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Pubertal Induction (pubertal + induction)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Improved final height in Turner's syndrome following growth-promoting treatment at a single centre

ACTA PAEDIATRICA, Issue 9 2003
EJ Gault
Aims: To examine the final height (FH) outcome of girls with Turner's syndrome (TS) treated at a single Scottish centre (Glasgow group), to compare it with an earlier national analysis (Scottish group) and to suggest reasons for any change. Methods: Retrospective growth and treatment data for 29 Glasgow patients were compared with those of 26 Scottish patients. Results: Age at GH start (mean ± SD) was 10.1 ± 2.6 vs 12.1 ± 1.7 y (p < 0.01) in the Glasgow versus Scottish groups, with overall duration of treatment 6.2 ± 2.4 vs 3.7 ± 1.1 y (p < 0.001) and years of GH treatment before pubertal induction 2.7 ± 2.8 vs 0.3 ± 0.8 y (p < 0.001), respectively. Pubertal induction was at a similar age: 12.7 ± 1.8 vs 12.8 ± 1.8 y (ns). FH was 151.1 ± 4.6 cm in the Glasgow group compared with 142.6 ± 5.6 cm in the Scottish group (p < 0.001), with FH -projected adult height (PAH) 5.7 ± 4.6 cm vs 0.6 ± 3.6 cm (p < 0.001), respectively. Univariate analysis of the Glasgow group's FH , PAH with a number of growth and treatment variables identified no statistically significant relationships. Conclusion: This group's improved FH and FH , PAH, relative to an earlier sample, are attributed to the introduction of GH treatment from a younger age and for longer, overall and before pubertal induction. In addition, the authors believe that compliance with treatment has been enhanced by this single centre's dedicated Turner clinic and the efforts of its established "growth team". These data demonstrate that a favourable FH can be achieved using a safe and financially viable dose of GH, while inducing puberty at a "normal" age. [source]

How do you initiate oestrogen therapy in a girl who has not undergone puberty?

CLINICAL ENDOCRINOLOGY, Issue 1 2009
Peter C. Hindmarsh
Summary The physiology of puberty needs to be taken into consideration in the induction of puberty. Puberty is a relatively slow process and replacement therapy should mimic this. Long-term maintenance requires careful monitoring and long-term assessment of risk-benefit. This has not been appreciably defined in the adolescent population. Options for fertility need careful consideration and may depend on the adequacy of pubertal induction in terms of uterine development. A number of regimens are available for pubertal induction but the lack of comparisons makes it difficult to advocate for a particular regimen. There remain a number of areas of uncertainty, and future studies need to consider these issues and whether there are cardiovascular risk factor advantages to certain preparations. The long-term risks of breast and gynaecological malignancy remain uncertain. Long-term cohort studies are required to address these issues. [source]

Poor uterine development in Turner syndrome with oral oestrogen therapy

CLINICAL ENDOCRINOLOGY, Issue 3 2002
Wendy F. Paterson
Summary OBJECTIVE To evaluate uterine development in Turner syndrome (TS) patients in relation to treatment with oral ethinyl oestradiol (E2) for pubertal induction. DESIGN AND PATIENTS Pelvic ultrasound data for 96 TS patients scanned since 1989 were analysed. Patients were classified into three groups: (1) untreated (n = 48); (2) complete spontaneous puberty (n = 10); and (3) treated with ethinyl oestradiol (n = 38). Uterine development was described in the three groups and compared with the normal data. MEASUREMENTS Uterine length, fundal-cervical ratio (FCR) and shape were recorded, and presence or absence of ovaries noted. In the treated group, cross-sectional and longitudinal data were combined to compare uterine development with Tanner breast stage. RESULTS In untreated girls up to age 10 years there was a variable distribution of uterine length and FCR about the mean. Thereafter, the uterus failed to grow and mature normally. Girls with complete spontaneous puberty had morphologically normal ovaries and uteri, but of 7 girls who attained menarche, 3 subsequently developed secondary oligomenorrhoea or amenorrhoea. In the treated group, in general, breast development and uterine length progressed with increasing E2 dose. However, only 50% of girls with complete secondary sexual development had a mature heart-shaped uterine configuration. CONCLUSIONS Our current E2 treatment regimen for TS girls gives rise to satisfactory pubertal induction and maintenance, but failed to induce a fully mature uterus in half the cohort. In view of the high risk of miscarriage in TS in both spontaneous and assisted pregnancies, the effect of more physiological methods of E2 replacement on uterine development should be investigated. [source]