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Mean final adult height showed a modest deficit compared with target height, but in one fifth of patients, final height was significantly less than target height. Earlier diagnosis and improved treatment of jejunal disease would be likely to improve final height.

Inflammatory diseases frequently impair linear growth. Crohn's disease inhibits growth in up to one third of affected children. In rats with trinitrobenzenesulphonic acid-induced colitis, 40% of growth impairment is attributable to inflammation, with the rest being due to undernutrition. In transgenic mice without inflammation, raised IL-6 retards growth, suppressing insulin-like growth factor (IGF)-I. We hypothesized that IL-6, induced by intestinal inflammation, suppresses growth and inhibits IGF-I expression. Therefore, an anti-IL-6 Ab was given to rats with trinitrobenzenesulphonic acid colitis. The Ab did not improve nutrient intake or decrease inflammation compared with untreated disease controls, but it significantly restored linear growth (P ‫؍‬ 0.023) and increased IGF-I (P ‫؍‬ 0.05). In humans, the IL-6 ؊174 G͞C promoter polymorphism affects IL-6 transcription, with the GG genotype inducing the greatest IL-6 levels. Because IL-6 is increased in Crohn's disease, we further hypothesized that growth failure would vary with the IL-6 ؊174 genotype. At diagnosis, among 153 children with Crohn's disease, those with the IL-6 GG genotype were more growthretarded than those with the GC or CC genotypes (height SD score, ؊0.51 vs. ؊0.10; P ‫؍‬ 0.031). Also, the patients with the IL-6 GG genotype had higher circulating levels of C-reactive protein, an IL-6-induced product (36 vs. 18 mg͞dl, P ‫؍‬ 0.028). However, their risk of developing Crohn's disease was similar to other genotypes when compared with 351 healthy controls (P ‫؍‬ 0.7). Thus, the IL-6 ؊174 genotype mediates growth failure in children with Crohn's disease.Crohn's disease ͉ height ͉ insulin-like growth factor I ͉ C-reactive protein ͉ food intake

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This is the first comprehensive review of the evidence base for the treatment of paediatric IBD, highlighting the paucity of trials of high methodological quality. As a result, the development of clinical guidelines for managing children and young people with IBD must be consensus based, informed by the best-available evidence from the paediatric literature and high-quality data from the adult IBD literature, together with the clinical expertise and multidisciplinary experience of paediatric IBD experts.

Background: There are no published data from Great Britain and Ireland detailing the initial management of children with inflammatory bowel disease (IBD). Aims: To prospectively record the initial investigation and treatment of children aged less than 16 years with newly diagnosed IBD. Methods: For 13 months, between June 1998 and June 1999, 3247 paediatricians, adult gastroenterologists, and surgeons across the UK and Ireland were prospectively surveyed each month and asked to report every newly diagnosed case of childhood IBD. Reporters subsequently completed a postal questionnaire about each case. Results: A total of 739 new IBD cases were reported from 172 institutions. Significant variations were observed in the investigation and treatment of these cases, when examined by number of cases reported per institution, or by the specialists providing care. There were wide regional variations in the proportion of children having access to paediatric gastroenterology services. Overall, one third of children received care from an adult service, and a tenth care exclusively from an adult gastroenterologist. Children with Crohn's disease who had some or all of their care from adult services were more likely to receive systemic steroids and less likely to receive dietary therapy; those with ulcerative colitis were more likely to receive rectal steroids and to have surgery. Height and weight were also less likely to be recorded in those whose care involved adult services. Conclusion: Current specialist provision, and initial investigation and treatment of IBD, is heterogeneous. Optimisation of care is likely to be achieved by greater access to specialist paediatric gastroenterology services for all those with suspected IBD.

We read with great interest the recently published guidelines on the management of osteoporosis associated with chronic liver disease (Gut 2002;50(suppl I):i1-9). However, we would like to add a few words of comment. Associations between coeliac disease (CD) and primary biliary cirrhosis in particular and other autoimmune liver diseases in general have been reported. 1-3 In addition, it has been suggested that these individuals should be considered as an at risk group for whom serological testing for CD is indicated. 1 Patients with CD are at high risk of developing low bone mineral density and bone turnover impairment, 1 and it has been shown that adherence to a gluten free diet has a significant positive impact on these parameters. 4 Thus we suggest that physicians caring for patients with the above mentioned liver diseases should screen them for CD in the presence of signs and symptoms suggestive of malabsorption such as osteoporosis. This seems a reasonable strategy as detection of CD will allow for a more rational therapeutic approach to the risks determined by this association. Complications due to the presence of CD, such as malnutrition, anaemia, and osteoporosis, may have a considerable impact on liver disease management and the need/success of transplantation. 5 6