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

关于幽门螺杆菌与循环中的生长激素的关系，有相互矛盾的报道。我们试图阐明幽门螺杆菌感染对人类胃和血浆Ghrelin动力学的影响。方法：采用实时定量聚合酶链式反应和放射免疫法分别检测56例幽门螺杆菌感染者和25例非幽门螺杆菌感染者胃黏膜组织中Ghrelin基因表达水平和胃Ghrelin多肽含量。我们还测量了血浆Ghrelin浓度，并分析了胃底腺区域Ghrelin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组成的7天三联疗法治疗。结果：幽门螺杆菌阳性患者胃Ghrelin基因表达水平(单位数1.64+/-1.27)显著低于Hp阴性患者(4.87+/-4.1，p&lt；0.0001)。Ghrelin pe…也出现了类似的趋势。肽含量较高(分别为31.2+/-27.5vs81.2+/-64.1 ng/mg蛋白质，p&lt；0.0001)。在H.plyori状态下，Ghrelin免疫反应细胞数/mm^2无显著差异。幽门螺杆菌感染者的血浆Ghrelin浓度(144.6+/-7.8.8fmol/ml)显著低于非感染者(196.1+/-97.2，p&lt；0.05)，感染治愈后血浆Ghrelin浓度升高。血浆Ghrelin水平与Ghrelin mRNA表达水平(r=0.583，p&lt；0.0001)和多肽产物表达水平(r=0.574，p&lt；0.0001)呈正相关。随着腺体萎缩程度的加重，胃Ghrelin mRNA表达(p&lt；0.05)、肽含量(p&lt；0.01)和Ghrelin免疫反应细胞密度(p&lt；0.05)逐渐降低。慢性炎症的组织学严重程度也对ghrelin mRNA的表达(p&lt；0.001)和多肽的产生(p&lt；0.005)产生了负面影响。结论：幽门螺杆菌感染对胃和血浆Ghrelin动力学有负面影响。与感染相关的慢性炎症和萎缩性改变可能影响胃Ghrelin的生物合成，导致循环水平低下。全胃切除或严重萎缩性胃炎患者出现体重减轻、食欲不振、骨软化等症状。作为一种较少的躯体更年期，Ghrelin的补充治疗可能对上述症状有利

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