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目的探讨不同铁状态母婴血清铁调素水平及其临床意义。方法健康足月产孕妇55例,依据血红蛋白(Hb)浓度、血清铁(SI)和血清铁蛋白(SF)水平分为三组:正常组(N组)23例,Hb≥100g/L,SF≥12μg/L;铁缺乏组(ID组)20例,Hb≥100g/L,SF<12μg/L;轻度缺铁性贫血组(IDA组)12例,90≤Hb<100g/L,SF<12μg/L。应用双抗夹心生物素-亲和素-酶联免疫吸附试验方法检测母婴血清铁调素。采用比色法测定SI,放射免疫法分析SF。结果随孕妇缺铁程度的加重,血清铁调素含量降低;IDA组孕妇血清铁调素含量低于N组[(147.62±37.77)ng/ml vs.(193.64±52.22)ng/ml](P<0.01)。三组孕妇所对应新生儿脐血铁调素浓度差异无统计学意义(P>0.05)。孕妇血清铁调素水平与孕妇Hb(r=0.412,P<0.01)、SI(r=0.360,P<0.01)和SF(r=0.315,P<0.05)均呈正相关。脐血铁调素与脐血Hb和SF无相关性(P>0.05)。结论随铁缺乏程度加重,孕妇血清铁调素浓度降低。孕妇血清铁调素浓度与Hb和SF呈正相关。母婴铁转运主要由孕妇血清铁调素调控,与胎儿血清铁调素水平无明显相关。
Objective To investigate the serum hepcidin levels and their clinical significance in different iron status. Methods According to the levels of hemoglobin (Hb), serum iron (SI) and serum ferritin (SF), 55 healthy pregnant women were divided into three groups: 23 cases in normal group (N group), Hb≥100 g / 12 cases of mild iron deficiency anemia group (IDA group), 90≤Hb <100g / L, SF≤12μg / L, iron deficiency group (ID group) 20 cases, Hb≥100g / <12μg / L. Application of double-antibody sandwich biotin-avidin-ELISA test method to detect serum hepcidin. SI was determined by colorimetry and SF was analyzed by radioimmunoassay. Results Serum hepcidin levels decreased with the increase of iron deficiency in pregnant women. The levels of serum hepcidin in IDA group were lower than those in N group [(147.62 ± 37.77) ng / ml vs (193.64 ± 52.22) ng / ml] <0.01). Three groups of pregnant women corresponding to newborns umbilical cord blood hepcidin concentration difference was not statistically significant (P> 0.05). Serum hepcidin levels in pregnant women were positively correlated with pregnant women Hb (r = 0.412, P <0.01), SI (r = 0.360, P <0.01) and SF (r = 0.315, P <0.05). There was no correlation between cord blood hepcidin and cord blood Hb and SF (P> 0.05). Conclusion With the aggravation of iron deficiency, serum hepcidin levels of pregnant women decreased. Serum hepcidin concentrations in pregnant women were positively correlated with Hb and SF. Maternal and infant iron transport is mainly regulated by serum hepcidin in pregnant women, but not significantly correlated with fetal hepcidin levels.