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SUMMARY A copy of the standardised classification (SC) proposed for assessing dysplasia in inflammatory bowel disease was circulated to six histopathologists who were asked to apply it to 40 slides from 34 patients with ulcerative colitis to test its reproducibility. The slides were relabelled and recirculated to the pathologists at least one month later. Each was asked to state whether or not key diagnostic features were present before giving a final dysplasia score for the second assessment. Only minor interobserver and intraobserver disagreements were recorded. Pathologists were most consistent at recognising back to back glands, villous mucosal architecture, hyperchromatic nuclei, stratification of nuclei, regenerative nuclei and loss of nuclear polarity. There was poor interobserver agreement in assessing dystrophic goblet cells and columnar mucous cells.Back to back glands, hyperchromatic nuclei, loss of nuclear polarity, stratification of nuclei and columnar mucous cells were considered to be the most important features for determining the severity of dysplasia.As there was poor interobserver agreement in assessing columnar mucous cells and dystrophic goblet cells these features need to be more clearly defined or should be removed from the SC.

During a three year period Giardia lamblia was found in duodenal juice of 154 children. Faecal examination alone would have led to a missed diagnosis in more than 50% of patients. Clinical features and mucosal damage seen in these 154 patients are reviewed. Diarrhoea, failure to thrive and abdominal distension were common and improved after treatment. Histological abnormality occurred in 70%, and disaccharidase depression in 48%. Mucosal damage responded to treatment in the majority. The improvement of clinical features and mucosal damage with treatment, suggests that G. lamblia was a pathogen in most of these children.

Studies by Thompson, 1 Carter et al, 2 MacDonald et al. and McCrae 4 have all shown a high familial frequency of coeliac disease (CD). The diagnostic criteria differed in each study; in Thompson's patients the diagnosis was based on clinical or historical data alone; in Carter's study response to a gluten-free diet was required, while in MacDonald's and McCrae's studies the diagnostic criteria included the demonstration of the lesion of CD by small bowel biopsy. In MacDonald's study some asymptomatic cases were discovered and a few of these had normal fat balance results. No hereditary pattern emerged from these studies though MacDonald postulated a dominant gene with variable penetrance while McCrae suggested that susceptibility to CD is inhereited multifactorially and that enviromental factors other than dietary gluten are of aetiological importance. Hoffman et al. 5, on the other hand, have described discordance for CD in identical twins.

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