The development of clinical science in Britain.
Explore the source record for details and available documents.
Education, Medical↗
Biomedical subjects
C C Booth
Publications and source records attributed to C C Booth.
Coeliac disease.
In coeliac disease there is an abnormality of the intestinal mucosa which is caused by ingesting gluten. The intestinal lesion affects predominantly the proximal small intestine and the ileum is either normal or less severely involved than the jejunum. In some cases adaptive changes occur in the ileum, producing enhanced absorption in that region when there is malabsorption in the jejunum. The characteristic absorptive abnormality in coeliac disease is therefore jejunal malabsorption and ileal hyperabsorption. When such a situitation develops it is possible that an indivisual with a flat jejunal mucosa may develop no symptoms of the disease, since the adaptive changes in the ileum compensate for the jejunal lesion. This may explain why in Western society there are probably more cases of coeliac disease undiagnosed in the community that have been treated by their doctors. The basic lesion in coeliac disease appears to be genetically determined and it is likely to be a failure to clear antigen which normally enters the lamina propria of the gut resulting in the formation of immune complexes with complement fixation at gut level.
Adult↗
Subepithelial collagen in intestinal malabsorption.
Intestinal biopsies from 146 patients with adult coeliac disease and 13 patients with intestinal villous atrophy of different aetiology were assessed for the presence of subepithelial collagen and compared with a group of 20 control subjects. Subepithelial collagen was a common and non-specific finding observed in intestinal biopsies from patients suffering from adult coeliac disease (36%) and tropical sprue. In adult coeliac disease the described subepithelial changes usually regress following treatment, though marked subepithelial collagen deposition may indicate a poor prognosis. The study showed that the presence of marked subepithelial collagen in a flat jejunal biopsy does not define a separate clinical entity.
Adult↗
Immunopathology of coeliac disease.
Coeliac disease may be defined as a condition in which there is an abnormal jejunal mucosa with loss of villi, which improves morphologically after treatment with a gluten-free diet. Pathologically, there is damage to the jejunal enterocytes, with hyperplasia of crypt cells so that overall enteropoiesis is increased. On conventional or scanning electron microscopy the enterocytes are markedly abnormal. Histochemically, the normal punctate appearance of the lysosomes is lost and sensitive lysosomal enzyme assays on mucosal biopsy samples using isopycnic centrifugation techniques show that there is an increase in total lysosomal activity with reduction in lysosomal latency. Studies following gluten feeding in patients whose mucosa has returned to normal after treatment with a gluten-free diet show that pathological abnormalities appear within 4--8 hours of gluten challenge. Complement together with extracellular IgM can be demonstrated in the lamina propria, suggesting the formation of immune complexes. In untreated coeliac disease there is a significant reduction in serum levels of C3 and C4. There is also evidence indicating the presence of immune complexes in the serum. Coeliac disease may therefore be an intestinal model of an immune complex disease, in which an antigen derived from gluten reacts with an antibody formed locally in the gut, fixing complement and causing damage to the enterocyte by activation of lysosomes.
Adult↗