PubMed1991
The secular trend toward an earlier age of puberty implicates health and nutrition as major determinants of the onset of sexual maturation. The pattern of hypothalamic stimulation of pituitary gonadotropin secretion causing gonadal steroid secretion that is active in the fetus, subdued in the child, and again awakened in the peripubertal period is well described, although the specific trigger of the initiation of puberty is unknown. Pubertal delay may have a cause in the CNS or in the gonad. Constitutional delay in pubertal development, a variant of normal, is difficult to differentiate from isolated gonadotropin deficiency, a permanent condition. However, a myriad of congenital defects, tumors, injuries, and infections can lead to hypogonadotropic hypogonadism, which may be diagnosed by associated physical findings. Gonadal abnormalities are characterized by elevated gonadotropin concentrations and often are associated with specific physical features. Early pubertal development may also be divided into etiologies based in the CNS or in other parts of the body. Idiopathic precocious puberty, in which the endocrine profile is identical to that of normal puberty, is seen in the early childhood period or as a minor variation from the normal range of the onset of pubertal development. Tumors of the CNS, however, are more often responsible for the youngest childhood cases of complete precocious puberty. Incomplete precocious puberty in boys can be caused by androgen production from the gonads or adrenal glands or can be caused by autonomous production of hCG. Variations of pubertal development are self-limited, although they may awaken parental or patient concerns. Thus, premature adrenarche is best differentiated from more serious and treatable causes of androgen production. Gynecomastia is usually treated with reassurance.