In its most severe form, called salt-wasting (or salt-losing) CAH, where there is a total or near total deficiency of the 21-hydroxylase enzyme, a life-threatening adrenal crisis can occur if the disorder is untreated.
Another type of CAH is characterized by only a slight deficiency in production of the 21-hydroxylase enzyme (nonclassic or late-onset form), in which symptoms occurs later in childhood or during young adolescence.
Prenatal therapy, in which a pregnant woman at risk for a second CAH child is given dexamethasone to decrease secretion of androgens by the adrenal glands of the female fetus, has been in use since 1994.
Congenital adrenal hyperplasia (CAH) is a form of adrenal insufficiency in which 21-hydroxylase, the enzyme that produces two important adrenal steroid hormones, cortisol and aldosterone, is deficient.
In the mild form of CAH, which occurs in late childhood or early adulthood, symptoms include premature development of pubic hair, irregular menstrual periods, unwanted body hair, or severe acne.
For some forms of CAH, prenatal diagnosis is possible through chronic villus sampling in the first trimester and by measuring certain hormones in the amniotic fluid during the second trimester.
Congenital adrenal hyperplasia (CAH) is a genetic disorder characterized by a deficiency in the hormones cortisol and aldosterone and an over-production of the hormone androgen.
It is also recommended that parents have a letter or information prepared concerning CAH and care needed so that this can be given to a new doctors who may treat the child.
This means that a number of fetuses are exposed to unnecessary steroid treatment in order to prevent the development of male-like genitals in female fetuses with CAH.
The acid renders it available as a manure by converting the calcium phosphate, Ca 3 P 2 O 8, that it contains into the soluble monocalcium salt, CaH 4 P 2 O 8, or "superphosphate."