Kondo M, Nishibori H, Ikezaki M, Takemura S, Masuda M
Gastroenterol Jpn. 1978;13(4):297-302. doi: 10.1007/BF02774053.
A 44-year-old man with Menetrier's disease associated with protein-losing gastropathy and with abnormal serum complement profile is reported. He was treated by an antifibrinolytic compound tranexamic acid (trans-AMCHA) since he was found to have elevated fibrinolytic activity in the biopsied gastric mucosa. The therapy brought his serum protein from 3.8 g/dl to 5.6g/dl, however could not reduce his mucosal disorder. Substitution of a placebo for trans-AMCHA resulted in marked depression of his serum protein to 3.7 g/dl. It was concluded that trans-AMCHA was effective in raising his serum protein to a certain extent but failed to block the vicious circle of "mucosal disorder", "increased tissue fibrinolysis" and "hypoproteinemia" (Kondo, M. et al. Gastroenterology 70, 1045, 1976). Abnormal serum complement profile seen in this patient was found to be due to cold activation of the classical complement pathway (Kondo, M. et al. J. Immunol. 117, 486, 1976). Although no correlation between the phenomenon and Menetrier's disease has been clarified yet, the appearance of wheezing as in asthma when exposed to cold suggested that cold activation of complement occurred in vivo and resulted in increasing of the vascular permeability in the lungs.
报告了一名44岁患有与蛋白丢失性胃病相关的胃黏膜巨肥厚症且血清补体谱异常的男性患者。由于在活检的胃黏膜中发现其纤溶活性升高,他接受了抗纤溶化合物氨甲环酸(反式 - 氨甲环酸)治疗。该治疗使他的血清蛋白从3.8g/dl升至5.6g/dl,但未能减轻其黏膜病变。用安慰剂替代氨甲环酸导致他的血清蛋白显著降至3.7g/dl。得出的结论是,氨甲环酸在一定程度上有效提高了他的血清蛋白,但未能阻断“黏膜病变”、“组织纤溶增加”和“低蛋白血症”的恶性循环(近藤,M.等人,《胃肠病学》70,1045,1976)。发现该患者出现的异常血清补体谱是由于经典补体途径的冷激活(近藤,M.等人,《免疫学杂志》117,486,1976)。尽管该现象与胃黏膜巨肥厚症之间的相关性尚未明确,但接触寒冷时出现类似哮喘的喘息表明补体的冷激活在体内发生,并导致肺部血管通透性增加。