论文部分内容阅读
目的探讨癌性贫血患者 EPO 生成及红系增生的变化,以及 TNF、IFN 等负调控细胞因子对 EPO 生成及红系增生的影响。方法对50例癌性贫血患者、15例癌症无贫血患者及对照组采用放射免疫法检测血清 EPO 水平,ELISA 方法检测血清可溶性转铁蛋白受体(sTIR)、TNF-α、IFN-γ水平,用直线回归方法及相关分析定量分析体内 EPO 生成、红系增生情况及其与 TNF-α、IFN-γ的关系。结果癌性贫血患者血清 EPO 水平为(23.11±10.00)IU/L,明显低于同等程度贫血的缺铁性贫血患者的(43.00±22.00)IU/L(P<0.01);实测值/预估值(O/P)EPO 为0.88(0.54～1.10),明显低于对照组及癌症无贫血患者,后二者之间的 O/P EPO 差异无统计学意义。癌性贫血患者的血清 sTfR 水平(30.8±16.95)nmol/L,高于健康对照组的(17.82±6.76)nmol/L,而低于溶血性贫血患者的(65.75±29.12)nmol/L,差异均有统计学意义(P<0.05);O/P sTIR 为0.89(0.57～1.22),明显低于对照组及癌症无贫血患者,后二者之间 O/P sTfR 差异无统计学意义。正常情况下存在于 log(EPO)与血红蛋白浓度之间以及 log(sTfR)与血红蛋白浓度之间的反比关系消失。癌性贫血患者血清 TNF-α、IFN-γ水平分别为(25.75±26.71)ng/L、(50.49±42.12)ng/L,均显著高于正常对照组及癌症无贫血组。TNF-α、IFN-γ水平与血红蛋白浓度之间呈负相关关系。TNF-α与 O/P EPO、O/P sTfR 之间呈负相关。血清 IFN-γ水平与 O/P EPO 之间无相关关系,与 O/P sTfR 呈负相关。结论 TNF-α、IFN-γ等负调控因子的作用下,内源性 EPO 对贫血的反馈性增生相对不足,以及骨髓红系对 EPO 的反应性增生相对不足参与癌性贫血的发病机制。
Objective To investigate the changes of EPO production and erythroid hyperplasia in patients with cancerous anemia and the effects of negative regulatory cytokines such as TNF and IFN on EPO production and erythroid hyperplasia. Methods Serum levels of EPO were measured by radioimmunoassay in 50 patients with cancer anemia, 15 patients without cancer and control group. Serum soluble transferrin receptor (sTIR), TNF-α and IFN-γ levels were measured by ELISA. Linear regression and correlation analysis were used to quantitatively analyze the in vivo EPO production, erythroid hyperplasia and its relationship with TNF-α, IFN-γ. Results The serum level of EPO in cancer patients with anemia was (23.11 ± 10.00) IU / L, which was significantly lower than that of patients with iron deficiency anemia (43.00 ± 22.00) IU / L (P <0.01) The value of O / P was 0.88 (0.54-1.10), which was significantly lower than that of the control group and the patients without cancer. There was no significant difference in O / P EPO between the two groups. The level of serum sTfR in patients with cancerous anemia (30.8 ± 16.95) nmol / L was significantly higher than that in healthy controls (17.82 ± 6.76 nmol / L), but lower than that in patients with hemolytic anemia (65.75 ± 29.12) nmol / L (P <0.05). The O / P sTIR was 0.89 (0.57-1.22), which was significantly lower than that of the control group and the patients without cancer. There was no significant difference in O / P sTfR between the two groups. The inverse relationship between log (EPO) and hemoglobin concentration and between log (sTfR) and hemoglobin concentration disappears under normal conditions. The serum levels of TNF-α and IFN-γ in patients with cancerous anemia were (25.75 ± 26.71) ng / L and (50.49 ± 42.12) ng / L, respectively, which were significantly higher than those in normal controls and those without cancer. TNF-α, IFN-γ levels and hemoglobin concentration was negatively correlated. TNF-α and O / P EPO, O / P sTfR was negatively correlated. There was no correlation between serum IFN-γ level and O / P EPO, but negatively correlated with O / P sTfR. CONCLUSION: Under the action of negative regulatory factors such as TNF-α and IFN-γ, the endogenous EPO is relatively deficient in the feedback-related hyperplasia of anemia, and the relative deficiency of erythroid hyperplasia in EPO is involved in the pathogenesis of cancerous anemia.