Iacopini Federico, Consolazio Adriana, Bosco Daniela, Marcheggiano Adriana, Bella Antonino, Pica Roberta, Paoluzi Omero A, Crispino Pietro, Rivera Margherita, Mottolese Marcella, Nardi Francesco, Paoluzi Paolo
Gastroenterology Unit, Department of Clinical Sciences, University La Sapienza of Rome, Italy.
Helicobacter. 2003;8(5):503-12. doi: 10.1046/j.1523-5378.2003.00172.x.
Helicobacter pylori is the main cause of gastritis and a primary carcinogen. The aim of this study was to assess oxidative damage in mucosal compartments of gastric mucosa in H. pylori positive and negative atrophic and nonatrophic gastritis.
Five groups of 10 patients each were identified according to H. pylori positive or negative chronic atrophic (Hp-CAG and CAG, respectively) and nonatrophic gastritis (Hp-CG and CG, respectively), and H. pylori negative normal mucosa (controls). Oxidative damage was evaluated by nitrotyrosine immunohistochemistry in the whole mucosa and in each compartment at baseline and at 2 and 12 months after eradication. Types of intestinal metaplasia were classified by histochemistry.
Total nitrotyrosine levels appeared significantly higher in H. pylori positive than in negative patients, and in Hp-CAG than in Hp-CG (p <.001); no differences were found between H. pylori negative gastritis and normal mucosa. Nitrotyrosine were found in foveolae and intestinal metaplasia only in Hp-CAG. At 12 months after H. pylori eradication, total nitrotyrosine levels showed a trend toward a decrease in Hp-CG and decreased significantly in Hp-CAG (p =.002), disappearing from the foveolae (p =.002), but remaining unchanged in intestinal metaplasia. Type I and II of intestinal metaplasia were present with the same prevalence in Hp-CAG and CAG, and did not change after H. pylori eradication.
Oxidative damage of the gastric mucosa increases from Hp-CG to Hp-CAG, involving the foveolae and intestinal metaplasia. H. pylori eradication induces a complete healing of foveolae but not of intestinal metaplasia, reducing the overall oxidative damage in the mucosa.
幽门螺杆菌是胃炎的主要病因及一级致癌物。本研究旨在评估幽门螺杆菌阳性和阴性的萎缩性及非萎缩性胃炎患者胃黏膜各层的氧化损伤情况。
根据幽门螺杆菌阳性或阴性的慢性萎缩性胃炎（分别为Hp-CAG和CAG）、非萎缩性胃炎（分别为Hp-CG和CG）以及幽门螺杆菌阴性的正常黏膜（对照组），将患者分为五组，每组10例。通过硝基酪氨酸免疫组化法在基线时以及根除治疗后2个月和12个月评估全层黏膜及各层的氧化损伤情况。通过组织化学方法对肠化生类型进行分类。
幽门螺杆菌阳性患者的总硝基酪氨酸水平显著高于阴性患者，Hp-CAG患者的总硝基酪氨酸水平高于Hp-CG患者（p <.001）；幽门螺杆菌阴性胃炎患者与正常黏膜之间未发现差异。仅在Hp-CAG患者的胃小凹和肠化生部位发现硝基酪氨酸。幽门螺杆菌根除治疗12个月后，Hp-CG患者的总硝基酪氨酸水平呈下降趋势，Hp-CAG患者的总硝基酪氨酸水平显著下降（p =.002），胃小凹部位的硝基酪氨酸消失（p =.002），但肠化生部位的硝基酪氨酸水平保持不变。Hp-CAG和CAG患者中I型和II型肠化生的发生率相同，幽门螺杆菌根除治疗后未发生变化。
胃黏膜的氧化损伤从Hp-CG到Hp-CAG逐渐增加，累及胃小凹和肠化生。幽门螺杆菌根除治疗可使胃小凹完全愈合，但不能使肠化生愈合，可降低黏膜的整体氧化损伤。
