Congenital toxoplasmosis presenting as central diabetes insi
In this disease, the severity of fetal damage depend on the stage of pregnancy when maternal infection occurs.

Although she looked apparently normal at birth, this patient presented in the neonatal period with nonspecific sepsis-like picture.

Later she showed predominant involvement of the central nervous system with seizures, hydrocephalus, chorioretinitis and spasticity.

These clinical features alerted physicians to the possibility of CTox, in which the detection of specific IgM or IgA antibodies that cannot cross the placental barrier, is a key marker of fetal infection.

Here, researchers report on a female infant who presented with fever, convulsions, and polyuria. Examination revealed weight and length below the 3rd centile along with signs of severe dehydration. Fundal examination showed bilateral chorioretinitis. This infant developed hypernatremia together with increased serum osmolality and decreased both urine osmolality and specific gravity consistent with central diabetes insipidus. Serology for toxoplasma specific immunoglobulin M was high for both the mother and the baby and polymerase chain reaction for toxoplasma deoxyribonucleic acid was positive in the infant confirming congenital toxoplasmosis. Brain computerized tomography scans demonstrated ventriculomegaly associated with cerebral and cortical calcifications. Fluid and electrolyte abnormalities responded to nasal vasopressin therapy.

It is known that congenital toxoplasmosis has a wide range of presentation at birth varying from severe neurological features such as hydrocephalus and chorioretinitis to a well appearing baby, who may develop complications late in infancy. While neuroendocrine abnormalities associated with congenital toxoplasmosis are uncommon, isolated central diabetes insipidus is extremely rare.

Conclusively, this report highlights central diabetes inspidus as a rare presentation of congenital toxoplasmosis.

Source: https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-7-184#Abs1
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