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PubMed2001

Intrauterine growth retardation and puberty in girls.

Some, albeit not all studies on the relationship between intrauterine growth retardation (IUGR) and female pubertal development have found an earlier and rapidly progressing puberty as well as concomitant disorders of related functional systems such as polycystic ovary syndrome and short stature. These pubertal changes are part of a growing list of IUGR-related diseases, which includes non-insulin dependent diabetes mellitus and coronary heart disease. A pulsatile release of gonadotropin releasing hormone is thought to be a conditio-sinne-qua-non for the initiation of puberty. In the absence of prospective studies on gonadotropin releasing hormone pulse patterns in IUGR-children other markers of pubertal development such as age at menarche have been deployed. From these studies it is not clear, however, whether the findings of an earlier onset of puberty in IUGR-girls merely reflect a more rapid progression of puberty. Both the role for IUGR and the mechanisms behind the onset of puberty are still elusive. Assuming a connection between IUGR and pubertal development, parallels can be drawn between hypotheses on the longterm consequences of IUGR and hypotheses on the initiation of puberty. For example, the somatometer concept proposes a role for fat mass in the initiation of puberty, which is compatible with the hypothesis on non-skeletal catch-up growth after IUGR. The debate on the origins of puberty and the role of IUGR mainly focuses on nature and nurture. Judgmentally, studies in mono- and dizygotic twins discordant for birth weight may be of particular help.

Adipose Tissue↗
PubMed2005

[Tintin in CMAJ].

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Growth Disorders↗
PubMed2005

Tintin in CMAJ.

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Growth Disorders↗
PubMed2005

Tintin in CMAJ.

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Animals↗
PubMed2005

Tintin in CMAJ.

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Human Growth Hormone↗
PubMed1993

Pulsatile LH-RH administration induces puberty in hypogonadotropic GH-deficient patients.

Three growth hormone (GH) deficient males with hypogonadotropic hypogonadism were treated with pulsatile luteinizing hormone-releasing hormone (LH-RH) administration. In two of them, the GH deficiency was idiopathic, but in the other it was secondary, caused by suprasellar germinoma. In response to LH-RH therapy, the serum testosterone (T), testicular volume, and body height increased in all three patients, and normal serum T levels and spermatogenesis were achieved in two patients. Gonadotropin responses to an LH-RH test preceding therapy did not seem to be an accurate predictor of the success of LH-RH therapy. We conclude that GH-deficient patients with hypogonadotropic hypogonadism can be expected to achieve normal pubertal development and spermatogenesis with pulsatile LH-RH administration.

Adolescent↗
PubMedDate not supplied

Determination of body composition in children and adolescents: validation of bioelectrical impedance with isotope dilution technique.

The determination of body composition as part of the clinical and auxologic follow up of childhood growth disorders necessitates the use of a quick, portable, reliable and simple non-invasive method. The present study was undertaken to validate bioelectrical conductance, height2/resistance (Ht2/R), against isotopically determined total body water (TBW) using heavy water tracer H2[18O]. The subjects (n = 56) consisted of normal children, children with various endocrine disorders, and young adults between the ages of 8-26 years. Isotopically determined TBW and fat free mass (FFM) were highly correlated with Ht2/R (r = 0.94, p = < 0.001, and r = 0.94, p = < 0.001, respectively). In a multiple regression analysis, 96% of the variability in FFM in normal subjects could be predicted by the following equation: FFM = 0.524 Ht2/R + 0.415 Wt-0.32, while in the group of patients by FFM = 0.659 Ht2/R + 0.254 Wt + 2.851. These data suggest that bioelectrical impedance measurements give valid and reliable estimates of FFM in children and adolescents. This easy technique could be incorporated in the auxologic follow up of children on hormone therapy.

Adolescent↗
PubMedDate not supplied

Bone age progression during five years of substitutive therapy for the induction of puberty in thalassemic girls--effects on height and sitting height.

UNLABELLED: It is known that in thalassemic patients there is a disproportion between lower and upper segments whose causes have not yet been identified. We evaluated whether the administration of estrogens to induce puberty in hypogonadic thalassemic girls caused an inappropriate acceleration of bone maturation and whether this had a negative influence on final and sitting height. MATERIALS AND METHODS: Twelve thalassemic patients with spontaneous puberty (Group A) and seven patients with hypogonadism (Group B) were studied. The mutations of the beta gene were identified by DNA analysis. We took into account four observations, ranging from the onset of spontaneous puberty in group A or the start of substitutive therapy in group B, to 5 years later. At each observation we considered: chronological age (CA), bone age (BA), height (Ht) expressed in cm and as standard deviation score (HtSDS) calculated with respect to CA (HtSDSCA) and BA (HtSDSBA), growth spurt, sitting height, expressed as SDS (SH-SDS), and height gain (HG). The delta BA and delta CA were calculated between the first and the final observation values to evaluate the bone age acceleration (delta BA/delta CA). RESULTS: No acceleration of BA was noted. delta BA/delta CA was 0.98 +/- 0.1 in group A and 0.89 +/- 0.1 in group B (p > 0.05). All patients in group B had the most severe form (beta degree/beta degree) of thalassemia. During the final observation, SH-SDS was -1.43 +/- 1.2 and -2.9 +/- 0.6 in group A and B respectively (p < 0.002), while no difference between the two groups for HtSDSCA and HtSDSBA was observed. HG was greater in group A than in group B (17.7 +/- 5.4 cm vs 10.8 +/- 5.2 cm) (p < 0.002), such as the spurt 8.6 +/- 1.4 cm (group A) and 6.1 +/- 2.6 cm (group B) (p < 0.05). CONCLUSIONS: Girls with hypogonadism did not show an inappropriate acceleration of BA, as they reached near final height similar to girls with spontaneous puberty. The auxological parameters showed a more severe body disproportion with the prevalence of the lower segment in the hypogonadic girls. This could be explained by a higher degree of bone marrow hyperplasia related to the most severe form of thalassemia and a higher blood consumption. As a consequence, damage at the vertebral level might determine an inability of the bone tissue to respond to estrogens. We suggest beginning estrogen therapy earlier in order to obtain better truncal growth.

Adolescent↗
PubMed2000

Osteopenia in children and adolescents with hyperprolactinemia.

Three patients with hyperprolactinemia due to pituitary adenomas (two patients) or empty sella (one patient) and osteopenia are described. Their ages at presentation ranged from 8 to 17 years. Each patient was treated with cabergoline. Serum prolactin levels became normal in all patients within one month. Bone density and pubertal stage improved after 12 months of treatment.

Adolescent↗
PubMed2005

Gonadal function of young patients with beta-thalassemia following bone marrow transplantation.

Bone marrow transplantation (BMT) can induce short- and long-term impairment of gonadal function. Patients with beta-thalassemia represent a special group, as their primary diagnosis and its treatment modalities are responsible for gonadal dysfunction. To address the effect of BMT on puberty and gonadal function, we investigated 25 patients (12 males) with thalassemia who received allogenic BMT during childhood or adolescence and at the post-transplant evaluation were at an age that the pubertal process should have started. Pubertal stage by Tanner of breast and pubic hair, as well as testicular volume were assessed pre-BMT once and post-BMT at least twice. Menstrual history was recorded. FSH, LH, testosterone and estradiol levels were also determined. The impact of BMT appears to be different in the two sexes. Males seem to have higher tolerance, as all males who were pubertal at the time of BMT had normal testosterone, and all but one normal gonadotropin levels. From those who were prepubertal at BMT, 62% proceeded to normal pubertal development. Post-menarcheal females seem to be an extremely sensitive group to the deleterious effect of the transplantation process, as 100% of the post-menarcheal females exhibited amenorrhea and elevated gonadotropin levels. These findings are important for pre- and post-BMT counseling.

Adolescent↗
PubMed2005

Hypogonadotropic hypogonadism associated with cleidocranial dysostosis.

BACKGROUND: Cleidocranial dysostosis (CCD) is a rare autosomal dominant disease with high penetrance and extremely variable expression. Some of the clinical manifestations include large, broad and short cranium with frontal and parietal bossing and a supraglabellar depression, facial part of the cranium relatively small with hypertelorism, absent or poorly defined superior and inferior clavicular depressions. PATIENT REPORT: A 17 year-old girl with CCD was referred to the pediatric endocrinology and metabolism clinic because she failed to reach any signs of puberty.

Adolescent↗
PubMed2006

A workshop on pubertal hormone replacement options in the United States.

BACKGROUND: The optimal pubertal hormone replacement therapy in females and males is unclear. OBJECTIVE: To review hormone replacement options for hypogonadal teenagers and to determine the relevant attitudes and practices of pediatric endocrinologists in the United States. DESIGN/METHODS: A workshop on pubertal hormone replacement options was held during the Lawson Wilkins Pediatric Endocrine Society meeting in 2004. A questionnaire was distributed to investigate the audience's attitudes and practices in inducing puberty. RESULTS: The majority of respondents used conjugated estrogens to treat hypogonadal girls with the primary aim of treatment being attainment of maximal adult height. The majority of respondents used depot testosterone to treat hypogonadal boys with the primary aim of treatment being pubertal development and virilization. CONCLUSIONS: The use of physiological sex hormone replacement to optimize the induction of puberty in hypogonadal adolescents was recommended. The workshop revealed striking differences between US and European pediatric endocrinologists regarding their practices and attitudes regarding the induction of puberty in hypogonadal females. Detailed studies are necessary to develop more uniform guidelines.

Adolescent↗
PubMed2001

Aspects of the treatment of Turner syndrome.

Several issues have to be considered when taking care of girls and women with Turner syndrome. During childhood, short stature is the primary concern and treatment with growth hormone (GH) is now widely used, often in conjunction with the androgen, oxandrolone. Recent studies indicate that doses used previously in the treatment of short stature have been too small. Induction of puberty should be performed at an appropriate age with reference to the peers of the patient. In adulthood, female sex hormone substitution should be offered to possibly prevent the increased morbidity seen in Turner syndrome, which consists of increased risk of fractures and osteoporosis, a clustering of diseases like ischaemic heart disease, hypertension, stroke and Type 2 diabetes, the latter entities being involved in the insulin resistance syndrome. Furthermore, hypothyreosis are often seen and the risk of Type 1 diabetes may also be increased. Congenital malformations of the heart are frequently seen in Turner syndrome, possibly increasing the risk of dissecting aorta aneurism. Liver enzymes are often elevated in Turner syndrome and there may be an increased risk of cirrhosis of the liver. Mortality does seem to be increased in Turner syndrome and women with the 'pure' 45,X karyotype do seem to be most severely affected. In the clinical practice of Turner syndrome, a careful monitoring of glucose and bone metabolism, weight, thyroid function and blood pressure should be performed. A cardiovascular risk profile should be determined and the patient informed concerning risks and benefits from sex hormone replacement therapy. Based on the available literature, sex hormone replacement therapy is highly recommended, although at present there are no longitudinal data documenting the long-term positive effect of sex steroid substitution. However, hypogonadism is expected to explain at least part of the decreased lifespan found in Turner syndrome. Since general physicians encounter Turner patients infrequently, it is recommended that the care and treatment of Turner syndrome is centralised.

Adolescent↗