Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study

Aim A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicoba cter pylori eradication has been described repeatedly, but the long-term pr ogression of such a decrease has been scarcely studied. We therefore studie d the effect of H. pylori eradication on basal and stimulated gastrin and P G levels for 1 year. Initially, the usefulness of measuring these parameter s for the noninvasive diagnosis of H. pylori eradication was validated. Fur thermore, an assessment was made of the association between H. pylori reinf ection and a re-increase in gastrin and PG values. Finally, an evaluation w as made of the variables influencing gastrin and PG concentration, with par ticular attention to H. pylori infection and histological lesions of gastri c mucosa. Methods Two-hundred and twenty-two patients with duodenal ulcer were studie d prospectively. Exclusion criteria were the administration of antibiotics, H-2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 mo nth after completing eradication therapy. In the successfully eradicated pa tients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef c ubes) and PGI (after injection of pentagastrin) were also performed. H. pyl ori-negative patients after therapy underwent a urea breath test at 6 and 1 2 months, and patients who had stimulated gastrin and PG concentration meas ured had also an endoscopy performed at 6 months. Results H. pylori was eradicated in 73% of patients. A histological improve ment was observed 1 month after completing H. pylori eradication therapy, b oth at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the differen t cut-off points for decreased basal and stimulated measurements for diagno sing H. pylori eradication, the best results were obtained, respectively, w ith PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after s timulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylon ' status correlated with gastrin, PGI and PGII after therapy (P < 0.001), w hile histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immedia tely after eradication (Wilcoxon test, P < 0.001), and an additional decrea se (at 6 months) was observed just in PGI (Friedman test, P < 0.01). Howeve r, gastrin and PGII values remained unchanged after the first month post-er adication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliabl e as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only i n one out of three with reinfection at 1 year did PGII rise at that stage. Conclusions (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication a fter therapy. (2) H. pylori eradication is associated with a significant de crease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains u nchanged for 1 year. However, the decrease in basal and stimulated PGI leve ls occurs progressively for 6 months, although such levels remain also unch anged afterwards. (3) Measurement of gastrin and PGI concentrations has a l imited usefulness in the diagnosis of H. pylori reinfections after successf ul eradication, although PGII determination could be more useful in this si tuation. (C) 1999 Lippincott Williams & Wilkins.