Transient Erythroblastopenia of Childhood Associated With Human Herpesvirus Type 6, Variant B

Penchansky, Lila; Jordan, Jeanne A.

doi:10.1093/ajcp/108.2.127

Cited by 29 publications

(20 citation statements)

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“…Although an association with viral infections has been proposed (some viral infection may induce a transient inhibition of erythroid cell formation) [1], the etiology of TEC remains unknown. TEC is usually observed in patients older than 6 months (generally between 1 and 4 years; range, 1 month to 6 years).…”

Section: Discussionmentioning

confidence: 99%

Onset of Afebrile Seizure in Transient Erythroblastopenia of Childhood

Watanabe¹,

Nagasawa²,

Matsuda³

et al. 2015

Int J Pediatr Neonat Care

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We describe a girl aged 2 years 2 months who presented with anemia and transient erythroblastopenia of childhood with the onset of afebrile seizure. She recovered spontaneously from transient erythroblastopenia of childhood 1 month after diagnosis without the need of any packed red cell transfusions. Although not a common disease, it was not very difficult to distinguish transient erythroblastopenia of childhood from other causes of anemia by patient history, physical examination, and limited blood testing. To our knowledge, this is one of the few documented cases of transient erythroblastopenia of childhood with neurological symptoms. Pediatricians should be aware of this disease to avoid unnecessary diagnostic procedures and treatment.

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Section: Discussionmentioning

confidence: 99%

Onset of Afebrile Seizure in Transient Erythroblastopenia of Childhood

Watanabe¹,

Nagasawa²,

Matsuda³

et al. 2015

Int J Pediatr Neonat Care

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“…HHV-6 has been associated with intussusception in a small number of infants and rare cases of meningoencephalitis or encephalopathy [29], exacerbation of idiopathic thrombocytopenic purpura (ITP) and fatal haemophagocytic syndrome. Transient erythroblastopenia of childhood, characterised by anaemia and reticulocytopenia in children aged 3 months to 4 years, is associated with HHV-6B infection [30]. Recently, a symptomatic primary infection with HHV-6A has been reported in an infant [31].…”

Section: Disseminated Infectionmentioning

confidence: 99%

Human herpesvirus 6: its impact and influence on infectious diseases and their management

Khare

2001

Expert Opinion on Pharmacotherapy

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Human herpesvirus (HHV)-6 was discovered 15 years ago and was then grouped as a member of the family human herpesviridae. Its first clinical manifestation was identified 2 years later as the agent responsible for exanthem subitum. With the advent of newer molecular techniques, its diagnosis is easier and prospective studies have shown that it is the most common pathogen responsible for febrile illness in infants. In some infants, it is associated with febrile convulsions. Two subtypes, A and B, have been identified, B subtype commonly being responsible for primary infection in infants. Primary infection in healthy adults is rare. Most of the clinical manifestations are mild, self-limiting and rarely fatal. Reactivation of HHV-6 is frequently found in bone marrow as well as solid organ transplant recipients. HHV-6 has been shown to be an independent risk factor responsible for recurrence of cytomegalovirus infection, especially in solid organ transplants. In bone marrow transplant recipients, HHV-6 has been associated with various manifestations like marrow suppression and graft versus host disease, although most infections present as usually mild febrile illness with or without rash. It has been reported to cause encephalitis in transplant recipients. Although HHV-6 has been shown to be responsible for upregulation of HIV in vitro studies, its exact role in AIDS is yet to be defined. In addition to its neurotropic manifestation of febrile convulsion in infancy, it has been found in plaques in the brain of multiple sclerosis and progressive multifocal leukoencephalopathy. Further studies are needed before its role in the pathogenesis of these neurological illnesses can be established. Its lymphotropic feature was responsible for its discovery and now it has only been detected in some lesions of primary ocular mucosa associated lymphoid tissue lymphoma. As HHV-6 is found to be responsible for more and more illnesses, especially causing serious illnesses in the immunocompromised, it is becoming necessary to find effective treatment. Some agents, like cidofovir and phosphonoformic acid, are effective in in vitro studies and some have shown effectiveness in a clinical setting. Further studies are needed to identify its role in the pathogenesis of various neurological and malignant lesions and AIDS. Various treatment regimens should be tested in clinical scenario and especially in immunocompromised transplant recipients.

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“…Infection in immunocompromised hosts can be more severe, frequently causing end organ damage . Given its pathogenic effects on bone marrow, a causative role of HHV‐6 in TEC has been explored with conflicting results . We describe a 2‐year‐old female child status post cardiac transplant on immunosuppression presenting with severe anemia who was subsequently found to have HHV‐6 infection isolated to the bone marrow.…”

mentioning

confidence: 99%

“…Viral infections including EBV, CMV, and parvovirus have classically been associated with PRCA and TEC . Penchansky first described TEC secondary to HHV‐6 in a series of 14 children with anemia . Two of the 14 were diagnosed with TEC, each having bone marrow infection with HHV‐6 (blood was not tested for concurrent viremia) .…”

mentioning

confidence: 99%

“…Penchansky first described TEC secondary to HHV‐6 in a series of 14 children with anemia . Two of the 14 were diagnosed with TEC, each having bone marrow infection with HHV‐6 (blood was not tested for concurrent viremia) . Subsequently, Skeppner prospectively tested 10 children with TEC for parvovirus B19, HHV‐6, CMV, and EBV in the blood, bone marrow, stools, and nasopharynx .…”

mentioning

confidence: 99%

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