Manabu Kimura

Increased serum pepsinogen I and recurrence of duodenal ulcer

To determine whether the serum pepsinogen I (PG I) level would be a suitable marker for selecting patients at risk for duodenal ulcer recurrence and, thus, would benefit from maintenance therapy, we treated duodenal ulcer patients with H2-receptor antagonists. After healing 140 ulcer patients we assessed the recurrence rate at 1 year with and without maintenance therapy. The annual recurrence rates in duodenal ulcer patients with hyper-PGI (95 ng/ml or more), with 66 ng/ml less than or equal to PGI less than 95 ng/ml, and with PGI less than 66 ng/ml were 87.0%, 27.3%, and 17.9%, respectively, when they did not receive maintenance therapy. In patients with hyper-PGI the recurrence rate was significantly lower in patients receiving maintenance therapy than in patients not receiving maintenance therapy, whereas in patients with PGI less than 66 ng/ml the recurrence rate was as low as 20% regardless of maintenance therapy. These results indicate that maintenance therapy with half the dose of H2-receptor antagonist is not required by patients with PGI less than 66 ng/ml, whereas those with hyper-PGI may be good candidates for long-term maintenance therapy.

Characteristics of Teen-age Patients with Juvenile Duodenal Ulcer Relation between Inherited Hyperpepsinogenemia I and Duodenal Ulcer

We analyzed environmental factors, family history of peptic ulcer, gastric acid secretion, and serum levels of pepsinogen I (PG I) and gastrin in 56 juvenile patients with duodenal ulcer and 39 normal teenage subjects. Basal acid output and maximal acid output were significantly higher in our duodenal ulcer patients than in controls without ulcer (both, p < 0.01), and patients with duodenal ulcer showed significantly higher serum levels of PG I and gastrin than the controls (both, p < 0.001). There were no significant differences in any environmental factor between the patients and controls. Fifteen of the 17 patients who had one or both parents with hyperpepsinogenemia I had high serum PG I levels. Over half of the duodenal ulcer patients had high serum gastrin levels, irrespective of family history of hypergastrinemia. Our findings suggest that hyperpepsinogenemia I and hypergastrinemia are important characteristics and that genetic background, particularly the inheritance of a gastric mucosal trait expressed as hyperpepsinogenemia I, is frequently involved in the pathogenesis of juvenile duodenal ulcer.

Multiplicative effect of hyperpepsinogenemia I and non-secretor status on the risk of duodenal ulcer in siblings.

SummaryIn a search for genetic markers of duodenal ulcer, serum pepsinogen I level, ABO blood groups and secretor status were determined in 89 siblings of 34 duodenal ulcer families. Duodenal ulcer patients were likely either to have hyperpepsinogenemia I or to be non-secretors on a familial basis, but not to have an increased frequency of blood group O. The frequency of duodenal ulcer in the siblings was highest in hyperpepsinogenemia I/non-secretor and lowest in normopepsinogenemia I/secretor. Therefore, the influence of two genes, hyperpepsinogenemia I and non-secretor, on the risk of duodenal ulcer is multiplicative. These results provide evidence on the hypothesis of polygenic inheritance of duodenal ulcer.