Androgen excess in childhood results in pseudoprecocious puberty, accelerated childhood growth with premature epiphyseal fusion, adult short stature, and unknown metabolic and psychological perturbations. Congenital adrenal hyperplasia (CAH) and familial male-limited precocious puberty (FMPP) are two genetic diseases that result in early childhood androgen excess, and CAH due to 21-hydroxylase deficiency is the most common cause of hyperandrogenism in childhood. This protocol will elucidate a comprehensive phenotypic profile for patients with CAH and FMPP. Data will be collected in a large cohort of patients regarding growth and development, hormonal and metabolic factors and psychological characteristics. This protocol will allow investigators to compare patients with androgen excess of different etiologies, elucidate androgen-mediated and disease-specific phenotypic characterizations, and allow the investigators to acquire further knowledge for use in the design of future therapeutic interventions.