Molecular pathological analysis of the ghrelin expression in H. Pylori associated diseases.

关于幽门螺杆菌与循环胃饥饿素之间的关系，有相互矛盾的报道。我们试图澄清幽门螺杆菌感染对人类胃和血浆胃饥饿素动力学的影响。方法：对56例幽门螺杆菌感染患者和25例未感染患者进行胃镜活检，采用实时聚合酶链反应法和放射免疫法分别测定胃饥饿素mRNA表达水平和胃饥饿素肽含量。我们还测量了血浆胃饥饿素浓度，并分析了底腺区域胃饥饿素免疫反应细胞的数量。51例幽门螺杆菌感染患者接受兰索拉唑、克拉霉素和阿莫西林的7天三联治疗。结果：幽门螺杆菌阳性组胃胃饥饿素mRNA表达水平（任意单位1.64 +/- 1.27）显著低于幽门螺杆菌阴性组（4.87 +/- 4.1,p<0.0001）。ghrelin的多肽含量也有类似的趋势（分别为31.2 +/- 27.5和81.2 +/- 64.1 ng/mg protein, p < 0.0001）。胃饥饿素免疫反应细胞数/mm^2在多殖梭菌状态方面无显著差异。幽门螺杆菌感染者血浆ghrelin浓度（144.6 +/- 7.8.8 fmol/ml）显著低于未感染者（196.1 +/- 97.2 fmol/ml, p < 0.05），感染治愈后升高。血浆ghrelin水平与ghrelin mRNA表达量（r=0.583, p<0.0001）和肽产物表达量（r=0.574, p<0.0001）呈正相关。胃饥饿素mRNA表达量（p<0.05）、肽含量（p<0.01）和胃饥饿素免疫反应细胞密度（p<0.05）随着腺体萎缩程度的加重而逐渐降低。慢性炎症的组织学严重程度也对胃饥饿素mRNA的表达（p<0.001）和肽的产生（p<0.005）产生负向影响。结论：幽门螺旋杆菌感染对胃和血浆胃饥饿素动力学有负面影响。与感染相关的慢性炎症和萎缩变化可能影响胃饥饿素的生物合成并导致低循环水平。全胃切除术或严重萎缩性胃炎患者表现为体重减轻、厌食、骨质疏松等。胃促生长素作为一种促生长激素，对上述症状可能有有益的治疗效果

There are contradictory reports on the relationship between Helicobacter pylori and circulating ghrelin. We sought to clarify the influence of H.pylori infection on gastric and plasma ghrelin dynamics in humans. METHODS : Using endoscopic biopsies from the corpus of 56 H.pylori-infected patients and 25 uninfected subjects, ghrelin mRNA expression levels and gastric ghrelin peptide contents were measured by real-time polymerase chain reaction and radioimmunoassay, respectively. We also measured plasma ghrelin concentrations and analyzed the numbers of ghrelin immunoreactive cells in the fundic gland area. Fifty-one patients with H. pylori infection were treated with a 7-day triple therapy consisting of lansoprazole, clarithromycin, and amoxicillin. RESULTS : The gastric ghrelin mRNA expression level of H.pylori-positive patients (1.64 +/- 1.27 in arbitrary units) was significantly lower than in H.pylori-negative subjects (4.87 +/- 4.1, p<0.0001). A similar trend was noted for ghrelin pe … More ptide contents (31.2 +/- 27.5 vs 81.2 +/- 64.1 ng/mg protein, respectively, p < 0.0001). There was no significant difference in the number of ghrelin immunoreactive cells/mm^2 in terms of H. plyori status. Plasma ghrelin concentrations in H.pylori-infected patients (144.6 +/- 7.8.8 fmol/ml) were significantly lower than in uninfected subjects (196.1 +/- 97.2, p < 0.05) and increased following cure of the infection. Plasma ghrelin levels correlated positively with the expression levels of ghrelin mRNA (r=0.583, p<0.0001) and peptide products (r=0.574, p<0.0001). There was a significant stepwise decrease in gastric ghrelin mRNA expression (p<0.05), peptide contents (p<0.01) and density of ghrelin immunoreactive cells (p<0.05) with progression of histological severity of glandular atrophy in the corpus. The histological severity of chronic inflammation also negatively influenced the ghrelin mRNA expression (p<0.001) and peptide production (p<0.005). CONCLUSIONS : H.pylori infection has a negative impact on gastric and plasma ghrelin dynamics. Chronic inflammatory and atrophic changes associated with the infection may affect gastric ghrelin biosynthesis and contribute to the low circulating levels.The patient with total gastrectomy or severe atrophic gastritis shows body weight reduction, anorexia, osteomalasia, etc. The ghrelin supply treatment might be beneficial effect for above symptoms as a kind of somatopause Less