Department of Gastroenterology, Rabin Medical Center, Tel Aviv University, Tel Aviv, Israel.
Digestion. 2012;86(3):258-63. doi: 10.1159/000341423. Epub 2012 Oct 16.
The incidence of Helicobacter pylori and non-steroidal anti-inflammatory drug (NSAID)-negative peptic ulcer disease has increased over the last two decades, especially in the Western world and in countries with low H. pylori infection rates. Idiopathic peptic ulcer disease is a recently described entity which relates to peptic ulcers not caused by H. pylori, NSAID/aspirin therapy, other ulcerogenic organisms and drugs, or other rare malignant and benign diseases. Structural and secreted mucins create the unstirred gastric mucus layer and maintain a stable pH above the gastric mucosa. This mucous layer prevents enzymatic attack by acid and pepsin. Inhibition of cyclooxygenase by NSAID and aspirin inhibits prostaglandin production, inhibits mucin and bicarbonate secretion, and exposes the mucosa to the toxic effects of acid and intragastric enzymes. There is also a complex relationship between H. pylori and different mucin subtypes which on one hand facilitates mucin invasion but on the other hand protects the gastric mucosa. Genetic and epigenetic changes in the mucin molecule may be responsible for idiopathic peptic ulcer disease, but this hypothesis must be further investigated. Herein, the mucin hypothesis of idiopathic peptic ulcer disease is explored.
在过去的二十年中，幽门螺杆菌（Helicobacter pylori）和非甾体抗炎药（NSAID）阴性消化性溃疡疾病的发病率有所增加，尤其是在西方国家和幽门螺杆菌感染率较低的国家。特发性消化性溃疡疾病是一种新近描述的疾病，它与由幽门螺杆菌、非甾体抗炎药/阿司匹林治疗、其他致溃疡生物和药物或其他罕见的恶性和良性疾病引起的消化性溃疡无关。结构性和分泌性粘蛋白构成未搅动的胃粘液层，并维持胃黏膜上方稳定的 pH 值。该粘液层可防止酸和胃蛋白酶的酶促攻击。NSAID 和阿司匹林对环氧化酶的抑制作用会抑制前列腺素的产生，抑制粘蛋白和碳酸氢盐的分泌，并使粘膜暴露于酸和胃内酶的毒性作用下。幽门螺杆菌和不同粘蛋白亚型之间也存在着复杂的关系，一方面有利于粘蛋白的侵袭，另一方面又保护胃黏膜。粘蛋白分子中的遗传和表观遗传变化可能是特发性消化性溃疡疾病的原因，但这一假设还需要进一步研究。本文探讨了特发性消化性溃疡疾病的粘蛋白假说。
