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Central diabetes insipidus
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Central diabetes insipidus
Central diabetes insipidus, also known as arginine vasopressin deficiency (AVP-D), is a form of diabetes insipidus that is due to a lack of vasopressin (ADH) production in the brain. Vasopressin acts to increase the volume of blood (intravascularly), and decrease the volume of urine produced. Therefore, a lack of it causes increased urine production and volume depletion.
It is also known as neurohypophyseal diabetes insipidus, referring to the posterior pituitary (neurohypophysis), which receives vasopressin from the hypothalamus in the brain, via the hypothalamo-hypophyseal tract in the pituitary stalk. This condition has only polyuria in common with diabetes. Although not mutually exclusive, with most typical cases, the name diabetes insipidus is misleading.
Untreated patients with central diabetes insipidus often experience polyuria, nocturia, and polydipsia due to the initial increase in serum sodium and osmolality. Central diabetes insipidus can be caused by various congenital or acquired lesions, and when the cause is unknown, it is classified as idiopathic.
The water deprivation test (WDT) is a commonly used test for diabetes insipidus, a two-step process involving parenteral desmopressin administration after an initial 8-hour water fast. It differentiates primary polydipsia from diabetes insipidus and central diabetes insipidus from nephrogenic diabetes insipidus. Diabetes insipidus is treated by restoring free water deficit, replacing the missing hormone, and addressing the underlying ailment. Desmopressin, an arginine vasopressin analog, is used to treat central diabetes insipidus.
Untreated central diabetes insipidus patients usually exhibit polyuria, nocturia, and polydipsia as a result of the initial rise of serum sodium and osmolality. Patients may also experience neurologic symptoms associated with the underlying illness, such as headaches and diplopia, depending on the exact origin of the central diabetes insipidus.
Even when their polyuria and polydipsia are adequately managed, patients with central diabetes insipidus frequently suffer psychological symptoms as elevated anxiety, social isolation, and an overall lower quality of life.
People with central diabetes insipidus also show oxytocin deficiency and have greatly blunted oxytocin increases and markedly reduced entactogenic effects such as euphoria, increased empathy, and reduced anxiety with MDMA.
The clinical manifestation of central diabetes insipidus is the lack of arginine vasopressin secretion as a result of the hypothalamus/posterior pituitary axis neurons being destroyed. Numerous different congenital or acquired lesions can cause the condition.
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Central diabetes insipidus
Central diabetes insipidus, also known as arginine vasopressin deficiency (AVP-D), is a form of diabetes insipidus that is due to a lack of vasopressin (ADH) production in the brain. Vasopressin acts to increase the volume of blood (intravascularly), and decrease the volume of urine produced. Therefore, a lack of it causes increased urine production and volume depletion.
It is also known as neurohypophyseal diabetes insipidus, referring to the posterior pituitary (neurohypophysis), which receives vasopressin from the hypothalamus in the brain, via the hypothalamo-hypophyseal tract in the pituitary stalk. This condition has only polyuria in common with diabetes. Although not mutually exclusive, with most typical cases, the name diabetes insipidus is misleading.
Untreated patients with central diabetes insipidus often experience polyuria, nocturia, and polydipsia due to the initial increase in serum sodium and osmolality. Central diabetes insipidus can be caused by various congenital or acquired lesions, and when the cause is unknown, it is classified as idiopathic.
The water deprivation test (WDT) is a commonly used test for diabetes insipidus, a two-step process involving parenteral desmopressin administration after an initial 8-hour water fast. It differentiates primary polydipsia from diabetes insipidus and central diabetes insipidus from nephrogenic diabetes insipidus. Diabetes insipidus is treated by restoring free water deficit, replacing the missing hormone, and addressing the underlying ailment. Desmopressin, an arginine vasopressin analog, is used to treat central diabetes insipidus.
Untreated central diabetes insipidus patients usually exhibit polyuria, nocturia, and polydipsia as a result of the initial rise of serum sodium and osmolality. Patients may also experience neurologic symptoms associated with the underlying illness, such as headaches and diplopia, depending on the exact origin of the central diabetes insipidus.
Even when their polyuria and polydipsia are adequately managed, patients with central diabetes insipidus frequently suffer psychological symptoms as elevated anxiety, social isolation, and an overall lower quality of life.
People with central diabetes insipidus also show oxytocin deficiency and have greatly blunted oxytocin increases and markedly reduced entactogenic effects such as euphoria, increased empathy, and reduced anxiety with MDMA.
The clinical manifestation of central diabetes insipidus is the lack of arginine vasopressin secretion as a result of the hypothalamus/posterior pituitary axis neurons being destroyed. Numerous different congenital or acquired lesions can cause the condition.