Does eradication of Helicobacter pylori reverse atrophic gastritis or intestinal metaplasia? Data from Japan

In Japan, more reports showing improvement of atrophy or IM after eradication have appeared than reports showing no change. Many authors take biopsy specimens from the lesser and greater curvatures of the antrum and body and incisura angularis and make a histologic assessment using the standardized Updated Sydney System. Sampling errors should be taken into account, however. Interobserver agreement is poor in grading of atrophy. Apart from these problems, it seems almost certain that some patients show improvement or regression of atrophy or IM after eradication. Takizawa et al, evaluating many gastritis specimens, observed that antral IM might regress after eradication in the antral mucosa, where some pyloric glands remained under IM because pyloric glands and IM shared the proliferative zone, and that body IM replacing total fundic glands might hardly regress (T. Takizawa, MD, personal communication). Suto et al showed in an animal model that pseudopyloric glands differentiated into chief and parietal cells. Watanabe et al examined the influence of gastric pH on IM in x-irradiated rats and showed that increased acid secretion was associated with partial disappearance of IM without Paneth cells. Because gastric acid secretion of hypochlorhydric patients with body-predominant gastritis increased into normal range 1 to 6 months after eradication, it is possible that IM may regress in human subjects whose acid-secreting capacity recovers after eradication. The point of no return at which eradication leads to regression of atrophy and IM is not known. It is unknown how long IM takes to regress after eradication. There may be some differences in the characteristics between patients with and without improvement. Factors other than H. pylori (e.g., environmental factors) also should be investigated.