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Biomedical subjects

C C Booth

Publications and source records attributed to C C Booth.

At least 37 records · Page 2Linked to original sources

Coeliac disease and malignancy.

Patients with coeliac disease are at greater risk than the general population for the development of malignant neoplasms, particularly lymphomas. Of 259 histologically confirmed malignancies in 235 patients with histologically proven coeliac disease, 133 were malignant lymphomas, the predominant histological type being malignant histiocytosis and the commonest site of this lesion the small intestine. Patients with coeliac disease also have a greatly increased risk for the development of small-intestinal adenocarcinomas. Among 116 invasive non-lymphomatous malignancies there were 19 small-intestinal adenocarcinomas, compared with 0 . 23 expected from national cancer registrations adjusted for sex and age. There were also more oesophageal and pharyngeal squamous carcinomas than expected.

Adenocarcinoma↗

HLA antigens in coeliac disease associated with malignancy.

Coeliac patients are at greater risk than the general population of developing malignant neoplasms, particularly lymphomas. The establishment at the Clinical Research Centre of a national collaborative study of coeliac patients with malignancy provided the opportunity to carry out HLA typing for 55 HLA-A, B and C and the 10 recognised DR antigens on a group of coeliac patients with malignancy. Study of a sample of 44 patients with biopsy proven coeliac disease and histologically confirmed malignancy, including 12 with malignant histiocytosis, and 57 coeliac patients without malignancy, failed to show any significant differences in antigen frequencies between patients with and without malignancy. These results indicate that there are no HLA genetic markers associated specifically with the development of malignancy in coeliac disease.

Adult↗

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↗