Hipergastrinemia em pacientes chagásicos: coinfecção pelo Helicobacter pylori, perfil sérico de citocinas e número de células G, D e enterocromafins

Abstract

Chagas Disease, mainly patients with digestive form presents a decrease of ganglion cells in the myenteric plexuses of the stomach leading to acid hyposecretion, one the main factor stimulating gastrin production. In addition, the gastrin levels as well known to be elevated in various conditions, including Helicobacter pylori (H. pylori) infection. It is not yet clear whether coinfection of H. pylori and Trypanosoma cruzi could influence the increase of the gastrin serum levels in patients as well as the number of gastrin-producing cells, somatostatinproducing cells, and histamine-producing cells. This study aimed to evaluate the number of G, D and enterochromaffin-like cells (ECL) in chagasic patients coinfected with H. pylori. A total of 73 outpatients who underwent endoscopy for histological analysis at the university hospital were included in the study. H. pylori infection was assessed by serology, histological analysis and 16S rRNA PCR test. Fasting serum gastrin concentration was measured by chemiluminescence assay. G, D and ECL cells in mucosa were analyzed by immunohistochemistry. Concentrations of IL-10, TNF and IFN-γ in serum were measured by ELISA. Gastric endoscopic was performed and histological features were also evaluated. The prevalence rates of H. pylori infection were similar (P>0.05) among the chagasic and control groups. The median serum gastrin concentration was significantly higher (P=0.008) in patients with Chagas disease compared to controls. The number of ECL cells were significantly higher among chagasic patients than controls (P=0.019) as well as among chagasic patients with the cardiac and indeterminate forms as compared with chagasic patients with the digestive form (P=0.020). There was no difference regarding the levels of serum cytokine between chagasic and control groups (P >0.05). In conclusion, the high level of gastrin that occurs in chagasic patients stimulates the proliferation of ECL cells, with a possible development of hyperplasia due to loss of parietal cells and consequently can lead to the hyperfunction of antral G cell.