Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease

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 (l6.4 (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.

Antral gastrin cell population in patients with chagasic megaesophagus and megacolon

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

Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

Patients with the digestive form of Chagas' disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4 neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9) while atrophic gastritis was present in 8 (47.1) patients. H. pylori was present on gastric mucosa of 8 (100) patients with atrophic gastritis and of 8 (88.8) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

Effect of chlorpromazine and biliary drainage on portal blood flow and mitochondrial function during extrahepatic cholestasis

The present study examines the effect of chlorpromazine and biliary drainage in cholestatic rats. The time course of portal blood flow was studied 24,48, and 72 h and seven days after bile duct ligation. Portal blood flow decreased after 72 h. Chlorpromazine reduced biliary hydrostatic pressure in sham-operated control rats, but 24-h obstruction was sufficient to prevent this effect in cholestatic rats. The drug ameliorated the mitochondrial and cell membrane function of cholestatic rats before and after drainage. The data present further support for the role of ischemia in cholestasis