We determined the effect of postgastrectomy
gastritis on serum
pepsinogen I and
pepsinogen II concentrations in 108 subjects with subtotal gastric resection. Eleven had normal remnant mucosa, 22 had superficial
gastritis, and 75 had
atrophic gastritis. In the subjects with superficial
gastritis, serum
pepsinogen I and II concentrations were significantly higher than in those with normal remnant mucosa, but the ratio of
pepsinogen I to II did not differ from normal. In
atrophic gastritis, serum
pepsinogen I concentrations fell with increasing severity of mucosal damage, but
pepsinogen II was persistently raised. Consequently, the ratio of
pepsinogen I to II in subjects with
atrophic gastritis was significantly lower than in those with superficial
gastritis or normal remnant mucosa. Discriminant function analysis revealed that the ratio of
pepsinogen I to II, in combination with the absolute level of
pepsinogen II, had a sensitivity of 80%, a specificity of 73%, and a positive predictive value of 87% for
atrophic gastritis in this population. We propose that the parallel increase in serum
pepsinogen I and II concentrations in postgastrectomy superficial
gastritis is because of an increased rate of endocrine release of both
zymogens from the fundic glands, and that the dichotomy in
pepsinogen I and II concentrations in postgastrectomy
atrophic gastritis results from the loss of fundic glands, which produce both
zymogens, and the appearance of metaplastic pyloric glands, which produce only
pepsinogen II.