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Clinical Aspects of Posterior Pituitary Hormones

المؤلف:  Norman, A. W., & Henry, H. L.

المصدر:  Hormones

الجزء والصفحة:  3rd edition , p87-88

2026-07-01

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A. Oxytocin

There are presently no clear clinical disorders that can be attributed to a mutation in the gene for oxytocin or for its receptor in humans, although it is conceivable that some social behaviors discussed above could be affected by such changes in oxytocin or the function of its receptor. That is not to say that oxytocin is of no clinical interest, as its use plays a critical role in the management of labor and delivery.

B. Diabetes Insipidus

 Lack of vasopressin action, due to damage to the hypothalamus or pituitary or a gene mutation in either the gene for the hormone or for the receptor in the kidney, leads to the condition known as diabetes insipidus (literally urine that is tasteless). This condition is to be distinguished from diabetes mellitus (urine that is sweet) which is due to lack of or resistance to insulin. Diabetes insipidus (DI) is characterized by polyuria (excessive urine volume) and polydipsia (excessive thirst/water intake).

The most common cause of hypothalamic DI in both children and adults is a primary brain tumor that impacts the hypothalamic magnocellular neurons that secrete vasopressin. Inherited forms of DI, resulting from defects in vasopressin gene expression, occur in both autosomal dominant and recessive forms; symptoms are generally recognized during the child’s second year of life when parents become more aware of the child’s need for water. In nephrogenic diabetes insipidus (NDI) the kidney is unresponsive to vasopressin, due to a defect in the receptor or the signaling path way. In congenital NDI, polyuria and polydipsia must be recognized at birth and treated immediately to avoid life-threatening dehydration. NDI can also be acquired through chronic renal disease, the use of one of several drugs including lithium and alcohol, and other disease states such as multiple myeloma and sarcoidosis.

Hypothalamic DI can be treated with replacement vasopressin or its therapeutic analog desmopressin, which has some beneficial pharmacokinetic proper ties. Dosages can be tailored to the individual by monitoring urine volume and osmolality. Treatment of nephrogenic DI is more complex since it is resistant to hormone replacement therapy. Most approaches involve treating the symptoms with low-sodium diet and drugs such as thiazide diuretics.