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PubMed1995

Primary empty sella: differences and similarities between children and adults.

To identify possible differences between empty sella in children and adults we studied 43 subjects (age 13.6 +/- 5.4 years, range 4.1-27 years) with hypothalamic-pituitary disorders and empty sella at magnetic resonance imaging. Pituitary function, presence of non-endocrine symptoms, perinatal history, sellar volume, pituitary height, midline or intrasellar anatomical abnormalities were evaluated. Twenty subjects had isolated growth hormone deficiency, 17 multiple pituitary hormone deficiency and 6 puberty disorders (3 precocious puberty, 2 idiopathic delayed puberty, 1 Kallmann syndrome). The group with multiple pituitary hormone deficiency had a higher percentage of subjects with complete empty sella, i.e. pituitary height < 2 mm (p = 0.016), or intrasellar anatomical abnormalities (p = 0.0002) than the other groups. The subjects with puberty disorders had a mean sellar volume higher than the other groups (p < 0.05). Apart from pituitary dysfunction, symptoms of the empty sella syndrome were infrequent (9.3% of cases) in our subjects. The age of our subjects, the frequent association between empty sella and pituitary dwarfism and the non-enlarged sellae suggest a different aetiology, perhaps congenital, for empty sella in our subjects. As in adults, empty sella may be associated with both pituitary hypo- and hyperfunction.

Adolescent↗

PubMed2006

Treatment with the aromatase inhibitor letrozole during adolescence increases near-final height in boys with constitutional delay of puberty.

OBJECTIVE: We investigated whether inhibition of oestrogen biosynthesis with the aromatase inhibitor, letrozole, during adolescence improves near-final height in boys with constitutional delay of puberty. PATIENTS AND METHODS: Seventeen boys with constitutional delay of puberty were randomized to receive testosterone (T) enanthate (1 mg/kg i.m.) every 4 weeks for 6 months in combination with placebo (Pl, n = 8), or the aromatase inhibitor letrozole (Lz, 2.5 mg/day orally) (n = 9), for 12 months. After treatment, patients were followed up until near-final height. Height discrepancy was calculated as near-final height minus mid-parental target height. MEASUREMENTS: The primary end point was the difference in near-final height between the groups treated either with T + Pl or T + Lz. Secondarily, height discrepancy and gain in height standard deviation score (SDS) were analysed in both groups. RESULTS: Boys treated with T + Lz reached a higher mean near-final height than did boys on T + Pl (175.8 vs. 169.1 cm, respectively, P = 0.04). In T + Lz-treated boys, mean near-final height did not differ from their mid-parental target height (175.8 vs. 177.1 cm, P = 0.38), whereas in T + Pl-treated boys, mean near-final height was lower than mid-parental target height (169.1 vs. 173.9 cm, P = 0.007). T + Lz-treated boys had a greater increment in height SDS over the pretreatment height SDS than T + Pl-treated boys (+1.4 SDS vs.+0.8 SDS, P = 0.03). CONCLUSIONS: Our findings indicate that in adolescent boys an increase in adult height can be attained by use of aromatase inhibitors.

Adolescent↗

PubMedDate not supplied

A practical GnRH analogue (triptorelin) stimulation test to distinguish constitutional delay of puberty from hypogonadotropic hypogonadism in prepubertal boys.

At present, no established practical and reliable endocrine test exists for differentiating between constitutional delay of puberty (CDP) and hypogonadotropic hypogonadism (HH). The most discriminating results have been reported by measuring LH and testosterone (T) responses to gonadotropin-releasing hormone (GnRH) analogues. In this study, 23 prepubertal boys aged 14 to 16.5 years underwent a modified triptorelin (a GnRH analogue) stimulation test, and they were followed clinically for up 24 to months. Sixteen subjects developed spontaneous puberty during the follow-up period and thus were diagnosed with CDP, and the remaining seven were diagnosed with HH. Retrospective evaluation of their LH, FSH and T responses revealed significant differences without any overlaps in serum LH levels at 4 h (CDP: 33.2 +/- 9.3 vs. HH: 3.3 +/- 2.6 mIU/ml, p < 0.0002) and in serum T levels at 24 h (CDP: 369.3 +/- 128.1 vs. HH: 61.4 +/- 22.6 ng/dl p < 0.0002). We conclude that CDP can be clearly differentiated from HH by the LH response at 4 h and/or T response at 24 h after a single-dose triptorelin administration.

Adolescent↗

PubMed1985

Differentiation of male hypogonadotropic hypogonadism and constitutional delay of puberty by pulsatile administration of gonadotropin-releasing hormone.

It is not possible to differentiate reliably between male idiopathic hypothalamic hypogonadism (HH) and severe constitutional delay of puberty (CD) on the basis of a standard GnRH bolus test (GBT) or other known endocrine or clinical parameters. Therefore, we studied the response of 17 hypogonadal men, 8 with a diagnosis of HH (age, 15.5-41; bone age, 12.5-19 yr; testes, 1-4 ml) and 9 with CD (age, 14.5-20; bone age, 11-15 yr, testes, 2-10 ml) to pulsatile GnRH stimulation. Basal and peak LH and FSH levels after a single dose of GnRH greatly overlapped between the two groups. In each patient, a spontaneous nocturnal plasma profile of LH and FSH, sampled every 20 min, was followed by a pulsatile GnRH stimulation (5 micrograms iv every 90 min) via a portable minipump for 36 h. Before and after this pulsatile GnRH stimulation, a GBT (60 micrograms/m2 iv) was performed and plasma LH, FSH, testosterone, androstenedione, and dehydroepiandrosterone sulfate were measured. Pulse analysis revealed 0-5 spontaneous nocturnal LH peaks in the CD patients but only one in all of the HH patients. During the 36 h of pulsatile GnRH, mean LH and FSH levels were significantly higher (P less than 0.0001) than during the spontaneous nocturnal profile in all patients (except 1 from each group for LH). The GBT after pulsatile stimulation caused significantly higher (P less than 0.001) LH increments in CD than in HH patients, with no overlap between the two groups (range, 4.1-15.6 in CD vs. 0.8-2.4 mIU/ml in HH). Plasma testosterone rose significantly (P less than 0.01) during pulsatile GnRH from 67 to 155 ng/dl (median) in the CD men, but did not change in the HH group (21 to 22.5 ng/dl). Plasma androstenedione and dehydroepiandrosterone sulfate did not rise in either group. We conclude that, in contrast to other parameters investigated so far, the LH increment in the second GBT after 36 h of pulsatile GnRH allows clear-cut differentiation between CD and HH. These results indicate significantly lower pituitary LH reserve in patients with permanent HH after short term priming of the pituitary by pulsatile GnRH administration.

Adult↗

PubMed1995

Short-term effect of testosterone treatment on reduced bone density in boys with constitutional delay of puberty.

We studied bone mineral content (BMC), bone mineral density (BMD), cortical thickness/total width (CT/TW) ratio and cortical area/total area (CA/TA) ratio in boys with constitutional delay of puberty and the effect of short-term testosterone treatment on bone mass. Seventeen boys (age 13.1-15.8 years) who met the family history and the clinical criteria of constitutional delay of puberty were selected and enrolled in the study. All subjects were eating a diet assuring an adequate intake of calories and calcium. A subset of 8 boys (group A) was treated with testosterone depot (100 mg/month x 6 months) while 9 boys (group B) were not. At inclusion, BMC and BMD were reduced in the patients according to their chronological age (BMC -4.04 +/- 1.34 standard deviation scores [SDS]; BMD -2.95 +/- 0.56 SDS), statural age (BMC -1.75 +/- 0.79 SDS; BMD -1.69 +/- 0.78 SDS), and bone age (BMC -1.80 +/- 0.65 SDS; BMD -1.86 +/- 0.68 SDS). No significant differences between the groups were found (group A: BMC 0.480 +/- 0.57 g/cm, BMD 0.488 +/- 0.037 g/cm2, CT/TW ratio 0.43 +/- 0.4, CA/TA ratio 0.68 +/- 0.04; group B: BMC 0.476 +/- 0.060, p = NS vs. group A; BMD 0.491 +/- 0.036 g/cm2, p = NS vs. group A). At 12 months of follow-up, BMC, BMD, CT/TW ratio, and CA/TA ratio significantly increased in group A (BMC 0.70 +/- 0.13 g/cm, delta +41.1 +/- 28.8%, p < 0.003 vs. 0 month; BMD 0.617 +/- 0.082 g/cm2, delta +26.2 +/- 13.6%, p < 0.005 vs. 0 month; CT/TW ratio 0.52 +/- 0.05, delta +20.59 +/- 10.65%, p < 0.001 vs. 0 month; CA/TA ratio 0.77 +/- 0.05 vs. 0 month; CT/TW ratio 13.60 +/- 6.65%, p < 0.004 vs 0 month), but not in group B (BMC: 0.48 +/- 0.05 g/cm; delta +5.1 7.8%, p = NS vs. 00 month; BMD: 0.492 +/- 0.037 g/cm2; delta +0.54 +/- 8.7%, p = NS vs. 0 month; CT/TW ratio 0.44 +/- 0.04, delta +4.04 +/- 6.75%, p = NS vs. 0 month; CA/TA ratio 0.68 +/- 0.05, delta +2.39 +/- 5.90%, p = NS vs. 0 month). We conclude that boys with constitutional delay of puberty have reduced BMC and BMD. The delay in statural and bone ages did not totally account for the decreased bone mass. Testosterone treatment for 6 months significantly increased BMC, BMD, CT/TW ratio, and CA/TA ratio in these patients, but definitive conclusions on the efficacy of the treatment in improving adult bone mass can be drawn only when our patients reach early childhood.

Adolescent↗

PubMed1986

Acceleration and delay of puberty in female mice via urinary chemosignals: age of the urine stimulus.

Five experiments were conducted to test the effects of the age of urine on the acceleration and delay of puberty in female mice resulting from treatment with urinary chemosignals. The chemosignal in the urine of male mice that accelerates female puberty was not affected by remaining exposed to the air at room conditions for up to 7 days, or when dried in air and reconstituted with water. The chemosignal in the urine of grouped female mice that delays puberty in females and the chemosignal present in the urine of pregnant and lactating female mice that accelerates female puberty were affected to varying degrees by exposure to room conditions; at 5-to-7 days of exposure the urine samples lost their capacity to delay or accelerate sexual maturation. These results are in agreement with earlier work indicating that the male chemosignal is not volatile, whereas the substances in urine from grouped females and pregnant or lactating females are more volatile. The results also have implications for interpretations of how the urinary chemosignals may affect the population biology of house mice under natural conditions.

Animals↗

PubMed1994

Predictive value of luteinizing hormone releasing hormone (LHRH) bolus testing before and after 36-hour pulsatile LHRH administration in the differential diagnosis of constitutional delay of puberty and male hypogonadotropic hypogonadism.

Intravenous LHRH bolus testing (100 micrograms) after 36 h of pulsatile LHRH administration (5 micrograms/90 min) preliminary has been reported to allow complete differentiation between constitutional delay of puberty (DP) and hypogonadotropic hypogonadism (HH) in a small group of sexually immature patients. So far, these data have never been confirmed. To assess the discriminatory power of the test, 33 patients with a presumptive diagnosis of either DP (n = 17) or HH (n = 16), confirmed by clinical follow-up, were studied accordingly. Both groups of patients had similar mean basal LH and FSH levels (P > 0.10). The mean basal plasma testosterone level was three times higher in DP than in HH (4.2 +/- 1.0 vs. 1.4 +/- 0.2 nmol/L, P* < 0.001), but there was a wide overlap. In response to the first LHRH bolus test, the mean LH increment was significantly lower in HH than in DP patients (P < 0.001), but, in 44% of the patients, the values overlapped. The FSH increments were similar in HH and DP. Pulsatile LHRH administration for 36 h similarly increased LH levels in HH and DP to values (2.7 +/- 0.4 and 3.8 +/- 0.5, respectively) slightly higher than before (P < 0.01), but again, not statistically significantly different from each other. The mean testosterone levels increased 2-fold in both groups and remained significantly higher in DP than in HH (7.6 +/- 2.1 vs. 2.8 +/- 0.5 nmol/L P* < 0.05). The mean FSH levels after priming also rose, however, to levels significantly higher in HH than in DP (5.2 +/- 0.8 vs. 3.5 +/- 0.4, P* < 0.05). In HH the ratio of FSH to LH almost doubled, whereas it virtually remained unchanged in DP. LHRH bolus testing after LHRH priming evoked a significantly lower LH response in both HH and DP than before priming despite only slightly higher baseline LH values. The LH increment in HH was five times lower in HH than in DP. In any of the 16 HH patients, the LH increment was < or = 3 IU/L, whereas in 15 out of 17 DP patients the increase was higher (sensitivity of the test 100%, specificity 88%, and diagnostic efficiency 94% after LHRH priming against 56%, 94%, and 75% respectively, before LHRH priming.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1991

Pubertal disorders. Psychology and clinical management.

The behavioral data reviewed herein must be viewed with caution. Although there are reports that adhere to rigorous methodology, these are the exception. Most reports do not adequately describe either the methodology used or their sample. Subjects are often of mixed endocrine diagnoses, and sometimes the results are of both boys and girls. All of these pitfalls make interpretation of results difficult and limiting. With this in mind, the following conclusions are offered. The majority of behavioral data on precocious puberty comes from studies of IPP in girls. Cognitively, IPP has been associated with average to high-average intelligence. Purportedly, the finding of lower visual-spatial skills than verbal skills in early maturing boys and girls has received equivocal support by cognitive studies of IPP individuals. Similarly, clear differences in hemispheric lateralization have not been demonstrated. Aside from increased somatic complaints during the nonmenstrual phases of their menstrual cycle, girls with IPP show a spectrum of behavior adjustments. Major psychopathology is rare. Clearly, their early development makes them look older than their actual age, which probably alters the expectations others have for them. Psychosexually, however, IPP girls develop in concert with their chronologic age and social experience, rather than their early biologic maturation. However, recent reports suggest a modest influence of hormones. In summary, these studies support an interactionist theory of human psychosexual development. Research data on IPP girls suggest that they do not significantly differ from girls who are early maturers but within the normal range. Research on these girls indicates that most negotiate their puberty without severe problems. There has been less research on IPP boys because it occurs so rarely. Most of what is understood about precocious puberty in boys comes from boys with precocious puberty secondary to poorly controlled CAH. Behavioral data on individuals with delayed puberty come almost exclusively from boys. Although CD appears to be the most frequently diagnosed form of delayed puberty and does not reflect a known pathologic process, men with CD as well as those with organic disorders appear to be at risk for psychosocial and psychosexual difficulties. These difficulties are not severe forms of psychopathology. Rather, they probably represent problems negotiating the expected adolescent lessons of psychosocial development with a physique that places them at a disadvantage. They clearly look younger than their actual chronologic age. Cognitively, as with the children with precocious puberty, there is no evidence of intellectual impairment associated with delayed puberty.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1976

Effect of synthetic luteinizing hormone-releasing hormone on the release of gonadotropins in hypophysogonadal disorders of children and adolscents. VII. Constitutional delay of puberty in males.

Serum gonadotropins (LH and FSH) were measured by radioimmunoassay before and after intravenous injection of 0.1 mg/m2 of synthetic luteinizing hormone-releasing hormone in 20 male patients, aged 15 to 18 years, with constitutional delay of puberty. Basal plasma levels of LH and FSH were in the prepubertal range. After administration of LH-RH, the increase in LH was significantly high than in prepubertal control subjects, aged 1 to 13 years; the difference between test patients and pubertal control subjects was not significant. The increase in FSH was in the prepubertal range, significantly lower than that in pubertal control subjects. This discrepancy between LH and FSH responses to LH-RH is similar to that observed in normal boys at the late prepubertal stage and suggests that an elevation of readily releasable pituitary stores of LH correlates with the first step of pubertal onset in males, even if puberty is delayed.

Adolescent↗

PubMed1986

Effects of restriction of dietary energy intake during the prepubertal period on secretion of luteinizing hormone and responsiveness of the pituitary to luteinizing hormone-releasing hormone in heifers.

The working hypothesis that a low plane of nutrition during the prepubertal period delays puberty in heifers by retarding the prepubertal increase in secretion of luteinizing hormone (LH) was investigated. Secretion of LH and the responsiveness of the pituitary to LH-releasing hormone (LHRH) were compared in heifers fed a growing diet (which allowed spontaneous occurrence of puberty; n = 12; control) or an energy deficient diet (which delayed puberty; n = 11; delayed) during the prepubertal period. The dietary treatments were initiated when the heifers were 299 +/- 14 (mean +/- SD) d of age (d 0 of the experiment) and continued until d 175 of the experiment (474 +/- 14 d of age). Weight gains were .79 +/- .05 (mean +/- SE) and .21 +/- .03 kg X head-1 X d-1 for control and delayed heifers, respectively. Puberty occurred on d 120 +/- 14 of the experiment (428 +/- 13 d of age) in control heifers, whereas none of the delayed heifers attained puberty during the feeding period. Serum concentration of LH and the frequency of LH pulses increased rapidly during the 175-d feeding period in control heifers. In delayed heifers, serum LH concentration increased less rapidly and no increase in pulse frequency was detected during the experimental period. Amplitude of LH pulses tended to be higher in control than delayed heifers. Responsiveness of LH secretion to LHRH was lower in delayed than control heifers. It is speculated that failure of secretion of LH to increase is the causative factor for delayed puberty when dietary energy is limited during the prepubertal period in heifers.

Animals↗

PubMed2002

Novel treatment of delayed male puberty with aromatase inhibitors.

BACKGROUND: As the evidence for the role of oestrogens in epiphyseal closure appears unequivocal, we hypothesized that boys with constitutional delay of puberty would attain greater adult height if oestrogen action was suppressed. METHODS: We conducted a randomized, double-blind, placebo-controlled study in which we treated boys with constitutional delay of puberty with testosterone plus placebo or testosterone plus a potent fourth-generation aromatase inhibitor, letrozole. FINDINGS: Letrozole effectively inhibited oestrogen synthesis. The 17beta-oestradiol concentrations increased in the untreated group and in the testosterone/placebo-treated group, but in the testosterone/letrozole-treated group no such increase was observed until letrozole treatment was discontinued. Testosterone concentrations were threefold higher in the testosterone/letrozole-treated group than in the other groups. Within 18 months, bone age had advanced by 1.1 +/- 0.3 years in the untreated group and by 1.7 +/- 0.3 years in the testosterone/placebo-treated group, but only by 0.9 +/- 0.2 years in the testosterone/letrozole-treated group (p = 0.02 between treatment groups). Predicted adult height did not change significantly in the untreated group and in the testosterone/placebo-treated group, whereas in the testosterone/letrozole-treated group the increase was 5.1 +/- 1.2 cm (p = 0.004). CONCLUSIONS: Our findings suggest that, if oestrogen action is inhibited in growing adolescents, adult height will increase. This observation provides a rationale for studies aimed at delaying bone maturation in several growth disorders.

Adolescent↗

PubMed1990

Environmental factors and age of puberty in female house mice.

Genetics, urinary chemosignals and related social influences, and ambient conditions affect reproduction in female mice. Five experiments tested the effects of environmental stressors on age at first vaginal estrus in female house mice. Environmental disruption in the form of changing the cage bedding and/or nesting material at various prescribed intervals resulted in different degrees of puberty delay relative to non-disrupted control mice. Disruption in the form of a male chasing the female for one to three 15-min intervals each day or the female being trapped and held in a live-trap for one to three 15-min intervals each day resulted in delays in puberty for treatments involving multiple daily disruptions. Food deprivation, but not water deprivation, influenced the onset of puberty. Variations in temperature and humidity resulted in differences in the age of puberty; low but not high temperatures and extremely low humidity levels delayed sexual maturation.

Animals↗

PubMed2003

Craniopharyngioma: presentation and endocrine sequelae in 36 children.

We studied the clinical presentation by age of 36 children with craniopharyngioma, and outcome by height and body mass index (BMI). Presenting symptoms included headache (51.4%), vomiting (31%), visual disturbances (22.9%), polyuria and/or polydipsia (17.1%), delayed puberty (19.4%), short stature (13.8%), and precocious puberty (2.7%). Growth deceleration was overlooked, as was diabetes insipidus (actual rate, 52% for both). Delayed puberty was observed in all patients of appropriate age. Mean height standard deviation score (SDS) at admission was significantly lower than mean target height SDS (p = 0.004), while mean final height SDS was similar (p = 0.14). BMI SDS at last follow-up was similar to mean parental BMI SDS. We conclude that although endocrinopathies are present in most patients with craniopharyngioma, they are rarely the reason for referral. While affected prepubertal children have non-endocrine complaints, most adolescents are referred because of delayed puberty. Diabetes insipidus may be more prevalent in craniopharyngioma than previously reported. When patients with hypothalamic obesity are excluded, mean BMI SDS remains within normal range and is influenced mostly by parental BMI SDS.

Adolescent↗

PubMed1998

Normal volumetric bone mineral density and bone turnover in young men with histories of constitutional delay of puberty.

It has been suggested that an appropriate timing of puberty is necessary for normal bone mineral density (BMD) acquisition, which may not be achievable in children with constitutional delay of puberty (CDP). To assess the effect of pubertal delay on BMD, we measured areal BMD (aBMD) at lumbar spine, by dual-energy x-ray absorptiometry (DEXA), in a group of patients with CDP (n=21; mean age, 21.8+/-1.7 yr) at final height and in healthy controls (n=12; mean age, 19.3+/-1.3 yr). A subset of seven patients (group a) were untreated, whereas six subjects (group b) had received im testosterone depot (100 mg/month, for 6-12 months) and 8 boys (group c) oral oxandrolone (1.25-2.5 mg/daily, for 6-28 months) for their pubertal delay. Volumetric BMD (vBMD) was calculated from DEXA measurements. aBMD was reduced in patients with CDP (1.101+/-0.134 g/cm2), in comparison with controls (1.222+/-0.091 g/cm2; P < 0.009); no significant differences were found among the groups (group a, 1.089+/-0.133 g/cm2; group b, 1.111+/-0.118 g/cm2; group c, 1.103+/-0.160 g/cm2). vBMD was not significantly different in patients with CDP (0.327+/-0.021 g/cm3) and in controls (0.337+/-0.017 g/cm3; P= not significant); no significant differences were found among the groups (group a, 0.326+/-0.016 g/cm3; group b, 0.332+/-0.022 g/cm3; group c, 0.330+/-0.021 g/cm3). No differences were found in mineral metabolism and in bone markers between patients and controls; patients did not report an increased fracture rate, compared with controls. Our data indicate that: 1) men with CDP have normal vBMD; 2) the reduced aBMD may be the result of uncritical use of DEXA measurements in subjects with altered growth pattern; and 3) androgen administration during pubertal years did not improve BMD in young men with a history of CDP.

Absorptiometry, Photon↗

PubMed1990

Delay of puberty and impairment of growth in female rats given a non competitive antagonist of NMDA receptors.

Reportedly, excitatory amino acids are involved in the control of gonadotropin secretion of rats and non-human primates. The aim of this study was to investigate the effect of chronic blockade of NMDA (N-methyl-D-aspartic acid) receptors by the non competitive receptor antagonist MK-801 on gonadotropin secretion and the onset of puberty in female rats. Moreover, since in humans alterations of the timing of puberty frequently coexist with disturbances of body growth, suggesting a common etiology for both events, we evaluated the effect of MK-801 also on the neural mechanisms controlling growth hormone (GH) secretion. Twenty-one-day-old female rats were treated with MK-801 (0.2 mg/kg ip, bid) or placebo for 10 days and were killed after 7 days of withdrawal. Administration of MK-801 induced a significant impairment of growth rate without altering food intake, and a delay in vaginal opening. Pituitaries from rats treated with MK-801 had a reduced luteinizing hormone (LH) content, and secreted in vitro lower amounts of LH both under basal and LHRH-stimulated conditions. MK-801 treated rats had a lower pituitary GH content and basal and GHRH-stimulated GH release and reduced plasma insulin-like growth factor-I levels. These data indicate that blockade of NMDA receptors in a critical period of the female rat life-span: 1) delays puberty by reducing gonadotropin secretion; 2) impairs growth rate by reducing GH secretion, with a mechanism still to be clarified.

Animals↗

PubMed1996

[Influence of physical activity upon bone mineralization of school age children of both sexes].

Obtention of an optimal peak bone mass decreases the risk of osteoporosis in adult life. An increase of physical activity favors bone mineralization in adults. However, in teenagers sports that could delay puberty can delay bone mineralization, while sports with a normal caloric intake favor mineralization. The objective of this study was to evaluate the effect of intensity of physical activity and the type of sport, upon bone mineralization before and during puberty. A sample of 144 normal school age children of both sexes aged 7 to 14 years, practicing various degrees of physical activity, was selected. Bone mineral density (BMD) of whole body, spine and hip was measured with a dual photon absorptiometry densitometer and compared with values of normal school children of similar ages. A better adequation of BMD of whole body and spine in school age children with increased physical activity was detected. Prepuberal female gymnasts had decreased BMD of whole body. Puberal school age children with decrease physical activity had diminished BMD. These results led us conclude that physical activity favors bone mineralization in spine and hip, specially during puberty.

Adolescent↗

PubMed1987

Suppression of plasma renin activity in a boy with chronic hyperkalemia.

Chronic hyperkalemia (6.8 mmol/L [6.8 mEq/L]) was discovered in a boy, aged 13 years 7 months, with short stature, delayed puberty, and normal blood pressure. Additional studies revealed hyperchloremic metabolic acidosis (serum values: sodium ion, 139 mmol/L [139 mEq/L]; chloride, 113 mmol/L [113 mEq/L]; bicarbonate, 18 mmol/L [18 mEq/L]), a normal glomerular filtration rate, a subnormal renal threshold for bicarbonate reabsorption, and normal serum thyroxine, growth hormone, and cortisol values. Renal excretion of potassium ion was subnormal for the prevailing serum concentration of potassium ion but was increased normally by infusion of sodium sulfate. The serum aldosterone concentration was appropriate for a normokalemic subject, despite marked suppression of plasma renin activity (PRA) (supine/upright: aldosterone, 140/580 pmol/L [5/21 ng/dL]; PRA, 0.0/0.03 ng/L X s [0.0/0.1 ng/mL/h]). Treatment with chlorothiazide and sodium chloride resulted in correction of the abnormal electrolyte concentrations and an increase in linear growth velocity. Serum aldosterone concentrations did not change significantly during treatment, even though the PRA had increased (supine/upright: aldosterone, 110/920 pmol/L [4/33 ng/dL]; PRA, 0.89/2.17 ng/L X s [3.2/7.8 ng/mL/h]). In this patient, we conclude that (1) hyperkalemia was due to inadequate renal excretion of potassium ion; (2) the serum potassium ion concentration was the major stimulus to aldosterone secretion before treatment; (3) suppression of PRA was more likely due to hyperkalemia than to extracellular volume expansion.

Acidosis↗

PubMed1992

Familial syndrome of endocrine and neuroectodermal abnormalities.

We report on a previously undescribed combination of endocrine and neuroectodermal abnormalities in four sibs from Burma. These abnormalities include low growth hormone levels in response to provocative stimuli, delayed puberty associated with prepubertal levels of gonadotropins in the males and pubertal levels of gonadotropins in the females, type II diabetes mellitus with elevated insulin levels, mild mental retardation, sensori-neural deafness, and alopecia without pili torti. They also had a characteristic facial appearance and fleshy hands and feet. This family appears to have a previously undescribed combination of endocrine and neuroectodermal abnormalities.

Adolescent↗