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A study of splenic function in 28 patients with adult coeliac disease showed no significant correlation between the half life of heat-damaged red cells and either the duration of pre-treatment exposure to gluten or the length of time on a gluten free diet. A significant correlation was found between splenic size and duration of treatment; those patients who had been taking a gluten free diet for the longest time had the smallest spleens. Blood films from 11 of these 28 patients taken before treatment with a gluten free diet were compared with those taken between two and 15 years after the start of treatment. There was no tendency for the hyposplenic changes to regress. In the majority, the changes became more prominent despite strict adherence to the gluten free diet. These findings suggest that splenic atrophy in adult coeliac disease is not reversed by treatment with a gluten free diet and is unlikely to be related to the state of the jejunal mucosa or the duration of initial exposure to gluten.

A new technique for measuring changes in the architecture of the small intestinal mucosa is described using a modification of the technique of television image analysis to measure the areas occupied by the surface and crypt epithelium in proximal jejunal biopsies. The ratios of these two areas to each other were then calculated. In 12 control mucosae, the mean ratio (+/-SD) was 2.27 +/- 0.41. In 12 untreated flat mucosae, by contrast, the mean ratio was only 0.24 +/- 0.07. This ten-fold difference, which was highly significant (p0.001), was greater than that for any similar measurements previously reported. This technique is intended for the measurement of changes in the mucosa too small for existing techniques to detect reliably rather than for the diagnosis of coeliac disease.

Mouth-caecum transit time (M-CTT) of a lactulose labelled liquid test meal has been measured in 27 coeliac patients and 10 healthy controls using the breath hydrogen technique. Although all patients were urged to maintain a gluten free diet, not all did, and there was, therefore, a wide range in the severity of fat malabsorption within the patient group. Gastric emptying of a 113Indium DTPA-labelled liquid test meal was also assessed in separate studies on six healthy controls and 11 of the coeliac patients. Fasting breath hydrogen concentrations and the response to lactulose, as assessed both by the rate of rise, and the peak breath hydrogen concentration reached, showed no difference between coeliacs and controls, regardless of the presence or absence of steatorrhoea. Mouth-caecum transit time in the 16 coeliac patients with steatorrhea (faecal fat greater than 7 g/24 h) was, however, significantly prolonged being 158 +/- 18 minutes (mean +/- SEM), compared with 70 +/- 9 minutes for the controls (p less than 0.02), and 83 +/- 15 minutes for the 11 coeliacs without steatorrhoea (p less than 0.002). Mouth-caecum transit time in the coeliac patients was linearly related to the 24 hour faecal fat excretion, r = 0.55, n = 27, p less than 0.01. Slow mouth-caecum transit in the coeliacs with steatorrhoea was not caused by delayed gastric emptying as the t1/2 for coeliacs with steatorrhoea was within the normal range. Coeliacs with delayed mouth-caecum transit had impaired insulin release but the postprandial profiles of the other peptides measured (cholecystokinin, GIP, secretin, motilin, neurotensin, enteroglucagon, and peptide YY) were all within the normal range in this group of partially treated coeliac patients.

A previously described technique for measuring changes in the architecture of the small intestinal mucosa was used to measure the long-term response in six patients with adult coeliac disease to treatment with a gluten-free diet. All had flat or flat-with-mosaic jejunal mucosae before treatment and were subsequently believed to keep strictly to a gluten-free diet. They were followed for between four and 14 months from the start of treatment. The ratio of the area of surface epithelium to that of crypt epithelium (;area ratio') invariably increased following gluten withdrawal, but did not begin to do so until after several weeks of treatment. No patient attained complete histological normality within the limited period of observation, which was never more than 14 months. In one of the three patients followed for a year or more the area ratio increased to within the control range, and in two of these three the ratio was about 10 times the pretreatment ratio. There was a highly significant linear correlation between area ratio and time on the diet (r = 0.775, p0.005). The surface cell height measurements for these patients, by contrast, rose steeply and almost invariably during the first few weeks of treatment, but after that they fluctuated without further significant change. It is suggested that the two methods of measurement were complementary to each other, surface cell height being useful while the patient was in hospital on a rigidly strict diet, and the area ratio after return home, when minor dietary lapses were almost invariable.