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Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B12 deficiency which results in a megaloblastic anemia and malabsorbtion of iron, leading to iron deficiency anaemia.〔Gut 2003;52:496-501 doi:10.1136/gut.52.4.496〕 It can be caused by persistent infection with ''Helicobacter pylori'', or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria. Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia. Type B gastritis primarily affects the antrum, and is more common with ''H. pylori'' infection. ==Pathophysiology== ''Autoimmune Metaplastic Atrophic Gastritis'' (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.〔(【引用サイトリンク】title=Autoimmune Metaplastic Atrophic Gastritis: Gastritis and Peptic Ulcer Disease: Merck Manual Professional )〕 The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cells, which leads to profound hypochlorhydria (and elevated gastrin levels). The inadequate production of intrinsic factor also leads to vitamin B12 malabsorption and pernicious anemia. AMAG is typically confined to the gastric body and fundus. Hypochlorhydria induces G Cell (Gastrin producing) hyperplasia, which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible for histamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Atrophic gastritis」の詳細全文を読む スポンサード リンク
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