Increased serum chromogranin a level after short-term proton-pump inhibitor therapy

Background: Chromogranin A (CgA) has been shown to be a useful marker in the diagnosis of neuroendocrine tumours (NETs). Enterochromaffin-like (ECL) cell hyperplasia secondary to hypergastrinemia also leads to increase of serum CgA. It's well established that medium- or long-term proton-pump inhibitor (PPI) therapy significantly increases serum CgA via hypergastrinemia, but the effect of short-term PPI treatment (as used during PPI-test) has been scarcely evaluated.

Aim: To analyze the effect of short-term PPI therapy on serum CgA levels.

Patients and methods: Fourteen patients with newly diagnosed erosive reflux esophagitis (5 males-9 females, mean age 50 years, range 30–68) were enrolled in this prospective study. Pathologic conditions associated with elevated CgA levels (e.g. renal insufficiency, malignancy, atrophic gastritis) were excluded. Esomeprazole therapy (40mg once daily) has been started after upper gastrointestinal endoscopy. Serum CgA levels were determined in all subjects after 12 hours fasting before (0. day), after one day (1. day), five days (5. day), ten days (10. day) and twenty-eight days (28. day) of PPI therapy. A solid phase, two site immunoradiometric assay (CIS Bio International, Gif-Sur-Yvette, France) was used for the determination of serum CgA levels. Statistical analysis with Kruskal-Wallis test (nonparametric ANOVA) was performed. P value of <0,05 was considered significant.

Results: CgA level (mean,±S.D.) was 62,03±46,14ng/ml before starting PPI therapy (0. day) and a significant stepwise increase was observed during the study period (1. day: 97,49 ±86,17ng/ml; 5. day: 132,73±132,2ng/ml; 10. day: 158,13±146,15ng/ml, 28. day: 193,53±181,1ng/ml, respectively) (Kruskall-Wallis, P=0.0027).

Conclusions: We demonstrate that CgA increases rapidly after PPI administration. This indirectly can suggest the rapid onset of gastric acid inhibition during PPI-test.