Gastroscopic and histochemical study of normal, atrophic and hypertrophic mucosa.

Abstract

The correlation between gastroscopic and histological findings was studied in atrophic and hypertrophic gastritis. The histochemical characteristics of these forms of gastritis were determined. 65 stomachs were studied: 15 cases of normal stomach, 40 cases of atrophic gastritis, and 10 cases of hypertrophic gastritis. The biopsy material was obtained in 33 cases by a Crosby capsule, in 5 cases by a Storz biopsy gastroscope, and in 27 cases by laparotomy. The following enzymes were researched: SDH; BDH; LDH; ICDH; G-6-PD; α-GPD; ATPase; Estα; AlkP; AcP. The correlation between gastroscopical observations and histology was excellent, in the cases of atrophic gastritis and of normal stomach, but not in hypertrophic gastritis where in no cases the gastroscopical diagnosis was confirmed by histology. This may be due, as suggested by Schindler, to the type of prelevement (Crosby capsule and biopsy gastroscope). The histoenzymatic study of atrophic gastritis shows: (1) A decrease, in the parietal cells, of the enzymatic activity of several enzymes in 82% of the cases. This decrease was roughly parallel to the intensity of the atrophic changes, and was not equal in the same stomach, and among the different cases. This might be due to the variability of the noxa playing a role in the genesis of gastritis. The reduction, in the parietal cells, of the activity of such enzymes as SDH, ATPase, IDH, and G-6-PD suggests that the lowering of acid output observed in atrophic gastritis may also be due to a lowering of the activity of enzymes playing a part in the energy producing metabolism. (2) The superficial epithelial cells show a decreased enzymatic activity in 65% of the cases. This reduction was also proportional to the importance of the atrophy. The metabolic activity of these cells is probably lessened and, therefore, the mucosa defends itself less firmly. (3) Intestinal metaplasia was found in 50% of the cases. The enzymatic characteristics of intestinal metaplasia were not homogenous, marked differences were observed among individual cases, in the location and the intensity of enzymatic activity. Thus intestinal metaplasia does not appear as an homogenous change. The intestinal metaplasia predisposition to carcinoma is discussed. (4) There was no difference between the enzymatic activity of the chief cells in atrophic gastritis, compared with normal stomach. (5) The enzymatic activity in hypertrophic gastritis was identical to the normal stomach.