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Advancements in Research on Necrotizing Enterocolitis Pathogenesis and Prevention Using PIGS
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Douglas Burrin, Juan Marini, Murali Premkumar, Barbara Stoll, Per Torp Sangild
Over the past few decades, strategies in the prevention of necrotizing enterocolitis (NEC), including the avoidance of infant formula, standardized feeding regimens, and infection control, have significantly reduced its incidence. However, due to the improved survival of extremely preterm infants, the advancing thresholds of prematurity, and poor understanding of its complex multifactorial pathophysiology, NEC is still fairly frequent and potentially deadly in the most premature infants. The incidence of necrotizing enterocolitis has remained steady at 3% to 10% in extremely low-birth-weight (ELBW) infants (1–3). The mortality can be as high as 40% in ELBW infants who are afflicted with severe forms of NEC.
The post pull-through Hirschsprung patient who is not doing well with obstructive or incontinence symptoms
Published in Alejandra Vilanova-Sánchez, Marc A. Levitt, Pediatric Colorectal and Pelvic Reconstructive Surgery, 2020
Jacob C. Langer, Marc A. Levitt
Although the exact cause of enterocolitis is unknown, certain factors, such as fecal stasis, can precipitate and aggravate the problem. It can occur after any of the HD operations (Figure 13.13). The stasis can result in proliferation and mucosal invasion by intraluminal flora resulting in a local and systemic inflammatory response and bacterial translocation. The clinical criteria for enterocolitis include fever, abdominal distention, and diarrhea; however, this broad definition makes it difficult to determine its actual incidence. Individual reports in the published data quote an incidence of up to half of patients. The presence of chronic enterocolitis can lead to failure to thrive. Enterocolitis may be present both before and after operative correction, and can range in severity from mild to life threatening. It is more common in younger children, longer segment disease, and trisomy 21. A reliable guide to defining enterocolitis is shown in Figure 13.14.
Paediatric Surgery: What the Adult Surgeon Needs to Know
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Marc A. Levitt, Richard J. Wood
Abdominal distention and enterocolitis can be due to either pathologic or anatomic problems. Enterocolitis may occur both before and after surgical correction of the disease and can be severe, even life-threatening. Although the clinical features of enterocolitis are generally agreed upon (fever, abdominal distention, diarrhoea), a precise definition has not been widely applied. Enterocolitis is thought to be caused by stasis resulting in bacterial proliferation and mucosa penetration (translocation) by intraluminal flora. Recurrent enterocolitis is more common in children with long-segment disease and those with trisomy 21.19
Prospective study reveals a microbiome signature that predicts the occurrence of post-operative enterocolitis in Hirschsprung disease (HSCR) patients
Published in Gut Microbes, 2020
Weibing Tang, Yang Su, Chen Yuan, Yuqing Zhang, Lingling Zhou, Lei Peng, Pin Wang, Guanglin Chen, Yang Li, Hongxing Li, Zhengke Zhi, Hang Chang, Bo Hang, Jian-Hua Mao, Antoine M. Snijders, Yankai Xia
Several small case–control studies have been conducted to retrospectively compare the enteric microbiome of HSCR patients with different HAEC status, reporting mixed findings.8,9,22,23 Two studies, including a total of 17 HSCR patients, observed increased Proteobacteria and decreased Bacteroidetes in HAEC cases vs. controls.8,9 Another study of 18 HSCR patients observed increased Proteobacteria and Bacteroidetes as well as decreased Firmicutes, comparing patients who had a history of HAEC to those who did not.22 It has also been reported that patients with a history of recurrent HAEC had increased Proteobacteria and Bacteroidetes, compared to those without a history.23 However, in all these studies, the enteric microbiome was measured after the occurrence of HAEC and could have been dramatically altered by the enterocolitis. In contrast, a prospective study design, such as that in our analyses, limits the likelihood of reverse causation by collecting tissue samples before the occurrence of HAEC, lending additional validity to the results.
Upper gastrointestinal symptoms and associated endoscopic and histological features in patients receiving immune checkpoint inhibitors
Published in Scandinavian Journal of Gastroenterology, 2019
Tenglong Tang, Hamzah Abu-Sbeih, Wenyi Luo, Phillip Lum, Wei Qiao, Robert S. Bresalier, David M. Richards, Yinghong Wang
ICIs have demonstrated efficacy in delaying disease progression in melanoma [7–9] and other types of cancer [10–19]. However, these agents can cause several side effects known as immune-related adverse events (irAEs), which may involve multiple organ systems, most commonly the skin, gastrointestinal (GI) tract, endocrine glands, lungs, and liver [20–23]. Most irAEs are mild (grade 1); however, more severe irAEs of grades 3 and 4 have been observed in up to 10% of patients treated with ICIs [24,25]. GI irAEs are among the most commonly reported severe adverse events that lead to the discontinuation of ICI treatments, especially anti-CTLA-4 medications [26–28]. ICI-induced enterocolitis can involve the colon and/or terminal ileum and has associated symptoms of diarrhea, abdominal pain, and blood or mucous in the stool [29]. Although ICI-induced enterocolitis has been studied extensively [25,30–35], very limited data are available about upper GI injury.
Increased prevalence of pathogenic bacteria in the gut microbiota of infants at risk of developing celiac disease: The PROFICEL study
Published in Gut Microbes, 2018
Marta Olivares, Alfonso Benítez-Páez, Giada de Palma, Amalia Capilla, Esther Nova, Gemma Castillejo, Vicente Varea, Ascensión Marcos, José Antonio Garrote, Isabel Polanco, Ester Donat, Carmen Ribes-Koninckx, Carmen Calvo, Luis Ortigosa, Francesc Palau, Yolanda Sanz
A previous study incluing of most of the cases enrolled in the PROFICEL project showed that breast-feeding promotes the colonization of Clostridium leptum group and Bifidobacterium species; whereas formula-feeding prometed that of C. coccoides-E. rectale group by quantitative PCR using genus- and group-specific primers.7 Here, using species-specific primers, we have analysed the prevalence of two potentially pathogenic species of the Clostridium genus. The increased prevalence of C. perfringens found at 7 days, 1 month and 4 months of age in the formula-fed infants of our cohort is in agreement with previous studies reporting that formula feeding promoted the presence of C. perfringens.37 This bacterial species has also been considered as a causal agent of necrotizing enterocolitis in infants.38 Similarly, a higher prevalence of C. perfringens has been proposed to possibly increase the risk of suffering other chronic intestinal disorders. Altogether, this evidence could support the protective role attributed to breast-feeding in reducing the rate of infections and, in turn, has been related to a reduced risk of developing CD in some studies.39