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Background: This study aimed to investigate the prevalence and clinicopathological correlates of intestinal endometriosis, amongst other extra-pelvic endometriosis foci, presenting as bowel obstruction in general surgery practice., Methods: A total of 23 female patients (mean ± SD age: 34.9 ± 6.5 years) who underwent abdominal surgery for acute bowel obstruction and received histopathological diagnosis of endometriosis were included in this retrospective case-series study. Data on patient characteristics, obstetric history, preoperative laboratory and imaging findings, preoperative provisional diagnosis, type of surgical intervention and the pathological diagnosis, and postoperative outcomes were recorded., Results: Definitive diagnoses on histopathological work-up involved intestinal endometriosis (52.2%), scar endometriosis (26.0%), ovarian endometriosis (13.0%) and inguinal endometriosis (8.7%). Postoperative complication, reoperation and recurrence rates were 8.7%, 8.7%, and 13.0%, respectively. Intestinal endometriosis, when compared to other extra-pelvic endometriosis foci (scar and inguinal), was associated with significantly higher preoperative platelet counts (332.0(284.0-528.0)vs. 239.0(223.0-370.0) 10 3 /µL, p = 0.010), lower albumin levels (4.0(2.7-4.7) vs. 4.5(4.2-4.9) g/dL, p = 0.029), higher rates of preoperative CT utilization (91.7% vs. 0.0%, p < 0.001) and emergent surgery (83.3% vs. 0.0%, p = 0.001) and longer LOS (median 4.5 (1.0-26.0) vs. 1.0(1.0-1.0) days, p = 0.001) along with a non-significant tendency for higher postoperative complication (16.7% vs. 0.0%) and ICU stay (25.0% vs. 0.0%) rates., Conclusion: Our findings revealed intestinal endometriosis, predominantly in the terminal ileum/appendix, was the most common extra-pelvic cause of acute bowel obstruction. The scar endometriosis, inguinal endometriosis and ovarian endometriosis appeared to be other potential but less prevalent aetiologies in this setting., Competing Interests: Declarations. Ethics approval and consent to participate: This study was conducted in accordance with the ethical principles stated in the “Declaration of Helsinki” and approved by the Bursa Uludag University Clinical Research Ethics Committee (Date of Approval: 08.07.2024, Protocol No: 2024-10-6). Written informed consent was obtained from each subject. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Coronavirus disease 2019 (COVID-19) vaccines are effective in reducing the prevalence of this disease. However, some patients develop autoimmune diseases after vaccination. We herein report a case of elderly onset intestinal Behçet's disease (BD) with trisomy 8 following COVID-19 vaccination in which the disease was exacerbated by COVID-19 infection. The patient developed refractory stomatitis and genital ulcers two weeks after receiving the second vaccination and presented with bloody stool two years later. Intestinal BD with trisomy 8, exacerbated by COVID-19, was treated with high-dose glucocorticoids and infliximab; however, surgical intervention was required. The findings of this case suggest that the COVID-19 vaccination may induce BD.

Background: Severe acute malnutrition (SAM) is the most life-threatening form of undernutrition, and children hospitalised with complications have unacceptably high mortality. Complicated SAM is a multisystem disease characterised pathophysiologically by muscle wasting, systemic inflammation, metabolic dysfunction, and malnutrition enteropathy including epithelial barrier dysfunction. There is a clear need for novel interventions to address the underlying pathogenic perturbations of complicated SAM., Methods: In this analysis of tertiary outcomes from a phase II multi-centre trial in Zambia and Zimbabwe, multiplex biomarkers were measured in 122 children (57% male) with SAM randomised following stabilisation ('baseline') to one of four interventions for 14 days to treat malnutrition enteropathy: budesonide, N-acetylglucosamine, colostrum, or teduglutide, compared with standard-of-care. Following measurement of 35 biomarkers from day 15 plasma samples using Luminex and ELISA, the dimensionality of biomarker data was reduced using principal component analysis., Findings: Both budesonide and colostrum reduced systemic inflammation (as measured by CD14, IL1-ra, CRP, and LBP), while children receiving colostrum had higher GLP2 and angiopoietin, and lower circulating lipopolysaccharide, suggesting better restoration of epithelial barrier function. N-acetylglucosamine, a precursor for epithelial glycosaminoglycan synthesis, increased biomarkers of epithelial regeneration (EGF, VEGF), and circulating growth factors (angiopoietin, IGFBP-3, and GCSF)., Interpretation: Interventions aimed at ameliorating malnutrition enteropathy showed plausible effects on biomarkers of inflammation and epithelial regeneration, demonstrating an interdependence of systemic inflammation and enteropathy markers seen in structural analysis. Given the interplay between inflammation and tissue restoration in malnutrition, this mechanism of action supports larger trials to determine the clinical benefits of interventions, either alone or in combination, in children with complicated SAM., Funding: This analysis of tertiary outcomes for the TAME trial was funded by a Wellcome grant to JPS (220566/Z/20/Z). The TAME trial was funded by a grant from the Medical Research Council (UK), number MR/P024033/1. AJP is funded by Wellcome (108065/Z/15/Z). Takeda UK provided teduglutide at a discounted price., Competing Interests: Declaration of interests RJP was previously an external consultant to Colostrum UK which provided the bovine colostrum used in these studies. RJP has also been an external consultant to Sterling Technology (USA) and an employee of Pantheryx Inc (USA) who produce and distribute bovine colostrum. There was no bovine colostrum company involvement in the production of this article or editing of its content. SH has had funding for teduglutide studies and lectured and participated in advisory boards on behalf of Takeda., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Purpose: This study aims to explore the value of multiple indicators in the evaluation of risk factors for intestinal adhesion (IA) after appendectomy in children with acute appendicitis (AA)., Methods: A retrospective study was conducted on 608 patients who underwent appendectomy in the Department of Pediatric Surgery, Children's Medical Center of Jilin Province from January 2017 to April 2023, with a one-year follow-up period to record the occurrence of IA after appendectomy. Univariate and multivariate analysis were used to screen the risk factors of postoperative IA, and a prediction model was established to predict postoperative IA., Results: There were 527 patients in the non-IA group and 81 patients in the IA group. Binary Logistic regression was used to determine the strength of correlation with postoperative intestinal adhesion. The risk factors identified were as follows: DS ≥ 43 h (OR = 3.903, 5points), CRP ≥ 65 mg/L (OR = 3.424, 4.5points), PCT ≥ 0.9 µg/L (OR = 8.683, 8points), Surgical duration ≥ 100 min (OR = 6.457, 7points), Appendiceal perforation (OR = 6.073, 6.5points), Postoperative exhaust time ≥ 55 h (OR = 14.483, 10points). After test, the nomogram drawn based on binary logistic regression can obtain good prediction efficiency. In the training set, the area under the curve was 0.960, the sensitivity was 0.898, and the specificity was 0.905. In the test set, the area under the curve was 0.957, the sensitivity was 0.864, and the specificity was 0.906., Conclusion: Postoperative exhaust time ≥ 55 h has a high risk of IA after appendicitis surgery in children. Early recovery of intestinal peristalsis function is essential. This scoring model is a novel and promising method for predicting postoperative IA., Competing Interests: Declarations Ethics approval and consent to participate The study was conducted in accordance with the 1975 Helsinki Declaration ethical guidelines and the study protocol was approved by the Ethics Committee of Children’s Medical Center of Jilin Province [Approval number: 2024-LW-020]. Due to the retrospective nature of the study, informed consent was waived. Consent for publication Not applicable. Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Background: The limited therapeutic options and inconsistent treatment efficacy of Intestinal Behçet's disease complicate its management, with the absence of standardized guidelines further exacerbating the challenges faced by clinicians., Case Presentation: In this case report, we present a patient with refractory intestinal Behçet's disease who experienced treatment failure with prior biologic agents. This case sheds light on managing this complex scenario with Janus kinase (JAK) inhibitors, the patient achieved mucosal healing after switching to Upadacitinib., Conclusion: This case underscores the potential of Upadacitinib as an effective alternative for managing difficult cases of intestinal Behçet's disease., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Sha, Xu, Wang, Qiao, Shi, Jiang, Quan and Liu.)

Background: Portal hypertensive enteropathy (PHE) is a small-bowel lesion observed in patients with portal hypertension. The clinical significance of endoscopic findings in PHE remains unclear. We aimed to clarify the clinical significance and predictive factors of capsule endoscopic findings in patients with PHE based on long-term outcomes., Methods: This retrospective study enrolled 55 patients with PHE (33 males and 22 females; median age, 64 years; range, 23-87) followed for > 3 years using capsule endoscopy (CE) between February 2009 and May 2023. We evaluated the clinical factors affecting PHE exacerbations and the effects of PHE exacerbations on gastrointestinal bleeding by comparing exacerbated and unchanged PHE groups., Results: Overall, 3 (5%) patients showed improvement, 33 (60%) remained unchanged, and 19 (35%) showed exacerbation on follow-up CE. In the exacerbated group, the rates of worsened fibrosis-4 index, exacerbated esophageal varices, and exacerbated portal hypertensive gastropathy were significantly higher than those in the unchanged group (21%, 32%, and 42% vs. 3%, 6%, and 12%, respectively; P < 0.05), and the rate of splenectomy was significantly lower in the exacerbated group than in the unchanged group (5% vs. 39%, respectively; P < 0.01). In multivariate analysis, exacerbation of esophageal varices and absence of splenectomy were significantly associated with PHE exacerbation. The rate of gastrointestinal bleeding after follow-up CE was significantly high in the exacerbated group (log-rank, P = 0.037)., Conclusions: Exacerbation of esophageal varices and splenectomy were significantly associated with exacerbation of PHE. Exacerbated PHE requires specific attention to prevent gastrointestinal bleeding., (© 2024. The Author(s).)

Hyperbaric oxygen (HBO) therapy can attenuate neurological impairment after traumatic brain injury (TBI) and alleviate intestinal dysfunction. However, the role and mechanism of HBO therapy in intestinal dysfunction following TBI remain unclear. Herein, by establishing a mouse model of controlled cortical impact (CCI), we found that HBO therapy reduced histopathological lesions and decreased the levels of inflammatory and oedema proteins in the intestinal tissues of mice 10 days after TBI. We also showed that HBO therapy improved microbiome abundance and probiotic (particularly g&#95;Bifidobacterium ) colonisation in mice post-CCI. Then, we identified that the m 6 A level imcreased notably in injured cortical tissue of CCI+HBO group compared with the CCI group following CCI. Thus, our results suggested that HBO therapy could alleviate TBI-induced intestinal dysfunction and m 6 A might participate in this regulation process, which provides new insights for exploring the specific mechanism and targets of HBO in the treatment of intestinal dysfunction after TBI, thereby improving the therapeutic effect of HBO., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Abstract: Sitosterolemia is a rare autosomal recessive genetic disorder in which patients develop hypercholesterolemia and may exhibit abnormal hematologic and/or liver test results. In this disease, dysfunction of either ABCG5 or ABCG8 results in the intestinal hyperabsorption of all sterols, including cholesterol and, more specifically, plant sterols or xenosterols, as well as in the impaired ability to excrete xenosterols into the bile. It remains unknown how and why some patients develop hematologic abnormalities. Only a few unrelated patients with hematologic abnormalities at the time of diagnosis have been reported. Here, we report on 2 unrelated pedigrees who were believed to have chronic immune thrombocytopenia as their most prominent feature. Both consanguineous families showed recessive gene variants in ABCG5, which were associated with the disease by in silico protein structure analysis and clinical segregation. Hepatosplenomegaly was absent. Thrombopoietin levels and megakaryocyte numbers in the bone marrow were normal. Metabolic analysis confirmed the presence of strongly elevated plasma levels of xenosterols. Potential platelet proteomic aberrations were longitudinally assessed following dietary restrictions combined with administration of the sterol absorption inhibitor ezetimibe. No significant effects on platelet protein content before and after the onset of treatment were demonstrated. Although we cannot exclude that lipotoxicity has a direct and platelet-specific impact in patients with sitosterolemia, our data suggest that thrombocytopenia is neither caused by a lack of megakaryocytes nor driven by proteomic aberrations in the platelets themselves., (© 2024 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)

Purpose: Studies on intestinal Behçet's disease (BD) complicated by myelodysplastic syndrome (MDS) are rare, and no established therapeutic guidelines exist. This study aimed to evaluate the clinical presentation and outcomes of patients with intestinal BD complicated by MDS (intestinal BD-MDS) and suggest a treatment strategy., Materials and Methods: Data from patients with intestinal BD-MDS from four referral centers in Korea who were diagnosed between December 2000 and December 2022 were retrospectively analyzed. Clinical features and prognosis of intestinal BD-MDS compared with age-, sex-matched intestinal BD without MDS were investigated., Results: Thirty-five patients with intestinal BD-MDS were included, and 24 (70.6%) had trisomy 8. Among the 35 patients, 23 (65.7%) were female, and the median age at diagnosis for intestinal BD was 46.0 years (range, 37.0-56.0 years). Medical treatments only benefited eight of the 32 patients, and half of the patients underwent surgery due to complications. Compared to 70 matched patients with intestinal BD alone, patients with intestinal BD-MDS underwent surgery more frequently (51.4% vs. 24.3%; p =0.010), showed a poorer response to medical and/or surgical treatment (75.0% vs. 11.4%; p <0.001), and had a higher mortality (28.6% vs. 0%; p <0.001). Seven out of 35 patients with intestinal BD-MDS underwent hematopoietic stem cell transplantation (HSCT), and four out of the seven patients had a poor response to medical treatment prior to HSCT, resulting in complete remission of both diseases., Conclusion: Patients with intestinal BD-MDS frequently have refractory diseases with high mortalities. HSCT can be an effective treatment modality for medically refractory patients with intestinal BD-MDS., Competing Interests: The authors have no potential conflicts of interest to disclose., (© Copyright: Yonsei University College of Medicine 2024.)

Background: Endoscopic features of intestinal transplant-associated microangiopathy (iTAM) have not been comprehensively investigated. This study aimed to examine the endoscopic characteristics of patients diagnosed with iTAM., Methods: This retrospective analysis included 14 patients pathologically diagnosed with iTAM after stem cell transplantation for hematolymphoid neoplasms (n = 13) or thalassemia (n = 1). The sex, age at diagnosis, endoscopic features, and prognosis of each patient were assessed. Serological markers for diagnosing transplant-associated thrombotic microangiopathy were also evaluated., Results: The mean age at the time of iTAM diagnosis was 40.2 years. Patients diagnosed based on the pathognomonic pathological changes of iTAM presented with diverse symptoms at the times of endoscopic examinations, including diarrhea (n = 10), abdominal pain (n = 5), nausea (n = 4), appetite loss (n = 2), bloody stools (n = 2), abdominal discomfort (n = 1), and vomiting (n = 1). At the final follow-up, six patients survived, while eight patients succumbed, with a median time of 100.5 days (range: 52-247) post-diagnosis. Endoscopic manifestations included erythematous mucosa (n = 14), erosions (n = 13), ulcers (n = 9), mucosal edema (n = 9), granular mucosa (n = 9), and villous atrophy (n = 4). Erosions and/or ulcers were primarily observed in the colon (10/14, 71%), followed by the ileum (9/13, 69%), stomach (4/10, 40%), cecum (5/14, 36%), duodenum (3/10, 30%), rectum (4/14, 29%), and esophagus (1/10, 10%). Cytomegalovirus infection (n = 4) and graft-versus-host disease (n = 2) coexisted within the gastrointestinal tract. Patients had de novo prolonged or progressive thrombocytopenia (6/14, 43%), decreased hemoglobin concentration (4/14, 29%), reduced serum haptoglobin level (3/14, 21%), and a sudden and persistent increase in lactate dehydrogenase level (2/14, 14%). Peripheral blood samples from 12 patients were evaluated for schistocytes, with none exceeding 4%., Conclusions: This study provides a comprehensive exploration of the endoscopic characteristics of iTAM. Notably, all patients exhibited erythematous mucosa throughout the gastrointestinal tract, accompanied by prevalent manifestations, such as erosions (93%), ulcers (64%), mucosal edema (64%), granular mucosa (64%), and villous atrophy (29%). Because of the low positivity for serological markers of transplant-associated thrombotic microangiopathy in patients with iTAM, endoscopic evaluation and biopsy of these lesions are crucial, even in the absence of these serological features., (© 2024. The Author(s).)

Background: Intussusception is one of the most common acute abdominal conditions in pediatric patients, and if left untreated, it may result in intestinal necrosis and even death. The etiology of the disease is unknown and may be related to a variety of factors, and there are only limited reports of small bowel necrosis secondary to abnormal Peyer's node hyperplasia after MMR vaccination., Case Presentation: In this report, we present two infants who had an abnormal proliferation of Peyer's nodes secondary to intussusception eventually leading to small bowel necrosis after MMR vaccination., Conclusions: Intestinal necrosis and infectious shock are the most common causes of infant mortality, and early detection and management are critical., (© 2024. The Author(s).)

BACKGROUND Neurological bowel dysfunction (NBD) due to spinal cord injuries (SCIs) is common and significantly impacts patients' quality of life. This study evaluated the efficacy of quantitative assessment-based nursing interventions on bowel function recovery, quality of life, and caregivers' satisfaction with SCI patients with NBD. MATERIAL AND METHODS The study included 418 SCI patients with NBD. Patients were categorized into 3 cohorts: quantitative assessment-based nursing intervention (QN, n=114), conventional nursing intervention (CN, n=125), or no nursing intervention (DN, n=189). The 3 cohorts were followed over a 6-month period. RESULTS At 6 months post-intervention, patients in the QN and CN cohorts showed significant reductions in symptoms of fecal incontinence, constipation, and abdominal distension compared to the DN cohort. Additionally, defecation time decreased significantly in the QN and CN cohorts compared to both initial measures and the DN cohort. Notably, patients in the QN cohort demonstrated substantial improvement in overall quality of life scores compared to baseline, CN, and DN cohorts. The QN cohort also reported marked improvement in caregivers' satisfaction, surpassing that of caregivers in the CN and DN cohorts. CONCLUSIONS Six months of quantitative assessment-based nursing interventions significantly improved bowel function, quality of life, and caregiver satisfaction in SCI patients with NBD. This intervention appears beneficial for managing NBD in SCI patients and improving their quality of life and caregiver satisfaction.

Background: Behçet's disease (BD) is a chronic systemic disease characterized by vasculitis as the basic pathological change. BD is rare, and gastrointestinal involvement occurs in 3% to 25% of affected patients. This article describes a rare case of intestinal BD along with a literature review of intestinal involvement in BD., Case Presentation: A 50-year-old Han woman from China presented with a > 6-month history of distending pain in the right upper abdomen. Because of mechanical obstruction secondary to stricture formation from an ileocecal ulcer, she underwent radical right colon resection, and postoperative pathologic examination indicated an ileocecal ulcer. The patient was readmitted to the hospital 6 months postoperatively for recurrence of the same symptoms. Colonoscopy indicated obvious narrowing of the anastomosis with an oval-shaped deep ulcer that could not be passed by the endoscope. Pathologic examination showed acute and chronic inflammation of the anastomotic mucosa and granulation tissue. In addition, gastroscopy showed a 3.0- × 4.0-cm giant ulcer at the junction of the descending bulb along with a sinus tract. Moreover, total gastrointestinal computed tomography angiography showed significant thickening of the intestinal wall near the transverse colon, forming a sinus tract at the junction of the antrum and duodenum with a length of about 1.3 cm and width of about 0.2 cm. Further inquiry regarding the patient's medical history revealed that she had developed repeated oral ulcers 3 years previously and repeated eye inflammation 5 years previously. Specimens of the right half of the colon removed 6 months previously were sent to Run Run Shaw Hospital Affiliated to Zhejiang University for consultation. The pathologic examination revealed vasculitis in the submucosa and subserosa, and the patient was finally diagnosed with BD. She began treatment with adalimumab, and repeat gastroenteroscopy revealed that the intestinal ulcer had significantly improved., Conclusions: An oval-shaped deep intestinal ulcer is a characteristic lesion in patients with BD and may involve the intestinal muscle layer. This case emphasizes that BD is a vasculitis affecting multiple organs and can present with a single, deep, clean-edged intestinal ulcer that penetrates the bowel wall to form a sinus tract. Therefore, careful examination and differential diagnosis should be carried out to prevent a poor prognosis. Adalimumab is effective for patients with intestinal BD., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Parenteral nutrition (PN) in children with short bowel syndrome is crucial and lifesaving. Taking care of such patients requires interprofessional practice and multiple team resource management. Home PN (HPN) usage allows patients and families to live regular lives outside hospitals. We share our experiences for the last two decades and identify the risk factors for complications and mortality. A retrospective study of HPN patients was conducted between January 2000 and February 2022. Medical records of age, body weight, diagnosis, length of residual intestines, HPN period, central line attempts, complications, weaning, and survival were collected and analyzed. The patients were classified as HPN free, HPN dependent, and mortality groups. A total of 25 patients received HPN at our outpatient clinic, and one was excluded for the adult age of disease onset. There were 13 patients (54.1%) who were successfully weaned from HPN until the record-enroled date. The overall mortality rate was 20.8% (five patients). All mortality cases had prolonged cholestasis, Child Class B or C, and a positive Pediatric End-Stage Liver Disease (PELD) score. For HPN dependence, extended resection and multiple central line placement were two significant independent factors. Cholestasis, Child Class B or C, and positive PELD score were the most important risk factors for mortality. The central line-related complication rate was not different in all patient groups. The overall central line infection rate was 1.58 per 1000 catheter days. Caution should be addressed to prevent cholestasis and intestinal failure-associated liver disease during the HPN period, to prevent mortality. By understanding the risks of HPN dependence and mortality, preventive procedures could be addressed earlier., Competing Interests: The authors declare no conflict of interest.

Background: Intestinal barrier integrity in the pathogenesis of sepsis is critical. Despite an abundance of evidence, the molecular mechanism of the intestinal barrier in sepsis pathology remains unclear. Here, we report a protective role of polo-like kinase 1 (PLK1) in intestinal barrier integrity during sepsis., Methods: Mice with PLK1 overexpression (CAG-PLK1 mice) or PLK1 inhibition (BI2536-treated mice) underwent caecal ligation and puncture (CLP) to establish a sepsis model. The intestinal barrier function, apoptosis in the intestinal epithelium, mitochondrial function and NF-κB signalling activity were evaluated. To suppress the activation of NF-κB signalling, the NF-κB inhibitor PDTC, was administered. The Caco-2 cell line was chosen to establish an intestinal epithelial injury model in vitro., Results: Sepsis destroyed intestinal barrier function, induced excessive apoptosis in the intestinal epithelium, and disrupted the balance of mitochondrial dynamics in wild-type mice. PLK1 overexpression alleviated sepsis-induced damage to the intestinal epithelium by inhibiting the activation of NF-κB signalling. PLK1 colocalized and interacted with TANK in Caco-2 cells. Transfecting Caco-2 cells with TANK-SiRNA suppressed NF-κB signalling and ameliorated mitochondrial dysfunction, apoptosis and the high permeability of cells induced by lipopolysaccharide (LPS). Furthermore, TANK overexpression impaired the protective effect of PLK1 on LPS-induced injuries in Caco-2 cells., Conclusion: Our findings reveal that the PLK1/TANK/NF-κB axis plays a crucial role in sepsis-induced intestinal barrier dysfunction by regulating mitochondrial dynamics and apoptosis in the intestinal epithelium and might be a potential therapeutic target in the clinic., (© 2022. The Author(s).)

Environmental enteric dysfunction (EED) is an elusive, inflammatory syndrome of the small intestine thought to be associated with enterocyte loss and gut leakiness and lead to stunted child growth. To date, the gold standard for diagnosis is small intestine biopsy followed by histology. Several putative biomarkers for EED have been proposed and are widely used in the field. Here, we assessed in a cross-sectional study of children aged 2-5 years for a large set of biomarkers including markers of protein exudation (duodenal and fecal alpha-1-antitrypsin (AAT)), inflammation (duodenal and fecal calprotectin, duodenal, fecal and blood immunoglobulins, blood cytokines, C-reactive protein (CRP)), gut permeability (endocab, lactulose-mannitol ratio), enterocyte mass (citrulline) and general nutritional status (branched-chain amino acids (BCAA), insulin-like growth factor) in a group of 804 children in two Sub-Saharan countries. We correlated these markers with each other and with anemia in stunted and non-stunted children. AAT and calprotectin, CRP and citrulline and citrulline and BCAA correlated with each other. Furthermore, BCAA, citrulline, ferritin, fecal calprotectin and CRP levels were correlated with hemoglobin levels. Our results show that while several of the biomarkers are associated with anemia, there is little correlation between the different biomarkers. Better biomarkers and a better definition of EED are thus urgently needed., Competing Interests: The authors declare no conflict of interest.

Intestinal Failure (IF) includes the loss of functional intestinal mass and the requirement of long term Parenteral Nutrition (PN) to achieve the development and growth in childhood., Objective: To evaluate the experience in a specialized unit for pediatric patients with IF, describing the clinical cha racteristics of those admitted from November 2009 to December 2019., Patients and Method: Retros pective and descriptive review from clinical records of 24 cases that matched the inclusion criteria. The following variables were recorded: gender, neonatal history, origin unit, patient age and anthropome tric diagnosis at admission to the unit, cause of IF, hospital stay, anthropometric data and parenteral nutrition dependency at discharge. In those patients with a diagnosis of short bowel syndrome (SBS), the cause of intestinal resection and the characteristics of the intestinal remnant were identified: ana tomical classification, remnant length (defining ultra-short as < 25 cm), presence of ileocecal valve, and characteristics of the colon., Results: The median age at admission was 7.8 months. Seventeen cases were preterm. Regarding IF etiology, 10 patients presented SBS, 6 patients with Intestinal Neuromus cular Disease (INMD), 7 children with SBS associated with INMD, and 1 case of intestinal lymphan giectasia. Within the SBS etiologies found in this group, intestinal atresia (8 cases) and necrotizing enterocolitis (9 patients) were the main causes with a similar proportion. Eight patients had no ileo cecal valve. According to anatomical classification, 1 case was Type I, 8 were Type II, and 8 were Type III. Related to bowel length, 3 were ultrashort, besides being Type II; in those with > 40 cm of bowel length, 7 were Type III. Overall average hospital stay was 456.4 days. Enteral autonomy was achieved in 16 patients and 8 cases required home parenteral nutrition., Conclusions: IF requires life support, PN and prolonged hospital stay. The principal etiology of IF is SBS caused by congenital intestinal atresia and necrotizing enterocolitis. Nevertheless, the high frequency of INMD could be attributed to the local protocol analysis. Most of our patients had poor prognosis factors, however, the management by a specialized team allowed the achievement of enteral autonomy in 66.7% of cases.

Despite advances in immunosuppressive prophylaxis and overall supportive care, gastrointestinal (GI) graft-versus-host disease (GVHD) remains a major, lethal side effect after allogeneic hematopoietic stem cell transplantation (allo-HSCT). It has become increasingly clear that the intestinal epithelium, in addition to being a target of transplant-related toxicity and GVHD, plays an important role in the onset of GVHD. Over the last two decades, increased understanding of the epithelial constituents and their microenvironment has led to the development of novel prophylactic and therapeutic interventions, with the potential to protect the intestinal epithelium from GVHD-associated damage and promote its recovery following insult. In this review, we will discuss intestinal epithelial injury and the role of the intestinal epithelium in GVHD pathogenesis. In addition, we will highlight possible approaches to protect the GI tract from damage posttransplant and to stimulate epithelial regeneration, in order to promote intestinal recovery. Combined treatment modalities integrating immunomodulation, epithelial protection, and induction of regeneration may hold the key to unlocking mucosal recovery and optimizing therapy for acute intestinal GVHD., (© 2022. The Author(s).)

Background: Sepsis is a troublesome syndrome that can cause intestinal injury and even high mortality rates. Omega-3 fatty acids (FAs) are known to protect against intestinal damage. Accordingly, the current study set out to explore if omega-3 FAs could affect sepsis-induced intestinal injury with the involvement of the microRNA (miR)-1-3p/Notch3-Smad axis., Methods: First, cecal ligation and perforation (CLP) was performed to establish septic mouse models in C57BL/6J mice, and mouse intestinal epithelial MODE-K cells were induced by lipopolysaccharide (LPS) to establish sepsis cell models. The CLP-induced septic mice or LPS-exposed cells were subjected to treatment with Omega-3 FAs and activin (Smad signaling activator), miR-1-3p inhibitor and over-expressed/short hairpin RNA (oe-/sh)-Notch3 to explore their roles in inflammation, intestinal oxidative stress and cell apoptosis. A dual-luciferase reporter gene assay was further performed to verify the regulatory relationship between miR-1-3p and Notch3., Results: Omega-3 FAs inhibited CLP-induced intestinal injury and ameliorated LPS-induced intestinal epithelial cell injury by down-regulating miR-1-3p, as evidenced by decreased levels of tumor necrosis factor-α, interleukin-1β (IL-1β) and IL-6, in addition to diminished levels of reactive oxygen species, malondialdehyde levels and superoxide dismutase activity. Furthermore, miR-1-3p could down-regulate Notch3, which inactivated the Smad pathway., Conclusion: Collectively, our findings indicated that omega-3 FAs elevate the expression of Notch3 by down-regulating miR-1-3p, and then blocking the Smad pathway to alleviate intestinal epithelial inflammation and oxidative stress injury caused by sepsis., (© 2022. The Author(s).)

Background: Radiotherapy or accidental exposure to ionizing radiation causes severe damage of healthy intestinal tissues. Intestinal barrier function is highly sensitive to ionizing radiation, and loss of epithelial integrity results in mucosal inflammation, bacterial translocation, and endotoxemia. Few studies have of epithelial integrity as a therapeutic target to treat radiation toxicity. Here, we examined the effects of pravastatin (PS) and the molecular mechanisms underlying epithelial integrity on radiation-induced enteropathy., Methods: The radio-mitigative effects of PS were evaluated in a minipig model by quantifying clinical symptoms, and performing histological and serological analyses and mRNA sequencing in intestinal tissues. To evaluate the role of intercellular junctions on radiation damage, we used tight junction regulator and metallothionein 2 (MT2) as treatments in a mouse model of radiation-induced enteropathy. Caco-2 monolayers were used to examine functional epithelial integrityand intercellular junction expression., Finding: Using a minipig model of pharmaceutical oral bioavailability, we found that PS mitigated acute radiation-induced enteropathy. PS-treated irradiated minipigs had mild clinical symptoms, lower intestinal inflammation and endotoxin levels, and improved gastrointestinal integrity, compared with control group animals. The results of mRNA sequencing analysis indicated that PS treatment markedly influenced intercellular junctions by inhibiting p38 MAPK signaling in the irradiated intestinal epithelium. The PS-regulated gene MT2 improved the epithelial barrier via enhancement of intercellular junctions in radiation-induced enteropathy., Interpretation: PS regulated epithelial integrity by modulating MT2 in radiation-damaged epithelial cells. These findings suggested that maintenance of epithelial integrity is a novel therapeutic target for treatment of radiation-induced gastrointestinal damage., Funding: As stated in the Acknowledgments., Competing Interests: Declaration of Competing Interest There are no conflicts of interest to declare., (Copyright © 2021 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Probiotics are widely used in intestinal microbiota imbalance caused by sepsis, however, the protective mechanism is still unclear. This study aimed to explore protective effect of Lacticaseibacillus rhamnosus TR08 on intestinal injury in septic mice., Results: The levels of serum inflammatory factors were reduced significantly in septic mice treated with L. rhamnosus TR08. The levels of sIgA in terminal ileum were significantly higher in probiotic treatment group than sepsis group. Intestinal pathological damage in septic mice improved and the expression of tight junction proteins increased after probiotic treatment. Sequencing of fecal microbiota showed that the abundance and diversity of probiotic treatment group were significantly better than those of sepsis group, and beneficial bacteria increased while some bacteria decreased in the phylum level., Conclusion: L. rhamnosus TR08 could improve the integrity of intestinal barrier, enhance the intestinal mucosal immunity in septic mice, and rebalance the intestinal microecosystem., (© 2021. The Author(s).)

Background: Environmental enteropathy (EE) contributes to growth failure in millions of children worldwide, but its relationship to clinical malnutrition has not been elucidated. We used RNA sequencing to compare duodenal biopsies from adults and children with EE, and from children with severe acute malnutrition (SAM), to define key features of these malnutrition-related enteropathies., Methods: RNA was extracted and sequenced from biopsies of children with SAM in hospital (n=27), children with non-responsive stunting in the community (n=30), and adults living in the same community (n=37) using an identical sequencing and analysis pipeline. Two biopsies each were profiled and differentially expressed genes (DEGs) were computed from the comparisons of the three groups. DEG lists from these comparisons were then subjected to analysis with CompBio software to assemble a holistic view of the biological landscape and IPA software to interrogate canonical pathways., Findings: Dysregulation was identified in goblet cell/mucin production and xenobiotic metabolism/detoxification for both cohorts of children, versus adults. Within the SAM cohort, substantially greater induction of immune response and barrier function, including NADPH oxidases was noted, concordant with broadly reduced expression of genes associated with the brush border and intestinal structure/transport/absorption. Interestingly, down regulation of genes associated with the hypothalamic-pituitary-adrenal axis was selectively observed within the cohort of children with stunting., Interpretation: Gene expression profiles in environmental enteropathy and severe acute malnutrition have similarities, but SAM has several distinct transcriptional features. The intestinal capacity to metabolise drugs and toxins in malnourished children requires further study., Funding: Bill & Melinda Gates Foundation (OPP1066118)., Competing Interests: Declaration of Competing Interest PIT is a consultant to, and holder of equity in MediBeacon Inc, which is developing novel technology to measure intestinal permeability in humans under a patent he partly owns. RDH and CS may receive royalty income based on the CompBio technology they developed, which was licensed by Washington University to PercayAI. All other authors declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.)

Environmental enteric dysfunction (EED) is a subclinical condition of intestinal inflammation, barrier dysfunction and malabsorption associated with growth faltering in children living in poverty. This study explores association of altered duodenal permeability (lactulose, rhamnose and their ratio) with higher burden of enteropathogen in the duodenal aspirate, altered histopathological findings and higher morbidity (diarrhea) that is collectively associated with linear growth faltering in children living in EED endemic setting. In a longitudinal birth cohort, 51 controls (WHZ > 0, HAZ > -1.0) and 63 cases (WHZ< -2.0, refractory to nutritional intervention) were recruited. Anthropometry and morbidity were recorded on monthly bases up to 24 months of age. Dual sugar assay of urine collected after oral administration of lactulose and rhamnose was assessed in 96 children from both the groups. Duodenal histopathology (n = 63) and enteropathogen analysis of aspirate via Taqman array card (n = 60) was assessed in only cases. Giardia was the most frequent pathogen and was associated with raised L:R ratio (p = 0.068). Gastric microscopy was more sensitive than duodenal aspirate in H. pylori detection. Microscopically confirmed H. pylori negatively correlated with HAZ at 24 months (r = -0.313, p = 0.013). Regarding histopathological parameters, goblet cell reduction significantly correlated with decline in dual sugar excretion (p< 0.05). Between cases and controls, there were no significant differences in the median (25th, 75th percentile) of urinary concentrations (μg/ml) of lactulose [27.0 (11.50, 59.50) for cases vs. 38.0 (12.0, 61.0) for controls], rhamnose [66.0 (28.0, 178.0) vs. 86.5 (29.5, 190.5)] and L:R ratio [0.47 (0.24, 0.90) vs. 0.51 (0.31, 0.71)] respectively. In multivariable regression model, 31% of variability in HAZ at 24 months of age among cases and controls was explained by final model including dual sugars. In conclusion, enteropathogen burden is associated with altered histopathological features and intestinal permeability. In cases and controls living in settings of endemic enteropathy, intestinal permeability test may predict linear growth. However, for adoption as a screening tool for EED, further validation is required due to its complex intestinal pathophysiology., Competing Interests: The authors have declared that no competing interests exist.

Chronic intestinal failure (CIF) is a rare but feared complication of Crohn's disease. Depending on the remaining length of the small intestine, the affected intestinal segment, and the residual bowel function, CIF can result in a wide spectrum of symptoms, from single micronutrient malabsorption to complete intestinal failure. Management of CIF has improved significantly in recent years. Advances in home-based parenteral nutrition, in particular, have translated into increased survival and improved quality of life. Nevertheless, 60% of patients are permanently reliant on parenteral nutrition. Encouraging results with new drugs such as teduglutide have added a new dimension to CIF therapy. The outcomes of patients with CIF could be greatly improved by more effective prevention, understanding, and treatment. In complex cases, the care of patients with CIF requires a multidisciplinary approach involving not only physicians but also dietitians and nurses to provide optimal intestinal rehabilitation, nutritional support, and an improved quality of life. Here, we summarize current literature on CIF and short bowel syndrome, encompassing epidemiology, pathophysiology, and advances in surgical and medical management, and elucidate advances in the understanding and therapy of CIF-related complications such as catheter-related bloodstream infections and intestinal failure-associated liver disease., Competing Interests: Conflict-of-interest statement: Aksan A reports congress expenses, consultancy fees and research funding from Vifor Pharma and Immundiagnostik AG. Farrag K reports speakers’ honoraria and congress expenses from Immundiagnostik AG, Janssen Cilag GmbH; consultancy honoraria from Vifor Pharma. Blumenstein I reports consultancy honoraria from AbbVie Deutschland, Amgen GmbH, Bristol Myers Squibb, Janssen Cilag GmbH, Fresenius Kabi Deutschland, Pharmacosmos GmbH, Pfizer GmbH, Shire Deutschland GmbH, Takeda Pharma GmbH; honoraria from AbbVie Deutschland, Biogen GmbH, DGVS, Dr. Falk Pharma GmbH, Endoakademie, Ferring Arzneimittel, Fraunhofer, Fresenius Kabi Deutschland, Kompetenznetz Darmerkrankungen, MSD Sharp Dome, Mylan GmbH, Pfizer GmbH, Janssen Cilag GmbH, Shire Deutschland GmbH, Takeda Pharma GmbH. Schroeder O reports congress expenses from Abbvie, Falk, Janssen, Takeda; speakers’ honoraria from Abbvie, Falk, Janssen, Takeda, Norgine, Pfizer. Dignass A reports consultancy honoraria from Abbott, Pharmacosmos, MSD, Ferring, Janssen, Pfizer, Otsuka, Roche/Genentech, Takeda, Falk; grants from Institut für Gemeinwohl & Stiftung Leben mit Krebs; Lecturing: Falk, Ferring, MSD, Abbott, Janssen, Pfizer, Otsuka, Vifor, Stiftung Leben mit Krebs, Kompetenznetz CED, Takeda, Pharmacosmos; Manuscript preparation: Falk. Education presentations: Abbott, Pharmacosmos, Falk, Ferring. Stein J reports personal fees from Abbvie, personal fees from Dr Schär, personal fees from Falk, personal fees from Ferring, personal fees from Fresenius Kabi, personal fees from Immundiagnostik AG, personal fees from Janssen, personal fees from Medice, personal fees from MSD, personal fees from Pfizer, personal fees from Pharmacosmos, personal fees from Shire, personal fees from Shield, personal fees from Takeda, personal fees from ThermoFisher, personal fees from Vifor Pharma, from NPS, outside the submitted work., (©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.)

The intestine can be the target of several immunologically mediated diseases, including graft-versus-host disease (GVHD) and inflammatory bowel disease (IBD). GVHD is a life-threatening complication that occurs after allogeneic hematopoietic stem cell transplantation. Involvement of the gastrointestinal tract is associated with a particularly high mortality. GVHD development starts with the recognition of allo-antigens in the recipient by the donor immune system, which elicits immune-mediated damage of otherwise healthy tissues. IBD describes a group of immunologically mediated chronic inflammatory diseases of the intestine. Several aspects, including genetic predisposition and immune dysregulation, are responsible for the development of IBD, with Crohn's disease and ulcerative colitis being the two most common variants. GVHD and IBD share multiple key features of their onset and development, including intestinal tissue damage and loss of intestinal barrier function. A further common feature in the pathophysiology of both diseases is the involvement of cytokines such as type I and II interferons (IFNs), amongst others. IFNs are a family of protein mediators produced as a part of the inflammatory response, typically to pathogens or malignant cells. Diverse, and partially paradoxical, effects have been described for IFNs in GVHD and IBD. This review summarizes current knowledge on the role of type I, II and III IFNs, including basic concepts and controversies about their functions in the context of GVHD and IBD. In addition, therapeutic options, research developments and remaining open questions are addressed., Competing Interests: RZ received honoraria from Novartis, Incyte and Mallinckrodt. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Haring, Zeiser and Apostolova.)

Background: Environmental enteric dysfunction (EED) may influence growth during and recovery from moderate acute malnutrition (MAM), however, biomarkers to assess these relations have yet to be identified., Objectives: The objectives of this study were to: 1) develop a score for EED based on host fecal mRNA transcripts, 2) compare biomarkers of EED with each other, and 3) examine associations between the EED biomarkers and recovery from MAM and growth outcomes., Methods: In a cohort of 520 Sierra Leonean MAM children, biomarkers of EED included the lactulose: mannitol (L: M) test, 15 host fecal mRNA transcripts, and host fecal proteins [α-1-antitrypsin (AAT), myeloperoxidase (MPO), neopterin (NEO)]. Anthropometry data were also collected and z scores were computed for length-for-age (LAZ) and weight-for-length (WLZ). Recovery from MAM was defined as midupper arm circumference ≥12.5 cm. Factor analysis was used to identify EED scores using the mRNA transcripts, and mixed effects regression was conducted to test for associations., Results: The 15 host fecal mRNA transcripts were clustered into 3 scores: gut inflammation (GI) score, gut structure (GS) score, and gut defense (GD) score. We found agreement between certain inflammation markers (GI score and MPO), and permeability markers (GS score and AAT; AAT and the L: M excretion ratio). Antimicrobial gut defense (GD score) was inversely associated with percent lactulose excreted, a measure of intestinal permeability. LAZ (β: -0.08; 95% CI: -0.14, -0.02) and WLZ (β: -0.03; 95% CI: -0.06, -0.01) were negatively associated with GI score. A high GD score (β: 0.36; 95% CI: 0.08, 0.64) and low AAT (β: -1.35; 95% CI: -2.35, -0.36) were associated with recovery from MAM., Conclusions: Scores derived from host fecal mRNA transcript variably correlated with the L: M test and host fecal proteins. Markers of intestinal inflammation, permeability, and defense were associated with growth outcomes and recovery from MAM., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background: Child stunting remains a poorly understood, prevalent public health problem. Environmental enteric dysfunction (EED) is hypothesized to be an important underlying cause., Objectives: Within a subgroup of 1169 children enrolled in the SHINE (Sanitation Hygiene Infant Nutrition Efficacy) trial in rural Zimbabwe, followed longitudinally from birth to 18 mo of age, we evaluated associations between the concentration of 11 EED biomarkers and linear growth velocity., Methods: At infant ages 1, 3, 6, 12, and 18 mo, nurses measured child length and collected stool and blood; the lactulose-mannitol urine test was also conducted at all visits except at 1 mo. Stool neopterin, α-1 antitrypsin, myeloperoxidase, and regenerating gene 1β protein; urinary lactulose and mannitol; and plasma kynurenine, tryptophan, C-reactive protein, insulin-like growth factor-1 (IGF-1), soluble CD14, intestinal fatty acid binding protein, and citrulline were measured. We analyzed the change in relative [∆ length-for-age z score (LAZ)/mo] and absolute (∆ length/mo) growth velocity during 4 age intervals (1-3 mo; 3-6 mo; 6-12 mo; and 12-18 mo) per SD increase in biomarker concentration at the start of each age interval., Results: In fully adjusted models, we observed only 3 small, statistically significant associations: kynurenine:tryptophan ratio at 12 mo was associated with decreased mean LAZ velocity during the 12-18 mo interval (-0.015 LAZ/mo; 95% CI: -0.029, -0.001 LAZ/mo); mannitol excretion at 6 mo was associated with increased LAZ velocity during the 6-12 mo interval (0.013 LAZ/mo; 95% CI: 0.001, 0.025 LAZ/mo), and plasma IGF-1 at 1 mo was associated with increased LAZ velocity during the 1-3 mo interval (0.118 LAZ/mo; 95% CI: 0.024, 0.211 LAZ/mo). Results for absolute growth velocity were similar, except IGF-1 was also associated with growth during the 12-18 mo interval. We found no other associations between any EED biomarker and linear growth velocity., Conclusions: None of 11 biomarkers of EED were consistently associated with linear growth among Zimbabwean children.This trial was registered at clinicaltrials.gov as NCT01824940., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Intestinal transplantation (ITx) is the treatment of choice for patients with intestinal failure who have developed life-threatening complications related to long-term parenteral nutrition. Patients may also undergo ITx as part of a combined liver-intestine or multivisceral transplant for a variety of indications, most commonly intestinal failure-associated liver disease or porto-mesenteric thrombosis. Endoscopy plays a critical role in the posttransplant management of these patients, most commonly in the diagnosis and management of rejection, which occurs in up to 30-40% of patients within the first-year posttransplant. With a lack of noninvasive biomarkers to identify the presence of rejection, endoscopy and biopsy remain the gold standard for its diagnosis. Endoscopic evaluation of the graft is also important in the identification of other complications post-ITx, including posttransplant lymphoproliferative disorder, graft-versus-host disease, and enteric infections. Each patient's posttransplant anatomy may be slightly different, making endoscopy sometimes technically challenging and necessitating clear and frequent communication with the surgical team in order to help identify the highest yield approach. Herein, we review the most common pathologies found endoscopically in the post-ITx patient and describe some of the unique challenges the endoscopist faces when evaluating these complex patients., (© 2020 The American Society of Transplantation and the American Society of Transplant Surgeons.)

Intestinal fibrosis is the most common complication of Crohn's disease (CD) that is one major disorder of inflammatory bowel disease (IBD), but the precise mechanism remains unclear. MiR-155 has been involved in fibrotic diseases. Here, we determined the role of miR-155 in regulating intestinal fibrosis. MiR-155 levels were significantly up-regulated in CD patients with intestinal stricture CD. The overexpression of miR-155 significantly aggravated TNBS-induced CD-associated intestinal fibrosis. Mechanistically, we identified that HBP1, a negative regulator of the Wnt/β-catenin signalling pathway, is a direct target of miR-155. Moreover, in vitro and in vivo experiments suggested that the miR-155/HBP1 axis activates Wnt/β-catenin signalling pathway to induce intestinal fibrosis. Taken together, we demonstrated that miR-155 directly targets HBP1 to induce CD-associated intestinal fibrosis via Wnt/β-catenin signalling pathway., (© 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Introduction: Objectives: in routine clinical practice many disorders are found that can disrupt the sequence of reactions in digestion and absorption, leading to malnutrition and requiring the use of oral nutritional supplements (ONS). The objective of our study was to evaluate in a real world setting the use of and compliance with a peptide-based ONS in malnourished adult patients with intestinal compromise after more than 14 days of parenteral nutrition. Material and methods: the study was carried out in 44 malnourished patients who required total parenteral nutrition for at least 14 days without using the oral route during their hospital stay. All patients were administered, on an outpatient basis, 1 brick per day of Vital 1.5® for 12 weeks. At the beginning of treatment and after the intervention period evaluated, the following variables were collected: weight, height, body mass index (BMI), global subjective assessment test, nutritional biochemistry, 3-day nutritional survey, adverse effects generated by the formula, and completion rate. Results: 44 patients were enrolled. Mean age was 70.4 ± 10.4 years (20 women & 24 men). After the intervention the following parameters had increased: BMI (0.51 ± 0.1 kg/m2; p = 0.02), weight (1.4 ± 0.3 kg; p = 0.03), prealbumin (3.5 ± 4.1 mg/dl; p = 0.01), albumin (1.3 ± 0.1 mg/dl; p = 0.03), and transferrin (71.5 ± 24.1 mg/dl; p = 0.02). Dietary intake of the ONS represented 14.4 % of the diet's total caloric intake at 3 months, 17.5 % of carbohydrates, 12.9 % of proteins, and 12.3 % of fats. Mean compliance was 87.7 ± 7.2 % of the prescribed intakes. In relation to the nutritional situation, at the beginning of the study, 52.3 % (n = 23) of patients were in the global subjective assessment test in category B (moderate malnutrition or nutritional risk), and 47.7 % (n = 21) in category C (severe malnutrition). After the intervention, 75 % of patients were in category A (n = 33), 13.6 % (n = 6) in category B, and 11.4 % (n = 5) in category C. Conclusions: the use of a peptide-based ONS with short-chain triglycerides in outpatients showed a beneficial effect on biochemical and anthropometric parameters, and improved the nutritional status of patients with high compliance and good tolerance rates.

Abstract: Factors related to developing postoperative ileus (POI) vary from pharmacologic, inflammatory, hormonal, metabolic, gastrointestinal physiology, neurologic, to psychological factors. Although orthopedic-related incidence of postoperative ileus is about 10%, these studies are limited to spine surgery and pelvic surgery. The purpose of this study was to investigate prevalence of POI and to analyze effect of chewing gum on POI and bowel function in elderly patients after hip fracture surgery.A prospective randomized controlled trial was conducted at the Gyeongsang National University Hospital. Elderly patients with hip fracture who underwent surgery from March 2017 to June 2018 were eligible to participate. Patients were excluded if they had a mastication disability, impaired cognitive function, previous history of gastrointestinal disease, respiratory disease and low oxygen saturation, hip arthroplasty with causes other than hip fractures, acetabular fractures, periprosthetic fractures, or pathological fractures. Patients with consciousness problem by excessive anesthesia were also excluded. Patients were classified into 2 groups by randomization. Group I received sugar-free gum and were encouraged to chew 6 hours following surgery until the first intestinal gas is released. Group II was given the same postoperative procedure and encouraged to consume water after 6 hours.After applying exclusion criteria, 74 patients were finally included. Thirty-one patients were classified to Group I and 43 patients were classified to the Group II. Prevalence of POI in all patients with hip fracture was 63.5% (47/74). Prevalence of POI in Group I was statistically significant lower than that in Group II (Group I: 41%, Group II: 79.1%, P = .01)The prevalence of POI in elderly patients with hip fracture was 63.5%. Chewing gum had a significant effect on reduction of POI in elderly patients with hip fractures., Competing Interests: The authors have no conflicts of interests to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Cancer cachexia is a multifactorial syndrome characterized by multiple metabolic dysfunctions. Besides the muscle, other organs such as the liver and the gut microbiota may also contribute to this syndrome. Indeed, the gut microbiota, an important regulator of the host metabolism, is altered in the C26 preclinical model of cancer cachexia. Interventions targeting the gut microbiota have shown benefits, but mechanisms underlying the host-microbiota crosstalk in this context are still poorly understood., Methods: To explore this crosstalk, we combined proton nuclear magnetic resonance ( 1 H-NMR) metabolomics in multiple compartments with 16S rDNA sequencing. These analyses were complemented by molecular and biochemical analyses, as well as hepatic transcriptomics., Results: 1 H-NMR revealed major changes between control (CT) and cachectic (C26) mice in the four analysed compartments (i.e. caecal content, portal vein, liver, and vena cava). More specifically, glucose metabolism pathways in the C26 model were altered with a reduction in glycolysis and gluconeogenesis and an activation of the hexosamine pathway, arguing against the existence of a Cori cycle in this model. In parallel, amino acid uptake by the liver, with an up to four-fold accumulation of nine amino acids (q-value <0.05), was mainly used for acute phase response proteins synthesis rather than to fuel the tricarboxylic acid cycle and gluconeogenesis. We also identified a 35% reduction in hepatic carnitine levels (q-value <0.05) and a lower activation of the phosphatidylcholine pathway as potential contributors to the hepatic steatosis present in this model. Our work also reveals a reduction of different beneficial intestinal bacterial activities in cancer cachexia. We found decreased levels of two short-chain fatty acids, acetate and butyrate (72% and 88% reduction in C26 caecal content; q-value <0.001), and a reduction in aromatic amino acid metabolites, which may contribute to the altered intestinal homeostasis in these mice. A member of the Ruminococcaceae family (ASV 2) was identified as the main bacterium responsible for the drop in butyrate. Finally, we report a two-fold intestinal transit acceleration (P-value <0.001) as a key factor shaping the gut microbiota composition and activity in cancer cachexia, which together lead to a faecal loss of proteins and amino acids., Conclusions: Our work highlights new metabolic pathways potentially involved in cancer cachexia and further supports the interest of exploring the gut microbiota composition and activity, as well as intestinal transit, in cancer patients with and without cachexia., (© 2021 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.)

Amino-acids (AAs) are the exclusive source of nitrogen for cells. AAs result from the breakdown of food proteins and are absorbed by mucosa of the small intestine that act as a barrier to harmful materials. The quality of food proteins may differ, since it reflects content in Essential-AAs (EAAs) and digestibility but, until now, attention was paid mainly to the interaction between indigested proteins as a whole and microbiota. The link between microbiome and quality of proteins has been poorly studied, although these metabolic interactions are becoming more significant in different illnesses. We studied the effects of a special diet containing unbalanced EAAs/Non-EAAs ratio, providing excess of Non-EAAs, on the histopathology of gut epithelium and on the microbiome in adult mice, as model of qualitative malnutrition. Excess in Non-EAAs have unfavorable quick effect on body weight, gut cells, and microbiome, promoting weakening of the intestinal barrier. Re-feeding these animals with standard diet partially reversed the body alterations. The results prove that an unbalanced EAAs/Non-EAAs ratio is primarily responsible for microbiome modifications, not vice-versa. Therefore, treating microbiota independently by treating co-existing qualitative malnutrition does not make sense. This study also provides a reproducible model of sarcopenia-wasting cachexia like the human protein malnutrition.

Small intestinal bacterial overgrowth (SIBO) occurs commonly, is difficult to treat, and frequently recurs. Bovine colostrum (BC) and chicken eggs contain immunoglobulins and other components that possess antimicrobial, immunoregulatory, and growth factor activities; however, it is not known if they have the ability to reduce injury caused by the presence of bacteria associated with SIBO ( Streptococcus , Escherichia coli , Staphylococcus , Bacteroides , Klebsiella , Enterococcus , and Proteus ) and infectious diarrhea (enteropathogenic Escherichia coli , Salmonella ). We examined the effects of BC, egg, or the combination, on bacterial growth and bacteria-induced changes in transepithelial electrical resistance (TEER) and bacterial translocation across confluent Caco-2 monolayers. BC, egg, or the combination did not affect bacterial growth. Adding bacteria to monolayers reduced TEER and (with minor variations among species) increased bacterial translocation, increased monolayer apoptosis (increased caspase-3 and Baxα, reduced Bcl2), increased intercellular adhesion molecule 1 (ICAM-1), and reduced cell adhesion molecules zonulin1 (ZO1) and claudin-1. BC, egg, or the combination reduced these effects (all p < 0.01) and caused additional increases in vascular endothelial growth factor (VEGF) and Heat Shock Protein 70 (Hsp70) expression. We conclude that BC ± egg strengthens mucosal integrity against a battery of bacteria relevant for SIBO and for infectious diarrhea. Oral BC ± egg may have clinical value for these conditions, especially SIBO where eradication of precipitating organisms may be difficult to achieve.

Loop ileostomy closure after colorectal surgery is often associated with Postoperative ileus, with an incidence between 13-20%. The aim of this study is to evaluate the efficacy and safety of preoperative stimulation of the efferent loop with probiotics prior to ileostomy closure in patients operated on for colorectal carcinoma. For this, a prospective, randomized, double-blind, controlled study is designed. All patients who underwent surgery for colorectal carcinoma with loop ileostomy were included. Randomized and divided into two groups, 34 cases and 35 controls were included in the study. Postoperative ileus, the need for nasogastric tube insertion, the time required to begin tolerating a diet, restoration of bowel function, and duration of hospital stay were evaluated. The incidence of Postoperative ileus was similar in both groups, 9/34 patients stimulated with probiotics and 10/35 in the control group (CG) with a p = 0.192. The comparative analysis showed a direct relationship between Postoperative ileus after oncological surgery and Postoperative ileus after reconstruction surgery, independently of stimulation. Postoperative ileus after closure ileostomy is independent of stimulation of the ileostomy with probiotics through the efferent loop. There seem to be a relationship between Postoperative ileus after reconstruction and the previous existence of Postoperative ileus after colorectal cancer surgery.

Introduction: Endometriosis is associated with a high number of chronic pelvic pain and reduced quality of life. Colorectal resections in case of bowel involvement of endometriosis are associated with an unneglectable morbidity in young and healthy patients. There is no linear correlation established between the degree of symptoms and stage of endometriosis. The aim of this study was to correlate the histological findings to preoperative pain scores in colorectal resected patients with endometriosis., Methods: Twenty-five patients who underwent laparoscopic colorectal resection for endometriosis between 2014 and 2019 were included in this retrospective study. Pain level was assessed preoperatively and postoperatively via phone call in May 2020. Histopathology was correlated to preoperative symptoms and postoperative outcome., Results: Average follow-up time was 38.68 months (± 19.92). Preoperative VAS-score was 8.32 (± 1.70). We observed a significant reduction of pain level in all patients after surgery (p ≤ 0.005). Pain levels were equal regarding the presence of satellite spots and various degrees of infiltration depth. The resection margins were clear in all patients. Postoperative complications occurred in 6 cases (24%) and anastomotic leakage was observed in 3 patients (12%). Average VAS-score at time of follow-up was 1.70 (± 2.54)., Conclusion: Our data demonstrate that adequate colorectal resection leads to reduction of pain and an increase of quality of life irrespective of histopathological findings. An experienced team is necessary to improve intraoperative outcome and to reduce postoperative morbidity in case of complication.

Backgroud: Exposure to high-dose radiation, such as after a nuclear accident or radiotherapy, elicits severe intestinal damage and is associated with a high mortality rate. In treating patients exhibiting radiation-induced intestinal dysfunction, countermeasures to radiation are required. In principle, the cellular event underlying radiation-induced gastrointestinal syndrome is intestinal stem cell (ISC) apoptosis in the crypts. High-dose irradiation induces the loss of ISCs and impairs intestinal barrier function, including epithelial regeneration and integrity. Notch signaling plays a critical role in the maintenance of the intestinal epithelium and regulates ISC self-renewal. Ghrelin, a hormone produced mainly by enteroendocrine cells in the gastrointestinal tract, has diverse physiological and biological functions., Purpose: We investigate whether ghrelin mitigates radiation-induced enteropathy, focusing on its role in maintaining epithelial function., Methods: To investigate the effect of ghrelin in radiation-induced epithelial damage, we analyzed proliferation and Notch signaling in human intestinal epithelial cell. And we performed histological analysis, inflammatory response, barrier functional assays, and expression of notch related gene and epithelial stem cell using a mouse model of radiation-induced enteritis., Results: In this study, we found that ghrelin treatment accelerated the reversal of radiation-induced epithelial damage including barrier dysfunction and defective self-renewing property of ISCs by activating Notch signaling. Exogenous injection of ghrelin also attenuated the severity of radiation-induced intestinal injury in a mouse model., Conclusion: These data suggest that ghrelin may be used as a potential therapeutic agent for radiation-induced enteropathy., (Copyright © 2020 The Authors. Published by Elsevier GmbH.. All rights reserved.)

Intestinal failure-associated liver disease (IFALD) remains one of the most common and serious complications of parenteral nutrition (PN), causing a wide spectrum of hepatic manifestations from steatosis and mild cholestasis to portal hypertension and end-stage liver failure. The prevalence of IFALD depends on the diagnostic criteria and ranges from 4.3% to 65%. Moreover, many factors are shown to contribute to its development, including nutrient deficiencies, toxicity of PN, infections, and alterations of bile acid metabolism and gut microbiota. Prevention and management of IFALD aim at ameliorating or eliminating the risk factors associated with IFALD. The use of PN formulations with a lower ratio omega-6-to-omega-3 polyunsaturated fatty acids, cycle PN, optimization of enteral stimulation and prevention and early treatment of infections constitute the main therapeutic targets. However, failure of improvement and severe IFALD with end-stage liver failure should be considered as the indications of intestinal transplantation. The aim of this review is to provide an update of the epidemiology, pathophysiology, and diagnosis of IFALD in the adult population as well as to present a clinical approach of the therapeutic strategies of IFALD and present novel therapeutic targets., Competing Interests: None

There are fewer than 100 documented cases of transanal small bowel evisceration in the literature. We report two cases of this rare surgical emergency in an 84-year old man and a 79-year old woman. Both patients required urgent laparotomy, resection of ischaemic bowel and transabdominal resection of the rectal defect with colostomy. Postoperative recovery was uneventful. Rare imaging and clinical photography are shared to highlight the extreme nature of this condition. We identified 38 relevant cases of reported bowel evisceration through our literature review. Most patients were elderly women with untreated rectal prolapse. Gynaecological comorbidity was another risk factor. The aetiological mechanism is suspected to stem from chronic ischaemic insult to the rectal wall, resulting in thinning and subsequent perforation. Surgical management may consist of primary suture repair of the rectal tear, or a Hartmann's procedure. Timely intervention is essential to minimise patient morbidity and mortality.

Posttransplant lymphoproliferative disorder is a serious, life-threatening complication in organ transplant patients receiving immunosuppressive therapy. Isolated posttransplant lymphoproliferative disorder of the gastrointestinal tract is rare. Posttransplant lymphoproliferative disorder encompasses a spectrum of clinical manifestations, in addition to a wide range of histopathological findings, from B-cell hyperplasia to lymphoma. Renal transplant patients with small intestinal posttransplant lymphoproliferative disorder are more likely to be of younger age, but less frequently represent Hodgkin and Hodgkin-like lesions. They also have better patient survival compared with transplant recipients with posttransplant lymphoproliferative disorder in other locations. We report on the treatment of a kidney transplant recipient with confirmed isolated posttransplant lymphoproliferative disorder in the small intestine. The patient presented with acute abdomen and small intestine perforation, 17 years after kidney transplant, despite being without calcineurin inhibitor in immunosuppressive therapy, to mitigate previous ductal breast carcinoma. Pathological examinations revealed isolated EpsteinBarr virus-positive diffuse large B-cell non-Hodgkin lymphoma of small intestine, clinical stage IV A E. The patient was treated with reduction of immunosuppression, rituximab, and the CHOP regimen (ie, cyclophosphamide, doxorubicin, vincristine, and prednisone). A complete remission was achieved. Kidney allograft function was stable throughout the follow-up period. Physicians should consider isolated gastrointestinal posttransplant lymphoproliferative disorder as a possible etiology in posttransplant, immunocompromised patients who present with different gastrointestinal symptoms. Given good clinical response to treatment, early identification of posttransplant lymphoproliferative disorder has a key role in monitoring and treatment.

Methods: A retrospective study on SJS patients was conducted at a tertiary medical center. All patients diagnosed as SJS, with available serum amylase index, were included. Clinical data of all subjects were retrospectively collected and analyzed. Colonic mucosal biopsies were obtained to measure tight junction protein expression., Results: A total of nine patients were included in the present study for study analysis. The average serum amylase of the study cohort was 228.78 ± 204.18 U/L. Among which, five patients had a positive fecal occult blood test (FOBT). Colonic mucosal biopsies were obtained and stained with occludin and zonula occludens-1 (ZO-1). The expression of occludin and ZO-1 was significantly downregulated in SJS patients ( p < 0.01), which was indicative of intestinal barrier dysfunction., Conclusion: Hyperamylasemia often extends beyond pancreatic diseases. Clinical awareness of asymptomatic hyperamylasemia secondary to other systemic diseases can help avoid unnecessary overexamination and overtreatment., Competing Interests: The author declares that there are no conflicts of interest., (Copyright © 2020 Yujen Tseng et al.)

Ischemic stroke is a major cause of death among patients with systemic hypertension. The narrowing of the lumen of the brain vasculature contributes to the increased incidence of stroke. While hyalinosis represents the major pathological lesions contributing to vascular lumen narrowing and stroke, the pathogenic mechanism of brain vascular hyalinosis has not been well characterized. Thus, the present study examined the postmortem brain vasculature of human patients who died of ischemic stroke due to systemic hypertension. Hematoxylin and eosin staining and immunohistochemistry showed the occurrence of brain vascular hyalinosis with infiltrated plasma proteins along with the narrowing of the vasa vasorum and oxidative stress. Transmission electron microscopy revealed endothelial cell bulge protrusion into the vasa vasorum lumen and the occurrence of endocytosis in the vasa vasorum endothelium. The treatment of cultured microvascular endothelial cells with adrenaline also promoted the formation of the bulge as well as endocytic vesicles. The siRNA knockdown of sortin nexin-9 (a mediator of clathrin-mediated endocytosis) inhibited adrenaline-induced endothelial cell bulge formation. Adrenaline promoted protein-protein interactions between sortin nexin-9 and neural Wiskott-Aldrich syndrome protein (a regulator of actin polymerization). Spontaneously hypertensive stroke-prone rats also exhibited lesions indicative of brain vascular hyalinosis, the endothelial cell protrusion into the lumen of the vasa vasorum, and endocytosis in vasa vasorum endothelial cells. We propose that endocytosis-dependent endothelial cell bulge protrusion narrows the vasa vasorum, resulting in ischemic oxidative damage to cerebral vessels, the formation of hyalinosis, the occurrence of ischemic stroke, and death in systemic hypertension patients.

Undernutrition is a global health issue leading to 1 out 5 all deaths in children under 5 years. Undernutrition is often associated with environmental enteric dysfunction (EED), a syndrome associated with increased intestinal permeability and gut inflammation. We aimed to develop a novel murine model of undernutrition with these EED features. Post-weaning mice were fed with low-protein diet (LP) alone or combined with a gastrointestinal insult trigger (indomethacin or liposaccharides). Growth, intestinal permeability and inflammation were assessed. LP diet induced stunting and wasting in post-weaning mice but did not impact gut barrier. We therefore combined LP diet with a single administration of indomethacin or liposaccharides (LPS). Indomethacin increased fecal calprotectin production while LPS did not. To amplify indomethacin effects, we investigated its repeated administration in addition to LP diet and mice exhibited stunting and wasting with intestinal hyperpermeability and gut inflammation. The combination of 3-weeks LP diet with repeated oral indomethacin administration induced wasting, stunting and gut barrier dysfunction as observed in undernourished children with EED. As noninvasive methods for investigating gut function in undernourished children are scarce, the present pre-clinical model provides an affordable tool to attempt to elucidate pathophysiological processes involved in EED and to identify novel therapeutic strategies.

Non-steroidal anti-inflammatory drugs (NSAIDs) induce ulcers in the gastrointestinal tract, including the stomach and small intestine. NSAID-induced gastric ulcers can be prevented by taking acid-neutralizing/inhibitory drugs and cytoprotective agents. In contrast, there are no medicines to control NSAID-induced small intestinal ulcers, which are accompanied by a mucosal invasion of bacteria and subsequent activation of immune cells. Galectin-3 (Gal3), an endogenous lectin, has anti-microbial and pro-inflammatory functions. In the small intestine, since Gal3 is highly expressed in epithelial cells constitutively and macrophages inducibly, the Gal3 level can affect microbiota composition and macrophage activation. We hypothesized that the modulation of Gal3 expression could be beneficial in NSAID-induced intestinal ulcers. Using Gal3 knockout (Gal3KO) mice, we determined whether Gal3 could be a therapeutic target in NSAID-induced intestinal ulcers. Following the administration of indomethacin, an NSAID, we found that small intestinal ulcers were less severe in Gal3KO mice than in wild-type (WT) mice. We also found that the composition of intestinal microbiota was different between WT and Gal3KO mice and that bactericidal antibiotic polymyxin B treatment significantly suppressed NSAID-induced ulcers. Furthermore, clodronate, a macrophage modulator, attenuated NSAID-induced ulcers. Therefore, Gal3 could be an exacerbating factor in NSAID-induced intestinal ulcers by affecting the intestinal microbiota population and macrophage activity. Inhibition of Gal3 may be a therapeutic strategy in NSAID-induced intestinal ulcers., Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT03832946., (Copyright © 2020 Park, Khadka, Sato, Omura, Fujita, Hsu, Liu and Tsunoda.)

Intractable gastrointestinal (GI) diseases often develop during infancy. Our group previously reported that natriuretic peptide receptor B (NPR-B)-deficient Npr2 slw/slw mice exhibit severe intestinal dysfunction, such as stenosis and distention, which resembles the dysfunction observed in Hirschsprung's disease-allied disorders. However, the root cause of intestinal dysfunction and the detailed of pathophysiological condition in the intestine are not yet clear. Here, we report that the intestine of preweaning Npr2 slw/slw  mice showed bloodless blood vessels, and nodes were found in the lymphatic vessel. Additionally, the lacteals, smooth muscle, blood vessel, and nerves were barely observed in the villi of preweaning Npr2 slw/slw mice. Moreover, intramuscular interstitial cells of Cajal (ICC-IM) were clearly reduced. In contrast, villi and ICC-IM were developed normally in surviving adult Npr2 slw/slw mice. However, adult Npr2 slw/slw mice exhibited partially hypoplastic blood vessels and an atrophied enteric nervous. Furthermore, adult Npr2 slw/slw mice showed markedly reduced white adipose tissue. These findings suggest that the cause of GI dysfunction in preweaning Npr2 slw/slw mice is attributed to defective intestinal development with microcirculation disorder. Thus, it is suggested that NPR-B signaling is involved in intestinal development and control of microcirculation and fat metabolism. This report provides new insights into intractable GI diseases, obesity, and NPR-B signaling.

Increased intestinal permeability (IIP) precedes several autoimmune disorders. Although Hashimoto’s thyroiditis (HT) is the most common autoimmune disorder, the role of IIP in its pathogenesis had received little attention. Zonulin plays a critical role in IIP by modulating intracellular tight junctions. Rise of serum zonulin levels were shown to indicate IIP in human subjects. In this case-control study, we examined the hypothesis that patients with HT have IIP. We studied 30 children and adolescents with HT, and 30 patients with congenital hypothyroidism (CH) matched for age, gender and body mass index (BMI). Serum zonulin levels, free thyroxine (fT4), thyroid stimulating hormone (TSH), anti-thyroglobulin antibody and anti-thyroid peroxidase antibody were measured. Zonulin levels were significantly higher in patients with HT than patients with CH (59.1±22.9 ng/mL vs. 43.3±32.9 ng/mL, p=0.035). In patients with HT, zonulin levels were positively correlated with weight (r=0.406, p=0.03), BMI (r=0.486, p=0.006) and levothyroxine dose (r=0.463, p=0.02). In patients with CH, zonulin levels were positively correlated with age (r=0.475, p=0.008), weight (r=0.707, p<0.001), BMI (r=0.872, p<0.001) and levothyroxine dose (r=0.485, p=0.007). After adjusting for age, weight, TSH and fT4 levels, serum zonulin was only associated with levothyroxine dose in patients with HT (R 2 =0.36, p=0.05). In patients with CH, only weight was associated with zonulin levels (R 2 =0.62, p<0.001). In conclusion, higher zonulin levels in children and adolescents with HT suggested IIP in these patients. Additionally, the association between zonulin levels and levothyroxine dose might imply a relationship between serum zonulin and disease severity.

(1) Background: Malnutrition in cancer patients impacts quality of life (QoL) and performance status (PS). When oral/enteral nutrition is not possible and patients develop intestinal failure, parenteral nutrition (PN) is indicated. Our aim was to assess nutritional status, QoL, and PS in hospitalised cancer patients recently initiated on PN for intestinal failure. (2) Methods: The design was a cross-sectional observational study. The following information was captured: demographic, anthropometric, biochemical and medical information, as well as nutritional screening tool (NST), patient-generated subjective global assessment (PG-SGA), functional assessment of cancer therapy-general (FACT-G), and Karnofsky PS (KPS) data. (3) Results: Among 85 PN referrals, 30 oncology patients (56.2 years, 56.7% male) were identified. Mean weight (60.3 ± 16.6 kg) corresponded to normal body mass index values (21.0 ± 5.1 kg/m 2 ). However, weight loss was significant in patients with gastrointestinal tumours ( p < 0.01). A high malnutrition risk was present in 53.3-56.7% of patients, depending on the screening tool. Patients had impaired QoL (FACT-G: 26.6 ± 9.8) but PS indicated above average capability with independent daily activities (KPS: 60 ± 10). (4) Conclusions: Future research should assess the impact of impaired NS and QoL on clinical outcomes such as survival, with a view to encompassing nutritional and QoL assessment in the management pathway of this patient group.

&lt;b&gt;Introduction:&lt;/b&gt; The complications of surgical treatment for rectal cancer, particularly anastomotic leaks after anterior resection, are a significant clinical problem. We retrospectively analysed preoperative factors that may affect the occurrence of complications. &lt;br&gt;&lt;b&gt;Meterial and Methods:&lt;/b&gt; A total of 392 rectal cancer patients were included in a retrospective analysis. A total of 257 anterior resections (AR) and 135 abdominoperineal resections (APR) were performed. The risk factors for early postoperative complications were analysed by logistic regression and receiver operating characteristic curves. &lt;br&gt;&lt;b&gt;Results:&lt;/b&gt; The significant risk factors for severe complications (grade 3B and higher on the Clavien-Dindo scale) in the multivariate analysis were neutrophil to lymphocyte ratio &gt; 5 (P = 0.047) in the AR group, age of the patients (P = 0.031) in the APR group, and coronary artery disease in both groups (P = 0.03, P = 0.011, respectively). There were no risk factors for anastomotic leaks in the AR group before the analysis was divided into early and late leaks. In the univariate analysis, the statistically significant risk factors for early leaks were preoperative neutrophil to lymphocyte ratio &gt; 5 and peripheral blood platelet count, while late leaks were associated with coronary artery disease; however, in the multivariate analysis, these factors were not statistically significant. &lt;br&gt;&lt;b&gt;Conclusions:&lt;/b&gt; The risk factors for severe postoperative complications were neutrophil to lymphocyte ratio &gt; 5, advanced age of the patients and coronary artery disease. The different risk factors for early and late anastomotic leaks after anterior resection may indicate their different aetiologies.

It had been reported miR-182 was down-regulated after intestinal ischaemia/reperfusion (I/R) damage. However, its role and potential mechanisms are still unknown. This study was aimed to elucidate the function of miR-182 in intestinal I/R injury and the underlying mechanisms. The model of intestinal injury was constructed in wild-type and Deptor knockout (KO) mice. Haematoxylin-eosin staining, Chiu's score and diamine oxidase were utilized to detect intestinal damage. RT-qPCR assay was used to detected miR-182 expression. Electronic microscopy was used to detect autophagosome. Western blot was applied to detect the expression of Deptor, S6/pS6, LC3-II/LC3-I and p62. Dual-luciferase reporter assay was used to verify the relationship between miR-182 and Deptor. The results showed miR-182 was down-regulated following intestinal I/R. Up-regulation of miR-182 reduced intestinal damage, autophagy, Deptor expression and enhanced mTOR activity following intestinal I/R. Moreover, suppression of autophagy reduced intestinal damage and inhibition of mTOR by rapamycin aggravated intestinal damage following intestinal I/R. Besides, damage of intestine was reduced and mTOR activity was enhanced in Deptor KO mice. In addition, Deptor was the target gene of miR-182 and was indispensable for the protection of miR-182 on intestine under I/R condition. Together, our research implicated up-regulation of miR-182 inhibited autophagy to alleviate intestinal I/R injury via mTOR by targeting Deptor., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)