title: Gastric secretory and hormonal patterns in end-stage chagasic achalasia.
abstract: Achalasia surgical treatment alters the esophagogastric junction anatomy (cardiomyotomy plus fundoplication or esophagectomy and gastric pull-up), thus favoring a certain degree of gastroesophageal reflux. Gastric secretory and hormonal functioning is not completely known in chagasic patients. The aim of this study was to evaluate the gastric secretory and hormonal response in patients with end-stage chagasic achalasia compared with normal subjects. Gastric secretion and hormonal response were assessed by estimation of gastric acid secretion (GAS) in basal condition and after pentagastrin stimulation, basal serum gastrin, and serum pepsinogen (SP) in basal condition and after betazole hydrochloride (Histalog; Eli Lilly and Company, Indianapolis, IN, USA) stimulation in 27 patients with chagasic achalasia. The results were then compared with those of 24 normal subjects. In the chagasic group, the mean basal and stimulated GAS were significantly lower than in the control group (basal: 1.277 vs. 3.13, P = 0.002; stimulated: 15.9 vs. 35.8, P = 0.0001). Chagasic patients' SG levels showed a significantly higher basal value than the control group (83.3 vs. 36.8, P = 0.0001). There was a significant increase of SP after stimulation compared with the basal levels in both chagasic and control groups. Although the chagasic patients' SP values were higher than the controls, this difference was not statistically significant, either in basal and stimulated conditions (basal: 122.0 vs. 108.9, stimulated 120 min: 177.1 vs. 158.9). In patients with chronic Chagas' disease (ChD), although autonomic denervation does not suppress the strength of the gastric mucosal cells' secretory response to stimulation, it reduces GAS (parietal cell) without, however, affecting SP production (chief cells). On the other hand, the gastrin-producing cells have continuously been stimulated by low GAS.
authors.affiliation: Digestive Surgery Division, Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, Brazil.
authors.forename: J R M
authors.initials: JR
authors.lastname: da Rocha
authors.forename: U
authors.initials: U
authors.lastname: Ribeiro
authors.forename: I
authors.initials: I
authors.lastname: Cecconello
authors.forename: R A A
authors.initials: RA
authors.lastname: Sallum
authors.forename: F
authors.initials: F
authors.lastname: Takeda
authors.forename: A
authors.initials: A
authors.lastname: Nasi
authors.forename: S
authors.initials: S
authors.lastname: Szachnowicz
mesh_terms: D000328:Adult; D000368:Aged; D001625:Betazole / Q000494:pharmacology; D014355:Chagas Disease / Q000503:physiopathology*; D002908:Chronic Disease; D004931:Esophageal Achalasia / Q000469:parasitology / Q000503:physiopathology* / Q000601:surgery; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005745:Gastric Acidity Determination; D017442:Histamine Agonists / Q000494:pharmacology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D055815:Young Adult
chemical_list: D017442:Histamine Agonists; D001625:Betazole; D020116:Pepsinogen A