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作 者:钱卫疆[1] 孟浦[1] 周东风[1] 桂敏 张志泉
出 处:《中国现代医学杂志》2007年第8期905-910,共6页China Journal of Modern Medicine
摘 要:目的通过应用染色体显带技术观察人巨细胞病毒(HCMV)感染致造血系统获得性染色体改变,为HCMV感染导致患儿造血功能紊乱的发病机制提供可能的遗传学基础,并进一步为抗HCMV感染的治疗和疗效判断提供遗传学依据。方法临床筛选造血系统2系或3系减少患儿52例,ELISA检测患儿血HCMV-IgG,HCMV-IgM;尿短时培养快速法检测HCMV即刻早期抗原(IEA);以及染色体G显带技术检测骨髓染色体畸变。结果①血清HCMV-IgM阳性52例,21例同时检出抗HCMV-IgG阳性。其中的38例患儿同期进行了尿HCMV快速培养检测HCMVIEA,37例尿HCMV快速培养为阳性,尿HCMV快速培养阳性率为97.4%,37例尿HCMV快速培养阳性患儿其IgM检测均为阳性。②37例活动性HCMV感染患儿中,外周血细胞形态学未见病态造血现象。骨髓细胞学检查中,红细胞系:37例存在红系造血增生,30例有较典型红系病态造血的特征性改变;粒系细胞有18例检出异常;巨核细胞系仅4例发现较典型改变。③骨髓培养及染色体检查,结果11例染色体核型异常,占29.7%,染色体核型异常呈非随机性改变。2例患儿经治疗后分别于3个月和6个月后复查骨髓染色体核型转为正常。结论HCMV感染可造成症状性造血功能紊乱并可能引起骨髓染色体畸变,是导致患儿造血功能紊乱可能的遗传学基础。[Objective] To use chromosome banding technique to observe the effect of acquired chromosomal change with HCMV infection, which may explain the possible mechanism of the HCMV-induced modifications of host hematological system function in genetic level, and provide genetic evidence of anti-HCMV therapy and judge its availability. [Methods] All the 52 cases underwent a clinical screening evaluation. Inclusion criteria were thrombocytopenia, neutropenia, and anemia. Serum HCMV-IgG and IgM were detected by ELISA; HCMV IEA in urine was detected by rapid cell culture technique (shell viral assay, SVA), and myelo-chromosomal aberration was detected by chromosome G-banding technique. [Results]① 52 cases of positive blood serum HCMV-IgM were detected, 21 cases of positive HCMV-IgG were detected simultaneously. 38 of 52 cases underwent SVA to detect HCMV IEA, 37 cases were positive, positive rate of SVA was 97.4%, 37 children whose SVA were positive simultaneously had a positive result of IgM test. ② The 37 cases with active HCMV infection had no sign of morphologic dyshaematopoiesis in peripheral blood. Detection of bone marrow cell: all the 37 cases had erythrocyte hyperplasy, comparatively typical dyshaematopoiesis; 18 cases had granulocytic series abnormality; only 4 cases had comparatively typical change of megakaryocytic series.③ In marrow culture and chromosomal test, 11 cases of chromosome caryotype abnormality were detected, 29.7%, chromosome caryotype abnormality presents nonrandomly change. 2 children were retested 3, 6 months after therapy respectively, their chromosome caryotype became normal. [Conclusion] HCMV infection can provoke semiological haematogenesis disorder and may provoke marrow chromosome aberration, which is a possible genetic foundation of semiological haematogenesis disorder of HCMV infected children.
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