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要旨 胃粘膜防御機構に関して,萎縮性胃炎,腸上皮化生,あるいは表層性胃炎といった慢性胃炎による変化を,全く除外して考えることは,困難である.AGMLを臨床病理学的に検討すると,慢性胃炎,腸上皮化生を背景にしては,発生しにくいことが明らかになった.また,粘膜血流,SOD(super oxide dismutase)の検討では,慢性胃炎,特に腸上皮化生粘膜は,barrier breaker投与によって引き起こされる粘膜の虚血に対して強い傾向がみられた.われわれは,AGMLは胃粘膜全域に及ぶ変化であり,その広汎な変化のなかに粘膜出血,びらん,潰瘍が局在的に形成される病態であると考えている.この局在して形成されるびらん,潰瘍の発生と程度は,慢性胃炎,特に腸上皮化生によって左右される可能性が大きいと推定している.
To investigate the gastric mucosal mechanism in clinical fields, we must consider the changes in chronic gastritis such as atrophic gastritis, superficial gastritis and intestinal metaplasia. By considering background gastric mucosa of AGML from the viewpoint of pathology, we know that acute gastric erosions and ulcers are frequently formed on the gastric mucosa without changes being brought about in the chronic gastritis especially in the case of intestinal metaplasia. After administration of bile acid under fiberoptical control, in chronic gastritis, gastric mucosal blood flow did not decrease as it does in normal gastric mucosa. The level of SOD (superoxide dismutase) was high in intestinal metaplasia.
We consider the change of AGML involves diffuse changes of the upper gastrointestinal tract. Among the diffuse changes are mucosal bleeding, erosions and ulcers which are formed locally. The progress and the degree of these localized erosions and ulcers depend on the degree of the background chronic gastritis especially intestinal metaplasia.
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