5 - Immunoassay Studies in Peptic Ulcer

Abstract

SUMMARY AND CONCLUSIONS The brief for this chapter has been the contribution of immunoassay to the pathophysiology of peptic ulcer. In this context, gastrin has been considered as a possible factor because of its known function as a stimulus to gastric acid secretion and because it is readily measured by immunoassay. A number of groups have reported serum gastrin levels in normals and peptic ulcer disease but variations in antisera and methodology have led to variable results. Employing an antiserum which specifically measures gastrin I, the majority of patients with duodenal ulcer have low basal serum gastrin levels which reflect acid inhibition, but also have a large gastrin-secreting cell mass. These findings have led to the thesis that both the increased G cell mass and increased parietal cell mass are a result of a common stimulus and this is probably the vagus. Occasional patients with duodenal ulcer have higher gastrin levels and these can be considered as being autonomous gastrin secretors. On the other hand, a number of groups employing antisera with a wider spectrum of immunogenicity to ‘gastrin’, have found normal or higher levels of basal gastrin in a majority of patients with duodenal ulcer. These findings indicate some autonomy of ‘gastrin’ secretion in duodenal ulcer and imply a failure of normal feedback inhibition of gastrin release in the face of high acid secretion. In gastric ulcer disease, gastrin levels are higher than normal and there is evidence that gastrin may be released in increased amounts from extra-antral sites. Damage to the gastric mucosa may make it more susceptible to further damage by gastrin-stimulated acid and pepsin, thus perpetuating the ulcer. That extragastric gastrin may be important in the pathogenesis of gastric ulcer is suggested by the observation of increased incidence of gastric ulcer after truncal vagotomy, particularly if the stomach is undrained. In summary, although controversy exists about basal serum gastrin levels in duodenal ulcer, there is some evidence for increased gastrin release in this disease in response to stimulation which undoubtedly contributes to the increased release of acid. Whether it is a key factor remains to be shown. On the other hand, gastrin, perhaps from extragastric sites, may have a role in the pathogenesis of gastric ulcer. The role of other hormones in the pathophysiology of peptic ulceration remains purely speculative.