historically , presence of heterotopic gastric mucosa in the intestinal tract has never aroused particular interest among clinicians .
apart from its occurrence in the meckel s diverticulum , the condition is regarded as clinically insignificant .
gastric metaplasia in the duodenum has been described by several authors , however , the significance of its occurrence remains unknown .
extensive use of gastroduodenal fibroscopy enabled the authors to obtain biopsies of the duodenal mucosa .
this paper will describe the incidence of gastric metaplasia in duodenum in various gastroduodenal diseases and discuss the pathogenetic role of gastric metaplasia in peptic ulcer .
the authors obtained two or three pieces of random biopsy specimens from apparently normal mucosa in the anterior wall of duodenal bulb using gastroduodenal fiberscope on 65 subjects .
all biopsies were immediately fixed in 10% formalin solution , embedded in paraffin , and 5 mm thick sections were stained with haematoxylin and eosine and pas , as described by mark and drysdale for sharp distinction of gastric metaplasia .
the authors attempted to locate the fundic gland in all specimens but failed . consequently , the possibility of gastric heterotopia was excluded .
the surface epithelium of gastric mucosa stained strongly with pas reaction contrasting sharply against the duodenal epithelium , where only goblet cells and the brush border disclosed a positive reaction ( fig .
duodenal ulcer and prepyloric ulcers are grouped together since they have the same pathogenetic mechanism as proposed by johnson .
the gastric ulcer group consisted solely of patients with ulcers located at the body , angle , or proximal antrum : two of the subjects in this group were additionally diagnosed with duodenitis . the incidence of gastric metaplasia according to its underlying diseases
gastric metaplasia was not observed in normal subjects with exception to one ( 5.2% ) . in patients with duodenal and/or prepyloric ulcer ( s ) ,
its incidence was 72.2% , which was higher than in normal controls ( 5.2% ) and those with gastric ulcer ( 36.4% ) , nevertheless the difference lacked statistical significance ( p<.25 ) .
three of 7 patients with duodenitis ( 42.8% ) , and one of 8 patients with gastric erosions ( 12.5% ) , had gastric metaplasia . the incidence of gastric metaplasia in the patients with gastic ulcer seemed to be varied according to the location of ulcer . although the number of cases was too low to evaluate it more thoroughly , the incidence of metaplasia was higher ( 66.7% ) in the patients with ulcers located in lower portion of the stomach ( prepyloric and pyloric ) than ulcers located in lower portion of the stomach ( prepyloric and pyloric ) than ulcers located in upper portion of the stomach ( 57.1% in those with ulcers located in angle and proximal antrum : 0% in those with body ulcer ) .
the gastric mucosa in the duodenum can be classified into congenital heterotopic gastric mucosa and acquired gastric metaplasia as shown in table 3 . until now
, many authors have made the mistake of combining metaplasia and true heterotopic gastric mucosa . since taylor reported earlier ( in 1927 ) two cases of gastric heterotopia in the duodenum , many authors described heterotopic gastric mucosa in duodenum as slightly raised patches consisting of chief cells and parietal cells .
as true gastric heterotopia is frequently seen in meckel s diverticulum , and occasionally in rectum and small intestine , it is usually regarded as congenital in origin .
the gastric metaplasia , a term which was first suggested by lessels , is an incomplete form of gastric heterotopia , and is composed of foveolar and pyloric gland : it can be identified only with microscopy .
the incidence of true gastric heterotopia is suggested to be present in approximately 2% of the population .
however , microscopic gastric metaplasia is far more frequently seen than true heterotopia and it is especially common in duodenal ulcer patients .
the incidence of gastric metaplasia in duodenal ulcer patients was reported to be 51.9% by johansen , 74.3% by urakami and 72.2% by these authors series , which was quite similar to previous reports .
it is unknown whether the gastric metaplasia has a protective role or a harmful effect in the formation of duodenal ulcer .
the presence of gastric epithelium in the duodenum could indicate a simple protective response to excessive acid secretion .
urakami reported that the gastric metaplasia is less frequent in the active stage of duodenal ulcer , and its incidence increases in the ulcer s healing stage .
jochi found that gastric metaplasia was frequently seen in the margin of the ulcer and appeared to occur with the healing process of the ulcer .
suzuki divided the gastric metaplasia into three types : foveolar cell metaplasia , parietal cell metaplasia , fully developed fundic gland metaplasia : he reported that each incidence had been 79.2% , 10.4% . and
this study was intended only to reveal the incidence of gastric metaplasia in various gastroduodenal disease patients .
the study could be expanded to clarify possible relations between acid secretion , stage of peptic ulcer , and stomach cancer .
 to investigate the incidence of duodenal gastric metaplasia and its underlying gastric or duodenal diseases , the authors obtained endoscopic biopsy specimens from the duodenal bulb at random sites during endoscopy from 19 normal subjects , 11 patients with gastric ulcer , 18 with duodenal and/or prepyloric ulcer ( s ) , 7 with duodenitis and 8 with gastric erosions . 
 the biopsy specimens were assessed with pas staining to confirm gastric metaplasia.the incidence of duodenal gastric metaplasia was 72.2% in patients with duodenal and/or prepyloric ulcer ( s ) , which contrasted with the patients with gastric ulcers ( 36.4% ) , duodenitis ( 42.9% ) , gastric erosions ( 12.5% ) , and normal subjects ( 5.3%).in conclusion , the results suggest that gastric metaplasia seen predominantly in patients with duodenal ulcer , seems to be related to hyperacidity and it plays some role in the pathogenesis of peptic ulcer in duodenum . 