Department of Medicine, National Yang-Ming University, School of Medicine, Taipei, Taiwan.
PLoS One. 2013 Apr 19;8(4):e61426. doi: 10.1371/journal.pone.0061426. Print 2013.
The pathogenesis of the higher occurrence of peptic ulcer disease in cirrhotic patients is complex. Platelets can stimulate angiogenesis and promote gastric ulcer healing. We compared the expressions of proangiogenic growth factors and their receptors in the gastric ulcer margin between cirrhotic patients with thrombocytopenia and those of non-cirrhotic patients to elucidate possible mechanisms.
Eligible cirrhotic patients (n = 55) and non-cirrhotic patients (n = 55) who had gastric ulcers were enrolled. Mucosa from the gastric ulcer margin and non-ulcer areas were sampled and the mRNA expressions of the proangiogenic growth factors (vascular endothelial growth factor [VEGF], platelet derived growth factor [PDGF], basic fibroblast growth factor [bFGF]) and their receptors (VEGFR1, VEGFR2, PDGFRA, PDGFRB, FGFR1, FGFR2) were measured and compared. Platelet count and the expressions of these growth factors and their receptors were correlated with each other.
The two groups were comparable in terms of gender, ulcer size and infection rate of Helicobacter pylori. However, the cirrhotic group were younger in age, had a lower platelet count than those in the non-cirrhotic group (p<0.05). The cirrhotic patients had diminished mRNA expressions of PDGFB, VEGFR2, FGFR1, and FGFR2 in gastric ulcer margin when compared with those of the non-cirrhotic patients (p<0.05). Diminished expressions of PDGFB and VEGFR2, FGFR1, and FGFR2 were well correlated with the degree of thrombocytopenia in these cirrhotic patients (ρ>0.5, p<0.001).
Our findings implied that diminished activity of proangiogenic factors and their receptors may contribute to the pathogenesis of gastric ulcers in cirrhotic patients.
肝硬化患者消化性溃疡病发病率较高的发病机制较为复杂。血小板可以刺激血管生成,促进胃溃疡愈合。我们比较了血小板减少症肝硬化患者和非肝硬化患者胃溃疡边缘的促血管生成生长因子及其受体的表达,以阐明可能的机制。
纳入了 55 例肝硬化患者和 55 例非肝硬化患者,这些患者均患有胃溃疡。从胃溃疡边缘和非溃疡区域采集黏膜,并测量和比较促血管生成生长因子(血管内皮生长因子[VEGF]、血小板衍生生长因子[PDGF]、碱性成纤维细胞生长因子[bFGF])及其受体(VEGFR1、VEGFR2、PDGFRA、PDGFRB、FGFR1、FGFR2)的 mRNA 表达。血小板计数和这些生长因子及其受体的表达相互关联。
两组在性别、溃疡大小和幽门螺杆菌感染率方面无差异。然而,肝硬化组年龄较小,血小板计数低于非肝硬化组(p<0.05)。与非肝硬化患者相比,肝硬化患者胃溃疡边缘的 PDGFB、VEGFR2、FGFR1 和 FGFR2 的 mRNA 表达减少(p<0.05)。PDGFB 和 VEGFR2、FGFR1 和 FGFR2 的表达减少与这些肝硬化患者血小板减少的程度密切相关(ρ>0.5,p<0.001)。
我们的研究结果表明,促血管生成因子及其受体活性降低可能导致肝硬化患者胃溃疡的发生。