Gastric and small intestinal lesions after partial stomach resection with Billroth II or Roux-en-Y reconstruction in the XXXX .

@entity5 @entity1711 @entity1373 @entity189 @entity1710 @entity3649 @entity3161 @entity35 @entity1412 @entity420 @entity356
The evolution and phenotypic expression of mucosal lesions of the @entity356 were investigated in male @entity35 submitted to gastric resection with reconstruction by the Billroth II technique (BII with biliopancreatic reflux, BPR) or by the Roux-en-Y procedure (without BPR). Animals were studied at 24, 36, 54 and 64 weeks after surgery and the phenotypic expression of lesions analysed using routine @entity1710 and @entity1711 staining, immunohistochemical staining for pepsinogen isoenzyme 1 and histochemical procedures for mucins (paradoxical concanavalin A, @entity3649 oxidase Schiff (GOS) and sialidase GOS reactions). BPR was found to be responsible for the formation of @entity1412 ( @entity1412 ), increasing in incidence and size with time, since the Roux-en-Y procedure failed to induce the @entity356 lesions observed after BII reconstruction. AHs always occurred in the transition of the @entity3161 , a site offering special conditions for BPR influence, and were classified as gastric (G), intestinal (I) and G+I types according to their phenotypic expression. No pure I type @entity1412 was diagnosed at any time point. The G and G+I types developed at approximately equal incidences (i.e., G type 7/17, G+I type 10/17 at the 64th week). It was suggested that both gastric and intestinal mucosal elements were stimulated to proliferate by BPR, with the @entity356 tending to demonstrate @entity1412 . Intestinal type components of @entity1412 were found adjacent to the jejunum and not at the stomach margin, indicating an origin from intestinal mucosa. No metaplasia of the @entity356 was observed in any animal after partial gastric resection. In 101 @entity35 submitted to the BII procedure, 5 mucinous @entity420 were eventually diagnosed, mostly located in the subserosa of the @entity3161 . All @entity189 expressed the phenotype of cells of the small intestine. Evidence of @entity1373 was not observed even at the 64th week. In conclusion, all lesions induced by BPR in the @entity35 remnant stomach are benign, and the few true @entity5 that arise in association are derived from the small intestine.
