Basso D, Stefani A L, Gallo N, Brigato L, Navaglia F, Fogar P, Piva M G, Greco E, Toma A, Plebani M
Dipartimento di Medicina di Laboratorio, Università, Padova.
Recenti Prog Med. 1999 Jun;90(6):342-6.
The serum determination of pepsinogen A (PGA) and pepsinogen C (PGC) might indicate gastric mucosal inflammation and atrophy. Body gastric mucosa produces both PGA and PGC, while antral mucosa produces only PGC. Therefore, diseases involving mainly the antrum, such as H. pylori infection, are mainly indicated by the variations in serum PGC than in serum PGA. In agreement, when the antral mucosa is infected by the more virulent cagA positive H. pylori strains, which cause severe inflammation, serum PGC significantly increases. Another indirect indicator of gastric inflammation is polymorphonuclear (PMN) oxidative burst after the stimulation with water extracts from H. pylori culture: this parameter is significantly increased in infected if compared to non-infected subjects. The higher oxidative burst response of peripheral PMN in infected patients, possibly consequent to the release of specific cytokines able to prime PMN towards H. pylori products, is unable to eliminate the infection, but it might concur in damaging the gastric mucosa.
血清胃蛋白酶原A（PGA）和胃蛋白酶原C（PGC）的测定可能提示胃黏膜炎症和萎缩。胃体黏膜同时产生PGA和PGC，而胃窦黏膜仅产生PGC。因此，主要累及胃窦的疾病，如幽门螺杆菌感染，主要通过血清PGC而非血清PGA的变化来提示。与此一致的是，当胃窦黏膜被更具毒性的cagA阳性幽门螺杆菌菌株感染时，会引发严重炎症，血清PGC会显著升高。胃炎症的另一个间接指标是用幽门螺杆菌培养物水提取物刺激后的多形核白细胞（PMN）氧化爆发：与未感染的受试者相比，感染患者的这一参数显著升高。感染患者外周PMN的氧化爆发反应较高，这可能是由于能够使PMN对幽门螺杆菌产物产生反应的特定细胞因子释放所致，虽然无法消除感染，但可能会导致胃黏膜损伤。
