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      Treatment of Pubertal Gynecomastia with the Specific Aromatase Inhibitor Anastrozole

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          Gynecomastia can be detected in up to 70% of boys during puberty and in about one third of adult males. An imbalance of estrogen to androgen tissue levels is believed to be the major reason for the development of gynecomastia; as a result most medical treatments so far have tried to lower the estrogen level. Five boys with pubertal gynecomastia and breast tenderness were treated for 6 months with the selective aromatase inhibitor anastrozole. Initial plasma levels of estradiol (E<sub>2</sub>), testosterone (T), androstenedione, dehydroepiandrosterone sulfate (DHEA-S) and gonadotropins were normal. DHEA-S showed a significant rise during treatment. T and androstenedione showed no significant change during treatment. E<sub>2</sub> decreased with therapy, although to no statistically significant extent. The E<sub>2</sub>/T ratio decreased significantly during the treatment. Breast size decreased in 4 out of 5 patients, and in 1 of these 4 boys glandular breast tissue disappeared completely. The longer the duration of gynecomastia before anastrozole administration, the smaller was the reduction of breast size. Breast tenderness was resolved in all boys within 4 weeks. No adverse effects were recorded. Since the aim of medical treatment is the total disappearance of breast tissue, anastrozole, as previous aromatase inhibitors, is of limited effect. However, anastrozole seems to be of benefit for the treatment of tenderness in gynecomastia and for patients in whom surgery is particularly risky. However, as spontaneous disappearance of pubertal gynecomastia is common, further double-blinded, placebo-controlled trials are necessary before a definite conclusion can be drawn about the effectiveness and the side effects of this therapy.

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          Aromatase inhibitors in breast cancer.

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              A specific aromatase inhibitor and potential increase in adult height in boys with delayed puberty: a randomised controlled trial.

              The role of oestrogens in the closure of growth plates in both sexes is unequivocal. We postulated that inhibition of oestrogen synthesis in boys with delayed puberty would delay maturation of the growth plates and ultimately result in increased adult height. We did a randomised, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone and placebo, or testosterone and letrozole. Boys who decided to wait for the spontaneous progression of puberty without medical intervention composed the untreated group. Letrozole effectively inhibited oestrogen synthesis and delayed bone maturation. Progression of bone maturation was slower in the letrozole group than in the placebo group. In 18 months, bone age had advanced 1.1 (SD 0.8) years in the untreated group and 1.7 (0.9) years in the group treated with testosterone and placebo, but only 0.9 (0.6) years in the letrozole group (p=0.03 between the treatment groups). Predicted adult height did not change significantly in the untreated group and in the placebo group, whereas in the group treated with letrozole the increase was 5.1 (3.7) cm (p=0.004). Our findings suggest that if oestrogen action is inhibited in growing adolescents, adult height will increase. This finding provides a rationale for studies that aim to delay bone maturation in several growth disorders.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                September 2004
                10 September 2004
                : 62
                : 3
                : 113-118
                Division of Pediatric Endocrinology, Department of Paediatrics, Christian-Albrechts-Universität Kiel, Kiel, Germany
                79882 Horm Res 2004;62:113–118
                © 2004 S. Karger AG, Basel

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                Figures: 2, Tables: 3, References: 23, Pages: 6
                Original Paper


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