gastrins and Chagas-Disease

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.

Topics: Case-Control Studies; Chagas Disease; Coinfection; Cross-Sectional Studies; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged

The aim of this study was to determine the contribution of preoperative gastric secretory and hormonal response, to the appearance of Barrett's esophagus in the esophageal stump following subtotal esophagectomy.. Thirty-eight end-stage chagasic achalasia patients submitted to esophagectomy and cervical gastric pull-up were followed prospectively for a mean of 13.6 +/- 9.2 years. Gastric acid secretion, pepsinogen, and gastrin were measured preoperatively in 14 patients who have developed Barrett's esophagus (Group I), and the results were compared to 24 patients who did not develop Barrett's esophagus (Group II).. In the group (I), the mean basal and stimulated preoperative gastric acid secretion was significantly higher than in the group II (basal: 1.52 vs. 1.01, p = 0.04; stimulated: 20.83 vs. 12.60, p = 0.01). Basal and stimulated preoperative pepsinogen were also increased at the Group I compared to Group II (Basal = 139.3 vs. 101.7, p = 0.02; stimulated = 186.0 vs. 156.5, p = 0.07. There was no difference in preoperative gastrin between the two groups. Gastritis was present during endoscopy in 57.1% of the Group I, while it was detected in 16.6% of the Group II, p = 0.014.. Barrett's esophagus in the esophageal stump was associated to high preoperative levels of gastric acid secretion, serum pepsinogen, and also gastritis in the transposed stomach.

Topics: Adult; Barrett Esophagus; Chagas Disease; Epithelium; Esophageal Achalasia; Esophagectomy; Female; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Pepsinogen A; Preoperative Period; Risk Assessment; Young Adult

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P > 0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (16.4 (6.9-54.4) vs 59.3 (29.6-113.8), P < 0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

Topics: Chagas Disease; Chronic Disease; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Pyloric Antrum; Somatostatin

1. Patients with chronic Chagas' disease have abnormally low gastric acid secretion and increased gastrin release both during fasting and after different stimuli. Regardless of the relationship between intragastric acidity and gastrin secretion, it is uncertain whether hypergastrinemia in Chagas' disease is caused by an increased population of antral gastrin (G) cells (hyperplasia) or by enhanced cell activity (hyperfunction). 2. We therefore estimated G cell number in antral biopsies from 16 chagasic patients and 13 control subjects using a peroxidase-anti-peroxidase immunohistochemical technique. All subjects underwent a gastric secretion test to determine peak acid output following intravenous pentagastrin instillation. 3. Antral G cell number in Chagas' disease patients was not significantly different from that observed in the control group (number of cells/mm2, median and (range): 128 (44-284) vs 138 (65-285)). 4. In chagasic patients, peak acid output was significantly lower than in controls (mmol/h, median and (range): 9.819 (3.024-21.564) vs 17.490 (9.423-25.848)). 5. These results suggest that the increase in gastrin release associated with reduced gastric acid secretion in Chagas' disease is mediated by antral G cell hyperfunction rather than by hyperplasia.

Topics: Adult; Cell Count; Chagas Disease; Chronic Disease; Esophageal Achalasia; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Megacolon; Middle Aged; Pyloric Antrum

Plasma gastrin and gastric acid responses to intravenous injection of insulin (0.2 IU/kg) were measured in 8 patients with Chagas' disease, which is known to be associated with extensive reduction of the intramural neurons of the digestive tract, and in 6 control subjects. All subjects developed hunger, sweating and tachycardia, and exhibited less than 50 mg/dl venous blood glucose. Plasma gastrin responses in Chagas' disease patients (median: 3.60 nmol L-1 min-1; range: 1:12 to 10.60 nmol L-1 min-1) were significantly higher than for control subjects (median: 0.52 nmol L-1 min-1; range: 0.25 to 1.09 nmol L-1 min-1). Gastric acid output was significantly lower in Chagas' disease patients (median: 3.5 mmol/h; range: 2.1 to 13.6 mmol/h) than in controls (median: 30.3 mmol/h; range: 7.3 to 38.2 mmol/h). These data show that chagasic patients have abnormally high gastrin release and low gastric acid secretion in response to insulin, and thus indicate that loss of intrinsic innervation of the stomach does not abolish the gastrin response to insulin hypoglycemia.

Topics: Adult; Blood Glucose; Chagas Disease; Female; Gastric Acid; Gastrins; Humans; Hypoglycemia; Insulin; Male; Middle Aged

Chagas' disease is known to be associated with extensive lesions of the intramural neurons of the digestive tract. In order to evaluate the contribution of the intramural plexuses to the control of plasma gastrin levels in man, we performed the following measurements: (a) fasting plasma gastrin in 18 chagasic patients and 16 control subjects; (b) integrated gastrin response to food in 9 chagasic patients and 10 controls, (c) basal acid secretion and gastric acid responses to graded doses of pentagastrin in 14 chagasic and 13 controls. Fasting plasma gastrin levels and integrated gastrin response were significantly higher in chagasics than in controls. Basal and maximal acid secretion and responsiveness of acid-secreting gastric cells were lower in chagasics. These results indicate that the intramural plexuses play a role in the control of gastrin release in man.

Topics: Adult; Chagas Disease; Fasting; Female; Food; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Pentagastrin