Abstract
Congenital adrenal hyperplasia (CAH) due to a deficiency of 21-hydroxylase is the most common inborn error of the adrenal steroid biosynthetic pathway. The considerable increase of 17α-hydroxyprogesterone (17-OHP) in the serum of CAH patients has been shown to be already evident at the neonatal period (Chaussain et al., 1974). Consequently, radioimmunoassays have been developed to measure 17-OHP in dried blood samples and have made neonatal screening programmes possible.
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