弓形体、人巨细胞病毒和人微小病毒B_(19)感染对新生儿畸形和生长发育的影响

探讨弓形体（TOXO）人巨细胞病毒（HCMV）及人微小病毒B（19）（HP—VB（19））对新生儿畸形及生长发育的影响。采取聚合酶链反应技术对42例畸形新生儿进行了TOXO—DNA、HCMV—DNA和HPVB（19）—DNA的检测，并对检测阳性与阴性畸形新生儿，用标准差记分法（SDS）衡量生长发育。PCR检测阳性率为18／42（42．86％），中枢及心血管系统畸形阳性率为12／18（66．67％），其他系统畸形阳性率为6／24（25．00％），P＜0．05。DNA阳性者，生长发育落后率为13／18（72．22％），阴性者生长发育落后率为20．83％，生后六个月稍有改善，与对照组比较P＜0．05。结果指出：TOXO、HCMV、HPVB（19）。可致新生儿畸形，以心血管畸形为主，并影响其生长发育。     

人类细小病毒B19感染与小儿急性特发性血小板减少性紫癜

目的 探讨人类细小病毒B19(HPVB19)感染与小儿急性特发性血小板减小性紫癜(ITP)发生的关系。方法对23例小儿急性ITP及17例对照组小儿用聚合酶链反应技术进行HPVB19一DNA的检测。结果 23例急性ITP患儿HPVB19一DNA阳性者7例,阳性率30.4％,17例对照组小儿HPVB19-DNA检测均阴性,两组间阳性率比较有非常显著性差异(x2=4.096,P<0.05)。结论小儿急性ITP的发生与HPVB19感染有关。     

人类细小病毒B19感染与新生儿高间接胆红素血症

目的 探讨人类细小病毒B19(HPVB19)感染与新生儿高间接胆红素血症(新生儿高胆)发生的关系。方法 对136例新生儿高胆及123例正常新生儿用聚合酶链反应技术进行血液HPVB19-DNA的检测。结果 136例新生儿高胆的患儿HPVB19-DNA阳性者48例，阳性率35．3％，123例正常新生儿HPVB19-DNA阳性者12例，阳性率9．8％，两组之间阳性率比较有非常显著性差异(x^2＝23．7，P＜0．005)。结论 新生儿高胆的发生与HPVB19感染有关。     

血细胞减少患儿血液标本中人微小病毒B19-DNA的检测

人微小病毒B19（HPVB19）可引起再生障碍性贫血，有时也可引起粒细胞减少、血小板减少及纯红细胞再生障碍性贫血。在接受化疗的患儿严重贫血时，也发现有HPVB19病毒血症。我们用PCR技术对1993年11月－1995年2月间20例血细胞减少和30例过敏性紫癜患儿的血清标本作了HPVB19－DNA检测，其中血小板减少9例，白血病4例，自身免疫性溶血性贫血2例，再生障碍性贫血2例，纯红细胞再生障碍性贫血2例，粒细胞缺乏1例。结果有2例阳性，1例为再生障碍性贫血，1例为急性粒细胞白血病M3型。阳性率为10％。30例过敏性紫癜均为阴性。     

病毒性心肌炎患儿微小病毒B19感染的研究

目的探讨病毒性心肌炎患儿微小病毒B19（HPV B19）感染的状况及其相关性。方法应用巢式聚合酶链反应法对60例病毒性心肌炎患儿（观察组）及30例健康体检儿童（对照组）血浆中微小病毒B19-DNA进行检测，并对观察组中HPV B19-DNA检测阳性与阴性两组中血CK、CK-MB及心功能指标进行比较。结果观察组B19-DNA检测阳性率为26．7％（16／60例），对照组B19-DNA检测均为阴性，两组比较差异有显著性（P〈0．01）。观察组中HPV B19-DNA检测阳性与阴性的两组中血CK、CK—MB值差异无显著性（P〉0．05）。心功能指标LVSF比较差异有显著性（P〈0．01），SV比较差异亦有显著性（P〈0．05）。结论小儿病毒性心肌炎与HPV B19感染有关，HPV B19可能是小儿病毒性心肌炎主要病原之一；HPV B19感染所致小儿病毒性心肌炎的心功能改变中左室功能受累程度较重。     

呼吸道感染儿童人细小病毒B19检测及临床意义

目的：了解呼吸道感染患儿是否存在人细小病毒B19(HPVB19)感染。方法：采用巢式PCR方法,对2 0 0 0年9月至2 0 0 1年8月2 5 6例临床诊断为呼吸道感染的儿童进行血清及咽分泌物HPVB19 DNA检测,并选择同期且检查前2～4月无呼吸道感染的 10 4例正常儿童为对照组。结果：①血清标本显示,观察组HPVB19 DNA阳性率18.8% (4 8/2 5 6 ),对照组HPVB19 DNA阳性率5 .8% (6 /10 4 ) ,二组相比差异有显著性 (P<0 .0 1) ;观察组4 8例阳性血清样本中,第1季度阳性者为15例,第2季度18例,第3季度7例,第4季度8例,第1,2季度阳性率高于第3,4季度阳性率(P <0 .0 1)。②咽分泌物标本显示,观察组阳性率2 0 .1% (5 4 /2 5 6 ) ,对照组阳性率 3.8% (4 /10 4 ) ,二组相比较差异具有显著性 (P <0 .0 1) ,观察组第1,2 ,3,4季度咽分泌物阳性例数分别为17,2 0 ,8,9例,第1,2季度阳性率高于第3,4季度 (P <0 .0 1)。结论：人类细小病毒B19可导致儿童呼吸道感染,说明HPVB19为儿童呼吸道感染的致病因素之一,对呼吸道感染儿童有必要进行HPVB19的检测;HPVB19所致的儿童呼吸道感染在第1,2季度高于第3,4季度。     

微小病毒B19宫内感染与早产儿、足月小于胎龄儿的相关研究

目的　观察人类微小病毒B19(HPVB19)宫内感染与早产儿、足月小于胎龄儿的关系。方法　采用ELISA方法对 35例早产儿、30例足月小于胎龄儿进行了血清HPVB19 IgM及IgG的检测 ,并将 4 8例正常新生儿脐血作为对照组。结果　 35例早产儿中HPVB19 IgM阳性率为 2 8 5 7% (10 /35 ) ,30例足月小于胎龄儿组HPVB19 IgM阳性率为 2 3 33% (7/30 ) ,4 8例正常对照组中HPVB19 IgM阳性率为 4 17% (2 /48)。两组与正常对照组比较 ,差异有非常显著性意义 [χ2 =7 87,P <0 0 1,相对危险度 (RR) =6 84 ;χ2 =4 90 ,P <0 0 5RR =5 6 ]。结论　微小病毒B19宫内感染与早产的发生、胎儿宫内生长迟缓相关。     

病毒性心肌炎患儿血清心肌钙蛋白Ⅰ检测阳性与时间的关系

目的探讨病毒性心肌炎（VM）患儿血清心肌钙蛋白Ⅰ（cTnI）检测阳性与时间的关系。方法临床诊断为急性VM患儿21例，分别于入院后不同时间静脉采血，动态检测血清cTnI，并与35例正常对照组比较。结果正常对照组血清cTnI均阴性；VM患儿刚入院时阳性6例（28．6％），至入院后6、12、18、24、48、72h，10～14d分别为7例（33．3％）、8例（38．1％）、9例（42．9％）、9例（42．9％）、13例（61．9％）、4例（19％）。入院后48、72h cTnI累计阳性率分别较刚入院时和入院后10～14d有显著性差异（P均〈0．05）。结论对临床上拟诊VM发病不久患儿，通过不同时间段反复多次采血，能提高cTnI检出阳性率。     

血液病患儿细小病毒B19感染的检测及临床意义

人细小病毒Ｂ１９（Ｈｕｍａｎ Ｐａｒｖｏｖｉｒｕｓ，Ｂ１９，ＨＰＶＢ１９）与人类多种疾病密切相关，可通过接触和使用血液制品等在人群中传播＾［１］，本文采用聚合酰链反应（ＰＣＲ）技术检测４５例血液病患儿血清ＨＰＶＢ１９－ＤＮＡ，结果总阳性率为２６．６％，其中急性白血病占３８．８％（７／１８），ＩＴＰ占４０．０％（４／１０），过敏性紫瘢占８．３％（１／１２），再障５例均为阴性；同时检测对照组１０名正常     

球蛋白生成障碍性贫血伴缺铁的发生率及意义

目的：了解球蛋白生成障碍性贫血（简称地贫）患儿伴缺铁的发生率，探讨其临床意义。方法：对127例确诊地贫儿进行铁指标（SF、SI、TIBC、FEP）的检测。结果：127例中缺铁者28例（22％），其中α型占19％（4／21），β型占22．6％（24／106），两者无显著差异（P＞0．5）。β型地贫并缺铁者HbF＜30％组占38．8％（19／49），HbF≥30％组占8．8％（5／57），差异显著（P＜0．005）。HbF＜30％组＜3a者的缺铁率明显高于＞3a者（53．3％vs15．8％，P＜0．01）。结论：地贫儿可能伴发铁缺乏，尤其是低HbF的婴幼儿缺铁率更高，有必要对其进行适当补铁治疗。     

幼年类风湿性关节炎与人细小病毒B19感染的关系及其临床特征

目的 探讨幼年类风湿性关节炎（ＪＲＡ）与人细小病毒Ｂ１９（Ｂ１９）感染的关系及其临床特征。方法 采用巢式ＰＣＲ方法对３０例ＪＢＡ患儿血清、２６例ＪＲＡ患儿骨髓、４例ＪＲＡ患儿关节液标本进行Ｂ１９－ＤＮＡ检测。结果 ⑴３０例ＪＲＡ患儿血清Ｂ１９－ＤＮＡ阳性１２例（４０％）,１０例对照组阳性１例（１／１０）,两组差异无显著性（Ｐ〉０．０１）。⑵２６例骨髓Ｂ１９－ＤＮＡ阳性１２例（４６％）,２５例对照组     

Life threatening parvovirus B19 and herpes simplex virus associated acute myocardial dysfunction in a child with homozygous sickle cell disease

Human parvovirus (HPV) B19, a common infection, frequently causes transient red cell aplasia in children with hemolytic anemia, such as sickle cell disease (SCD). It was considered to be a self-limited condition, easily treated with blood transfusion. However, acute splenic sequestration, acute chest syndrome, nephrotic syndrome, and stroke have been reported in SCD patients following HPV B19 infection. We report a 3-year-old child with SCD who developed fulminant myocarditis following HPV B19-related aplastic crisis. The diagnosis of myocarditis should be considered in a patient with hemolytic anemia with an infection with HPV B19 who develops signs of cardiopulmonary failure despite correction of anemia.     

Classic transient erythroblastopenia of childhood with human parvovirus B19 genome detection in the blood and bone marrow

The etiology of transient erythroblastopenia of childhood (TEC) remains unknown, although an association with viral infections has been proposed. The authors describe a 3.5-year-old girl with classic TEC concomitantly with human parvovirus B19 (HPV) infection. The infection was evident by detection of HPV genome in the blood and the bone marrow by polymerase chain reaction. Viral genome was no longer detected when the TEC resolved clinically. The patient was immunocompetent and the anemia has not recurred. To the authors' knowledge, this is one of the few documented cases of classic TEC attributable to HPV infection.     

人细小病毒B19 VP1独特区基因变异的研究

目的：获取人细小病毒B19(HPV B19)VP1独特区基因,并进行序列测定及变异分析,为研制诊断试剂及预防疫苗创造条件。方法：应用聚合酶链反应（PCR）技术从1例急性特发性血小板减少性紫癜患儿的血清中扩增HPV B 19VP1独特区基因片段,将其克隆至pGEM-T easy载体,转化大肠杆菌DH5α,筛选阳性克隆,测定目的基因的序列。结果：成功地扩增到HPV B19 VP1独特区全长基因,长度为705个核苷酸,测定结果与Genbank中Gallinella G和Venturoli S所发表的HPV B19 VP1独特区全长基因序列比较,有2处核苷酸发生突变,但所编码的氨基酸均未发生变化。结论：（1）HPV B19 VP1独特区有基因变异;（2）构建了HPV B19 VP1独特区基因的重组质粒,所获实验结果为深入研究奠定了基础。     

24 cases of human parvovirus B19 infection in children]

From January 1, 1987 through December 31, 1990, twenty-four pediatric patients with human parvovirus B19 (HPV B19) infection were seen. In every case the diagnosis was established by a positive capture immunoassay for IgM antibodies against the HPV B19. Four patients had hematologic manifestations, including one case of transient bone marrow aplasia revealing hereditary spherocytosis, one case of autoimmune hemolytic anemia with beta-thalassemia, and two cases of peripheral thrombocytopenia. Eight patients had skin lesions, with a morbilliform rash in six cases, erythema nodosum in one case, and Gianotti-Crosti syndrome in one case. No patients had erythema infectiosum. Seven patients developed joint manifestations: Henoch-Sch?nlein purpura in two cases, arthralgia in four cases, and polyarticular disease progressing to severe rheumatoid arthritis in a thirteen-year-old girl. Unremarkable symptoms of viral disease were seen in three patients. A five-month-old infant developed severe acute myocarditis. One patient with hepatitis A had acute liver failure. This study confirms the broad spectrum of clinical manifestations of HPV B19 infection. There were a number of unusual findings, including the high rate of joint manifestations (29%) and the severe course of some hematologic and myocardial manifestations. These results raise the question of whether the HPV B19 may be involved in the genesis of chronic juvenile arthritis.     

A CHILD WITH HUMAN PARVOVIRUS B19 INFECTION INDUCED APLASTIC ANEMIA AND ACUTE HEPATITIS: Effectiveness of Immunosuppressive Therapy

Human parvovirus B19 (HPV B19) infections are usually asymptomatic or benign and self-limiting. In immunocompromised patients and patients with chronic hemolytic anemia, it can lead to transient red cell aplasia. Few reports in the literature have implicated HPV B19 as the possible cause of acute hepatitis and severe aplastic anemia in immunocompetent patients. Here, the authors report a previously healthy 6-year-old girl with acute hepatitis and severe aplastic anemia associated with HPV B19 infection diagnosed by serology (ELISA). Other common causes of these manifestations were ruled out. The clinical manifestations subsequently improved significantly with the use of immunosuppressive therapy confirming an autoimmune mechanism.     

A child with human parvovirus B19 infection induced aplastic anemia and acute hepatitis: effectiveness of immunosuppressive therapy

Human parvovirus B19 (HPV B19) infections are usually asymptomatic or benign and self-limiting. In immunocompromised patients and patients with chronic hemolytic anemia, it can lead to transient red cell aplasia. Few reports in the literature have implicated HPV B19 as the possible cause of acute hepatitis and severe aplastic anemia in immunocompetent patients. Here, the authors report a previously healthy 6-year-old girl with acute hepatitis and severe aplastic anemia associated with HPV B19 infection diagnosed by serology (ELISA). Other common causes of these manifestations were ruled out. The clinical manifestations subsequently improved significantly with the use of immunosuppressive therapy confirming an autoimmune mechanism.     

A case of prolonged human parvovirus B19 DNA-emia associated with polyclonal B cell activation

The current paper reports an 8 year old girl with arthralgia and polyclonal B cell activation induced by human parvovirus B19 infection (HPV B19). The infection was diagnosed by the presence of the virus genome in sera. The patient presented with transient arthritis in the wrist, ankle joint and neck and elevation of immunoglobulin IgM antibodies to HPV B19 and rubella, antibodies to Mycoplasma and antistreptolysin O but without the typical clinical features of erythema infectiosum. The polyclonal B cell activation was paralleled by the presence of the virus genome of HPV B19 in sera. In some children with arthralgia, it is important to examine the genomes of viruses that may cause arthritis as well as the antibody titers to the viruses.     

Neonatal erythema infectiosum

A report is presented of a patient with neonatal erythema infectiosum who developed petechiae, transient thrombocytopenia and transient cardiac failure due to transplacental transmission of human parvovirus B19 (HPV B19) infection. It is suggested that the thrombocytopenia was caused by platelet-associated IgG produced by the patient, and that the cardiac failure may have been caused by direct entry of HPV B19 into the cardiac tissue.