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PubMed1980

Treatment of anorchia with oral testosterone undecanoate: pharmacodynamics and clinical effectiveness.

The pharmacodynamics of plasma testosterone (T) and androstenedione (A) levels were studied in ten hypogonadal boys after oral administration of testosterone undecanoate (TU). Plasma T and A levels were measured by specific radioimmunoassays. Six hours after a single dose of 120 mg TU, there was a significant increase (P < 0.005) in plasma T and A with a median T peak level of 940 ng/100 ml. Furthermore, twelve agonadal boys treated with a mean dose of 60 mg TU/day were examined over a period of 18-24 months. During this therapy, plasma T and A levels were significantly higher than before (P < 0.005), whereas plasma levels of LH and FSH did not decrease significantly. With the exception of one anorchic boy, all patients showed signs of sexual maturation, such as growth of pubic and axillary hair, and steady development of bone age during oral TU treatment.

Administration, Oral↗
PubMed2004

Effect of long-term L-thyroxine treatment on bone mineral density in young adults with congenital hypothyroidism.

OBJECTIVE: To evaluate whether long-term L-thyroxine therapy in young adults with congenital hypothyroidism may affect bone mineral density (BMD). DESIGN: Thirty-seven subjects with congenital hypothyroidism, detected by neonatal screening and longitudinally followed from the time of diagnosis and treatment (26+/-4 days) up to the age of 17.8+/-1.0 years, were studied. METHODS: Spinal (L2-L4) BMD, measured by dual-energy X-ray densitometry, and bone quality, measured as amplitude-dependent speed of sound (Ad-SoS) by quantitative ultrasound, were evaluated. RESULTS: Z-score mean values (+/-s.d.) of BMD (-0.3+/-0.7) and Ad-SoS (-0.7+/-1. 1) were slightly below the average but within the normal range. Ad-SoS resulted in a z-score below -1 in 38% of patients as compared with BMD which resulted in a z-score below -1 in only 13.5% of subject. No significant differences were observed between males (BMD, -0.3+/-0.7; Ad-SoS, -0.9+/-1.0) and females (BMD, -0.3+/-0.7; Ad-SoS, -0.5+/-1.2) or when dividing patients on the basis of aetiological defects; ectopic gland (BMD, -0.3+/-0.6; Ad-SoS, -0.8+/-0.9), athyreosis (BMD, -0.3+/-0.9; Ad-SoS, -0.8+/-1.0) and eutopic gland (BMD, -0.3+/-0.8; Ad-SoS, -0.4+/-1.3). No significant relationships were observed between BMD or Ad-SoS z-score and hormonal status or L-thyroxine dosages at the time of the study or during the pubertal period. CONCLUSIONS: The careful monitoring of serum thyroid-stimulating hormone and adjustment of l-thyroxine dosage avoided the significant deleterious effects of prolonged L-thyroxine replacement therapy on bone tissue in adolescents and young adults with congenital hypothyroidism treated from the neonatal period.

Absorptiometry, Photon↗
PubMed1985

Photoperiodic regulation of reproductive development in male white-footed mice (Peromyscus leucopus) born at different phases of the breeding season.

Male white-footed mice were maintained from birth in chambers equipped with latitudinal timers programmed to simulate the natural progression of daylengths at 42 degrees N latitude. Mice were born into photoperiods starting on 1 April, 15 July, 15 September or 27 October. Testes and seminal vesicles of April- and July-born mice were mature at 60 days of age; puberty was delayed by several months in animals born into the September and October photoperiods but these mice became fecund at about 3.5 months of age, independent of current photoperiod. Therefore, increasing daylengths of late winter do not appear to synchronize the reproductive development of overwintering juveniles born at different times during the previous breeding season.

Animals↗
PubMed1990

Effects of treatment of male and female rats in infancy with mifepristone on reproductive function in adulthood.

Treatment of neonatal male and female rats with mifepristone (1 mg s.c. every 2 days from Day 1 to 15 or Day 4 to 18 of life) interfered with the normal development of their reproductive capacities and of the adrenal glands. The effect on the adrenal glands seemed only temporary. Effects on reproductive functions seemed permanent. Female rats developed abnormalities in structure of the oviduct and ovarian capsule reminiscent of effects reported after perinatal treatment with androgen or oestrogen. During adulthood, anovulatory polyfollicular ovaries developed, reminiscent of rats treated with a small dose of androgen in infancy. Males showed retardation of testicular growth and delay of puberty. During adulthood testes did not grow beyond 65% that of normal rats. Sexual behaviour was deficient in that ejaculations occurred only rarely; when ejaculations did occur, fertility was unimpaired. Males treated with mifepristone in infancy exhibited female sexual behaviour as adults after castration and injections of testosterone and oestradiol. All effects pointed to an insufficient action of testicular hormones in infancy to bring about normal 'masculinization'. Mifepristone therefore appears to show 'teratogenic' actions in rats which affect female reproductive tract development and, in males and females, development of the systems underlying normal reproductive activity and functions in adulthood.

Adrenal Glands↗
PubMed1999

Pregnancy in female house mice exposed to urinary chemosignals from other females.

Seven experiments were performed to investigate pregnancy termination, urinary chemosignals, and litter sex ratio variation in female house mice. Experiments tested the effects of urine from adult and prepubertal females, housed individually or in groups, on successful insemination and litter production by females treated at different times and for different periods during the 3 weeks before mating and during gestation. Treatment of females with urine from adult females housed eight per cage or with urine pooled from eight adult females housed individually for 2 or 3 weeks before mating resulted in fewer successful pregnancies and significantly more female-biased litters. Treatment with urine from adult or prepubertal females housed eight per cage or with urine pooled from eight mice housed individually for the first 6 days of gestation or throughout pregnancy resulted in a significant increase in the rate of pregnancy termination. These treatments resulted in lower body weights at birth and slower growth rates in all males and in some females. Puberty was delayed in female progeny from urine-treated dams in five of seven experiments, and these young females attained first oestrus at greater mean body weights than mice in other treatments. These findings indicate that, in mice, at high population density, communication via a urinary chemosignal can alter reproduction in recipient females. Availability of, and competition for, resources such as food would be greater at higher densities, possibly lowering the probability of reproductive success. Pregnancy termination and delays in reproduction and attainment of sexual maturity might lead to greater successful reproduction at a later time.

Animals↗
PubMed2000

IGF-I stimulation of luteinizing hormone secretion, IGF-binding proteins (IGFBPs) and expression of mRNAs for IGFs, IGF receptors and IGFBPs in the ovine pituitary gland.

Circulating concentrations of insulin-like growth factor-I (IGF-I) are reduced in juvenile sheep during nutritional growth restriction and the associated delay in puberty. Since exogenous IGF-I has been shown to stimulate luteinizing hormone (LH) secretion, it is postulated that endogenous IGF-I may act as a stimulatory metabolic signal to the pubertal ovine hypothalamo-pituitary axis, yet its site of action is unknown. Using coronal hypothalamic and pituitary sections from pubertal ewe lambs, in vitro autoradiography was used to localise 125I-labelled IGF-I binding, and gene expression for components of the IGF system was localised by in situ hybridisation using oligonucleotide probes. High concentrations of 125I-IGF-I binding were seen in the pars tuberalis (PT) and pars distalis (PD) of the pituitary, and relatively little in the hypothalamus; binding in the PT but not the PD was displaced by excess unlabelled IGF-I. Large amounts of mRNA were detected for the type-1 receptor (IGF-1R) and for IGF-binding protein (IGFBP)-5, localised to the PT and PD, and less intense specific hybridisation signals were obtained with mRNAs for IGF-II, type-2 receptor (IGF-2R) and IGFBP-3. There was some evidence for specific hybridisation to IGFBP-4 mRNA in the PT. IGF-I, IGFBP-1 and IGFBP-2 mRNAs were not detected in PT and PD. None of the genes were expressed in hypothalamic tissue. Western-ligand binding on PD extracts from male castrates revealed by their molecular weights the likely presence of IGFBPs-2, -3, and -5. Finally, cultured PD cells from abattoir-killed sheep were challenged with IGF-I (0.1, 1, 10 or 30 nM) or luteinizing hormone-releasing hormone (LHRH, 10 nM) alone, or both together. Basal LH output was stimulated by 10 nM IGF-I (120+/-11.2%, P>0.05), 30 nM IGF-I (148+/-12.8%, P<0.01), and LHRH alone (200+/-16.1%, P<0.001); there was no additive or subtractive effect of LHRH and IGF-I given together. Thus, an intrapituitary IGF system exists in sheep and the present results are consistent with an endocrine role for IGF-I in nutritional modulation of LH secretion at the level of the pituitary gland.

Analysis of Variance↗
PubMed1998

Sex steroid metabolism and menstrual irregularities in the exercising female. A review.

This article aims to clarify why, and by which mechanisms, exercise may influence the normal menstrual cycle. Therefore, the vast amount of literature on this subject is reviewed and a critical appraisal of the most widespread hypotheses if offered. The strikingly low body mass which frequently accompanies exercise-related menstrual irregularities (ERMI) has led some authors to develop a hypothesis which postulates that a critical percentage of body fat is essential to trigger normal menstruation. The relevance of any reference to anorexia nervosa to support this view lacks consistency: female athletes differ in many ways from patients with anorexia nervosa, not least in their excellent physical status which is essential to deliver first-class performances. ERMI is not identical to the so-called female athlete triad, a complicated pathology that involves ERMI, premature osteoporosis and disordered eating. ERMI itself does not seem to have any substantial pathological effects as long as attention is paid to preventing osteoporosis or stress fractures which may result from prolonged hypo-estrogenaemia. In the female athlete with ERMI who wishes to conceive, the accompanying subfertility may necessitate a response other than a prompt reduction in training intensity, as this is hardly a first choice for any top athlete. During recent years, a number of prospective studies have greatly contributed to our understanding of the complexity of the mechanisms involved in ERMI. Older hypotheses, such as those considering hyperprolactinaemia as the cornerstone of ERMI, have now been firmly rejected. The present hypotheses emphasise the importance of caloric deficiency and limited energy availability, although they still fail to identify the actual mechanism that causes ERMI. There is, however, evidence that ERMI is produced by a disturbance of the hypothalamic gonadotrophin-releasing hormone oscillator. This disturbance is caused by either an insufficient estrogen or progesterone feedback or by an imbalance of local opioid peptide and catecholamine activities mediated by gamma-aminobutyric acid (GABA), corticotrophin-releasing hormone and insulin-like growth factor-1. More recent experiments have also linked ERMI with changes in steroid metabolism, in particular, an increasing activity of catecholestrogens possibly leading to enhanced intracerebral noradrenaline (norepinephrine) levels that may interfere with normal gonadotrophin release. This article demonstrates that the outcome of the many studies of ERMI is characterised by much controversy and numerous methodological flaws. The importance and complexity of some recent findings necessitate a comprehensive study which links older and newer findings within a critical perspective.

Adipose Tissue↗
PubMed1998

Cat eye syndrome with hypogonadotropic hypogonadism.

A 17-year-old male diagnosed as having Cat Eye Syndrome (CES) with hypogonadotropic hypogonadism showed short stature and no development of secondary sex characteristics. Exogeneous gonadotropin replacement therapy combining human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) was started. As a result, the short stature and androgen deficiency were relieved. The critical region of CES was tetrasomy of 22 pter-->q11. Abnormalities of other chromosomes which cause hypogonadotropic hypogonadism may exist, thus further investigation is needed.

Abnormalities, Multiple↗
PubMed1996

Personality development of adolescents with hypogonadotropic hypogonadism.

Hypogonadotropic hypogonadism is a disorder of puberty characterized by absence of spontaneous sexual maturation. 8 male adolescents with this disorder, who were treated with pulsatile GnRH administration, were examined psychologically by means of standardized interviews. Problems were found in the development of independence (specifically relating to own body image and social functioning) and in identity development (particularly on personal characteristics).

Adolescent↗
PubMed1986

Effects of pulsatile injection of GnRH into 6- to 14-wk-old Holstein bulls.

With the goal of hastening puberty, we evaluated the effects of dose of gonadotropin releasing hormone (GnRH) during pulsatile injection on luteinizing hormone (LH) secretion in bulls 6, 10 or 14 wk old, and of pulsatile administration of GnRH every 2 h to bulls from 6 to 12 wk of age on reproductive development. Based on response to the last three of 12 bihourly injections of 20, 200 or 2,000 ng GnRH/kg, only the two higher doses of GnRH induced secretion of LH at 6 wk. At all ages, 200 ng GnRH/kg induced maximal discharges of LH. Based on comparisons between seven treated bulls and their identical twins, bihourly injections of GnRH starting on d 42 elicited discharge of LH for less than or equal to 4 d in progeny of one sire and greater than 28 d but less than 42 d in progeny of another sire. After 14 d of treatment, both elicited and spontaneous discharges of LH were smaller in all treated bulls. Within 2 d after cessation of GnRH injections on d 84, LH discharges were similar in frequency and amplitude in treated and control twins. Testicular and body growth were similar in treated and control bulls, but puberty was delayed (P less than .05) in bulls in which exogenous GnRH suppressed endogenous discharges of LH.

Aging↗
PubMed1984

Induction of male puberty by long-term pulsatile subcutaneous LH-RH therapy.

Prolonged low dose LH-RH treatment was given to induce puberty in a 17.8-year-old male with hypogonadotrophic hypogonadism. The patient had developed panhypopituitarism after transcranial surgery of a craniopharyngioma at the age of 16.8 years. One year after the operation he had no signs of pubertal development and was of short stature. A small portable automatically-timed infusion pump, connected to a subcutaneous (s.c.) catheter, was used for the 328-day-long treatment, which was given in periods of between 16 to 185 days. Twenty micrograms of LH-RH s.c. was given every 90 min. Growth hormone therapy, 8 IU intramuscularly (i.m.) twice weekly, was instituted at the same time. During the prolonged LH-RH treatment the gonadotrophin secretion normalized. The serum concentration of testosterone increased to the normal range of adult males. Rapid pubertal progression occurred with development of pubic hair to adult type and increase in size of the penis. Testicular volume increased from 2 to 12 ml. Nocturnal emissions occurred after 30 weeks of pulsatile LH-RH treatment and sperms were found in the ejaculate after 43 weeks. The height of the patient increased from 162 to 176 cm. Thus, chronic pulsatile low dose LH-RH treatment can induce normal pituitary - gonadal function with pubertal maturation and spermatogenesis in primary male hypogonadotrophic hypogonadism.

Adolescent↗
PubMedDate not supplied

Beta-thalassemia alleles in Aegean region of Turkey: effect on clinical severity of disease.

Beta (beta) globin gene analysis was performed in 54 homozygous beta-thalassemia patients followed up in the Pediatric Hematology Department of Medical School of Ege University. The spectrum of beta-thalassemia alleles and their effect on clinical severity of disease were investigated. Twelve different mutations were determined in our patients. The six most frequent alleles, IVSI-110 (G-A), IVSI-6 (T-C), IVSI-I (G-A), IVSII-745 (C-G), Cd39 (C-T), and FSC8, account for 80.6% of all the disease genes. Eleven percent of the chromosomes could not be identified with the probes used in this study. In 38 patients both of whose beta-thalassemia alleles were identified, the beta-thalassemia alleles were found to be the major determinant of the clinical severity of disease. The clinical progress of disease was also closely related to the degree of iron overload.

Adolescent↗
PubMed1987

Double-stimulation with LH-RH in primary amenorrhea caused by chronic internal hydrocephylus: a case study.

A 19-year-old female patient with primary amenorrhea and pubertas tarda due to chronic internal hydrocephalus presented with normal hormonal findings except for low estradiol and a prepubertal type of reaction in the double-stimulation test with LH-RH. After successful operative treatment with a Spitz-Holter high-pressure valve, the intracranial decompression was promptly followed by pubertal development, she began to menstruate, and the LH-RH double-stimulation test showed an adult pattern of response. The results of the test support the view that a partial deficiency in the secretion of LH-RH is the cause of hypogonadism in such a case.

Adult↗
PubMed2005

A novel mutation (A148V) in the glucose 6-phosphate translocase (SLC37A4) gene in a Korean patient with glycogen storage disease type 1b.

We report a Korean patient with glycogen storage disease type 1b (GSD-1b) whose diagnosis was confirmed by liver biopsy and laboratory results. The patient presented with delay of puberty and short stature on admission and had typical clinical symptoms of GSD as well as chronic neutropenia and inflammatory bowel disease. Mutation analysis of the glucose 6-phosphate translocase 6-phosphate translocase (SLC37A4) gene revealed that the patient was a compound heterozygote of two different mutations including a deletion mutation (c.1042_1043delCT; L348fs) and a missense mutation (A148V). The L348fs mutation was inherited from the patient's father and has been reported in an Italian family with GSD-1b, while the A148V mutation was transmitted from the patient's mother and was a novel mutation. To the best of our knowledge, this is the first report of genetically confirmed case of GSD-1b in Korean.

Antiporters↗