Toljamo Kari T, Niemelä Seppo E, Karvonen Anna-Liisa, Karttunen Tuomo J
Department of Internal Medicine, Division of Gastroenterology, University of Oulu, Finland.
Scand J Gastroenterol. 2005 Nov;40(11):1275-83. doi: 10.1080/00365520510023594.
Gastric erosions are mainly associated with Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs), but there has been no information available on the long-term evolution of gastritis in subjects with erosions.
A series of 117 patients with gastric erosions without peptic ulcer disease and matched controls without erosions or ulcers were studied. Available subjects underwent endoscopy and biopsy 17 years later. Parietal cell antibodies were analysed at the first visit.
Fifty-two patients and 67 controls were available for follow-up. Since H. pylori was a major determinant of gastritis, only subjects with unchanged H. pylori status were included in the evaluation of gastritis progression. At the follow-up visit, gastric erosions were present in 38% (16/42) of the patients and 11% (5/46) of the controls (p=0.005). In H. pylori-negative subjects, no evolution of histological changes was seen. In H. pylori-positive subjects, body gastritis was initially less active in the erosion group. With time, antral gastritis worsened only in the erosion group. Parietal cell antibodies were more common in the control group (23%; erosion patients 0%; p=0.01), which also showed worsening of gastritis (p=0.003) and aggravation of atrophy (p=0.002) in the body mucosa.
Gastritis in H. pylori-positive subjects with gastric erosions shows evolution of antral predominance, body predominance including development of atrophic changes being rare. Accordingly, patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype. These findings support the importance of H. pylori and acid in the pathogenesis of gastric erosions in H. pylori-positive patients.
胃糜烂主要与幽门螺杆菌感染和非甾体抗炎药（NSAIDs）相关，但关于有糜烂的受试者胃炎的长期演变情况尚无可用信息。
对117例无消化性溃疡病的胃糜烂患者及117例无糜烂或溃疡的匹配对照进行了研究。17年后对所有可用受试者进行了内镜检查和活检。首次就诊时分析了壁细胞抗体。
52例患者和67例对照可进行随访。由于幽门螺杆菌是胃炎的主要决定因素，因此仅将幽门螺杆菌状态未改变的受试者纳入胃炎进展评估。随访时，患者中有38%（16/42）存在胃糜烂，对照组中有11%（5/46）存在胃糜烂（p = 0.005）。在幽门螺杆菌阴性的受试者中，未观察到组织学变化的演变。在幽门螺杆菌阳性的受试者中，糜烂组胃体部胃炎最初活动性较低。随着时间推移，仅糜烂组胃窦部胃炎恶化。壁细胞抗体在对照组中更常见（23%；糜烂患者为0%；p = 0.01），对照组胃体黏膜的胃炎也有恶化（p = 0.003）和萎缩加重（p = 0.002）。
幽门螺杆菌阳性且有胃糜烂的受试者的胃炎表现为胃窦部优势的演变，胃体部优势包括萎缩性改变的发展较为罕见。因此，有糜烂的患者具有十二指肠溃疡表型胃炎的特征。这些发现支持了幽门螺杆菌和胃酸在幽门螺杆菌阳性患者胃糜烂发病机制中的重要性。
