[Gastrin secretion in patients with functional dyspepsia].

UNLABELLED: The pathogenesis of functional dyspepsia is very complicated and its etiology is still not clear. One of the supposed pathophysiological mechanisms are disturbences of gastric acid secretion and gastric motility. Recently, it has been recognized, that in the pathogenesis of above disturbances may play a role enterohormones, like gastrin.

AIM: To establish if in patients with functional dyspepsia the level of gastrin concentration changes and wheather it correlates with type and grade of symptom's intensity.

MATERIAL AND METHODS: The study included 50 subjects between of 20 to 54 years with diagnosed functional dyspepsia (according to the Rome III Criteria). The study group was divided into two subgroups: group I--25 subjects with Epigastric Pain Syndrome--EPS and group II--25 subjects with Postprandial Distress Syndrome--PDS. Control group comprised 20 healthy subjects (without any clinical or morphological symptoms of digestive tract disease). In each patient due to gastrointestinal tract organic disease exclusion the gastroscopy, histological examination of gastric mucosa, ultrasonography of abdomen and laboratory tests were performed. H. pylori infection was detected using fast urea test (CLO-test), confirmed by histopathological examination (stained Giemsa method) and non-invasive urea breath test (UBT-13C) using mass spectrophotometer FANci 2 (Fisher Analyser Instrumente GmbH). In each patient the level of gastrin concentration in blood serum, in fasting state, was determined, based on ELISA method considering the length of the weave lamda=430 nm. The study group was also divided into 3 subgroups, using 10-points scale of symptom's intensity: --grade 1--mild (1-3 points); --grade 2--moderate (4-6 points); --grade 3--severe (7-10 points).

RESULTS: The concentration of gastrin in blood serum in healthy subjects was 2.4 +/- 1.23 pmol/L. In patients with functional dyspepsia was significantly higher; in patients with Epigastric Pain Syndrome--7.51 +/- 2.46 pmol/L (p < 0.05), in patients with Postprandial Distress Syndrome - 6,92 +/- 2.18 pmol/L (p < 0.05). There were no significant differences in dependence on pain's intensity in EPS--the concentrations in subgroups 1, 2 and 3 were: 7.36 +/- 1.4 pmol/L, 7.53 +/- 2.43 pmol/L and 7.64 +/- 2.55 pmol/L. The gastrin concentration in PDS in dependence on symptom's intensity in subgroup 1 was 6.34 +/- 1.2 pmol/L, in subgroups 2 and 3 were higher: 6.99 +/- 2.31 pmol/L and 7.42 +/- 2.2 pmol/L, but the differences were not statistically significant. In patients with functional dyspepsia, infected with H. pylori the gastrin concentration was significantly higher and was 15.28 +/- 5.3 pmol/L (p < 0.05). There were no significant differences in dependence on type of dyspepsia.

CONCLUSIONS: The gastrin concentration in blood serum in fasting state in patients with functional dyspepsia is higher than in control subjects, both in patients with Epigastric Pain Syndrome--EPS as well as with Postprandial Distress Syndrome--PDS. The grade of symptom's intensity does not correlate with increase of gastrin concentration.