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 13 C-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.
Background: Acid inhibition from chronic proton pump inhibitor use and a possible increase in gastrin can lead to changes in the regulation of hydrochloric acid production. However, it has not known whether such chronic use changes the presence of gastrin, delta, and enterochromaffin-like cells in the stomach or the relationship between gastrin and delta cells. Aim: To analyze the number of gastrin-producing gastrin cells, somatostatin-producing cells, and histamine-producing cells in patients who were chronic users of proton pump inhibitor, with or without related Helicobacter pylori infection. Methods: Biopsies from 105 patients, including 81 chronic proton pump inhibitor users (experimental group) and 24 controls, were processed immunohistochemically and subjected to counting of gastrin, delta, and enterochromaffin-like cells in high-magnification microscopic fields and in 10 glands. Results: Gastrin cell, delta cell, and enterochromaffin-like cells counts were similar across the groups and appeared to be unaffected by Helicobacter pylori infection. The ratio between gastrin cells and delta cells was higher in the chronic users of proton pump inhibitor group than in controls. Conclusion: Chronic users of proton pump inhibitor does not affect gastrin cell, delta cell, and enterochromaffin-like cell counts significantly, but may alter the ratio between gastrin cells and delta cells.
Helicobacter pylori is a Gram-negative bacterium that colonizes around 50% of world population. It is frequently associated with gastrointestinal diseases such as gastritis, peptic ulcer, and in some cases, can favour the development of gastric cancer. After the host colonization, H. pylori can cause chronic infection and disease in less than 10% of symptomatic individuals after several years. Thus, the apparent colonization of H. pylori requires a long time of establishment and the continuous stimulation of the inflammatory response to produce enough histological deterioration for disease expression [1].Several virulence factors of H. pylori have been described (i.e. cagA and vacA genes). The presence of these factors can contribute to the development of a more aggressive form of the disease, although strains not carrying these virulence factors were also recovered from stomach of infected patients. As the colonization of H. pylori can be asymptomatic for decades, most cases of the disease (i.e. peptic ulcers) occur in patients older than 40 years, and around 1% of these individuals can evolve to gastric cancer [2]. Due to its long latent period of infection, the small numbers of cases of that evolve to gastric cancer and the detection of H. pylori in the faeces of mummified humans around 3,000 years ago some authors have hypothesized that this pathogen cold be, in fact, more an ancestral commensal microorganism of humans than a true pathogen [3]. Reinforcing this hypothesis is the fact that the infection is transmitted early in life and is mainly in a family setting.
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