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Results for “Puberty, Delayed”

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At least 1,405 records · Page 78Linked to original sources
PubMed1997

Can we predict and prevent adult morbidity in males with childhood-onset growth hormone deficiency?

In order to achieve an optimal quality of life and minimize morbidity in adulthood, the therapeutic management of patients with childhood-onset growth hormone deficiency (GHD) should follow strict guidelines. Optimal final height should be obtained by the early diagnosis of GHD and subsequent adequate growth hormone (GH) dosing and duration of treatment. Moreover, particularly in males with associated gonadotrophin deficiency, the psychosexual maladjustment could be prevented by the earlier induction of puberty, completion of the male phenotype and testicular stimulation with gonadotrophins or luteinizing hormone-releasing hormone. Finally, a satisfactory peak bone mass could be attained by continuation of GH treatment for some years after cessation of linear growth.

Adult↗
PubMed1974

Peromyscus: effect of early pairing on reproduction.

Sibling mating in prairie deer mice (Peromyscus maniculatus bairdi) results in poor reproductive performance. Siblings experimentally paired before puberty exhibit delayed reproduction when adult. A behavioral mechanism is involved in this reproductive delay, since prepubertal familiarity also delays reproduction in nonsibling pairs. Such a reproductive delay may act to reduce inbreeding depression and regulate population growth.

Age Factors↗
PubMed1981

Familial cytomegalic adrenocortical hypoplasia: an X-linked syndrome of pubertal failure.

Five boys with familial cytomegalic adrenocortical hypoplasia have been followed up for an average of 19 years. Despite treatment with replacement corticosteroids, all 5 failed to show a spontaneous onset of puberty and, when assessed at ages 13 to 19 years, all had both sexual infantilism and skeletal immaturity. Hypogonadism was confirmed by low levels of plasma testosterone, and pituitary reserve of gonadotrophin was shown to be inadequate by testing with gonadotrophin-releasing hormone. Two boys, both with adequate testosterone output on human chorionic gonadotrophin stimulation, were given gonadotrophin therapy, whereas the other 3 were treated with parenterally administered testosterone. With treatment, all 5 patients showed advances in pubertal staging. Although the mechanism of the hypogonadotropism remains unclear, the association of hypogonadotrophic hypogonadism with familial cytomegalic adrenocortical hypoplasia appears to be a constant one and may be considered as a treatable inherited syndrome of pubertal failure.

Adolescent↗
PubMed1983

Method for the earlier recognition of abnormal stature.

Two hundred and twenty seven children with a height below the 3rd or above the 97th centile were seen consecutively in the Oxford growth clinic. Their referral ages were analysed to determine the pattern of referral. Eighty seven per cent of the children had short stature. In 40% of these there was an organic reason for abnormal growth--the most common conditions being growth hormone deficiency, hypothyroidism, and Turner's syndrome--but the rest had genetic short stature or 'constitutional' delay in puberty. Many children who could have been treated effectively were referred too late, for effective treatment to ensure normal adult height because of this we have developed full sized percentile charts to screen populations of children so that abnormal stature can be recognised immediately.

Adolescent↗
PubMed1984

Patterns of growth in the hepatic glycogenoses.

Longitudinal growth data from 31 patients with hepatic glycogen storage disease (type I (8 patients), type Ib (three patients), type III (13 patients), and type IX (phosphorylase kinase deficiency) (7 patients) ) have been reviewed. All patients were below the mean for height at presentation; the mean height standard deviation scores were -2.13 (type I), -2.0 (type Ib), -2.4 (type III), and -1.6 (type IX). Untreated, most patients with type I and Ib grew slowly with no catch up growth but three patients with mild disease grew normally. Most children with type III disease grew at a normal velocity throughout childhood. Puberty was delayed and final height normal. Some of the children with type III and all of those with type IX had catch up growth throughout childhood. Intensive treatment of patients with severe forms of type I and Ib disease resulted in catch up growth, but this was not complete if the treatment was started late.

Body Weight↗
PubMed1994

Effect of alpha thalassaemia trait and enhanced gamma chain production on disease severity in beta thalassaemia major and intermedia.

One hundred and twenty patients with homozygous beta thalassaemia were selected to determine the clinical effects of certain genetic factors which may modify disease severity. Genetic analysis defined specific beta thalassaemia mutations, the alpha thalassaemia genotype, and the presence of an XmnI restriction enzyme site, associated with increased fetal haemoglobin (HbF) production under certain conditions. Genotypic data with globin chain synthesis were related to the age when regular transfusions began and subsequent pubertal development. This study showed that the major determinants of disease severity in beta thalassaemia were the beta thalassaemia mutations, with co-inheritance of alpha thalassaemia trait and coinheritance of a high HbF determinant acting as ameliorating factors. The presence of an alpha thalassaemia deletion significantly reduced initial disease severity, although the effect on pubertal development was less clear. It is concluded that detailed genetic analysis should be performed in all newly diagnosed patients with thalassaemia. This, in conjunction with clinical assessment, will help to predict disease severity and prognosis.

Adolescent↗
PubMed1995

Renal transplantation and osteoporosis.

A cross sectional study assessed the bone mineral density (BMD) of 20 young adult patients who received a renal transplantation in childhood. The BMD of the lumbar spine, mainly trabecular bone, and of the total body, mainly cortical bone, were measured and expressed as an SD score. Fourteen patients (70%) had a BMD SD score of the lumbar spine below -1, of whom six patients were below -2. Fifteen patients (75%) had a BMD SD score of the total body below -1, of whom seven patients were below -2, Both trabecular and cortical bone appeared to be involved in the osteopenic process. The cumulative dose of prednisone was inversely correlated to both lumbar spine and total body BMD SD score. In a multiple regression analysis the cumulative dose of prednisone appeared to be the only factor with a significant effect on BMD SD score. Most young adult patients who had received a renal transplantation in childhood had moderate to severe osteopenia. Corticosteroid treatment played a major part in the development of osteopenia in these patients.

Adult↗
PubMed1995

Osteopenia in Crohn's disease.

A 16 year old boy presented soon after diagnosis of Crohn's disease with diffuse osteopenia of the lumbar spine with collapse of three vertebral bodies and grossly reduced bone mineral density noted on dual energy x ray absorptiometry scan. Treatment of the underlying Crohn's disease and induction of puberty resulted in marked improvement in bone mineralisation.

Absorptiometry, Photon↗