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Neonatal Type I diabetes associated with maternal echovirus 6 infection: a case report
T Otonkoski1, M Roivainen, O Vaarala
1Hospital for Children and Adolescents and Haartman Institute, Transplantation Laboratory, University of Helsinki, Finland.
Insights
Neonatal diabetes mellitus can be caused by in utero enteroviral infections triggering beta-cell autoimmunity. This case study found evidence of echovirus 6 infection and associated autoantibodies in a growth-retarded infant with permanent diabetes.
Area of Science:
- Endocrinology
- Virology
- Immunology
Background:
- Neonatal diabetes mellitus is rare and typically not linked to beta-cell autoimmunity.
- Enteroviral infections during pregnancy are a suspected risk factor for later Type 1 diabetes development.
Observation:
- A severely growth-retarded infant presented with neonatal insulin-deficient diabetes.
- The infant exhibited multiple diabetes-associated autoantibodies (insulin, islet cell, GAD65) postnatally.
- Infant's T-cells responded to insulin and enterovirus antigens; mother showed no autoantibodies.
Findings:
- Serological evidence suggested echovirus 6 infection during pregnancy as the trigger.
- The infant developed permanent diabetes and exocrine pancreatic insufficiency.
- Infant's T-cells demonstrated reactivity to both insulin and enterovirus.
Implications:
- Enteroviral infections may induce beta-cell autoimmunity in utero.
- This finding expands the understanding of neonatal diabetes mellitus etiology.
- Highlights the potential role of prenatal viral exposure in autoimmune diabetes development.
Aims/Hypothesis:
Neonatal diabetes mellitus is rare, and it has not been associated with beta-cell autoimmunity. Enteroviral infections during pregnancy 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 was 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 several types of islet cell reactive autoantibodies. The infant's T-cell responses to insulin and enterovirus antigens were recorded and enterovirus antibodies 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 autoantibodies and glutamic acid decarboxylase antibodies, whereas no autoantibodies were observed in the mother. The infant's T-cells showed reactivity to insulin and purified enterovirus particles. Based on serological studies, the pathogenetic process could have been triggered by an echovirus 6 infection during pregnancy. The patient's diabetes has been permanent, although there were signs of endogenous insulin production for several months. Exocrine pancreatic insufficiency was diagnosed at the age of 1 year.
Conclusion/Interpretation:
These observations suggests that enteroviral infections may induce beta-cell autoimmunity even in utero.