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At least 1,207 records · Page 67Linked to original sources
PubMed2001

Sickle cell disease and age at menarche in Jamaican girls: observations from a cohort study.

AIMS: (1) To investigate the distribution of age at menarche in a representative sample of 99 patients with homozygous sickle cell (SS) disease, 69 with sickle cell haemoglobin C (SC) disease, and 100 controls with a normal haemoglobin (AA) genotype followed in a cohort study from birth. (2) To explore the determinants of the age at menarche. METHODS: Children ascertained in a newborn screening programme were followed prospectively from birth to age 18-26.5 years with regular assessments of height, weight, pubertal stage, and haematological indices at the Sickle Cell Clinic of the University Hospital of the West Indies. RESULTS: All subjects have now reached menarche and the mean age in normal controls (13.0 years) was significantly earlier than in SC disease (13.5 years) or SS disease (15.4 years). Greater weight and earlier age at menarche was the only association significant across all genotypes although additional contributions occurred from fetal haemoglobin and red cell count in SS disease. Alpha thalassaemia, which ameliorates many of the effects of SS disease, had no discernible effect on menarche. CONCLUSIONS: Mean age at menarche is delayed by 0.5 years in SC disease and by 2.4 years in SS disease. Weight appears to be the principle determinant of age at menarche.

Adolescent↗
PubMedDate not supplied

Testosterone induced priapism in two adolescents with sickle cell disease.

Priapism is common in pubertal males with sickle cell disease, but the association between low-dose exogenous testosterone administration and priapism in such patients has not been well documented. Two adolescents with homozygous sickle cell disease (SCD) and delayed maturation with behavioral problems developed priapism about one week after receiving an intramuscular injection of testosterone enanthate. Neither had a previous history of priapism. We conclude that testosterone should not be administered to male patients with SCD because of the risk of inducing priapism and possible impotence.

Adolescent↗
PubMedDate not supplied

Delayed sexual development.

Sexual maturation can occur at an early age, at the expected or average time, or late. In adolescents who mature late, osseous development may be delayed. A variety of causes for delayed growth and sexual development should be evaluated. Constitutional delay is a nonpathogenic variation within normal growth parameters. The Tanner criteria should be used in assessing sexual maturation and bone age evaluation for skeletal growth. These criteria are based on the fact that sexual growth follows predictable patterns. Children need reassurance about their developmental growth, and subsequent growth should be monitored carefully.

Adolescent↗
PubMed2004

Alterations in serum growth hormone (GH)/GH dependent ternary complex components (IGF-I, IGFBP-3, ALS, IGF-I/IGFBP-3 molar ratio) and the influence of these alterations on growth pattern in female rhythmic gymnasts.

BACKGROUND AND AIM: Normal growth in children is regulated to a great extent through the actions of the GH/IGF-I axis, a system consisting of GH and its mediators (ternary complex) that modulate growth in many tissues. The ternary complex (IGF-I/IGFBP-3/ALS) provides an acute regulatory mechanism in which IGF-I may be mobilized from the circulating reservoir of 150 kDa complexes to the tissues. Acute exercise is known to be a stimulus for GH secretion. The beneficial effects of scheduled exercise on body composition are also well established. However, the impact of strenuous exercise on the pubertal development of child athletes is still not well understood. The first goal of this study was to assess the acute effects of high intensity exercise training on GH-dependent ternary complex components in female rhythmic gymnasts compared to age-matched healthy female controls with normal physical activity. The second goal was to explore the influence of these exercise-induced changes on skeletal and pubertal growth in the same group prospectively over a period of 4 years. SUBJECTS AND METHODS: Seventeen female rhythmic gymnasts, aged 11.4 +/- 0.9 years, who had 10 h per week intense exercise for at least 4 months volunteered to participate in this study. Anthropometric measurement of height (Height SDS for chronological age [HtSDS(CA)], parentally adjusted height, predicted adult height), bone age and weight (BMI) were made using standard techniques in gymnasts and controls (aged 12.5 +/- 3.0 years, n = 12). Gymnasts were followed up to 4 years to observe growth velocity and pubertal progression. In order to determine the acute impact of exercise on levels of GH and GH-dependent ternary complex component (IGF-I, IGFBP-3, ALS, IGF-I/IGFBP-3 molar ratio), blood samples were obtained from gymnasts after a routine 2-h high-intensity training program and then after a 2-day rest period. These results were compared with age-matched controls with no scheduled sports activity. RESULTS: Despite the significant increment in serum GH and GH-dependent components immediately following the exercise, serum GH/IGF-I levels showed a significant decrement (p < 0.01) after a 2-day rest in gymnasts, to a nadir as low as those of the control subjects' baseline levels (p < 0.01). There was no difference in anthropometric characteristics of gymnasts and controls except BMI; gymnasts were leaner than controls. During a 4-year follow up, there were no differences between the gymnasts and controls in regard to skeletal growth and reaching their predicted height. However, in gymnasts there was a delay in pubertal tempo but not in growth. CONCLUSION: Intense exercise induces an acute rise in GH levels, but this acute elevation rapidly normalizes after a 2-day rest in female rhythmic gymnasts. These fluctuations in serum GH and GH-dependent ternary complex components had no reflection on the skeletal growth patterns in gymnasts over the 4-year follow up but there was a delay in their pubertal progression.

Adolescent↗
PubMed1992

[Clinical polymorphism of the XYY syndrome].

The XYY syndrome presents with a wide variation in the clinical features, both of the physical and behavioral nature. We report two new cases which illustrate this statement. The first case presented with aggressive behaviour and cryptorchidism. The second case was associated with pathological short height, pubertal delay and cardiac features (extrasystoles and short PR interval). We revise some of the aspects of XYY syndrome.

Adolescent↗
PubMedDate not supplied

Short stature at the University College Hospital, Ibadan, Nigeria.

Twenty four patients were evaluated for short stature at the University College Hospital, Ibadan, Nigeria, over a seven year period. Fourteen were males, 10 were females and their ages ranged from 6 to 23 years at first presentation. Nine out of the 10 females came to the hospital primarily because of failure of sexual development whereas only 1 of the 14 males presented with this complaint. The causes of short stature were as follows: idiopathic hypopituitarism in 5 (20.8%) patients (4 males, 1 female), gonadal dysgenesis in 5 patients (all females), syndrome of hepatosplenomegaly, dwarfism and poor sexual development in 5 patients (all males); 2 (8.3%) patients had hypothalamic-pituitary lesions, 2 had juvenile hypothyroidism and 1 (4.2%) had sickle cell hemoglobinopathy; the cause of the short stature was not certain in 4 (16.7%) patients. This is perhaps the first time that the syndrome of hepatosplenomegaly of uncertain etiology with delayed growth and sexual maturation previously reported in Iranian and Egyptian adolescents, is being described in black Africans. Although comprehensive hormonal data were not available in most of these patients, this clinical descriptive study is the first attempt at reporting some of the causes of short stature in Nigerians.

Adolescent↗
PubMed1989

Amplitude modulation of the nightly melatonin rise in the neonatal lamb and the subsequent timing of puberty.

Spring-born female lambs require a decrease in day length for the normal timing of puberty the following autumn. If this decrease occurs early in postnatal life (i.e. 0-10 weeks), puberty is delayed. This study tested the hypothesis that failure of the neonatal lamb to respond to the critical long-day to short-day signal is due to inadequate nocturnal melatonin secretion. The approach was to artificially increase, to adult levels, the low nighttime rises of melatonin during the early postnatal period. Eight female lambs served as controls; they were raised on short days until 17 wk of age, and then exposed to 5 wk of long days, after which they were returned to short days. This alternating sequence of photoperiods during mid-development would be expected to induce normal puberty. Sixteen experimental females were exposed to the critical block of long days much earlier; they were placed in long days between 2 and 7 wk of age and in short days thereafter. Half (n = 8) received no further treatment. The other half (n = 8) were infused nightly with melatonin during the 8-h dark phase of the 5-wk, long-day photoperiod. This increased the amplitude of the natural nighttime melatonin rises 3- to 4-fold, well into the adult range.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1989

Small penis and the male sexual role.

We interviewed and examined 20 patients with the primary diagnosis of micropenis in infancy. The patients were divided into 2 groups: 8 prepubertal (10 to 13 years old) and 12 postpubertal (17 to 43 years old). All but 1 had been given human chorionic gonadotropin, testosterone or cortisone during childhood. Only 1 child in the prepubertal group had a stretched penile length above the 10th percentile. All postpubertal patients were below the 10th percentile. Puberty was delayed in only 2 patients in the older group. All patients were heterosexual and they had erections and orgasms. Eleven patients had ejaculations, 9 were sexually active and reported vaginal penetration, 7 were married or cohabiting and 1 had fathered a child.

Adaptation, Psychological↗
PubMed1993

Long-term complications following bone marrow transplantation in children.

Seventeen children who underwent bone marrow transplantation (BMT) between 1975 and 1985 and survived for more than 2 years were evaluated for growth and development. The patients had a follow up of 2.1-13.1 years. Prior to transplant, children with malignancy had received multi-agent chemotherapy and nine had also received central nervous system irradiation. Transplant preparation for malignancy (group 1; n = 13) included high-dose cyclophosphamide (CPA) 120-200 mg/kg and total body irradiation (TBI) 10-13.2 Gy, whereas conditioning for non-malignant disorders (group 2; n = 4) included high-dose CPA 200 mg/kg with or without busulphan. Patients in group 1 showed a steady decline in height velocity following initial chemotherapy and cranial irradiation and the decline was even greater following BMT. Growth hormone (GH) deficiency developed in eight of nine children tested, hypergonadotrophic hypogonadism developed in 11 who reached puberty, thyroid hormone abnormalities were encountered in four out of 10 tested and 11 of 13 developed cataracts. Patients in group 2 did not show decline in linear growth rate, thyroid hormone abnormalities or cataracts after BMT. The only child tested had normal GH levels and the two patients who reached puberty showed delayed but complete gonadal recovery. Our data demonstrate that TBI leads to significant late effects on growth and gonadal function. Contrary to previous reports, a high incidence of cataract formation is observed after fractionated TBI. Conditioning regimens TBI should be considered in children undergoing BMT.

Adolescent↗
PubMed1996

[Osteopenia in beta-thalassemia major].

Regular blood transfusions in patients with beta-thalassaemia major lead to secondary hemochromatosis in the majority of cases. As a consequence of chronic iron overload, many endocrinopathies may occur. The most frequent endocrine dysfunction is hypogonadotropic hypogonadism, which is mainly responsible for osteopenia in as much as 80% of thalassemic patients. The frequencies of other endocrine disorders (hypothyroidism, diabetes mellitus and hypoparathyroidism) are lower. We investigated 5 female patients aged 22-25 years for endocrine dysfunction and bone density. All presented with hypogonadotropic hypogonadism and amenorrhea (four primary and one secondary). 4 patients showed absent or delayed pubertal development and short stature (below 10th percentile). In all five, hypogonadism is the most relevant cause of osteopenia as demonstrated by osteodensitometry. Endocrine disorders, especially absent pubertal development, should be detected in good time and treated with hormonal replacement. Established osteopenia is treated hormonally and with vitamin D3 and calcium.

Adult↗
PubMed1994

Delayed somatic growth and pubertal development in human immunodeficiency virus-infected hemophiliac boys: Hemophilia Growth and Development Study.

As part of the Hemophilia Growth and Development Study, we investigated the impact of human immunodeficiency virus (HIV) infection on statural growth, weight gain, and skeletal and sexual maturity in more than 300 boys with moderate to severe hemophilia, of whom 62% were infected with HIV. Age-adjusted height and weight were reduced in the HIV-infected subjects (p < 0.001). However, mean weight for height and triceps skin-fold thickness of the infected-boys closely resembled those of the uninfected group. In HIV-infected boys, height for age was positively related to the CD4+ lymphocyte count when the count was < 200 cells/mm3. Age-adjusted serum testosterone levels did not differ by HIV status, but in the infected participants the mean age-adjusted bone age was significantly reduced (p = 0.038) and the distribution of Tanner stages, adjusted for age, differed significantly (p = 0.003). The probability of advancing one or more Tanner stages in the first study year was significantly slowed in HIV-infected boys more than 14 years of age (p = 0.0003). We conclude that linear growth was significantly impaired in boys with hemophilia and HIV infection, but the wasting of malnutrition was not found. The delays in bone age and pubertal maturation strongly suggest that part of the growth failure seen in acquired immunodeficiency syndrome can be attributed to pubertal delay. We speculate that the lack of demonstrable difference in age-adjusted testosterone concentrations might reflect subtle differences in the pattern of secretion of testosterone or in the concentration of sex-hormone binding globulin.

Adolescent↗
PubMed1994

Management of the short stature due to pubertal delay in boys.

Boys with constitutional pubertal delay who present with decreased growth rate pose diagnostic and therapeutic problems. Ninety-one boys seen after the age of 14 yr for height for age less than -2 SD, growth rate less than 5 cm/yr, and pubertal delay were evaluated. The GH peak after the arginine-insulin stimulation test was less than 10 micrograms/L in 35 of the subjects; these boys differed from the 56 others in having a GH peak of 10 micrograms/L or more, their higher body mass index (-0.27 +/- 0.2 vs. -0.85 +/- 0.1 score; P < 0.05), and lower plasma insulin-like growth factor-I (IGF-I; 1.2 +/- 0.2 vs. 1.8 +/- 0.2 U/mL; P < 0.05). The GH peak correlated negatively with the body mass index (P < 0.01), but not with plasma levels of testosterone and IGF-I or its GH-dependent binding protein (BP-3). At a second GH evaluation, performed with testosterone priming (21 boys; 100 mg testosterone heptylate/15 days, im; four doses) or without (6 boys), 23 patients had increased their GH peak to above 10 micrograms/L, and 4 had not. Three of these were treated with human (h) GH, and a third GH evaluation, performed after full pubertal development, showed a normal GH peak. The growth rate during the year preceding the GH evaluation was 3.8 +/- 0.1 cm (1-7 cm). During the year after the GH evaluation, it was 6.8 +/- 0.3 cm in the 32 patients followed without therapy, 7.3 +/- 0.3 cm in the 25 patients given testosterone (25 mg testosterone heptylate/15 days, im), and 7.3 +/- 1.4 cm in the 3 treated with hGH. Spontaneous growth during the 2 periods was correlated with testicular volume (P < 0.01) and the plasma testosterone level (P < 0.05), but not with the GH peak, plasma IGF-I, or BP-3. The final height (n = 49) was -1.0 +/- 0.1 SD, below target height (-0.4 +/- 0.1 SD; P < 0.0001). It was similar in patients with a GH peak below or equal to or above 10 micrograms/L and in those given or not given testosterone therapy. We conclude that the growth rate of boys with constitutional pubertal delay depends on the testicular volume and plasma testosterone level, but not on the GH peak, plasma IGF-I, or BP-3 levels. Final height is not altered by a transient drop in GH or by low dose testosterone therapy.

Adolescent↗
PubMed1982

The onset of menarche: a late event in pubertal progression to be affected by physical training.

Several studies have shown that involvement in certain sports activities could lead to a significant delay in the onset of menarche. It is here emphasized that the latter constitutes a late pubertal event and that research in kinanthropology should now focus on processes underlying menarche. Some findings indeed suggest an influence of certain physical activities upon the maturation rate of endocrine axes which lead to the onset of the first menses.

Adrenal Glands↗
PubMed1983

Endocrine profiles in pediatric andrology. II. Insulin-dependent diabetic adolescents.

Seventy-five diabetic male and female children and 75 matched controls were classified according to pubertal staging. Blood samples were assayed for gonadotropins and gonadal hormones. The ultimate adult height in diabetic patients was 5 cm less than that of controls. Almost all diabetic children had a retarded bone age. Levels of serum gonadotropins and gonadal hormones did not differ markedly between diabetic and healthy children. The delay in growth and maturation was not due to hormonal failure, but probably to chronic undernutrition of body cells and failure to utilize the amino acids for protein anabolism related to relative insulin deficiency.

Adolescent↗
PubMed1999

Effect of short-term testosterone treatment on leptin concentrations in boys with pubertal delay.

Testosterone administration increases growth hormone (GH) secretion and decreases the plasma leptin concentration in men. We evaluated the effect of increased GH secretion due to short-term testosterone treatment on leptin concentrations. Ten boys aged 14.8 +/- 0.2 (mean +/- SE) years with transient GH deficiency caused by pubertal delay were evaluated before and after (3 months) 4 intramuscular injections of 100 mg testosterone heptylate, given at 15-day intervals. The leptin concentration decreased from 5.4 +/- 1.3 to 3. 6 +/- 1.1 microgram/l (p < 0.001), despite a weight gain of 3.4 +/- 0.5 kg. There were significant increases in body mass index (BMI), from -0.2 +/- 0.5 to 0.2 +/- 0.5 SD, p < 0.005, in GH peak after stimulation test, from 6.3 +/- 0.5 to 21.7 +/- 2.9 microgram/l, p < 0. 0003, in plasma testosterone, from 0.6 +/- 0.1 to 6.5 +/- 1.3 microgram/l, p < 0.001, in insulin-like growth factor-I (IGF-I), from 152 +/- 21 to 330 +/- 30 microgram/l, p < 0.0001, and in IGF-binding protein-3 (IGFBP-3), from 4.2 +/- 0.5 to 5.4 +/- 0.4 mg/l, p < 0.01. But there were no changes in blood glucose (4.7 +/- 0.1 and 4.8 +/- 0.1 mmol/l), or plasma fasting insulin (9.0 +/- 1.2 and 8.1 +/- 1.3 mIU/l). The leptin concentrations were positively correlated with the BMI before (p < 0.03) and after (p < 0.04) testosterone, but not with the GH peak after stimulation, or with plasma testosterone, IGF-I or IGFBP-3. The leptin and insulin concentrations after testosterone treatment were positively correlated (p < 0.04). Thus, short-term testosterone treatment of boys with pubertal delay decreases their leptin concentrations. The lack of correlation with GH secretion or with its changes, despite the dramatic increase in GH secretion, and the lack of change in insulin are additional features suggesting that testosterone increases the leptin concentration mainly by an effect on adipose tissue.

Adolescent↗
PubMed1999

Amenorrhea in the athlete.

Amenorrhea in the athlete is commonly encountered in clinical practice. The work-up of an athlete with amenorrhea should include consideration of all the physiological and pathological conditions that give rise to amenorrhea in any adolescent. Delay or failure to recognize and manage these patients may result in the emergence of athletic triad with potential serious consequences of increased stress fractures, scoliosis, and thin body mass. This article reviews amenorrhea in the adolescent athlete with respect to body composition, disordered eating, osteoporosis, psychological factors, warning signs, treatment, and outcomes. Need for further strategies specific to prevention, surveillance, research, health consequences, medical care, and public and professional education is addressed.

Adolescent↗
PubMed1987

Treatment of short stature and delayed adolescence.

The treatment of growth failure in children with documented GH deficiency remains the only noncontroversial indication for GH therapy. There are increasing data suggesting that GH may be useful in treating some children with Turner's syndrome and with NVSS. Further studies, however, are necessary to evaluate the long-term efficacy and safety of GH therapy in these children. The treatment of non-GH deficient children whose heights are within two standard deviations of the mean height for age is clearly inappropriate and should be avoided, despite parental protests.

Adolescent↗
PubMedDate not supplied

[The HLA system antigens in delayed sexual development].

Frequency distribution of HLA antigens of A and B loci was examined in 138 adolescent boys aged 14-18 with delayed sexual development (DSD) of stages I-III, residing in the north-eastern region of Ukraine. Increase of A28- and B40-antigens and haplotypes A1-B40, A28-B40, A10-B40 determination frequencies was established. There were revealed positive and negative correlation between some of HLA antigens and DSD. Relative and attributive risks of DSD formation were calculated.

Adolescent↗