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SUMMARY Fifty seven children with dermatitis herpetiformis, 18 from Finland and 39 from Hungary, were studied. Diagnostic criteria included the finding of granular IgA deposits in the skin of all patients. The mean age at onset of the rash was 7-2 years and favoured sites were the elbows, knees, and buttocks. Symptoms suggesting small intestinal disease were rare but in 35 (61%) of the children subtotal villous atrophy and in 16 (28%) partial villous atrophy were found on jejunal biopsy.Eighteen children underwent a second biopsy after a mean of 21 months on a gluten free diet; villous height was found to be increased and the intraepithelial lymphocyte count decreased in all these patients. Gluten challenge caused a reversal in the two children who underwent a third biopsy. The effect of the gluten free diet on the rash was examined in Finnish children by observing the daily requirements of dapsone, a drug used to control the rash at the beginning of the diet. Eight (67%) of the 12 children were able to stop taking dapsone after a mean of 11 months on the diet and all three patients treated with diet alone became asymptomatic after three to 6 months on the diet.These results confirm that most children with dermatitis herpetiformis have jejunal villous atrophy, though they rarely have gastrointestinal symptoms. The central role of gluten in childhood dermatitis herpetiformis is evidenced by the fact that a gluten free diet helps the damaged jejunal mucosa to recover and controls the rash even in those children who do not have an abnormal jejunal biopsy.Dermatitis herpetiformis in adults is characterised by a pruritic, blistering rash and is associated with coeliac disease which is mostly subclinical in these patients.' Gluten plays an important role in adult dermatitis herpetiformis; both the enteropathy and rash respond to gluten withdrawal and relapse on gluten challenge.2-4 Dermatitis herpetiformis in

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(CMI) and 12 of these on a cow's milk free diet were compared with 47 children with untreated coeliac disease, with 15 of these on a gluten free diet, and with 15 controls. The total number of cells in the crypts of the patients with CMI was 1 8 times (p<0.001) and in patients with coeliac disease 2-4 times (P < 0.001) that seen in the controls. During the elimination diet the total number of cells in the crypts returned to the level seen in the controls. The mitotic indices, both crude and corrected, were significantly higher (P < .001) in untreated patients with CMI and those with coeliac disease than in the controls. During dietary treatment the indices fell, but not quite to the level of the controls. These small differences between the two groups may be due to the difference in the causative agents or to the different ages of the patients.Cell renewal in the healthy normal human small intestine was studied by Bertalanffy and Nagy.3 From counts of mitoses in adults these workers calculated that the whole epithelium lining the human duodenum is completely renewed in about two days. In adult coeliac disease the mitotic index in the jejunal epithelium of the small intestinal mucosa was found to be increased two-fold45 During the elimination diet the mitotic index returned to the level seen in the normal small intestinal mucosa.5In 1973 Wright et al.2 described a new method for analysing cell kinetics in the small intestinal crypts from sections of peroral biopsy specimens. They showed that, in adult and childhood coeliac disease and in adults with gluten-sensitive enteropathy of dermatitis herpetiformis, there was a marked increase in the number of the proliferating cells per crypt as well as in the mitotic index in the 'flat' mucosa. These findings are consistent with Booth's6 suggestion that the characteristic changes in crypt morphology are a direct consequence of 'enteroblastic hyperplasia' compensating for excessive loss of surface enterocytes.