Intestinal permeability to sugar has been used as an objective measure of small bowel integrity to assess the efficacy of an elemental diet as the sole treatment or Crohn's disease of the small bowel. Fourteen children aged 11-17 years with active small bowel Crohn's disease were given an elemental diet for six weeks. Investigations with iso-osmolar oral test solutions before and after this treatment showed that all 14 children had abnormally raised lactulose/L-rhamnose permeability ratios, which fell significantly after the elemental diet. This change coincided with marked clinical improvement, as assessed by a disease activity index score.

Publisher Summary This chapter describes the delayed recovery after gastroenteritis. In developed countries, acute gastroenteritis is usually a self-limiting illness with an uneventful recovery. Some children however suffer a significant persistence or return of diarrhea, despite treatment, and experience a delayed recovery. This can extend into the post-enteritis syndrome if the symptoms continue for 14 days or longer. In a study reviewed in the chapter, 334 patients were admitted for the treatment of gastroenteritis. The association of lactose intolerance with delayed recovery and the way that intercurrent hospital-acquired infection can complicate clinical evaluation is exemplified by the case of a 1-month-old boy admitted with a 2-day history of loose stools and vomiting after feeds. He had been breast-fed for 3 weeks and then bottle-fed with a cow's-milk-based formula feed. Initially no infective organisms were detected in the stool. A regrade was started, however, it was deemed to have failed because of a return of vomiting. The regrading procedure was restarted with thickened feeds, but failed on full strength feeds when stool frequency increased, vomiting recurred, and 1% reducing substances were found in the stool. A third regrade failed because of the repeated lactose intolerance and weight loss. A small bowel biopsy was performed which showed a patchy enteropathy, a probable cow's-milk-sensitive enteropathy was diagnosed, and the child thrived on a cow's-milk-free diet.

Evidence for autoimmunity in diarrhoeal disease is reviewed. Firstly, coeliac disease (CD) is considered. The incidence of tissue-reactive autoantibodies in both adults and children with CD (68% and 65%, respectively) is higher than the incidence of these autoantibodies in controls (6% in normal adults, and 14% and 9% in disease controls drawn respectively from adult and child populations). The R1 antireticulin antibody, when present, was found to disappear after several weeks on a gluten-free diet, but in contrast, other autoantibodies persisted. Secondly, a case is argued for a new disease category, namely "autoimmune enteropathy." Seven cases are reviewed in which patients presented with protracted diarrhoea, a small intestinal enteropathy which failed to heal during periods of total parenteral nutrition, and evidence of a predisposition to autoimmunity (namely, the presence of high titre autoantibodies including one specific for gut epithelium, and/or the presence of associated diseases regarded to be autoimmune). Thirdly, evidence for autoimmunity in inflammatory bowel disease is reviewed and includes discussion of serum goblet cell antibodies and of circulating T cells which participate in antibody-dependent cellular cytotoxicity in vitro using colonic epithelial cells as targets. Finally, an unusual child is described who presented with chronic diarrhoea and a flat small intestinal mucosa, who responded to gluten withdrawal but who later relapsed spontaneously during a strict gluten-free diet. Her mucosa healed only after a period of total parenteral nutrition and treatment with oral steroids. This child's enteropathy was also associated with thyrotoxicosis and a microscopic colitis.

Brush border membrane proteins from a child with congenital microvillus atrophy were analysed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and compared with brush border membrane proteins from normal and disease controls. A predominant band of MW 200K was present in all preparations with the exception of the membrane preparation from the child with congenital microvillus atrophy. Although the band was present in the latter case, it was grossly diminished. The diminished 200K MW band may result in the abnormality of brush border structure. This could account for the involution of the microvilli, the distinguishing feature of congenital microvillus atrophy, and could be the underlying defect in this disease.

Gastrointestinal food allergies may be defined as clinical syndromes which are characterised by the onset of gastrointestinal symptoms following food ingestion where the underlying mechanism is an immunologically mediated reaction within the gastrointestinal tract. These gastrointestinal symptoms, principally vomiting and diarrhoea, sometimes abdominal colic, may be accompanied by other symptoms outside the alimentary tract. The clinical spectrum of these disorders ranges from acute anaphylaxis (rarely leading to death in infancy) to relatively minor symptoms which are difficult to distinguish from other disorders such as toddler's diarrhoea or psychologic disorders. The same food, e.g. cow's milk, may produce a wide range of clinical manifestations. In the one individual, clinical features may change with age. The incidence of gastrointestinal food allergic disease is greatest in the first year of life and decreases with age. There are, broadly speaking, two categories of clinical syndromes which are related to speed of onset of symptoms: immediate and delayed. Those syndromes which manifest immediately after food ingestion are usually easy to diagnose and specific IgE tests and skin prick tests are frequently positive. Those which have a delayed onset of up to several days are difficult to diagnose, and currently available investigations may be unsatisfactory for routine use. In current clinical practice, gastrointestinal syndromes which can be manifestations of food allergy, may be grouped as follows: 1) immediate syndromes, including anaphylaxis and b) acute vomiting +/- diarrhoea in association with cutaneous and respiratory manifestations; and 2) delayed syndromes, including a) food-sensitive small intestinal enteropathies, b) food-sensitive colitis, c) multiple food allergy +/- enteropathy, and d) infantile colic.(ABSTRACT TRUNCATED AT 250 WORDS)

The precise specificity of the R1 anti-reticulin antibody (ARA) associated with untreated gluten sensitive enteropathy (GSE) is unknown. Collagen type III, fibronectin and the non-collagenous reticulin component (NCRC) of Pras & Glynn (1973) co-distribute in tissues in a manner consistent with their being components of reticulin. We therefore used purified preparations of these connective tissue components in studies of the specificity of the ARA. Our results show that the ARA found in GSE does not react with collagen type III, fibronectin or NCRC.

A male infant, aged 1 year 3 months, was admitted to the hospital with protracted diarrhoea, vomiting, and weight loss. The diarrhoea and vomiting coincided with an outbreak of acute diarrhoea and vomiting affecting other family members. Biopsy showed a flat small intestinal mucosa which did not respond to a diet free of gluten, cow's milk, and eggs, or during 8 weeks of intravenous alimentation. Steroids were given, and courses of nalcrom and later cimetidine, but these did not produce any significant improvement. A rare IgG autoantibody specific for gut epithelium was found, which, when present, was associated with a cytological abnormality of crypt enteroblasts. The autoantibody disappeared after treatment with cyclophosphamide, and the cytological abnormality subsequently diminished. However, the mucosa remained severely abnormal and has been so for 23 months. It is possible that an autoimmune reaction against the patient's small intestinal mucosa has led to persistence of the enteropathy.

Here is yet another contribution to the rapidly expanding literature on paediatric gastroenterology.This book is based on a postgraduate course held on 24-25 April 1978 in Manhasset, New York.As a result there are no fewer than 31 contributions.Inevitably this leads to unevenness of style and some topics, inflammatory bowel disease for example, are covered in 3 different chapters.The aim of the book is to focus on current concepts in pathophysiology and management of gastrointestinal and nutritional disorders commonly en- countered in paediatrics.It is in 5 sections: hepatobiliary disorders, gastrointestinal disorders, intestinal absorption disorders, diarrhoeal disorders, and consequences of gastrointestinal disorders.As can be seen some topics overlap.Many of the review articles are valuable and comprehensivefor example, Alan Walker's chapter on 'Intestinal defences in health and disease',

Thirty-nine infants suspected of having cow's milk protein intolerance (C.M.P.I.) were investigated, and jejunal biopsies were performed before and after challenge with cow's milk. Thirty patients had significant jejunal mucosal damage after milk challenge, but symptoms of diarrhœa and vomiting developed in only twenty-two. The patients with symptoms were subsequently managed on a diet free from cow's milk until tolerance developed. However, the eight infants without symptoms (but with jejunal mucosal damage) made satisfactory clinical progress, with adequate weight-gain, on a diet of cow's milk. Repeat jejunal biopsy specimens from two of these patients showed that there had been a definite improvement since the immediate post-challenge biopsy specimens were taken. Most patients with C.M.P.I. who need to be treated with a diet from which cow's milk has been eliminated may be detected by clinical means alone, and the remainder may continue on a cow's milk diet unless or until symptoms develop. There seems to be no clinical justification for routine jejunal biopsy in infants in whom C.M.P.I. is suspected.