The diagnostic value in coeliac disease of circulating antibodies to casein, crude gliadin, and a gliadin was assessed using an adaption of the enzyme linked immunosorbent assay system. a Gliadin was the only antigen which consistently separated 26 patients with untreated coeliac disease from 26 normal controls and 13 patients with chronic inflammatory bowel disease. The mean assay index for the 26 patients was 3-1 (SD 1-2) compared with 1-05 (0-5) for the normal controls and 1-1 (0-6) for patients with chronic inflammatory bowel disease. The a gliadin antibody levels of six patients with coeliac disease who had maintained a gluten free diet for at least two years were not significantly higher than normal (10 (0-4)). The validity of the test was determined in 90 consecutive patients who were being investigated for the presence of coeliac disease. Levels of a gliadin antibody were raised in 36 out of 44 patients found to have histologically proved coeliac disease and in six out of 46 subjects whose jejunal mucosa was normal. Serial a gliadin concentrations were measured in 12 patients with coeliac disease who had repeat jejunal biopsies performed six months after starting a gluten free diet. The levels of antibody fell in seven of the eight patients whose jejunal mucosa improved on maintaining the
SUMMARY In vitro cytotoxicity of four different gluten fractions was tested in organ culture for up to 48 hours using flat intestinal biopsies from children with coeliac disease. The fractions were (1) a peptic-tryptic digest of gliadin containing a moderate amount of alpha-gliadin, (2) a peptic-tryptic digest of gluten (Frazer fraction III) from a strain of wheat with a high content of alpha-gliadin, (3) alpha-gliadin, and (4) alpha-GT-18 000, a tryptic fragment of alpha-gliadin. The latter three fractions were toxic to coeliac patients in vivo. In vitro, however, none of these fractions proved to be cytotoxic. When added to the culture medium they were not capable of inhibiting the regeneration of the surface epithelium as visualised by histology and electron microscopy. The only difference between cultures with and without gluten fractions was that the former produced slightly more mucus when maintained in vitro as observed in the dissecting microscope. Furthermore, for Frazer fraction III the absence of apparent toxicity was confirmed by the behaviour of brush border enzyme activities during culture. Our results are not in accordance with those reported in the literature. We believe that the criteria used at the present time for the assessment of gluten toxicity in vitro should be extended to include the process of enterocyte desquamation.
A computer simulation model is presented of the gastric phase regulation of gastric acid secretion in humans. The model is based on experimental data from the literature and includes terms representing gastric pH and gastric volume-dependent gastrin secretion, gastrin-dependent acid secretion, food storage in the stomach, and gastric emptying. We have explored the predictive value of the model in assessing the relative importance of gastric pH-dependent and gastric volume-dependent acid secretion mechanisms under various conditions. Similarly we have studied the role of gastric acid deregulation in achlorhydria, the Zollinger-Ellison syndrome, and duodenal ulcer, and the influence of the antacid drugs cimetidine and ranitidine under duodenal ulcer conditions. Model analysis of normal gastric acid regulation suggests that gastric volume-controlled acid secretion is of major importance during eating and predicts that pH-dependent gastrin secretion is of major importance in preventing excessively low pH levels between meals and during the night.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.