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目的 探讨粒系集落刺激因子 (G CSF)的调节机制及代谢途径。方法 本文运用酶联免疫吸附试验 (ELISA)检测 61例慢性肾功能衰竭 (CRF) +/ 血液透析患者血清G CSF水平。结果 CRF患者血清G CSF水平明显升高。CRF非血透患者血清G CSF检出率为 80 65% ,血清G CSF水平为566 4 0± 2 0 7 98ng/L。CRF血透患者G CSF检出率为 93 33% ,血透前和血透后G CSF水平分别为 12 55 36±611 2 5ng/L和 1151 61± 599 4 7ng/L。血透组G CSF水平略高于非血透组 ,但两组无明显差异。血透前与血透后患者G CSF水平无明显差异。进一步分析表明 ,G CSF水平与WBC ,BUN或Scr水平无关 (P >0 0 5)。结论 CRF患者血清G CSF水平升高可能是由于肾功能不全导致G CSF清除减少或 /和G CSF产生增加。
Objective To investigate the regulatory mechanism and metabolic pathway of granulocyte colony stimulating factor (G CSF). Methods Serum G-CSF levels in 61 patients with chronic renal failure (CRF) + hemodialysis were measured by enzyme linked immunosorbent assay (ELISA). Results Serum G CSF levels in patients with CRF were significantly higher. The detection rate of serum G-CSF in non-hemodialysis patients was 80 65%, and the serum G CSF level was 566 40 ± 2 0 7 98 ng / L. The detection rate of G CSF in CRF hemodialysis patients was 93 33%. The levels of G CSF before hemodialysis and after hemodialysis were 12 55 36 ± 611 2 5 ng / L and 1151 61 ± 599 47 ng / L, respectively. The level of G CSF in the hemodialysis group was slightly higher than that in the non-hemodialysis group, but there was no significant difference between the two groups. There was no significant difference in G CSF levels between hemodialysis and hemodialysis patients. Further analysis showed that G CSF level had no relation with WBC, BUN or Scr levels (P> 0.05). Conclusions Elevated serum CSF-CSF levels in patients with CRF may be due to reduced renal clearance of G CSF or / or increased G CSF production due to renal insufficiency.