RESUMO
BACKGROUND: Ingestion of magnets carries risks for significant morbidity. We propose a new protocol designed to reduce the need for surgery, shorten length of stay, and decrease morbidity. METHODS: The Early Colonic-preparation and Salvage Laparoscopic Appendectomy (ECSLA) protocol includes initiating colonoscopy preparation upon admission in asymptomatic patients if magnets are not amenable to removal by gastroscopy, and laparoscopic magnets retrieval via appendectomy if surgery is eventually needed. The protocol was initiated in May 2023. A retrospective study of all cases of ingested magnets in children in our institution during July 2020 - January 2024 was conducted to retrieve and analyze demographic, clinical, imaging, management, and outcome data. RESULTS: During the 3.5-year study period, 13 cases of ingested multiple magnets were treated, including 7 cases since initiation of ECLSA protocol, with no complications. Since initiation of ECSLA protocol, Early colonic preparation resulted in spontaneous passage of magnets (two cases) and successful colonocsopic removal (three cases), with two cases in which magnets were retrieved via gastroscopy upon admission, and no patients needing surgical intervention. Length of stay (LOS) was short (1-3 days). CONCLUSIONS: The ECSLA protocol is a promising tool for preventing surgical intervention and complications and for possibly shortening LOS in children who have ingested multiple magnets.
RESUMO
Cholestatic injuries are accompanied by ductular reaction, initiated by proliferation and activation of biliary epithelial cells (BECs), leading to fibrosis. Sortilin (encoded by Sort1) facilitates IL-6 secretion and leukemia inhibitory factor (LIF) signaling. This study investigated the interplay between sortilin and IL-6 and LIF in cholestatic injury-induced ductular reaction, morphogenesis of new ducts, and fibrosis. Cholestatic injury was induced by bile duct ligation (BDL) in wild-type and Sort1-/- mice, with or without augmentation of IL-6 or LIF. Mice with BEC sortilin deficiency (hGFAPcre.Sort1fl/fl) and control mice were subjected to BDL and 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet (DDC) induced cholestatic injury. Sort1-/- mice displayed reduced BEC proliferation and expression of BEC-reactive markers. Administration of LIF or IL-6 restored BEC proliferation in Sort1-/- mice, without affecting BEC-reactive or inflammatory markers. Sort1-/- mice also displayed impaired morphogenesis, which was corrected by LIF treatment. Similarly, hGFAPcre.Sort1fl/fl mice exhibited reduced BEC proliferation, but similar reactive and inflammatory marker expression. Serum IL-6 and LIF were comparable, yet liver pSTAT3 was reduced, indicating that sortilin is essential for co-activation of LIF receptor/gp130 signaling in BECs, but not for IL-6 secretion. hGFAPcre.Sortfl/fl mice displayed impaired morphogenesis and diminished fibrosis after BDL and DDC. In conclusion, sortilin-mediated engagement of LIF signaling in BECs promoted ductular reaction and morphogenesis during cholestatic injury. This study indicates that BEC sortilin is pivotal for the development of fibrosis.