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目的：观察ＣＲＦ患者血透治疗过程中细胞免疫功能的变化及与ＰＴＨ的关系。方法：４４例患者按血透治疗时间长短分为４组，于透前、中、后检测ＰＨＡ刺激的淋巴细胞转化；Ｔ细胞亚群；可溶性白细胞介素２受体（ＳＩＬ２Ｒ）的表达；Ｔ细胞内静止水平的钙［Ｃａ２＋］ｉ及血清ＰＴＨ。结果：血透患者血清ＰＴＨ明显高于正常（Ｐ＜０００１）。ＰＨＡ刺激的淋巴细胞转化明显低于正常对照组（Ｐ＜０００１）。淋巴细胞转化率降低与ＰＴＨ值升高无相关性。血透患者的ＣＤ２淋巴细胞低于正常（Ｐ＜００５），与ＰＴＨ值无相关性。ＣＤ４／ＣＤ８比值较正常对照组降低（Ｐ＜００１），与ＰＴＨ值呈负相关（Ｐ＜００５）。细胞内的［Ｃａ２＋］ｉ在血透治疗１年以上组明显高于正常和血透＜６月组（Ｐ＜００１），ＳＩＬ２Ｒ浓度高于正常（Ｐ＜０００１）。单次血透前、中、后，以上各项检测结果均无显著差异。结论：ＣＲＦ血透患者存在Ｔ细胞功能低下及ＰＴＨ增高，ＰＴＨ值与Ｔ细胞功能呈负相关。细胞免疫低下在血透治疗后有所改善，尤以血透半年内改善最为明显。血透一年以上组Ｔ细胞内静止［Ｃａ２＋］ｉ升高，可能是高ＰＴＨ慢性作用于Ｔ细胞，使Ｔ细胞内的［Ｃａ２＋］ｉ增加，干扰了?
Objective: To observe the changes of cellular immune function and the relationship with PTH in hemodialysis patients with CRF. Methods: Forty-four patients were divided into 4 groups according to the duration of hemodialysis. PHA-stimulated lymphocyte transformation, T lymphocyte subsets, soluble interleukin 2 receptor (SIL-2R) ; T-cell resting levels of calcium [Ca2 +] i and serum PTH. Results: Serum PTH in hemodialysis patients was significantly higher than normal (P <0001). PHA stimulated lymphocyte transformation was significantly lower than the normal control group (P <0 001). There was no correlation between the decrease of lymphocyte conversion and the increase of PTH. CD2 lymphocytes in hemodialysis patients were lower than normal (P <005), and had no correlation with PTH. The CD4 / CD8 ratio was lower than that of the normal control group (P <001) and negatively correlated with PTH (P <005). The intracellular [Ca2 +] i in hemodialysis group was significantly higher than that in normal group and hemodialysis group <6 months (P <001), and SILR concentration was higher than normal (P <0001). Single hemodialysis before, during, after the above test results were no significant differences. CONCLUSION: T-cell dysfunction and PTH are elevated in patients with CRF hemodialysis, and PTH is negatively correlated with T cell function. Cellular immunity improved after hemodialysis treatment, especially in the hemodialysis within six months to improve the most obvious. In the hemodialysis group more than one year, the increase of [Ca2 +] i in T cells may be due to the chronic action of high PTH on T cells and the increase of [Ca2 +] i in T cells.