Aims/hypothesis. Neonatal diabetes mellitus is rare, and it has not been as
sociated with beta-cell autoimmunity. Enteroviral infections during pregnan
cy have been implicated as a risk factor for the later development of Type
I (insulin-dependent) diabetes mellitus. We now report of a baby girl who w
as born severely growth-retarded with neonatal insulin-deficient diabetes,
and look for evidence of intrauterine enteroviral infections and beta-cell
targeted autoimmunity.
Methods. Diabetes-associated autoimmunity was studied by measurement of sev
eral types of islet cell reactive autoantibodies. The infant's T-cell respo
nses to insulin and enterovirus antigens were recorded and enterovirus anti
bodies were measured both from the mother and the child.
Results. Several types of diabetes-associated autoantibodies were detected
postnatally, including insulin autoantibodies, conventional islet cell auto
antibodies and glutamic acid decarboxylase antibodies, whereas no autoantib
odies were observed in the mother. The infant's T-cells showed reactivity t
o insulin and purified enterovirus particles. Based on serological studies,
the pathogenetic process could have been triggered by an echovirus 6 infec
tion during pregnancy. The patient's diabetes has been permanent, although
there were signs of endogenous insulin production for several months. Exocr
ine pancreatic insufficiency was diagnosed at the age of 1 year.
Conclusion/interpretation. These observations suggests that enteroviral inf
ections may induce beta-cell autoimmunity even in utero.