Fred Hunter

Serum pepsinogens as markers of response to therapy for Helicobacter pylori gastritis.

We have investigated the effect of therapy forHelicobacter pylori gastritis on serum concentrations of pepsinogen I and II in 43 patients. In the 22 patients in whom therapy resulted in dramatic decrease in gastritis scores and in clearance of the bacteria, there was a highly significant (P=0.0001) fall in mean serum pepsinogen II from 13.3±0.8 to 7.9±0.7 μg/liter, and a less pronounced fall in pepsinogen I from 89.0±5.9 to 78.5±0.4 μg/liter (P=0.01). These changes resulted in a significant (P=0.01) increase in the pepsinogen I/II ratio. In contrast, nonsignificant declines of 3.5% and 11.6% were observed in mean pepsinogen I and II levels in the 21 patients whose gastritis failed to resolve histologically and whose infection did not clear. These findings suggest that serum pepsinogen levels, especially pepsinogen II, are a new tool that may be found to be clinically useful in evaluation of treatment outcome in patients withH. pylori-associated gastritis.

Helicobacter pylori-associated gastritis and the ascorbic acid concentration in gastric juice.

Patients infected with Helicobacter pylori have abnormally low ascorbic acid concentration in gastric juice. Low vitamin C intake and Helicobacter pylori infection have been related to an increased risk of gastric carcinoma. This report examines the association between ascorbic acid and Helicobacter pylori in patients referred for upper gastrointestinal endoscopy. Elevated gastric pH and the damage to the gastric surface epithelium were inversely associated with the ascorbic acid concentration in gastric juice. We postulate that these two factors mediate the ascorbic acid-decreasing effect of Helicobacter pylori. Patients with nonpremalignant conditions (normal gastric histology, diffuse antral gastritis, or duodenal ulcer) had lower gastric pH, less damage to the gastric epithelium, and higher levels of ascorbic acid in gastric juice than patients with atrophic gastritis, intestinal metaplasia, or dysplasia.

Ascorbic acid, Helicobacter pylori and Lewis phenotype among blacks and whites in New Orleans

Gastric juice ascorbic acid concentrations were examined in black and white patients. Significantly lower concentrations were found in blacks, in the absence of a significant difference in the plasma concentration of vitamin C between races. Blacks had higher prevalence of Helicobacter pylori infection, higher gastric pH, more severe acute and chronic inflammation of the gastric mucosa and higher frequency of Lewis (a-b-) phenotype. Although most of these factors have been related to low ascorbic acid levels in gastric juice, none of them could account entirely for the difference between races either individually or after joint consideration. These observations may help to explain the high incidence of gastric carcinoma among the black population in southern Louisiana.

Clinical Trials as Etiologic Research Tools in Helicobacter-Associated Gastritis

The role of clinical trials as tools to elucidate the etiology of chronic gastritis is discussed. Three areas are briefly explored. The first one concerns the classification of chronic gastritis, a constellation of interconnected nosologic entities. The second refers to the histopathologic factors of chronic gastritis; preliminary results show that clearance of Helicobacter pylori decreases the inflammatory infiltrate and suggest that H. pylori alters cell ploidy. The third area refers to the multifactorial etiology of chronic gastritis and the role that clinical trials could play in its elucidation.