中华检验医学杂志
中華檢驗醫學雜誌
중화검험의학잡지
CHINESE JOURNAL OF LABORATORY MEDICINE
2008年
2期
143-147
,共5页
李智%李晶华%许丙根%成佳景%吴逸%顾小萍
李智%李晶華%許丙根%成佳景%吳逸%顧小萍
리지%리정화%허병근%성가경%오일%고소평
高血压,妊娠性%幼红细胞%淋巴细胞亚群%细胞因子类%流式细胞术
高血壓,妊娠性%幼紅細胞%淋巴細胞亞群%細胞因子類%流式細胞術
고혈압,임신성%유홍세포%림파세포아군%세포인자류%류식세포술
Hypertension,pregnancy-induced%Erythroblasts%Lymphocyte subsets%Cytokines%Flow cytometry
目的 研究孕妇外周血中胎儿细胞种类、数量及免疫状况与妊娠高血压综合征(PIH)的关系,探讨PIH的发病机制.方法 (1)采用流式细胞术比较3种不同方法:CD71、HbF/I抗原(血红蛋白F/血型I抗原)和HbF/CA(血红蛋白F/碳酸酐酶)分别检测孕妇外周血中胎儿有核红细胞(fNRBCs).(2)同时检测孕妇组和PIH组的免疫学指标:淋巴细胞亚群、细胞因子等.结果 (1)3种方法CD71、HbF/I抗原、HbF/CA检测胎儿红细胞PIH患者组[百分比中位数(95%可信上限)分别为6.56(11.37)%、0.09(0.16)%、0.6(0.11)%]与正常孕妇组[分别为1.58(3.35)%、0.04(0.08)%、0.02(0.06)%]差异均具有统计学意义(Z值分别为:-5.31、-2.97、-4.13,P值均＜o.01).(2)PIH组的淋巴细胞亚群和TNFα及IL-6,除CD8 (30.2±7.1)%与正常孕妇组(31.0±7.1)%差异无统计学意义(P=0.620)外,CD3(76.4±8.5)%、CD4(42.6±6.4)%、CD4/CD8(1.5±0.4)%、CD19(10.5±3.9)%、CD16/CD56(12.2±7.7)%、TNF-α(1.4±0.6)μg/L及IL-6(89.6±12.9)μg/L和正常孕妇组[分别为CD3(70.4±8.3)%、CD4(35.3±6.9)%、CD4/CD8(1.2±0.4)%、CD19(8.2±2.8)%、CD16/CD56(20.5±8.9)%、TNF-α(0.5±0.2)μg/L及IL-6(22.0 4±5.7)μg/L]之间差异均具有统计学意义(P＜0.001).结论 孕妇外周血中fNRBCs的数量增多引起的免疫状况的改变均可能是PIH发生发展的重要因素.
目的 研究孕婦外週血中胎兒細胞種類、數量及免疫狀況與妊娠高血壓綜閤徵(PIH)的關繫,探討PIH的髮病機製.方法 (1)採用流式細胞術比較3種不同方法:CD71、HbF/I抗原(血紅蛋白F/血型I抗原)和HbF/CA(血紅蛋白F/碳痠酐酶)分彆檢測孕婦外週血中胎兒有覈紅細胞(fNRBCs).(2)同時檢測孕婦組和PIH組的免疫學指標:淋巴細胞亞群、細胞因子等.結果 (1)3種方法CD71、HbF/I抗原、HbF/CA檢測胎兒紅細胞PIH患者組[百分比中位數(95%可信上限)分彆為6.56(11.37)%、0.09(0.16)%、0.6(0.11)%]與正常孕婦組[分彆為1.58(3.35)%、0.04(0.08)%、0.02(0.06)%]差異均具有統計學意義(Z值分彆為:-5.31、-2.97、-4.13,P值均＜o.01).(2)PIH組的淋巴細胞亞群和TNFα及IL-6,除CD8 (30.2±7.1)%與正常孕婦組(31.0±7.1)%差異無統計學意義(P=0.620)外,CD3(76.4±8.5)%、CD4(42.6±6.4)%、CD4/CD8(1.5±0.4)%、CD19(10.5±3.9)%、CD16/CD56(12.2±7.7)%、TNF-α(1.4±0.6)μg/L及IL-6(89.6±12.9)μg/L和正常孕婦組[分彆為CD3(70.4±8.3)%、CD4(35.3±6.9)%、CD4/CD8(1.2±0.4)%、CD19(8.2±2.8)%、CD16/CD56(20.5±8.9)%、TNF-α(0.5±0.2)μg/L及IL-6(22.0 4±5.7)μg/L]之間差異均具有統計學意義(P＜0.001).結論 孕婦外週血中fNRBCs的數量增多引起的免疫狀況的改變均可能是PIH髮生髮展的重要因素.
목적 연구잉부외주혈중태인세포충류、수량급면역상황여임신고혈압종합정(PIH)적관계,탐토PIH적발병궤제.방법 (1)채용류식세포술비교3충불동방법:CD71、HbF/I항원(혈홍단백F/혈형I항원)화HbF/CA(혈홍단백F/탄산항매)분별검측잉부외주혈중태인유핵홍세포(fNRBCs).(2)동시검측잉부조화PIH조적면역학지표:림파세포아군、세포인자등.결과 (1)3충방법CD71、HbF/I항원、HbF/CA검측태인홍세포PIH환자조[백분비중위수(95%가신상한)분별위6.56(11.37)%、0.09(0.16)%、0.6(0.11)%]여정상잉부조[분별위1.58(3.35)%、0.04(0.08)%、0.02(0.06)%]차이균구유통계학의의(Z치분별위:-5.31、-2.97、-4.13,P치균＜o.01).(2)PIH조적림파세포아군화TNFα급IL-6,제CD8 (30.2±7.1)%여정상잉부조(31.0±7.1)%차이무통계학의의(P=0.620)외,CD3(76.4±8.5)%、CD4(42.6±6.4)%、CD4/CD8(1.5±0.4)%、CD19(10.5±3.9)%、CD16/CD56(12.2±7.7)%、TNF-α(1.4±0.6)μg/L급IL-6(89.6±12.9)μg/L화정상잉부조[분별위CD3(70.4±8.3)%、CD4(35.3±6.9)%、CD4/CD8(1.2±0.4)%、CD19(8.2±2.8)%、CD16/CD56(20.5±8.9)%、TNF-α(0.5±0.2)μg/L급IL-6(22.0 4±5.7)μg/L]지간차이균구유통계학의의(P＜0.001).결론 잉부외주혈중fNRBCs적수량증다인기적면역상황적개변균가능시PIH발생발전적중요인소.
Objective To investigate various types and quantities of fetal cells getting into peripheral blood of pregnant women and immune status related to pregnancy induced hypertension syndrome (PIH) and analyze the etiology of PIH.Methods (1) Three markers of fetal nucleated red blood cells (fNRBCs) in normal pregnant women(n=43)and PIH patients (n=39)were measured by flow cytometry: CD71,HbF/iAg and HbF/CA.(2)We detected the levels of sub-groups of lymphocytes and some plasma cytokines.such as TNF-α and IL-6.The blood samples were from normal pregnant subjects and patients of PIH.Results In the peripheral blood of patients of PIH and normal pregnant subjects,(1) The quantities of fetal cells using three different methods in PIH [6.56(11.37)%、0.09(0.16)%、0.06(0.11)%]were significantly different from normal pregnant subjects[1.58(3.35)%、0.04(0.08)%、0.02(0.06)%],Z= -5.31,-2.97,-4.13 respectively,P＜0.01.(2)Except CD8,the levels of CD3 (76.4±8.5)%,CD4(42.6±6.4)%,CD4/CD8(1.5±0.4)%,CD19(10.5±3.9)%,CD16/CD56 (12.2±7.7)%,TNF-α (1.4 ±0.6)μg/L and IL-6(89.6±12.9)μg/L in PIH were significantly different from normal pregnant subjects[CD3(70.4±8.3)%,CD4(35.3±6.9)%,CD4/CD8(1.2±0.4)%,CD19(8.2±2.8)%,CD16/CD56(20.5±8.9)%,TNF-α(0.5±0.2)μg/L and IL-6(22.0±5.7)μg/L,respectively,P＜0.001].There were no significant differences observed in the level of CD8(P＞0.05).Conclusion The increment of fNRBCs getting into peripheral blood of pregnant women and associated immune status were implicated in the development of PIH.
