Background: Cows' milk sensitive reflux oesophagitis is an emerging clinical entity in children, normally indistinguishable from primary gastro-oesophageal reflux (GOR) apart from the response to dietary antigen exclusion. It is conjectural whether a tendency towards mucosal eosinophilia distinguishes this group from primary GOR. Aims: To determine whether there may be differences in the mucosal lesion within the oesophagus in those children with reflux in association with cows' milk induced small bowel pathology, particularly in relation to the eosinophil chemokine eotaxin. Methods: A total of 29 children underwent endoscopic assessment, including nine with cows' milk sensitive enteropathy (CMSE) and associated GOR, seven histologically normal controls, six with primary GOR, and seven disease controls. Oesophageal biopsy specimens were examined immunohistochemically for the chemokines eotaxin and MCP-2, and T cell lineage and activation markers. Results: Strong upregulation of eotaxin expression, limited to basal and papillary epithelium, occurred in all CMSE patients. By contrast, weak expression was seen in a minority of controls and in 50% of primary GOR patients. Infiltration of CD3, CD4, and CD8 lymphocytes occurred in similar distribution in CMSE patients, significantly increased above controls. Significant upregulation of activation markers (CD25, HLA-DR) was also seen in the CMSE group within basal and papillary epithelium compared to controls and primary GOR. Conclusion: Basal and papillary epithelial eotaxin expression, with focal lymphocyte activation, was seen in infants with CMSE associated GOR. This preliminary study provides early evidence to suggest a pathogenesis distinct from primary GOR, in which specific recruitment of T cells and eosinophils may contribute to oesophageal dysmotility.

85 Microvillous atrophy [MVA] is a definitive diagnosis within the intractable diarrhoea of infancy syndrome. Patients are managed on TPN and the only treatment currently available is intestinal transplantation. The underlying pathogenesis is unclear, although a cytoskeletal myosin deficiency has been found. The aim of this work was to investigate the glycobiological nature of the epithelial accumulation of periodic acid Schiff [PAS] positive material (a diagnostic characteristic of MVA) using histochemical techniques. Small intestinal tissue was available from two cases of MVA who had undergone intestinal transplantation. Histologically normal and abnormal (coeliac disease, autoimmune enteropathy, idiopathic intractable diarrhoea) small intestinal mucosal biopsy samples were used as controls. Alcian blue[AB]/PAS staining showed that the accumulated material in MVA was a neutral glycosubstance. Saponification (which makes acetyl groups PAS +ve) prior to AB/PAS demonstrated a high degree of acetylation, and saponification with phenylhydrazine blocking (to stop neutral sugar staining) indicated the presence of acetylated sialic acids. Removal of acetylated sialic acids using saponification and neuraminidase or sulphuric acid digestion showed a marked reduction in positive staining. Control samples demonstrated the same phenomena, but these were restricted to the brush border region and were not identified intracellularly. These result indicate that MVA involves a defect in exocytosis of the glycocalyx as acetylated sialic acids are one of its integral components. The glycocalyx forms a hydrophilic polyanionic gel coat on the enterocyte surface and is considered to maintain cell surface charge, protect against physical trauma, regulate ionic & macromolecular access. and form a cationic store. Thus, the absence of the glycocalyx would have profound consequences on normal cell function.

Journal of Pediatric Gastroenterology and NutritionVolume 28, Issue 5 p. 557-557 E S P G H A N 32nd Annual Meeting; Warsaw, Poland, June 2-5, 1999 EFFECT OF ENTEROAGGREGATIVE ESCHERICHIA COLI PLASMID-ENCODED TOXIN [PET] ON HUMAN INTESTINE S Hicks, S Hicks University Dept of Paediatric Gastroenterology, Royal Free Hospital, London, UKSearch for more papers by this authorI R Henderson, I R Henderson University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorF Navarro-Garcia, F Navarro-Garcia University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorJ P Nataro, J P Nataro University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorA D Phillips, A D Phillips University Dept of Paediatric Gastroenterology, Royal Free Hospital, London, UKSearch for more papers by this author S Hicks, S Hicks University Dept of Paediatric Gastroenterology, Royal Free Hospital, London, UKSearch for more papers by this authorI R Henderson, I R Henderson University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorF Navarro-Garcia, F Navarro-Garcia University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorJ P Nataro, J P Nataro University of Maryland School of Medicine, Baltimore, USASearch for more papers by this authorA D Phillips, A D Phillips University Dept of Paediatric Gastroenterology, Royal Free Hospital, London, UKSearch for more papers by this author First published: 01 May 1999 https://doi.org/10.1002/j.1536-4801.1999.tb02228.xRead the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume28, Issue5May 1999Pages 557-557 RelatedInformation

BACKGROUND/AIM:The aim of this study was to investigate epithelial cell turnover in childhood enteropathy to establish whether common disease related mechanisms operate. Levels of epithelial cell proliferation were measured in children with food intolerance (cows' milk protein intolerance and coeliac disease), and after infection with Giardia lamblia, Cryptosporidium, and enteropathogenic Escherichia coli.METHODS:Comparative measures of epithelial cell proliferation were performed by recording mitotic activity and MIB-1 immunoreactivity in proximal small intestinal biopsy specimens.RESULTS/CONCLUSIONS:A hyperplastic crypt response was evident in all of the disease states examined and was particularly pronounced in coeliac disease and in infection with enteropathogenic E coli, where mitotic and MIB-1 labelling indices were significantly raised above control values. In contrast with coeliac disease, increased crypt cell production rates in enteropathogenic E coli infection were also due to an expansion of the crypt proliferation compartment, without a comparable increase in crypt cell numbers. Crypt hyperplasia is therefore a common tissue response to mucosal damage in food allergy and infection, although disease specific mechanisms are evident.