Patients with megaesophagus (ME) have increased prevalence of cancer of the esophagus. In contrast, a higher incidence of colorectal cancer is not observed in patients with megacolon (MC). MC is very common in some regions of Brazil, where it is mainly associated with Chagas disease. We reviewed the pathology records of surgical specimens of all patients submitted for surgical resection of MC in the Hospital das Clínicas of the Faculty of Medicine of Ribeirão Preto (HC-FMRP), from the University of São Paulo. We found that 894 patients were operated from 1952 until 2001 for MC resection. Mucosal ulcers, hyperplasia and chronic inflammation were frequently found, while polyps were uncommon. No patients with MC presented any type of colonic neoplasm. This observation reinforces the hypothesis that MC has a negative association with cancer of the colon. This seems to contradict the traditional concept of carcinogenesis in the colon, since patients with MC presents important chronic constipation that is thought to cause an increase in risk for colon cancer. MC is also associated with other risk factors for cancer of colon, such as hyperplasia, mucosal ulcers and chronic inflammation. In ME these factors lead to a remarkable increase in cancer risk. The study of mucosal cell proliferation in MC may provide new insights and useful information about the role of constipation in colonic carcinogenesis.

Purpose: Develop an experimental model to study esophageal preneoplastic lesions induced by diethylnitrosamine in rats with achalasia. Methods: Male Wistar rats were divided into four groups: control -C (n=8); rats with megaesophagus -B (n=8); rats treated with DEN -D (n=15) and rats with megaesophagus plus DEN -BD (n=15). Megaesophagus can be experimentally obtained in rats by topical application of benzalkonium choride. The morphology and PCNA labeling index of the epithelium were evaluated. Results: The morphometric analysis showed an increase in epithelial thickness in the animals of group BD (2166±1012mm 2 ) when compared to the other groups (C = 878±278mm 2 ; B = 1746±144mm 2 and D = 1691±697mm 2 ), mainly due to basal layer hyperplasia, besides an increase in the keratin of the superficial layer. The PCNA labeling index in the basal layer was significantly higher in the group BD (0,695±0,111) when compared to the other groups (C = 0,490±0,132; B = 0,512±0,215 and D = 0, 477±0,198). Conclusions: Our data confirm in an experimental model the previous observation in humans of increased epithelial cell proliferation during the esophageal carcinogenic process in achalasia and may be useful to further studies on the mechanisms of the esophageal carcinogenesis and the the design of follow-up endoscopic studies for patients with achalasia. Key words: Esophageal Achalasia. Animal experimentation. Rats. RESUMOObjetivo: Desenvolver um modelo experimental que permitisse o estudo de lesões preneoplásicas induzidas por diethylnitrosamina em ratos com acalasia. Métodos: Ratos Wistar machos foram distribuídos em quatro grupos: controle -C (n=8); ratos com megaesôfago -B (n=8); ratos tratados com DEN -D (n=15) e ratos com megaesôfago mais DEN -BD (n=15). O megaesôfago pode ser obtido experimentalmente através da aplicação tópica de cloreto de benzalcônio. Foi avaliada a morfologia do epitélio e a proliferação celular do epitélio pelo método do PCNA. Resultados: A análise morfométrica mostrou aumento da espessura epitelial no grupo BD (2166±1012mm ), principalmente devido a uma hiperplasia da camada basal e um aumento na queratina da camada superficial. O índice de marcação pelo PCNA na camada basal foi significantemente maior neste mesmo grupo (0,695±0,111) quando comparado com os outros (C-0,490±0,132; B-0,512±0,215 e D-0,477±0,198). Conclusões: Estes dados confirmam através de um modelo experimental o aumento proliferativo celular durante o processo de carcinogênese na acalasia do esôfago e podem ser úteis durante estudos de endoscopia realizados em pacientes que possuem acalasia. Descritores: Acalasia Esofágica. Experimentação animal. Ratos.