To cast light on tumorigenesis in the remnant stomach after distal gastrectomy for peptic ulcer or gastric cancer, 45 cases in gastroduodenostomy (Billroth I, 17 cases) and gastrojejunostomy (Billroth II, 28 cases) groups were compared for a series of parameters. Cancers in Billroth II were significantly more predominant in the anastomosis area and more frequently associated with Epstein-Barr virus infection. Active gastritis, accelerated epithelial cell turnover (as assessed by measurements of apoptosis and cell proliferation), DNA damage, and foveolar cell hyperplasia were all greater in anastomotic areas after Billroth II than in proximal areas after Billroth II or either area after Billroth I. K-ras mutations were rare, but Epstein-Barr virus infection in cancers was seen frequently in anastomosis cases. In conclusion, active gastritis, possibly induced by enterogastric reflux, is linked to tumorigenesis in anastomosis sites in Billroth II cases.
Intestinal arterio-venous malformation (AVM) is one of the uncommon causes of gastrointestinal hemorrhage and is usually difficult to diagnose before pathological study. Five operated cases with the AVM were presented. The vascular lesions were studied by barium-gelatin injection and routine histological procedures. The AVM lesion was detected in the proximal jejunum and in the distal ileum in each one case, respectively. In two other cases the AVM lesion was observed as a protruded tortuous vascular plexus in colonic mucosa. By the microangiographical study, it was confirmed that the main lesion of AVM was located in submucosal layer with complicating minute AVM in lamina propria of intestinal mucosa. In the mucosal lesion of AVM it was disclosed that arterialization of precapillary arterioles was a remarkable finding. Thickened intimal layer and duplication of internal elastic lamina were recognized in these arteriolar lesions. Two kinds of intestinal AVM were classified, one is located in the submucosal layer and another one is located in mucosal layer. It was suggested that a marked ectasia of mucosal vessels seemed to be a secondary change of the submucosal AVM. The pathogenesis of the mucosal AVM was discussed.
Abstract Background : Our previous study showed that L ‐cysteine (Cys) and methylmethionine sulfonium chloride (MMSC) inhibited ethanol‐induced gastric mucosal damage and increased the amount of surface mucin in rats. This study examined whether Cys and MMSC augmented mucin secretion and changed distribution of mucin vesicles ultrastructurally in mucous cells by using primary cultured mucous cells from rabbit glandular stomach. Changes in intracellular cyclic adenosine 3′,5′‐monophosphate (cAMP) and in levels of cytosolic free Ca 2+ were investigated by treatment with Cys and MMSC. Methods : Mucin content was measured by an enzyme‐linked lectin assay. Transmission electron micrography was used to examine ultrastructural distribution of mucin granules. The amount of cAMP or levels of free Ca 2+ were measured by enzyme immunoassay or by fura‐2. 16,16‐Dimethyl prostaglandin E 2 (dmPGE 2 ) or ATP was used as the positive control. Results : L ‐Cysteine and MMSC increased mucin secretion and decreased cellular mucin content. The same was noted for dmPGE 2 . Accelerated mucin granule movements toward the plasma membrane were shown by these agents. Intracellular cAMP increased with exposure to dmPGE 2 for 20 min, while neither Cys nor MMSC increased cAMP. No increase in cytosolic free Ca 2+ levels occurred after treatment with Cys or MMSC, but an increase was induced 10 s after the addition of ATP. Conclusions : The present findings indicate that the increase in mucin secretion by Cys and MMSC was not mediated through the cAMP or Ca 2+ signal transduction pathway, but might occur through non‐receptor‐mediated mechanisms.
