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Studies are reported on a 19-month-old boy with hydrocephalus and severe central nervous system infection, who developed sustained hyponatremia and water intoxication with maximally concentrated urine, urinary sodium loss, and no clinical signs of contraction of the extracellular fluid volume. Inappropriate secretion of antidiuretic hormone was postulated as the cause of this syndrome. The increased levels of antidiuretic activity in the plasma, its suppression after ethanol administration, and failure to dilute the urine after a water load confirmed this contention. Though the neurohypophysis was not sensitive to changes in plasma osmolality, the mechanism of suppression of the secretion of antidiuretic hormone in response to an acute expansion of the extracellular fluid volume was intact. After water loads ethanol administration invariably caused water diuresis. The hyponatremia was corrected by a regime of restricted water intake and increased sodium intake. However, the child recovered from this syndrome only with proper treatment of his central nervous system infection.
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Mangos et al. (1964) studied this question.
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