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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.)