Enterovirus-associated haemophagocytic syndrome in a neonate

A 3‐d‐old neonate presented with fever, hepatosplenomegaly, coagulopathy, thrombopenia and anaemia. Secondary haemophagocytic lymphohistiocytosis was suspected, as persistent cytopenias were associated with hypofibrinogenaemia, haemophagocytosis in bone marrow and decreased NK cell. There was no pos...

Full description

Saved in:
Bibliographic Details
Published in:Acta Paediatrica 1998-04, Vol.87 (4), p.469-471
Main Authors: Barre, V, Marret, S, Mendel, I, Lesesve, JF, Fessard, Cl
Format: Article
Language:English
Subjects:
Biological and medical sciences
Enterovirus
Enterovirus Infections - complications
Enterovirus Infections - transmission
Female
histiocytosis
Histiocytosis, Non-Langerhans-Cell - congenital
Histiocytosis, Non-Langerhans-Cell - diagnosis
Histiocytosis, Non-Langerhans-Cell - etiology
Histiocytosis, Non-Langerhans-Cell - physiopathology
Human viral diseases
Humans
Infant, Newborn
Infectious Disease Transmission, Vertical
Infectious diseases
macrophage activation
Male
Medical sciences
newborn
Pregnancy
Pregnancy Complications, Infectious
Remission, Spontaneous
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:A 3‐d‐old neonate presented with fever, hepatosplenomegaly, coagulopathy, thrombopenia and anaemia. Secondary haemophagocytic lymphohistiocytosis was suspected, as persistent cytopenias were associated with hypofibrinogenaemia, haemophagocytosis in bone marrow and decreased NK cell. There was no positive family lymphohistiocytosis history or parental consanguinity. Bacterial investigation proved negative. The diagnosis of enterovirus maternofoetal infection was carried out. The infant's condition improved with symptomatic therapy from day 7. Follow up at 1 y was normal without relapse. This is the first report of a neonatal enteroviral infection that was responsible for excessive macrophage activation.
ISSN:0803-5253
1651-2227
DOI:10.1111/j.1651-2227.1998.tb01482.x