Increased serum gastrin in patients with different clinical forms of Chagas disease coinfected with Helicobacter pylori

• Autor(a) principal: Sousa, Jacqueline Batista
• Data de Publicação: 2019
• Outros Autores: Etchebehere, Renata Margarida, Queiroz, Dulciene Maria de Magalhães, Fonseca, Fernanda Machado, Batista, Bianca Bontempi, Junqueira, Iracema Saldanha, Camilo, Sílvia Maria Perrone, Oliveira, Adriana Gonçalves de
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Revista do Instituto de Medicina Tropical de São Paulo
• Texto Completo: https://www.revistas.usp.br/rimtsp/article/view/154491
• topic: Helicobacter pylori; Chagas disease; Gastrin; Chronic gastritis; Acid secretion; Gastric physiology

Trypanosoma cruzi and Helicobacter pylori (HP) are pathogens that cause chronic diseases and have been associated with hypergastrinemia. The aim of this study was to evaluate the fasting gastrin levels in patients with different clinical forms of Chagas disease (CD), coinfected or not by HP. The enrolled individuals were outpatients attending at the university hospital. HP infection was assessed by serology and 13C-urea breath test. Fasting serum gastrin concentration was measured by chemiluminescence assay. Gastric endoscopic and histological features were also evaluated. Associations between CD and serum gastrin level were evaluated in a logistical model, adjusting for age, gender and HP status. A total of 113 patients were evaluated (45 with Chagas disease and 68 controls). In the multivariate analysis, increasing serum gastrin levels (OR= 1.02; 95% CI= 1.01-1.12), increasing age (OR= 1.05; 95% CI= 1.02 - 1.09) and HP-positive status (OR = 2.88; 95% CI = 1.10 - 7.51) remained independently associated with CD. The serum gastrin levels were significantly higher in the group of patients with the cardiodigestive form (P = 0.03) as well as with digestive form (P = <0.001) of Chagas disease than in the controls. In conclusion, patients with cardiodigestive and digestive clinical forms of CD have increased basal serum gastrin levels in comparison with controls. Moreover, we also demonstrated that H. pylori coinfection contributes to the hypergastrinemia shown in CD.