Published online Apr 15, 2003. doi: 10.3748/wjg.v9.i4.836
Revised: November 26, 2002
Accepted: December 3, 2002
Published online: April 15, 2003
AIM: To explore the pathophysiologibasis for the fact that patients with digestive tract symptoms do not necessarily have gastric mucosal pathology and those without clinical symptoms do not necessarily have no gastric mucosal pathology.
METHODS: The ultrastructure, trace elements, cAMP, DNA, SOD and LPO in the gastric mucosa and its epithelial cells of 188 patients without organic lesions of heart, lung, liver, gallbladder, pancreas, kidney or intestine and basically histopathological normal persons (F) were detected synchronously by SEM, TEM, EDAX, Image analysis system RIA and 3H-TdR Lymphocyte Transfer Test.
RESULTS: The content of Zn, Cu, cAMP and 3H-TdR LCT in gastric mucosa and the content of Zn, Cu, DNA and LPO in gastric mucosa epithelial nuclei of each group were shown as belows: Normal control (4.1 ± 1.0, 5.2 ± 0.8, 15.9 ± 1.5, 1079.7 ± 227.4, 7.6 ± 0.4, 58.4 ± 0.3, 12.6 ± 2.7, 2.6 ± 0.6); CSG without symptoms group (3.7 ± 1.2, 5.1 ± 1.8, 15.6 ± 0.9, 924.5 ± 234.9, 7.8 ± 0.3, 58.6 ± 0.4, 13.0 ± 3.1, 2.9 ± 0.4); CAG without symptoms group (3.3 ± 1.0, 4.8 ± 0.9, 14.9 ± 0.7, 887.7 ± 243.6, 7.8 ± 0.3, 58.7 ± 0.3, 14.3 ± 2.8, 3.1 ± 0.4); F type with symptoms group (3.5 ± 1.4, 4.5 ± 1.0, 15.7 ± 1.4, 932.1 ± 2449.3, 7.9 ± 0.4, 58.7 ± 0.5, 13.5 ± 4.6, 2.9 ± 0.7); CSG with symptoms group (2.8 ± 1.9, 4.0 ± 1.5, 14.2 ± 1.8, 867.3 ± 240.5, 8.1 ± 0.5, 58.9 ± 0.5, 15.2 ± 3.2, 4.2 ± 0.7); CAG with symptoms group (2.0 ± 1.8, 3.4 ± 1.5, 13.4 ± 1.8, 800.9 ± 221.8, 8.6 ± 0.4, 59.3 ± 0.5, 16.5 ± 3.1, 4.5 ± 0.6). The contents of Zn, Cu in mitochonondria and SOD in gastric mucosa of each group were shown as belows: Normal control group (9.2 ± 0.5, 58.3 ± 0.3, 170.5 ± 6.1), CSG without symptoms group (8.9 ± 0.5, 58.2 ± 0.3, 167.2 ± 5.3), CAG without symptoms group (8.8 ± 0.4, 57.5 ± 0.2, 166.1 ± 4.2); F type with symptoms group (8.9 ± 0.5, 58.0 ± 0.3, 167.9 ± 5.7), CSG with symptoms group (8.6 ± 0.5, 57.8 ± 0.3, 163.3 ± 5.6); CAG with symptoms group (8.3 ± 0.4, 57.5 ± 0.3, 161.2 ± 4.3). There were significant differences in these cases, P < 0.05-0.001. There were synchronous changes of gastric mucosa epithelial cellular ultrastructure. The “background lesions” (focal atrophic gastritis, focal intestinal metaplasia, micro-ulcer) in nonfocal gastric mucosa of all groups had significant differences (P < 0.05-0.001).
CONCLUSION: Disease with symptoms, disease without symptoms, nondisease with symptoms occur on the basis of the quantitative changes of gastric mucosa epithelial cellular ultrastructure and related bioactive substances.