Of the abnormal conditions associated with micropenis, most are conditions of reduced prenatal androgen production or effect, such as abnormal testicular development, Klinefelter syndrome, Leydig cell hypoplasia, specific defects of testosterone or dihydrotestosterone synthesis, androgen insensitivity syndromes, inadequate pituitary stimulation, and other forms of congenital hypogonadism. Micropenis can also occur as part of many genetic malformation syndromes that do not involve the sex chromosomes. It is sometimes a sign of congenital growth-hormone deficiency or congenital hypopituitarism. Several homeobox genes affect penis and digit size without detectable hormone abnormalities. In addition, in utero exposure to some estrogen based fertility drugs like diethylstilbestrol has been linked to genital abnormalities or a smaller than normal penis. After evaluation to detect any of the conditions described above, micropenis can often be treated in infancy with injections of various hormones, such as human chorionic gonadotropin and testosterone. Most eight- to fourteen-year-old boys referred for micropenis do not have the micropenis condition. Such concerns are usually explained by one of the following:
a penis concealed in suprapubic fat
a large body and frame for which a prepubertal penis simply appears too small
Growth of the penis both before birth and during childhood and puberty is strongly influenced by testosterone and, to a lesser degree, the growth hormone. However, later endogenous hormones mainly have value in the treatment of micropenis caused by hormone deficiencies, such as hypopituitarism or hypogonadism. Regardless of the cause of micropenis, if it is recognized in infancy, a brief course of testosterone is often prescribed. This usually induces a small amount of growth, confirming the likelihood of further growth at puberty, but rarely achieves normal size. No additional testosterone is given during childhood, to avoid unwanted virilization and bone maturation. Testosterone treatment is resumed in adolescence only for boys with hypogonadism. Penile growth is completed at the end of puberty, similar to the completion of height growth, and provision of extra testosterone to post-pubertal adults produces little or no further growth.
Surgery
Because hormone treatment rarely achieves average size, several surgical techniques similar to phalloplasty for penis enlargement have been devised and performed; but they are not generally considered successful enough to be widely adopted and are rarely performed in childhood. In extreme cases of micropenis, there is barely any shaft, and the glans appears to sit almost on the pubic skin. From the 1960s until the late 1970s, it was common for sex reassignment and surgery to be recommended. This was especially likely if evidence suggested that response to additional testosterone and pubertal testosterone would be poor. With parental acceptance, the boy would be reassigned and renamed as a girl, and surgery performed to remove the testes and construct an artificial vagina. This was based on the now-questioned idea that gender identity was shaped entirely from socialization, and that a man with a small penis can find no acceptable place in society. Johns Hopkins Hospital, the center most known for this approach, performed twelve such reassignments from 1960 to 1980, most notably that of David Reimer, overseen by John Money. By the mid-1990s, reassignment was less often offered, and all three premises had been challenged. Former subjects of such surgery, vocal about their dissatisfaction with the adult outcome, played a large part in discouraging this practice. Sexual reassignment is rarely performed today for severe micropenis
