SYNOPSIS Jejunal lamina propria plasma cells and eosinophils and intraepithelial lymphocytes were raised in coeliac children on gluten-containing diets, but only intraepithelial lymphocytes were increased in patients on gluten-free diets. In contrast, lamina propria lymphocytes were reduced in children with coeliac disease on gluten-containing diets but were normal in patients on gluten-free diets. In children with coeliac disease who were studied serially, lamina propria plasma cells and eosinophils and intraepithelial lymphocytes increased, and lamina propria lymphocytes decreased, within three months of the reintroduction of gluten to the diet. These observations are essentially similar to those made in the adult form of the disease and suggest that more than one type of immunological reaction is involved in the pathogenesis of the jejunal lesion.

the Institute of Child Health, London sumxARY Thirty-two children with a past diagnosis of coeliac disease were reinvestigated by means of gluten challenge. They had received a gluten-free diet for a mean period of 6 5 years (range 0 25-11 .0) before gluten challenge, and had a mean age of 9 9 years (range 3.0-15.3) at the onset of challenge.Small intestinal biopsies were performed before and after the gluten challenge (at least 10 g natural gluten per day for 3 months in the majority) and, as judged by light microscopy and morphometric techniques, coeliac disease was confirmed in 25 (78%.) of the 32 patients; challenge was continued in the remaining 7 for a total period of 2 years when biopsies were repeated in 6 children and all were normal. Serum and RBC folate, serum iron, Hb level, and clinical symptoms were unpredictable variables in identifying children who developed gluten-induced enteropathies. The social and emotional effects of gluten challenge are discussed. The results highlight the importance of gluten challenge and intestinal biopsy in the diagnosis of coeliac disease and strongly suggest that a normal biopsy after a 3-month gluten challenge (as described above) excludes coeliac disease.Intolerance to dietary gluten is a permanent phenomenon in true coeliac disease (Mortimer et al., 1968;Sheldon, 1969;Young and Pringle, 1971;Hamilton and McNeill, 1972) and there is an increased risk of neoplasia in affected adult patients (Harris et al., 1967;Barry and Read, 1973) which may be reduced by treatment with a strict gluten-free diet (Harris et al., 1967;Holmes et al., 1976). The application of strict diagnostic criteria (Meeuwisse, 1970) is thus of paramount importance to both child and family, and includes demonstration of abnormalities of the small intestinal mucosa induced by the ingestion of gluten. The timing of diagnostic biopsies during a gluten challenge is largely empirical particularly in those patients who remain asymptomatic, and the optimum duration of a gluten challenge has not been established.We present results of a study designed to reappraise a past diagnosis of coeliac disease in a group of children who were being treated with a gluten-free diet. The effects of a gluten challenge on the intestinal mucosa and the clinical, emotional, and haematological effects of the challenge are reported.

Jejunal mucosal immunoglobulin-containing cells of all three major classes (IgA, IgM, IgG) were increased in coeliac children on gluten-containing diets but only IgM cell numbers were raised in those on gluten-free diets. Patients with subtotal villous atrophy had greater numbers of immunoglobulin-containing cells than patients with normal mucosa. In previously treated patients studied before and after three months on a gluten-containing diet ther was an increase in all three classes of cell, IgM containing cells showing the greatest proportional rise. Basement membrane staining with anti-IgA serum occurred in coeliacs and was most intense in untreated patients. Apart from one patient with very low levels of serum IgA, serum immunoglobulins did not differ from normal. However, after reintroduction of gluten to the diet a significant fall in serum IgM concentrations occurred compared with levels in the same patients while on gluten-free diets. It seems probable that both IgA and IgM systems are important in the immunopathogenesis of the small intestinal lesion of childhood coeliac disease.

790. Urinary outputs of oxalate, calcium, and magnesium in children with intestinal disorders: potential cause of renal calculi. 24-hour urinary outputs of oxalate, calcium, and magnesium have been determined in a total of 62 children aged 3 months to 17 years who fell into the following groups: (i) 16 normal controls, (ii) 3 with primary hyperoxaluria, (iii) 9 with small and/or large intestinal resections, (iv) 9 with untreated coeliac disease, (v) 5 with pancreatic dysfunction, and (vi) a miscellaneous group of 20 children with a variety of intestinal disorders.Taken as a whole, 58% of patients with intestinal disorders had hyperoxaluria, and of these 7 % had urinary outputs of oxalate which fell within the range seen in primary hyperoxaluria. The proportion of children with hyperoxaluria in the different diagnostic groups was as follows: intestinal resections (78%), coeliac disease (67%), pancreatic dysfunction (80%), and miscellaneous (45%). 35% of the patients with hyperoxaluria had hypercalciuria, whereas magnesium excretion was normal in all subjects studied. In 2 patients treatment of the underlying condition was accompanied by a return of oxalate excretion to normal.These results indicate that hyperoxaluria and hypercalciuria are common in children with a variety of intestinal disorders, and that such children may be at risk of developing renal calculi without early diagnosis and treatment.Hyperoxaluria is common in adult patients with ileal disease or resection, and a proportion of these patients develop oxalate renal calculi (Dowling, Rose, and Sutor, 1971; Smith, Fromm, and Hofmann, 1972;Chadwick, Modha, and Dowling, 1973

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