequently reported in Japan. This case report describes a 3-year-old Japanese girl who developed FPIES triggered by multiple seafoods, including swordfish, cod, and squid. The diagnosis was confirmed through oral food challenge tests (OFC), which led to repeated vomiting and an increase in thymus and activation-regulated chemokine (TARC) levels. This case highlights the importance of considering fish-induced FPIES in the differential diagnosis of recurrent vomiting in children and suggests the potential utility of TARC levels in diagnosing and monitoring FPIES.

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BACKGROUND: Necrotising enterocolitis (NEC) is a critical gastrointestinal emergency affecting premature and low-birth-weight neonates. Serum amyloid A (SAA), procalcitonin (PCT), and high-mobility group box 1 (HMGB1) have emerged as potential biomarkers for NEC due to their roles in inflammatory response, tissue damage, and immune regulation. AIM: To evaluate the diagnostic value of SAA, PCT, and HMGB1 in the context of NEC in newborns. METHODS: The study retrospectively analysed the clinical data of 48 newborns diagnosed with NEC and 50 healthy newborns admitted to the hospital. Clinical, radiological, and laboratory findings, including serum SAA, PCT, and HMGB1 Levels, were collected, and specific detection methods were used. The diagnostic value of the biomarkers was evaluated through statistical analysis, which was performed using chi-square test, t-test, correlation analysis, and receiver operating characteristic (ROC) analysis. RESULTS: The study demonstrated significantly elevated levels of serum SAA, PCT, and HMGB1 Levels in newborns diagnosed with NEC compared with healthy controls. The correlation analysis indicated strong positive correlations among serum SAA, PCT, and HMGB1 Levels and the presence of NEC. ROC analysis revealed promising sensitivity and specificity for serum SAA, PCT, and HMGB1 Levels as potential diagnostic markers. The combined model of the three biomarkers demonstrating an extremely high area under the curve (0.908). CONCLUSION: The diagnostic value of serum SAA, PCT, and HMGB1 Levels in NEC was highlighted. These biomarkers potentially improve the early detection, risk stratification, and clinical management of critical conditions. The findings suggest that these biomarkers may aid in timely intervention and the enhancement of outcomes for neonates affected by NEC.

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INTRODUCTION: Optimal oxygen saturation targets remain unknown for extremely preterm infants. METHODS: Cohort analysis of eligible preterm infants born <29 weeks' gestation admitted between 2011 and 2018 to centers submitting data to the Canadian Neonatal Network (CNN) database. Site questionnaires to determine saturation targets, alarm settings, and date of change, allowed assignation of centers to intermediate (88-93%) or high (90-95%) saturation targets. A 6-month washout period was applied to sites which switched targets during the study period. Our primary outcome was survival free of major morbidity. Secondary outcomes were death, necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), treated retinopathy of prematurity, and evidence of brain injury during admission. Generalized estimating equations were applied to compensate for demographic differences and site practices. RESULTS: There were 2,739 infants in the high (mean gestational age [GA] 26 ± 1.6 weeks) and 6,813 infants in the intermediate (mean GA 26.2 ± 1.6 weeks) saturation target group. Survival without morbidity was higher in the intermediate target group (adjusted odds ratio [aOR] 1.59; 95% CI: 1.04, 2.45). There was no difference in mortality between groups (aOR 0.81; 95% CI: 0.59, 1.11), in NEC, treated retinopathy, or brain injury. On subgroup analysis, restricting data to sites which switched targets during the study, intermediate saturation targets were associated with lower rates of BPD (aOR 0.45; 95% CI: 0.28, 0.72). CONCLUSION: For neonates <29 weeks' gestation, intermediate saturation target was associated with higher odds of survival without major morbidity compared to higher oxygen saturation target.

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The aim of this study was to compare sequelae and acute kidney injury (AKI) occurrence among patients with necrotizing enterocolitis (NEC) after changing institutional guidelines replacing vancomycin with ampicillin for gram-positive coverage. This was a retrospective, single-center cohort analysis of patients from 2016-2020 (n = 73) with NEC at a surgical neonatal intensive care unit with a high community prevalence of methicillin-resistant Staphylococcus aureus (MRSA). Multivariate logistic regression was utilized to assess associations. Twenty-five (34%) patients had at least 1 sequela related to NEC. Ampicillin containing regimens were not associated with any sequelae type or AKI. Postmenstrual age < 29 weeks at diagnosis ([OR] 5.8 [1.2-28.8], P = .03; and receipt of vasopressors [OR] 3.3 [1.1-10.2], P = .04) were independently associated with sequalae. Stage III NEC was independently associated with AKI, OR 10.6 (2-55.6), P = .005. In conclusion, ampicillin-containing regimens are effective for NEC management at our institution despite a high prevalence of MRSA.

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Objectives: To explore risk factors for Stage-III necrotizing enterocolitis (NEC-III) in preterm neonates. Methods: This was a retrospective case-control study of neonates born <33 weeks gestational age (GA) who were admitted to a tertiary neonatal intensive care unit, between 2015 and 2018. NEC-III cases were compared with Stage-II NEC (NEC-II) and non-NEC controls. Two to four non-NEC controls were matched by GA ± 1 week and date of birth ± 3 months, to one NEC-III case. Univariate and multivariate analyses were used to examine risk factors for NEC-III. Results: Of 1360 neonates born <33 weeks, 71 (5.2%) had NEC-II and above, with 46% being NEC-III. Mean age of onset of NEC-III was 13.7 days versus 23.9 days for NEC-II (p = 0.01). Neonates with NEC-III were of lower GA (NEC-III 25.4 weeks, NEC-II 27.3 weeks, and non-NEC 26 weeks; p = 0.0008) and had higher Score for Neonatal Acute Physiology Perinatal Extension-II scores (NEC-III 47.5, NEC-II 28.4 and non-NEC 37, p = 0.003). Multivariate analysis showed duration of umbilical arterial catheter (UAC) >5 days was significantly associated with the development of NEC-III with adjusted odds ratio (AOR) 3.8; 95% confidence interval (CI) (1.05-13.66) for NEC-III versus non-NEC and AOR 5.57; 95% CI (1.65-18.73), p = 0.006 for NEC-III versus NEC-II. Rupture of membranes (ROM) >1 week was associated with NEC-III (AOR 6.93; 95% CI [1.56-30.69] vs. non-NEC and AOR 11.74; 95% CI [1.14-120.34] vs. NEC-II). Conclusion: The increased association of NEC-III with duration of UAC and ROM could be further examined in prospective studies, and an upper limit for UAC duration could be considered in NEC prevention bundles.

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Reduction-oxidation (redox) chemistry plays a vital role in human homeostasis. These reactions play critical roles in energy generation, as part of innate immunity, and in the generation of secondary messengers with various functions such as cell cycle progression or the release of neurotransmitters. Despite this cornerstone role, if left unchecked, the body can overproduce reactive oxygen species (ROS) or reactive nitrogen species (RNS). When these overwhelm endogenous antioxidant systems, oxidative stress (OS) occurs. In neonates, OS has been associated with retinopathy of prematurity (ROP), leukomalacia, and bronchopulmonary dysplasia (BPD). Given its broad spectrum of effects, research has started to examine whether OS plays a role in necrotizing enterocolitis (NEC). In this paper, we will discuss the basics of redox chemistry and how the human body keeps these in check. We will then discuss what happens when these go awry, focusing mostly on NEC in neonates.

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Preterm newborns represent a population at risk of developing intestinal dysbiosis as well as being predisposed to sepsis and Necrotizing Enterocolitis. Necrotizing Enterocolitis is a condition burdened by many complications and mortality due to an alteration of the intestinal barrier, an immaturity of the immune system, and intestinal dysbiosis. Low gestational age at birth, low birth weight, and early use of antibiotics are other predisposing factors. Instead, breast milk and probiotics are protective factors in providing intestinal homeostasis and microbiome regulation. In this mini-review, we analysed the protective role of probiotics in the onset of Necrotizing Enterocolitis in preterm populations.

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INTRODUCTION: Although pneumoperitoneum from necrotizing enterocolitis or spontaneous intestinal perforation is a surgical emergency, risk stratification to determine which neonates benefit from initial peritoneal drainage (PD) is lacking. METHODS: Using a single-center retrospective review of very low birth weight neonates under 1500 g who underwent PD for pneumoperitoneum (January 2015 to December 2023) from necrotizing enterocolitis or spontaneous intestinal perforation, two cohorts were created: drain "responders" (patients managed definitively with PD; includes placement of a second drain) and "nonresponders" (patients who underwent subsequent laparotomy or died after PD). Antenatal/postnatal characteristics, periprocedural clinical data, and hospital outcomes were compared between responders and nonresponders using Student's t-test, chi-squared test, or Kruskal-Wallis test as appropriate, with P < 0.05 considered significant. RESULTS: Fifty-six neonates were included: 31 (55%) drain responders and 25 (45%) nonresponders. Birth weight, gestational age, sex, ethnicity, use of postnatal steroids, and enteral feeds were similar between the cohorts. Nonresponders had higher base deficits (-3.4 versus -5.0, P = 0.032) and FiO2 (0.25 versus 0.52, P = 0.001) after drain placement. Drain responders had significantly shorter lengths of stay (89 versus 148 days, P = 0.014) and lower mortality (6.4% versus 56%, P < 0.001). A subgroup analysis of the nonresponders showed no differences in birth weight, vasopressor requirement, FiO2, or postdrain base deficit between nonresponders who had a drain alone versus laparotomy following drain placement. CONCLUSIONS: PD remains a viable initial therapy for pneumoperitoneum in premature very low birth weight neonates (< 1500 g), demonstrating clinical response in more than half. Ongoing clinical assessment and judgment is imperative after drain placement to ensure continued clinical improvement.

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BACKGROUND: Necrotizing enterocolitis (NEC) is an inflammatory and necrotizing intestinal emergency that occurs in preterm infants and low birth weight newborns; however, no specific serum biomarkers for the diagnosis of NEC has been identified so far. METHODS: Serum samples were collected from healthy neonatal controls and patients with NEC newly admitted to the Children's Hospital of Chongqing Medical University. ELISA was used to measure serum PK2 levels, and ROC curve analysis was sued to evaluate the diagnostic efficacy of PK2 and other clinical biomarkers. RESULTS: Serum PK2 levels in the NEC group (n = 53) were significantly lower than those in the control group (n = 18), but increased to near-normal levels after the postoperative recovery period. The NLR value of NEC group was higher than that of control group (P < 0.05). There was no significant difference in WBC and PLT count between NEC group and control group (P > 0.05). Serum CRP and PCT levels in NEC group were significantly higher than those in control group (P < 0.001 for CRP and P < 0.05 for PCT, respectively). After surgery, serum CRP, NLR and PCT levels were lower than before surgery, while serum PK2 levels were higher than before surgery (P < 0.05). The areas under the ROC curve (AUC) of PK2, PCT and CRP for the diagnosis of NEC were 0.837, 0.662 and 0.552, respectively. The AUC of PK2 combined with PCT, PK2 combined with CRP, and PK2 combined with PCT and CRP were 0.908, 0.854 and 0.981, respectively. PK2 exhibited the highest diagnostic efficacy for NEC. CONCLUSION: PK2 has higher diagnostic efficacy than PCT and CRP in the diagnosis of NEC; the combination of PK2 and PCT or CRP can significantly improve its diagnostic efficiency, especially when the three are combined at the same time.

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BACKGROUND: Necrotizing enterocolitis is the most severe life-threatening acquired gastrointestinal disorder among preterm neonates. We describe here an outbreak of Clostridium butyricum-related necrotizing enterocolitis in preterm neonates that occurred in three different neonatal centres, in southeast France. METHODS: We defined a confirmed case of C. butyricum-related necrotizing enterocolitis in preterm neonates by the presence of clinical signs according to modified Bell criteria and C. butyricum identified from stool samples using real-time polymerase chain reaction or culture. A phylogenetic analysis of the isolated strains by whole-genome sequencing was also performed. RESULTS: Between 5th and 27th January 2022, we identified 10 confirmed cases of C. butyricum-related necrotizing enterocolitis, including five from Neonatal Centre 1, four from Neonatal Centre 2, and one from Neonatal Centre 3. The attack rate of necrotizing enterocolitis in Neonatal Centre 1 was 7.1% (5/70). The positivity rate of C. butyricum detected from stool samples was higher during the outbreak period (37/276; 13.4%) than outside this period (7/369; 1.9%), while systematic screening was maintained (P<0.001). Phylogenetic analysis showed a clonality between strains inside four clusters. Two clusters included neonates hospitalized in different neonatal centres, suggesting the transmission of C. butyricum strains during the transfer of neonates between neonatal centres. CONCLUSIONS: This outbreak of C. butyricum-related necrotizing enterocolitis confirms a cross-transmission between preterm neonates, including twin or triplet siblings, and involving necrotizing enterocolitis cases together with asymptomatic carriers. After three months of follow-up, no further cases were identified following the implementation of contact precautions with sporicidal agents.