Presotto Fabio, Sabini Beatrice, Cecchetto Attilio, Plebani Mario, De Lazzari Franca, Pedini Beniamino, Betterle Corrado
Department of Medical and Surgical Sciences, University of Padua School of Medicine, Padua, Italy.
Helicobacter. 2003 Dec;8(6):578-84. doi: 10.1111/j.1523-5378.2003.00187.x.
Helicobacter pylori is thought to be involved in atrophic body gastritis. We explored the prevalence of H. pylori infection in asymptomatic subjects with gastric parietal cell antibodies, as well as in patients with pernicious anemia, to evaluate a possible role of H. pylori gastric infection in gastric autoimmunity.
We studied 79 consecutive asymptomatic subjects with parietal cell antibodies, 24 patients with pernicious anemia, and 66 parietal cell antibody-negative controls. All patients underwent gastric biopsies for histology and detection of H. pylori. Red blood cell count and volume, serum levels of gastrin, pepsinogen I, iron, folic acid, vitamin B12, and circulating antibodies to H. pylori and to intrinsic factor were also determined.
We found an atrophic body gastritis in 14 of the 79 asymptomatic subjects with parietal cell antibodies (18%) and in 2 of the 66 controls (3%) (p =.01). Mean levels of gastrin were increased (p <.0001), while those of pepsinogen were reduced (p <.001) compared with controls. H. pylori was identified at the gastric level and/or circulating anti-H. pylori antibodies were detected in 46 parietal cell antibody-positive subjects (58%) compared with 26 controls (39%) (p =.03). In patients with pernicious anemia we found an atrophic body gastritis in 18 of 24 cases (75%) (p <.001 vs. controls). Mean levels of gastrin were markedly increased (p <.0001) and those of pepsinogen I decreased (p <.0001) relative to controls. Only five of these patients (21%) had evidence of H. pylori infection compared with 46 of the parietal cell antibody-positive subjects (58%) (p =.003) and 26 of the controls (39%). Considering all patients with gastric autoimmunity (i.e. with parietal cell antibodies and/or with pernicious anemia), H. pylori was found in 44 of 72 of those without atrophy (61%) but in 6 of 31 with gastric body atrophy (19%) (p <.001), indicating that H. pylori infection is greatly reduced when gastric acid secretion decreases.
The frequent detection of H. pylori infection in subjects with early gastric autoimmunity, indicated by the presence of parietal cell antibodies, suggests that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level.
幽门螺杆菌被认为与萎缩性胃体胃炎有关。我们探究了无症状胃壁细胞抗体阳性受试者以及恶性贫血患者中幽门螺杆菌感染的患病率，以评估幽门螺杆菌胃部感染在胃自身免疫中可能发挥的作用。
我们研究了79例连续的无症状胃壁细胞抗体阳性受试者、24例恶性贫血患者以及66例胃壁细胞抗体阴性对照者。所有患者均接受了胃活检以进行组织学检查和幽门螺杆菌检测。还测定了红细胞计数和体积、血清胃泌素、胃蛋白酶原I、铁、叶酸、维生素B12水平以及针对幽门螺杆菌和内因子的循环抗体。
我们发现，79例无症状胃壁细胞抗体阳性受试者中有14例（18%）存在萎缩性胃体胃炎，66例对照者中有2例（3%）存在萎缩性胃体胃炎（p = 0.01）。与对照组相比，胃泌素平均水平升高（p < 0.0001），而胃蛋白酶原水平降低（p < 0.001）。在胃水平检测到幽门螺杆菌和/或检测到循环抗幽门螺杆菌抗体的胃壁细胞抗体阳性受试者有46例（58%），而对照者有26例（39%）（p = 0.03）。在恶性贫血患者中，24例中有18例（75%）存在萎缩性胃体胃炎（与对照组相比，p < 0.001）。相对于对照组，胃泌素平均水平显著升高（p < 0.0001），胃蛋白酶原I水平降低（p < 0.0001）。这些患者中只有5例（21%）有幽门螺杆菌感染的证据，而胃壁细胞抗体阳性受试者中有46例（58%），对照者中有26例（39%）。在所有有胃自身免疫的患者（即有胃壁细胞抗体和/或恶性贫血）中，72例无萎缩者中有44例（61%）发现有幽门螺杆菌，但31例有胃体萎缩者中有6例（19%）发现有幽门螺杆菌（p < 0.001），这表明胃酸分泌减少时幽门螺杆菌感染显著降低。
胃壁细胞抗体的存在表明，在早期胃自身免疫受试者中频繁检测到幽门螺杆菌感染，提示幽门螺杆菌可能在胃水平自身免疫的诱导和/或维持中起关键作用。
