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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.

Trypanosoma cruzi presents a high degree of intraspecific variability, with possible implications for the pathogenesis of Chagas disease. The aim of this study was to evaluate T. cruzi kDNA minicircle gene signatures using the low-stringency single-specific-primer PCR technique in both peripheral blood and oesophageal mucosa from chronic chagasic patients, with or without megaesophagus, alone or in combination with cardiopathy and megacolon. It was not possible to identify a uniform pattern of shared bands between blood and oesophageal mucosa samples from individuals with the same clinical form or mixed forms, suggesting multiple T. cruzi infections with differential tissue tropism. Thus, the results indicate that there is an intense intraspecific variability in the hypervariable regions of T. cruzi kDNA, which has so far made it impossible to correlate the genetic profile of this structure with the clinical manifestations of Chagas disease.

We have previously amplified Trypanosoma cruzi DNA by polymerase chain reaction (PCR) from the oesophagus of chagasic patients with megaoesophagus, whilst immunohistochemical analysis failed to detect T. cruzi antigen in the oesophagus of chagasic patients without megaoesophagus. During 2000-01, we tested for the presence of T. cruzi DNA in oesophageal tissue from 9 chronic chagasic patients without megaoesophagus and 5 were positive by PCR, which suggests that other factors, besides simply the presence of the parasite, should be considered in the understanding of the pathogenesis of megaoesophagus.

The authors report a case of schistosomiasis of uncommon location. A patient submitted to esophagectomy for Chagas' megaesophagus was found to have eggs of Schistosoma mansoni upon pathologic examination of the surgical specimen. The authors discuss the anatomopathological aspects of schistosomiasis, as well as its occurrence in other rare sites. To date, no references in literature have been found on the existence of esophageal schistosomiasis, and its association to Chagas' megaesophagus has never been described.

Two stocks of Trypanosoma cruzi isolated from patients with advanced megaoesophagus produced megastomach in chronically infected mice. The mice showed evidence of stomach dilatation and a delay in intestinal transit time. These findings are discussed in the light of the hypothesis that regional variations in T. cruzi determines mega formation in man.