Nardone G, Staibano S, Rocco A, Mezza E, D'armiento F P, Insabato L, Coppola A, Salvatore G, Lucariello A, Figura N, De Rosa G, Budillon G
Dipartimento di Patologia Sistematica, Cattedra di Gastroenterologia, Università degli Studi "Federico II", via Pansini 5, 80131 Naples, Italy.
Gut. 1999 Jun;44(6):789-99. doi: 10.1136/gut.44.6.789.
Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability.
To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression.
METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer.
All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged.
Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.
幽门螺杆菌是慢性胃炎的主要病因，是I类胃致癌物。慢性胃炎通过萎缩、化生和发育异常发展为癌症。癌前表型表达通常与获得性基因组不稳定有关。
评估幽门螺杆菌感染及其根除对胃组织学、细胞增殖、DNA状态和癌基因表达的影响。
方法/研究对象：采用形态计量学和免疫组化技术检查8名对照、10名幽门螺杆菌阴性慢性胃炎患者、53名幽门螺杆菌阳性慢性胃炎患者和11名胃癌患者的胃黏膜活检标本。
所有慢性胃炎患者均处于与黏膜炎症相关的增殖亢进状态，无论是否感染幽门螺杆菌。10名幽门螺杆菌阴性慢性胃炎患者中有3例出现萎缩，53名幽门螺杆菌阳性慢性胃炎患者中有26例出现萎缩，其中18例伴有肠化生。仅11例萎缩且感染幽门螺杆菌的患者DNA含量异常；其中8例也有c-Myc表达，6例与p53表达相关。对53名幽门螺杆菌阳性慢性胃炎患者进行抗生素治疗后随访12个月：3例退出；45例感染被根除，其细胞增殖随胃炎活动度降低而下降；45例中先前检测到萎缩的21例，5例萎缩消失，9例从重度减轻至轻度，7例保持不变；14例完全化生中有4例消失，先前存在的基因组不稳定标志物消失。5例幽门螺杆菌持续存在的患者，萎缩、化生、发育异常和基因组不稳定标志物保持不变。
慢性幽门螺杆菌感染似乎是幽门螺杆菌阳性慢性萎缩性胃炎部分病例基因组不稳定的原因；根除幽门螺杆菌感染可逆转炎症及相关的萎缩、化生和基因组不稳定。
