Xiao Yan, Lin Wen, Liu Qin, Jin Run-ming, Fei Hong-bao
Department of Pediatrics, Xiehe Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Zhonghua Er Ke Za Zhi. 2006 May;44(5):346-9.
Idiopathic thrombocytopenic purpura (ITP) is a hemorrhagic disease in children with blood platelets redundant destruction caused by chaotic immunological mechanism. However, some patients with ITP with negative platelet-associated antibody and ineffective adrenal cortical hormone therapy probably have special pathogenesis. It is indicated that the human cytomegalovirus (HCMV) can incubate in haemopoietic stem cell/ancestral cell to inhibit its generation and differentiation. Therefore, the study was designed to investigate HCMV-late mRNA expression in megakaryoblast for the purpose of examining the pathogenesis of ITP and to examine the effectiveness of ganciclovir on ITP.
Colony forming unit-megakaryocyte (CFU-MK) of 46 ITP patients with HCMV infection were incubated. Reverse transcription-polymerase chain reaction (RT-PCR) was subsequently used for HCMV-late mRNA detection. Ganciclovir therapy was given to both positive group and negative group for comparison of therapeutic effectiveness.
Nineteen out of 46 CFU-MK culture cell specimens with positive HCMV-DNA by PCR or positive CMV-IgM by enzyme linked immunosorbent assay (ELISA) from serum of peripheral blood showed positive for HCMV-late mRNA. While, the remaining 27 were negative. Sixteen positive responders to ganciclovir therapy were observed amongst those with positive HCMV-DNA. Whereas, only 4 positive responders to ganciclovir therapy were noticed amongst those with negative HCMV-DNA. The curative effectiveness in positive group was significantly higher than that in negative group (P < 0.01).
HCMV can directly infect CFU-MK, which might be one of the mechanisms responsible for ITP. Ganciclovir is an effective therapy resulting in an increase in thrombocyte in ITP patients whose HCMV-late mRNA was positive in their CFU-MK.
特发性血小板减少性紫癜(ITP)是一种儿童出血性疾病,由免疫机制紊乱导致血小板过度破坏。然而,一些血小板相关抗体阴性且肾上腺皮质激素治疗无效的ITP患者可能具有特殊的发病机制。有研究表明,人巨细胞病毒(HCMV)可在造血干细胞/祖细胞中潜伏,抑制其生成和分化。因此,本研究旨在检测巨核母细胞中HCMV晚期mRNA的表达,以探讨ITP的发病机制,并观察更昔洛韦对ITP的治疗效果。
对46例合并HCMV感染的ITP患者的巨核细胞集落形成单位(CFU-MK)进行培养,随后采用逆转录-聚合酶链反应(RT-PCR)检测HCMV晚期mRNA。对HCMV晚期mRNA检测阳性组和阴性组均给予更昔洛韦治疗,比较治疗效果。
46例CFU-MK培养细胞标本中,PCR检测HCMV-DNA阳性或酶联免疫吸附测定(ELISA)检测外周血血清CMV-IgM阳性的标本中有19例HCMV晚期mRNA呈阳性,其余27例为阴性。HCMV-DNA阳性者中观察到16例对更昔洛韦治疗有反应,而HCMV-DNA阴性者中仅4例对更昔洛韦治疗有反应。阳性组的治疗效果显著高于阴性组(P<0.01)。
HCMV可直接感染CFU-MK,这可能是ITP的发病机制之一。更昔洛韦对CFU-MK中HCMV晚期mRNA呈阳性的ITP患者是一种有效的治疗方法,可使血小板计数增加。