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.     

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 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.     

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。     

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.     

Parvovirus B19 infection in pediatric solid-organ and bone marrow transplantation

The clinical significance of parvovirus B19 infection in pediatric solid-organ and bone marrow transplanted patients is unclear. The overall prevalence of parvovirus B19 infection in these patients is about 1-2% during the first year after transplantation. The most common symptom is anemia, but leukopenia and thrombocytopenia have also been observed. Rare cases of hepatic dysfunction, myocarditis, vasculitis and respiratory failure have also been reported. Whereas serology is of limited value around the time of transplantation, it is recommended that a search for B19 DNA is included in first-line investigations in any transplanted patient with unexplained anemia. Specific antiviral therapy is not available, however, intravenous immunoglobulin produces rapid improvement in most cases. Although relatively rare, the severe complications following parvovirus B19 infection in the transplant setting can be avoided by early diagnosis and treatment.     

Leukophagocytosis in human parvovirus B19-induced transient bicytopenia in a healthy child

A previously healthy 11 year old boy had transient leukopenia and thrombocytopenia associated with human parvovirus B19 (B19) infection. This case suggested that low-grade hemophagocytosis can be involved in developing B19-related cytopenia even in an otherwise healthy child. Bone marrow aspiration at an early stage could reveal the underlying mechanism of B19-related cytopenia.     

Human parvovirus B19-associated thrombocytopenic purpura

Abstract We report two patients who presented with thrombocytopenic purpura (TP) associated with primary human parvovirus B19 (B19) infection. One patient also had transient Liver dysfunction. In both cases, B19-DNA was detected in serum and bone marrow by polymerase chain reaction. Six months after the illness in patient 1 and 8 months after the illness in patient 2, B19-DNA disappeared from the serum. Serum immunoglobulin (Ig)G antibody to B19 remained positive in both cases, but B19 IgM antibody became negative 3 months after the onset in case 1 and 4 months after the onset in case 2. The mechanism of TP by B19 infection is unknown.     

Severe Shwachman-Diamond Syndrome and Invasive Parvovirus B19 Infection

Parvovirus B19 (PVB19) is the causative agent of infectious erythema. In healthy children the virus causes transient erythroid aplasia, whereas in children with chronic hemolytic anemias it can cause severe aplastic crises, and in immunodeficient individuals it can produce chronic red cell aplasia. If contracted during pregnancy, the infection may induce serious damage to the fetus (abortion or hydrops fetalis). Shwachman-Diamond (S-D) syndrome, a rare autosomal recessive condition, consists of exocrine pancreatic insufficiency plus neutropenia; many patients develop either anemia or thrombocytopenia or both. We describe a newborn baby with severe congenital bone marrow failure who was diagnosed with S-D syndrome and persistence of PVB19 virus contracted by the mother in the third trimester of pregnancy.     

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。     

血液病患儿细小病毒B_(19)感染的检测及临床意义

人细小病毒B19（HumanParvovirrusB19，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］，本文采用聚合酶链反应（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），过敏性紫癜占8．3％（1／12），再障5例均为阴性；同时检测对照组10名正常儿童均为阴性。将病例组与对照组进行比较有显著意义（P＜0．05）。     

A case of transient neonatal diabetes mellitus

We present a case of an 8-day-old infant boy with transient neonatal diabetes mellitus who presented to our emergency department with profound dehydration, failure to thrive, and hyperglycemia. The initial ill appearance of the patient required attention to a broad differential diagnosis including cardiac, metabolic, endocrine, and infectious processes. Transient neonatal diabetes mellitus is one of several causes of severe hyperglycemia in the neonatal period and is caused by genetic imprinting at the 6q24 region. It requires specific genetic testing for diagnosis. This case illustrates initial management of and recommended laboratory testing in neonates presenting with possible transient neonatal diabetes mellitus.     

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。     

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     

The renal effects of radiocontrast administration during cardioangiography in two different groups with congenital heart disease

Renal effects of the administration of contrast media during cardiac catheterisation were compared in two groups of patients with congenital heart diseases. Group A consisted of 21 patients with cardiac malformations, characterised primarily by left ventricular valvular defects. Group B consisted of 23 patients with lesions affecting the right ventricle which are rarely associated with left heart failure, such as: Tetralogy of Fallot and Pulmonic stenosis.Patients in Group A showed a significant increment in both plasma creatinine and uric acid levels in the 24 h following heart catheterisation. This observation was significantly more prominent in the older age group (above the age of 5 years). In Group B no changes in these parameters were encountered. Plasma renin activity and fractional sodium excretion increased and decreased respectively, by a similar degree in both groups in the 24h following contrast media administration. No difference in renal tubular handling of uric acid was observed between both groups, nor did any of the patients studied demonstrate any degree of proteinuria or abnormality in the urine sediment, prior to or following heart catheterisation.We suggest that chronic pre-existing left ventricular overload should be considered a risk factor among the other known risk factors which promote the incidence of acute renal failure after contrast media administration. We also suggest that the reduction in glomerular filtration rate as evidenced in Group A by the increase in plasma creatinine and uric acid levels could be attributed to indirectly renin-mediated changes in systemic haemodynamics, probably induced by the high osmotically active contrast media. Patients with chronic pre-existing left ventricular volume overload are probably more prone to develop transient cardiac decompensation due to the transient hyper-osmolar state caused by the contrast media and which results in renal function impairment. Older children who have longstanding left ventricular overload are more prone to develop this transient cardiac decompensation, resulting in renal function impairment, than younger ones with the same cardiac lesions.Abbreviations GFR glomerular filtration rate - FeNa fractional sodium excretion - FeUa fractional uric acid excretion     

PARVOVIRUS B19-INDUCED PERSISTENT PURE RED CELL APLASIA IN A CHILD WITH T-CELL IMMUNODEFICIENCY

Persistent pure red cell aplasia can be a manifestation of parvovirus B19 infection in immunocompromised hosts. Failure of the humoral immune response to clear parvovirus B19 in such patients results in persistent pure red cell aplasia. The authors describe a child who had T-cell immunodeficiency and persistent pure red cell aplasia due to parvovirus B19 infection. Interestingly, they detected human parvovirus B19 genome by polymerase chain reaction (PCR) not in the peripheral blood, but in the bone marrow specimen of the patient. In their patient, T-cell immunodeficiency may have caused impaired B-cell activation and failure of effective humoral immune response to neutralize the virus. Additionally, before the diagnosis of pure red cell aplasia, IVIG treatment given at a dosage of 400 mg/kg/day with 3-week intervals may result in sufficient neutralization of peripheral blood parvovirus B19, whereas it may not be sufficient for the neutralization of parvovirus B19 genome in bone marrow. Thus, peripheral blood parvovirus B19 serology (IgM and IgG) and PCR were negative, whereas bone marrow aspiration sample was positive for parvovirus B19 PCR in this patient. Reticulocytopenia and severe anemia may warn the physicians of parvovirus B19 infection, especially in immunocompromised children. Diagnosis may require demonstration of absence of late erythroid precursors in the bone marrow as well as serologic testing and detection of parvovirus B19 genome by PCR in the serum and/or bone marrow samples of the patient.     

A Case of Severe Thrombocytopenia Due to Parvovirus B19 Virus

A 9-year-old girl admitted with generalized skin, mucosa, and genitourinary system bleeding had anemia and thrombocytopenia. Her bone marrow was normocellular. Parvovirus B19 IgM and IgG were positive. An absence of reticulocytopenia suggested that the virus affected only the megakaryocytic cell line and the anemia was due to generalized bleeding resulting from thrombocytopenia. Intravenous immunoglobulin treatment was instituted. On the tenth day of hospitalization the patient recovered from anemia and thrombocytopenia. IgM antibodies disappeared.     

NEONATAL ALLOIMMUNE THROMBOCYTOPENIA DUE TO ANTI-HUMAN LEUKOCYTE ANTIGEN ANTIBODY: A Case Report

Anti-HLA antibodies reportedly exist in 31% of pregnant women. However, few occurrences of neonatal alloimmune thrombocytopenia (NAIT) causedby anti-HLA antibody have been reported. In this study, maternal anti-HLA B60 and B61 antibodies were identified in patient serum at birth, but no anti-platelet antibodies were present. No maternal anti-HLA A2, A24, B51, or B52 antibodies were detected in patient serum. Platelet transfusion from the third donor was effective because these platelets expressed HLA A24 and B52 but not B60 or B61. Cross-matching tests between patient leukocytes or platelets and maternal serum were strongly positive, indicating that maternal anti-HLA antibodies were responsible for NAIT. This report is the first to demonstrate NAIT probably caused by maternal anti-HLA A24 and B52.