Using r and om-effects models , estrogen replacement therapy showed an increase in bone mineral density [ weighted mean change from baseline 0.09 g/cm2 ( 0.04–0.14 ) ] that differed by type of estrogen but not route of administration .
Oral estrogen replacement therapy showed a higher increase in high density lipoprotein cholesterol levels when compared to transdermal [ weighted mean difference 9.33 mg/dl ( 4.82–13.85 ) ] with no significant effect on other lipid fractions .
The current evidence suggests possible benefit of estrogen replacement therapy  on bone mineral density and high density lipoprotein cholesterol .
Patients with Turner syndrome have adverse bone and cardiovascular outcomes from chronic estrogen deficiency .
Hence , long-term estrogen replacement therapy is the cornerstone treatment .
The estimates of its effect and optimal use , however , remain uncertain .
We aim ed to summarize the benefits and harms of estrogen replacement therapy on bone , cardiovascular , vasomotor and quality of life outcomes in patients with Turner syndrome .
Decreased bone mass despite long-term estrogen replacement therapy in young women with Turner's syndrome and previously normal bone density.
OBJECTIVE To determine whether young women with Turner 's syndrome who had normal bone mineral density ( BMD ) before the induction of puberty maintain normal BMD in young adulthood . DESIGN Controlled clinical study . SETTING A private hospital clinical research setting . PATIENTS Young women with Turner 's syndrome in Tanner stage V of puberty with previously normal BMD . INTERVENTIONS Oral conjugated estrogens and progesterone acetate were administered continuously for a mean ( + /-SD ) of 4.1+/-1.0 years . Bone mineral densities and blood sample s were evaluated . MAIN OUTCOME MEASURE(S ) The BMD of the lumbar spine and the femoral neck was determined during young adulthood . The change in BMD over the previous 6 years also was evaluated . Serum concentrations of the carboxy-terminal propeptide of type 1 collagen and of the carboxy-terminal cross-linked telopeptide of type 1 collagen were measured . RESULT ( S ) The BMD of the lumbar spine was reduced significantly in our patients . There was no change in the BMD of the femoral neck or lumbar spine over a period of 6.1 years . Concentrations of the carboxy-terminal propeptide of type 1 collagen were decreased , whereas concentrations of the carboxy-terminal cross-linked telopeptide of type 1 collagen were increased . CONCLUSION ( S ) Young women with Turner 's syndrome do not attain normal peak bone mass even when estrogen replacement therapy is begun in adolescence . Their low BMD seems to be due to decreased bone formation and increased bone resorption
Using r and om-effects models , estrogen replacement therapy showed an increase in bone mineral density [ weighted mean change from baseline 0.09 g/cm2 ( 0.04–0.14 ) ] that differed by type of estrogen but not route of administration .
Oral estrogen replacement therapy showed a higher increase in high density lipoprotein cholesterol levels when compared to transdermal [ weighted mean difference 9.33 mg/dl ( 4.82–13.85 ) ] with no significant effect on other lipid fractions .
The current evidence suggests possible benefit of estrogen replacement therapy  on bone mineral density and high density lipoprotein cholesterol .
Patients with Turner syndrome have adverse bone and cardiovascular outcomes from chronic estrogen deficiency .
Hence , long-term estrogen replacement therapy is the cornerstone treatment .
The estimates of its effect and optimal use , however , remain uncertain .
We aim ed to summarize the benefits and harms of estrogen replacement therapy on bone , cardiovascular , vasomotor and quality of life outcomes in patients with Turner syndrome .