: 84 In girls with Turner syndrome who do not experience spontaneous puberty, exogenous estrogen is used to induce and maintain feminization. Estrogen replacement is recommended to begin at around age 11–12, although some parents prefer to delay the induction of puberty in girls with lower social and emotional preparedness. The dose of estrogen in induced puberty begins at 10% of adult estrogen levels and is steadily increased at six-month intervals, with a full adult dose attained two to three years after the beginning of treatment. Estrogen replacement may interfere with growth hormone therapy, due to the closing effects of estrogen on growth plates; individuals must weigh up their preferences for taller height versus greater feminization. : 97–103

Fertility
Women with Turner syndrome are infertile. Only 2%–5% are capable of pregnancy without fertility treatment, most with mosaic karyotypes. Early in gestation, fetuses with Turner syndrome have a normal number of gametes in their developing ovaries, but this starts decreasingly rapidly as early as 18 weeks of pregnancy; by birth, girls with the condition have markedly reduced follicular counts. Women with Turner syndrome who wish to raise families but are incapable of conception with their own oocytes have the options of adoption or of pregnancy with donor eggs; the latter has a comparable success rate to donor pregnancy in women with 46,XX karyotypes.Pregnancy in Turner syndrome is inherently high-risk; the maternal death rate is 2%.Usually, estrogen replacement therapy is used to spur the growth of secondary sexual characteristics at the time when puberty should onset.
Estrogen replacement therapy can promote development of the breasts and hips. Medical care is often required to manage other health problems with which Turner syndrome is associated.Turner syndrome occurs in between one in 2,000 and one in 5,000 females at birth. All regions of the world and cultures are affected about equally. Generally people with Turner syndrome have a shorter life expectancy, mostly due to heart problems and diabetes. American endocrinologist Henry Turner first described the condition in 1938. In 1964, it was determined to be due to a chromosomal abnormality. Presentation
Turner syndrome has a number of physical and psychological impacts, including short stature, heart defects, neck webbing, delayed or absent puberty, and infertility. The phenotype of Turner syndrome is affected by mosaicism, where cell lines with a single sex chromosome are combined with those with multiple. Around 40%–50% of cases of Turner syndrome are true "monosomy X" with a 45,X0 karyotype, while the remainder are mosaic for another cell line, most commonly 46,XX, or have other structural abnormalities of the X chromosome. The classic features of Turner syndrome, while distinctive, may be rarer than previously thought; incidental diagnosis, such as in biobank samples or prenatal testing for older mothers, finds many girls and women with few traditional signs of Turner syndrome. Physiological
Height
Turner syndrome is associated with short stature. The mean adult height of women with Turner syndrome without growth hormone therapy is around 20 cm (8 in) shorter than the mean of women in the general population.