Hypopituitarism and the CHARGE association.
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Child↗
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Results for “Puberty, Delayed”
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Physiologic testosterone or estradiol induction of puberty increases plasma somatomedin-C.
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Adolescent↗
Identical twins discordant for the "rudimentary testes" syndrome.
A 20-year-old man was found to have rudimentary testes, microphallus and minimal evidence of sexual maturation, along with low serum testosterone and high serum gonadotropin levels, consistent with the syndrome of rudimentary testes and microphallus. His identical twin brother was unaffected, confirming that this unusual congenital disorder does not have a genetic basis in all cases.
Adult↗
Gluten-sensitive enteropathy in childhood.
Genetic and environmental factors (breast feeding, probably viral infections) play a role in the expression of the disease. Prevalence of GSE in childhood did not substantially decrease in the last 15 years in all European countries, where GSE is still more common in infantile age and presents frequently gastrointestinal symptoms. A decrease has been reported in childhood in several United Kingdom areas and in Finland, where the clinical presentation is changing, shifting upward with age and coming closer to the adult type of the disease. The following clinical problems have been reported in the recent literature: enamel hypoplasia; monosymptomatic short stature; arthritis and other immunologic diseases; association with diabetes, atopy, Iga deficiency, and probably Down's syndrome. Delay in puberty and other peculiar problems of the disease have been described in adolescents. Tests assessing the permeability of the small intestine and the blood levels of antigliadin antibodies have recently gained success as noninvasive tools for the diagnosis of the GSE. The gluten should be withdrawn from the diet and the challenge with gluten should be performed not before 12 months of gluten-free diet with an accurate timing of the biopsy on the basis of the antigliadin and antireticulin antibodies, to avoid clinical and growth damage. Celiac children do require a permanent gluten-free (and not poor) diet. In reality, too many celiac adolescents are off-diet.
Adolescent↗
Androgen and progestagen effects on plasma lipids.
Androgens are 19-carbon steroid rings. Progestagens include both 19-carbon and 21-carbon steroid rings; the 19-carbon progestagens are generally more androgenic than are the 21-carbon compounds. Both androgens and progestagens are physiological regulators of plasma lipids, particularly high-density lipoprotein (HDL) cholesterol. The structure of a particular hormonal preparation, as well as its route of administration, modulates its regulatory effects. Both endogenous and exogenous androgens have a suppressive effect on HDL cholesterol in males, with little effect on other plasma lipoproteins. Oral and nonaromatizable androgens have a greater suppressive effect on HDL cholesterol, particularly on HDL2, than do aromatizable androgens. Cross-sectional studies in males generally show a positive relationship between serum T and plasma HDL levels; data in females suggest an inverse relationship between androgens and HDL cholesterol. Medroxy-progesterone acetate and related progestagens have a mild suppressive effect on plasma HDL levels. The C-19 compounds have a greater suppressive effect on HDL cholesterol and the HDL2 density subfraction.
Aging↗
Plasma prolactin concentration in gilts reared in confinement.
Plasma prolactin concentrations were determined in confinement-reared gilts, which were subsequently exposed to boars and/or relocated to pasture lots. At an average age of 181 days, an indwelling vascular cannula was surgically implanted, and 28 gilts were assigned randomly to either control (remained in confinement) or treatment (relocated to pasture) groups. Nine of the gilts in each group were exposed to a mature boar twice daily. Furthermore, the experiment was divided between April (n=17 gilts) and September (11 gilts). Blood samples were drawn at the time of surgical implantation and twice daily thereafter. Plasma concentrations of prolactin were quantified by validated radio-immunoassay procedures. Samples which were collected at surgery had significantly more prolactin than post-surgical samples in 25 of 28 gilts. The overall average for the post-surgical concentration of prolactin was 2.7 ng/ml, and there was no effect of continued confinement versus relocation to pasture lots. There was a tendency for boar exposure to reduce prolactin levels in relocated gilts but not in control gilts. There was also a tendency for plasma prolactin to be greater in September than in April, especially in control gilts. Overall these results indicate that plasma prolactin levels do not reflect the delay of puberty in confinement-reared gilts or the induction of puberty caused by relocation to pasture lots.
Journal Article↗
Growth and development: physical, mental, and social aspects.
This article details normal adolescent growth and development, including Tanner staging. Problems of abnormal adolescent growth and development are also discussed, along with treatment of short stature. Tables and graphs outlining these topics are included.
Adolescent↗
Role of hormones in puberty.
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Adolescent↗
Role of hormones in puberty.
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Body Height↗
Does growth hormone cause relapse of brain tumours?
Tumour relapse rates in 14 patients with medulloblastoma, 8 with glioma, 2 with ependymoma, 6 with leukaemia, and 1 with T-cell lymphoma who received growth hormone (GH) treatment for growth failure secondary to cranial irradiation were compared with rates among patients treated with radical radiotherapy for the same types of tumour. Five relapses (in 5 patients) occurred (1 optic nerve glioma, 2 medulloblastomas, and 2 ependymomas), three during and two after completion of GH treatment. Patients with medulloblastoma and ependymoma who relapsed were older at tumour diagnosis, underweight at the start of GH therapy, and entered puberty later than similar relapse-free patients. The late relapse rate of medulloblastoma and glioma was unaltered by GH therapy. Ependymoma carries a poor prognosis, and of the 4 late survivors, the 2 who received GH relapsed. No leukaemic relapse has been associated with GH treatment. The findings indicate that GH therapy does not increase the relapse rate of medulloblastoma, glioma, and leukaemia.
Adolescent↗
Effects of pubertal timing on EEG coherence and P3 latency.
Neurodevelopmental approaches to schizophrenia emphasise the role of late brain maturational events. Abnormalities here may account for both the putative cortico-cortical underconnectivity in schizophrenia and its typical onset in late adolescence. Saugstad hypothesised that maturational rate at puberty may lead to an extension of normal maturational processes such as synaptic pruning. In extreme late maturers pruning was thought to be prolonged, leading to reduced numbers of synapses and an increased risk for schizophrenia. Here we assessed the effects of pubertal timing extremes on EEG coherence and P3 latency as putative measures of brain development in N = 37 healthy adults. During photic stimulation late maturing males showed increased left-hemispheric coherence compared with male early maturers. This was in line with earlier findings (Kaiser, J., Gruzelier, J.H., 1996. Timing of puberty and EEG coherence during photic stimulation. Int. J. Psychophysiol. 21, 135-149). As expected, P3 latency was shorter in late compared with early maturers. However, this was true only for females, whereas there was no difference in males. These results are consistent with the notion of an exaggeration of normal maturational changes in slow maturation, whereby the underlying process appears to be different for males and females.
Adult↗
Timing of puberty and syndromes of schizotypy: a replication.
The view of schizophrenia as a neurodevelopmental disorder involving an abnormality in the programmed elimination of excitatory synapses during puberty has been supported by recent neuroimaging studies suggesting disordered functional connectivity in schizophrenia. We investigated a model predicting dysfunctionally high or low synaptic density in extreme early or late maturers at puberty, respectively (Saugstad, L.F., 1989. Clin. Genet. 36, 156-167; Saugstad, L.F., 1994. Int. J. Psychophysiol. 18, 189-203). In an earlier study (Gruzelier, J.H., Kaiser, J., 1996. Schizophr. Res. 21, 183-194), we found increased psychosis proneness scores in both extremes of the pubertal timing spectrum in the normal population. Here we present a replication study where N = 100 healthy adults completed a retrospective pubertal timing scale and the 'Personality Syndrome Questionnaire' measuring schizotypy syndromes. The following relationships were replicated: (1) elevated scores on scales of the total Unreality syndrome and the Ideas of Reference subscale in both maturation extremes; and (2) a trend for a positive correlation between the Withdrawal scale and the composite maturation score in males. Cognitive Unreality and Suspiciousness were higher in early than late maturing females. Social Anxiety was elevated in female extreme maturers compared with average maturers, but the opposite was found for males, where average maturers had higher scores than early or late maturers. Active syndrome findings were confined to the male subsample with late maturing males showing higher scores on the Cognitive Failures and Odd Speech subscales than early maturers. As in the previous study, there was no relationship between a global psychosis proneness scale and maturational rate. These findings support a neurodevelopmental model of psychosis-proneness and show the importance of adopting a syndromal view.
Adult↗
Central administration of an antisense oligodeoxynucleotide against type I pituitary adenylate cyclase-activating polypeptide receptor suppresses synthetic activities of LHRH-LH axis during the pubertal process.
Central administration of an antisense oligodeoxynucleotide against type I pituitary adenylate cyclase-activating polypeptide receptor suppresses synthetic activities of LHRH-LH axis during the pubertal process In the present study, we determined the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) and PACAP receptor type I (PAC1) genes during juvenile development and the pubertal process. Female rats were assigned--based on uterine weights, the presence and abundance of uterine fluid, and their vaginal patency--to one of the following: anestrus (AE), early proestrus (EP), late proestrus (LP) or first estrus (E). The hypothalami from 22-, 24- and 26-day-old animals and from those in the peripubertal phases of AE, EP, LP and E were collected, and the content of PACAP and PAC1 mRNA was assessed. These levels were found to decrease in EP and LP. To determine the effect of PACAP on prepubertal luteinizing hormone-releasing hormone (LHRH) and LH synthesis through PAC1, a PAC1 antisense oligodeoxynucleotide (ODN) was i.c.v.-administered, and mRNA levels of LHRH, LH beta, and LHRH receptor (LHRH-R) were determined. Prepubertal increases in LHRH, LH beta, and LHRH-R mRNA levels were markedly suppressed, and the onset of puberty was delayed by the i.c.v. injection of the antisense PAC1 ODN. These data suggest that PACAP may play a role in the regulation of hypothalamic LHRH neurons, through which it regulates synthetic machinery of pituitary LH, during the pubertal process.
Animals↗
Diabetes mellitus and its effects on menarche.
In a combined mail and medical record survey of 121 non-diabetic and 90 diabetic girls greater than or equal to 9 years of age, the mean age of menarche in the control non-diabetic population was 13.0 +/- 1.2 years and 13.4 +/- 1.2 years in the diabetics. The diabetic group was divided into those whose onset was before or after age 11 years (DM less than 11, DM greater than or equal to 11). The DM greater than or equal to 11 group had a mean menarchal age of 14.0 +/- 1.2 years and the DM less than 11 group, 13.1 +/- 1.2 (p less than 0.005). The DM greater than or equal to 11 group also differed significantly from the control group. The difference between the two groups suggests that the onset of diabetes near the onset of puberty may have a more disruptive effect on hypothalamic-pituitary-gonadal axis maturation that does the prepubertal onset of diabetes.
Adolescent↗
Enzyme therapy for Gaucher disease: the first 5 years.
Gaucher disease was first described by Philippe Gaucher in his 1882 medical thesis. Gaucher's original concept was of an unusual epithelioma of the spleen. By the early 1900s, Mandelbaum recognized the systemic nature of the disease. Several children with Gaucher disease were described at the turn of the century, but Rusca described a rapidly progressive fatal neurodegenerative type of disease, i.e. type 2, in the 1920s. The 'juvenile' form (type 3) of the disease was described in Sweden in the 1950s. In 1965, the deficient enzyme, acid beta-glucosidase, was discovered and the lysosomal nature of the disease was elucidated. Currently, three variants of Gaucher disease have been defined clinically and are distinguished by the presence and severity of neuronopathic involvement (Table 1). Each of these clinical types has substantial phenotypic variation, but types 1 and 3 have significantly heterogeneous rates of disease progression and degrees of visceral organs involvement. The neuronopathic involvement in type 3 also has substantial variation in the age of onset and disease progression even within relatively isolated communities. An extensive review of the clinical and pathologic involvement by Gaucher disease is available.
Animals↗
Late effects in children treated with radiation therapy for Wilms' tumor.
PURPOSE: To determine the frequency and types of late effects in children receiving radiation therapy (RT) for Wilms' tumor. MATERIALS AND METHODS: From 1968 to 1994, 55 children received megavoltage RT at our institution as part of treatment for Wilms' tumor. A total of 42 (76.4%) have survived and have a minimum follow-up of 5 years. There were 25 female and 17 male patients with a median age at diagnosis of 48 months (range, 7-126 months). There were 12 Stage I, eight Stage II, 15 Stage III, six Stage IV, and one Stage V patient. RT was delivered to the hemiabdomen in 36 and whole abdomen in six patients. RT dose was 1000-1200 cGy (Group A) in 12, 1201-2399 cGy (Group B) in 11, and 2400-4000 cGy (Group C) in 19. Whole-lung RT was delivered to 13 patients either at diagnosis or pulmonary relapse. All patients received chemotherapy; the most common agents were actinomycin-D/vincristine/adriamycin in 13 and actinomycin-D/vincristine in 18. Median follow-up was 181 months (range, 60-306 months). RESULTS: Of 42 patients, 13 (31.0%) did not have late effects of treatment. The number of patients who developed muscular hypoplasia, limb length inequality, kyphosis, and iliac wing hypoplasia were seven (16.7%), five (11.9%), three (7.1%), and three (7.1%), respectively. Scoliosis was seen in 18 (42.9%) with only one patient requiring orthopedic intervention. Median time to development of scoliosis was 102 months, with a range of 16-146 months. The actuarial incidence of scoliosis at 5, 10, and 15 years after RT was 4.8 +/- 3.3%, 51.8 +/- 9.0%, and 56.7 +/- 9.3%, respectively. Only one of 12 Group A patients developed scoliosis. The 10- and 15-year actuarial incidences of scoliosis for Group A and B patients were 37.7 +/- 12.4% and 37.7 +/- 12.4%, whereas for Group C patients the incidences were 65.8 +/- 12.0% and 74.4 +/- 11. 7% (p = 0.03, log rank test). The actuarial incidence of bowel obstruction at 5, 10, and 15 years was 9.5 +/- 4.5%, 13.0 +/- 5.6%, and 17.0 +/- 6.5%. Of 23 patients, five irradiated within 10 days of surgery and one of 19 irradiated after 10 days developed bowel obstruction (p = 0.09, log rank test). Three patients developed hypertension with normal blood urea nitrogen (BUN) and creatinine levels; another patient had chronic renal insufficiency in a nonirradiated kidney. One patient developed diffuse interstitial pneumonitis. Of the 19 female patients who have reached puberty, three have given birth, and 15 have regular and one has irregular menstrual periods. Four patients developed benign neoplasms; three were in the RT field (two osteochondroma, one lipoma) and one outside (cervical intraepithelial neoplasia II). There were three second malignancies (chronic myelogenous leukemia at 9 years, osteosarcoma at 11 years, and breast cancer at 25 years after initial diagnosis of nephroblastoma); both solid malignancies occurred in the RT field. CONCLUSIONS: Late effects of therapy were seen in more than two thirds of children treated for Wilms' tumor. Children treated with lower doses (<2400 cGy) had a lower incidence of scoliosis compared with those who received more than 2400 cGy. There is also a suggestion that the incidence is lower in patients who received 1000-1200 cGy. Severe physical and functional deformity from RT was uncommon.
Child↗
Assessment of pubertal development in juvenile male rats after sub-acute exposure to bisphenol A and nonylphenol.
The effects of bisphenol A and nonylphenol on pubertal development in the intact juvenile/peripubertal male Sprague-Dawley rats was observed in this study from PND23-52/53. Two groups of rats were administered orally with either 100 mg/kg body weight of nonylphenol or bisphenol A. Another group of rats were administered orally with a mixture of 100 mg/kg body weight of nonylphenol and bisphenol A. Control group was administered with the vehicle of Tween-80 with corn oil (1:9 v/v). Observations made in this study included growth, age at preputial separation, thyroid, liver, testis and kidney weight and histology, epididymal and seminal vesicle plus coagulation gland weight. Nonylphenol and bisphenol A have been observed to cause delay in puberty onset as well as testicular damage in the treatment groups when compared to the control; spermatogenesis was affected in most treated rats. Bisphenol A also caused the enlargement of the kidney and hydronephrosis. Administration of nonylphenol and bisphenol A as a mixture has caused less than additive effects.
Animals↗
mtDNA nt3243 mutation, external ophthalmoplegia, and hypogonadism in an adolescent girl.
A 14-year-old girl presented with a 3-month history of easy fatigue and exercise intolerance, especially when climbing stairs. She had a mild ptosis and mild limitation of upward gaze. Her puberty was delayed, and she manifested hypogonadotrophic hypogonadism. Serum lactic and pyruvic acids were elevated. Cranial magnetic resonance imaging was normal. Muscle biopsy documented typical ragged-red fibers. A point mutation at nucleotide 3243 in the tRNALeu(UUR) (typical mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) mutation) was detected in mitochondrial DNA from both blood and muscle tissues, indicating that our patient was suffering from a mitochondrial myopathy. Hypogonadism may be a manifestation of the MELAS nucleotide 3243 mutation.
Adolescent↗