[Benign delayed puberty in boys].
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Adolescent↗
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Delayed puberty in girls and primary amenorrhea.
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Adolescent↗
[Idiopathic delayed puberty--female].
The developmental changes during puberty occur over a period of 3 to 5 years, usually between ages 9 and 14. The age of onset of puberty is influenced by genetic and environmental factors. Delayed puberty is a rare condition in girls, and a genetic problem or hypothalamic-pituitary-ovarian disorder can be suspected. In addition, anatomic abnormalities of the uterus and ovaries are rare but important factors to consider. The history and physical examination are useful in the diagnostic work-up. Pelvic examination and U.S. should be completed. Also, hormonal analysis should be recommended with diagnostic plan. Although, the possibility of rare diagnoses should always be kept in mind.
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[Chronic giardiasis with intestinal dwarfism and delayed puberty in immunoglobulin deficiency syndrome: complete catch-up growth after therapy].
A 10-year-old, previously healthy Swiss boy suffered from repeated episodes of watery diarrhea for some months following a summer camp holiday. No etiology was found, and except for symptomatic treatment no other therapy was necessary. Five years later he was investigated because of growth failure, with a bone age of 11.5 years, but the correct diagnosis was not established. Only when he was reinvestigated at the age of 20 years, because of persistent growth failure and a bone age of 14 years, were Giardia lamblia trophozoites seen microscopically on the surface of duodenal mucosa biopsy specimens. At the same time dysgammaglobulinemia was detected which may have predisposed the gastrointestinal tract to chronic giardiasis. After a 10-day course of metronidazole the patient experienced catch-up growth and completed his pubertal development. The dysgammaglobulinemia persisted after therapy. This case showed that in patients with intestinal growth failure, catch-up growth and completion of pubertal development are possible even after the age of 20 years if nutritional supply is sufficient. Bone age determinations serve to indicate remaining growth potential.
Adolescent↗
[Delayed puberty (in a boy)].
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Adolescent↗
Precocious and delayed puberty. Studies of FSH and LH production and metabolism.
We measured the production rates and metabolic clearance, disappearance and excretion rates of FSH and LH as well as plasma testosterone and delta 4-androstenedione in males with precocious and delayed puberty. In precocious puberty, we found modestly elevated FSH production early in puberty, reaching adult levels by midpuberty and remaining constant thereafter. LH production was low early in puberty, reached high levels at midpuberty and then fell. The plasma testosterone concentrations paralleled the changes in LH. This suggests that moderate FSH production is achieved by early puberty and adult levels are reached by midpuberty. On the other hand LH production is low early in puberty, reaches high levels by midpuberty and then falls again towards the end of puberty. Constitutional delay in sexual development probably consists of several syndromes due either to a delay in LH production or to FSH production or to both. One patient with hypogonadotrophic hypogonadism was also studied. He showed relatively normal LH production but very low FSH production.
Adolescent↗
Effect of increased haemoglobin levels on growth hormone (GH) secretion in beta-thalassaemia major: differences between prepubertal subjects and patients with delayed puberty.
Basal and L-dopa-stimulated secretion of growth hormone (GH) was investigated in 10 patients with beta-thalassaemia major. Five patients were prepubertal (chronological age 8 to 12 years), whereas 5 patients had delayed puberty (chronological age 15 to 19 years). Ten normal prepubertal subjects (chronological age 8 to 11 years) served as the control group. Each thalassaemic patient was subjected to two L-dopa tests (0.5 g L-dopa plus 0.7 mg/Kg body weight propranolol, orally): one was performed under conditions of low haemoglobin (Hb) levels (30 days after the last blood transfusion), and the second in the presence of increased Hb concentrations (10 days after the transfusion of packed red blood cells). Before the transfusion of packed red blood cells, basal GH concentrations were significantly higher in the patients with delayed puberty (4.3 +/- 1.6 ng/ml), than in prepubertal thalassaemic (1.8 +/- 0.9 ng/ml, p less than 0.05) and control (1.9 +/- 1.0 ng/ml, p less than 0.02) subjects. In contrast, the pituitary responsiveness to L-dopa, expressed as the relative maximum response for GH (GH delta %), was significantly higher in the latter two groups (8.5-fold, p less than 0.05, and 10.9-fold, p less than 0.02, respectively). The transfusion of packed red blood cells increased significantly Hb concentrations in both groups of thalassaemic patients (prepubertal +27%, p less than 0.05, delayed puberty +33%, p less than 0.025, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Evaluation of delayed puberty in the female adolescent with chronic renal failure.
The purpose of this report is to discuss the differential diagnosis of delayed puberty in the adolescent female with chronic renal failure. The appropriate therapy varies depending on the etiology of the delay. Frasier syndrome--chronic renal failure with true gonadal dysgenesis--should be considered in the diagnosis of a normal phenotypic female with end-stage renal disease and delayed puberty.
Adolescent↗
Autoimmune polyglandular endocrinopathy and anterior hypophysitis in a 14 year-old girl presenting with delayed puberty.
We report a 14 year-old peripubertal girl who presented at our clinic with the primary complaint of delayed puberty. She was asymptomatic except for vague complaints of fatigue. Physical examination was significant for mucosal hyperpigmentation and lack of secondary sexual characteristics. Laboratory evaluation revealed a morning cortisol concentration of <0.1 microg/dl (normal range [n.r.]: 4.3-22.4 microg/dl) and a simultaneous ACTH concentration of 2 pg/ml (n.r. 25-62 pg/ml); FSH 66.8 IU/l (n.r. for age: 1-12.8 IU/l); LH 41.1 IU/l (n.r. for age: 1-12 IU/l); E2 38 pg/ml (n.r. for age: 7-60 pg/ml). She had a flat cortisol response to an ACTH stimulation test. MRI of the pituitary gland failed to reveal a lesion. Plasma renin activity, thyroid function tests, parathyroid hormone, prolactin, IGF-I, IGFBP-3 concentrations and serum electrolytes were normal. However, her urinary sodium concentration was high. She was diagnosed with autoimmune polyglandular endocrinopathy including ovarian failure, adrenal failure and autoimmune anterior hypophysitis presenting as isolated ACTH deficiency. We emphasize that autoimmune etiology should be considered in the differential diagnosis of delayed puberty and ovarian failure and that the presence of other endocrinopathies should be searched for even in asymptomatic patients.
Adolescent↗
Treatment of constitutional delayed puberty with a combination of testosterone esters.
Thirteen boys with constitutional delayed puberty (CDP) were treated with a combination of short and long-acting testosterone esters (testosterone propionate, testosterone phenylpropionate, testosterone isocaproate). Mean age at the onset of treatment was 14.9 +/- 0.6 years and bone age delay was -2.7 +/- 0.9 years. The dose of testosterone used was 200 mg intramuscularly four times at three week intervals, and the treated CDP boys were followed for two years. All the boys with CDP entered puberty after the last dose (testicular volume > or = 4 ml), and growth rate increased from 4.5 +/- 0.5 cm/year, pretreatment, to 8.4 +/- 1.6 cm/year, posttreatment, at the two year follow-up. Height for bone age SD score did not change significantly from a mean of -1.1 before treatment to -1.3 after treatment, nor did predicted height before treatment (173.5 +/- 6.6 cm) and after treatment (173.3 +/- 4.9 cm). Combination of testosterone esters in a given dose and schedule is a safe and effective treatment for prepubertal boys with constitutional delayed puberty.
Adolescent↗
Reversible growth hormone deficiency and delayed puberty triggered by a stressful experience in a young adult.
Growth retardation and delayed puberty developed in a young man after emotional trauma at age 12 years, three months. He had an eating disorder, was profoundly malnourished for several months, and then resumed eating spontaneously. Deficient secretion of growth hormone was documented during multiple arginine-insulin tolerance tests, and gonadotropin levels were low. These hormonal deficits persisted for many years in spite of good nutrition and lack of abuse, a course inconsistent with psychosocial dwarfism or effects of malnutrition per se. Later the patient spontaneously achieved normal height and secondary sexual characteristics. Apparently, psychic trauma induced a deranged hormonal state that persisted for several years.
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Quantitative bone SPECT in young males with delayed puberty and hypogonadism: implications for treatment of low bone mineral density.
UNLABELLED: Constitutional delayed puberty (DP) and idiopathic hypogonadotropic hypogonadism (IHH) lead to osteoporosis in adult men. We were interested in whether response to treatment of these conditions by testosterone could be predicted by in vivo quantitative bone SPECT (QBS) measurement of bone turnover and whether testosterone administration affects bone mineral density (BMD) in these subjects. METHODS: In vivo QBS and BMD measurements were performed in the lumbar spine (LS) and femoral neck (FN) of 29 young men with DP and 16 young men with IHH. In vivo QBS and BMD values in these patients were compared to the values obtained from 27 age-matched normal controls. The effect of testosterone treatment was determined by measuring changes in QBS and BMD, before and after treatment of 22 patients with DP and of all 16 patients with IHH. Seven patients with DP were not treated. RESULTS: In vivo QBS values in patients with DP were significantly higher than those in controls (8.44% +/- 2.55%ID/ml compared to 5.63% +/- 1.12%ID/ml x 10(-3), p < 0.001, for the LS; and 7.86% +/- 3.01%ID/ml compared to 4.29% +/- 1.25%ID/ml, p < 0.001, for the FN). One year after testosterone treatment, QBS values in DP were significantly reduced. Pretreatment BMD values in patients with DP were significantly lower than those in normal subjects (0.77 +/- 0.11 g/cm2 compared to 1.03 +/- 0.14 g/cm2, p < 0.0001, for the LS; and 0.89 +/- 0.11 g/cm2 compared to 1.08 +/- 0.18 g/cm2, p < 0.006, for the FN). One year after treatment, BMD values increased significantly (0.91 +/- 0.14 g/cm2, p < 0.0001, for the LS; and 0.97 +/- 0.11 g/cm2, p < 0.0001, for the FN). The seven untreated young men with DP still had significantly lower-than-normal BMD values (0.82 +/- 0.08 g/cm2, p < 0.008, for the LS; and 0.89 +/- 0.05 g/cm2, p < 0.04, for the FN). In patients with IHH, QBS values were not significantly different from those found in normal controls. The values for BMD were significantly lower for both the LS (p < 0.0001) and the FN (p < 0.001). After treatment, BMD values in patients with IHH were still significantly lower than those of normals (p < 0.009 for the LS; and p < 0.006 for the FN). CONCLUSION: Young men with maturation abnormalities show low bone density. Patients with DP and high bone turnover, as revealed by high QBS values, respond to testosterone treatment. Patients with IHH have normal bone turnover and do not respond to testosterone.
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Serum immunoreactive somatomedin-C levels in growth failure and delayed puberty associated with chronic hepatosplenic schistosomiasis.
Eleven patients, five males, six females, aged 14-20 years with hepatosplenic schistosomiasis (HSS), growth failure and delayed puberty were submitted to endocrine evaluation. All patients had well preserved parenchymal liver function although several changes were present in the portal system, showing a poorly vascularized liver. Bone age was retarded, thyroid function was normal, the human growth hormone response to hypoglycaemia was within the normal limits and the prolactin response to TRH was normal. LH and FSH basal levels were normal and a normal rise was observed after a provocative test with LHRH. Gonadal function, expressed as serum testosterone or oestradiol levels, was abnormally low for the chronological age. Serum somatomedin-C levels were also low (range 0.11-2.10 U/ml) for the respective Tanner stage or bone age of each individual patient. One year after a splenorenal shunting in the three patients that returned for follow-up, it was observed that sexual maturation reached Tanner stage III, linear growth increment ranged from 9.0 to 11.5 cm and serum somatomedin-C levels increased to 4.3-5.6 U/ml. We concluded that a combination of undernutrition and marked vascular changes in the liver, present in HSS, are associated with decreased serum sex steroids and somatomedin-C concentrations, resulting in growth failure and delayed puberty in these patients.
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Constitutional delayed puberty in males and hypogonadotropic hypogonadism: a reliable and cost-effective approach to differential diagnosis.
Forty-six male teenagers 13-19 years old with delayed puberty (DP) underwent gonadotropin releasing hormone (GnRH) and human chorionic gonadotropin (HCG) stimulation as part of their work-up. All were followed to age 18 and beyond. Thirty-seven had constitutional delayed puberty (CDP). Nine had hypogonadotropic hypogonadism (HH). At referral 34 youngsters with CDP were properly diagnosed when the lower limit for the luteinizing hormone (LH) response to GnRH (Factrel 0.1 mg i.v.) was set at 12 IU/l. Three boys with CDP failed to reach that level and were not assigned appropriately. All nine patients with HH had basal serum testosterone (T) < 50 ng/dl when first seen and LH responses to GnRH stimulation < 8.0 IU/l. In the late 1970s, five subjects with DP were given HCG 3,000 IU (two patients daily for 5 days; three on 3 alternate days). Serum T was measured before the first, and 48 hours after the last injection (day 7). With recognition of the long biological half-life of injected HCG and receptor downregulation by daily doses, the protocol was changed. In the early 1980s, the dose of HCG was randomized to either 500 IU or 1,000 IU given on 3 alternate days. T was measured before the first injection (basal), 48 hours later (day 3) and 48 hours after the third injection (day 7). At referral 35 patients with CDP, including one GnRH failure, met the criterion for a positive response to HCG stimulation based on their own reactions (T > 170 ng/dl on day 3; > 200 on day 7). Eleven patients with DP failed the test. Nine had HH and two had CDP. The nine patients with HH included the two given daily injections and the three given HCG 3,000 IU on 3 alternate days. Of the two with CDP, one, an obese boy with a normal GnRH test, only received 500 IU HCG (5.6 IU/kg), which may have been inadequate. The other failed both tests. Of the 35 responders, 17 (group 1) were given HCG 500 IU and 18 (group 2) were given 1,000 IU i.m. on 3 alternate days. Seven boys in group 1 and 12 in group 2 had serum T determined on day 3, and all 35 had T measured on day 7. There was no significant difference between the basal T levels in the two groups or in their responses to HCG, and the results were pooled. The combined data in the patients with CDP were then compared with those of the nine patients with HH, recognizing that the result on day 7 in the two patients given daily injections may reflect receptor down-regulation. Setting the limit for a normal T response at > 170 ng/dl 48 hours after a single injection of HCG and > 200 ng/dl after the third injection assigned all the patients with CDP appropriately. The data on the patients with HH are less complete, with only three T values 48 hours after the first injection However, even after three injections of HCG on alternate days, only one of nine patients with HH approached the lowest level achieved by the patients with CDP after a single injection. The data confirm that a basal serum T 50 ng/dl is evidence of the onset of puberty. In those with serum T < 50 ng/ dl our data suggest that a single injection of HCG 15 IU/kg, with serum T determined 48 hours later, is more discriminatory and offers the most reliable, easy to perform, least painful, and by far the most cost effective test to differentiate CDP from HH.
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Evaluation of the buserelin stimulation test in diagnosing gonadotropin deficiency in males with delayed puberty.
OBJECTIVE: To assess the efficacy of the gonadotropin-releasing hormone (GnRH) agonist buserelin in a stimulated gonadotropin test for the investigation of delayed puberty in males. STUDY DESIGN: Prepubertal males (n = 31; age range, 10.3 to 17.2 years) were studied; buserelin (100 microg) was administered subcutaneously, with blood sampling at 0 and 4 hours for serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH). At follow-up (mean, 4.2 years), 8/31 (26%) failed to progress into puberty, constituting hypogonadotropic hypogonadism (HH), but 23/31 (74%) had testicular enlargement (> or =8 mL) consistent with a normal hypothalamic-pituitary-gonadal (HPG) axis. RESULTS: Stimulated serum LH response to buserelin was lower in males with HH (mean +/- standard error under the mean for HH, 1.4 +/- 0.5 U/L, compared with a normal HPG axis of 17.4 +/- 2.0 U/L; P < .0001). Stimulated serum FSH response was nondiscriminatory (HH, 7.7 +/- 2.2 U/L; normal HPG axis, 11.5 +/- 1.6 U/L; P = .27). All males with HH had a stimulated serum LH level <5 U/L, whereas only 1/23 with a normal HPG axis had a stimulated serum LH below this level. Using this value as the criterion for diagnosing HH, the buserelin stimulation test yielded a sensitivity of 100%, specificity of 96%, and positive predictive value of 89%. CONCLUSIONS: The buserelin stimulation test is a highly specific and sensitive GnRH agonist test for the investigation of males with delayed puberty.
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[A prolactin-producing microadenoma as the cause of galactorrhea and delayed puberty in an adolescent boy].
The case history of a 16 years old boy with delayed puberty and the sudden onset of galactorrhea is presented. Prolactin analyses and X-ray studies of the sella turcica lead to the diagnosis of a pituitary tumor. A prolactin producing microadenoma was selectively excised via the transsphenoidal route. Serum prolactin resumed normal concentrations within hours after the operation. During the next months the boy showed the signs of normal puberty with increasing concentrations of serum testosterone. Because serum prolactin concentrations remained within the normal range, therapy with bromocriptine was not necessary. A spermiogram however, performed seven months after the operation, showed signs of a viscosipathy and terato-asthenozoospermia.
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Leptin and thyroxine during sexual development in male monkeys: effect of neonatal gonadotropin-releasing hormone antagonist treatment and delayed puberty on the developmental pattern of leptin and thyroxine secretion.
OBJECTIVE: Neonatal treatment of male monkeys with a gonadotropin-releasing hormone antagonist (Ant) increased the incidence of delayed puberty. Using blood samples that had been collected from monkeys with normal or delayed puberty, we assessed the potential involvement of leptin and thyroxine (T4) in sexual development. DESIGN AND METHODS: Monkeys were treated from birth until 4 months of age with vehicle, Ant or Ant/androgen and blood samples were drawn from 10 to 62 months of age. RESULTS: Serum leptin and total T4 concentrations declined in parallel throughout adolescence in all treatment groups. There was no transient rise in leptin before or in association with the onset of puberty. Also, leptin did not differ during the peripubertal period between animals experiencing puberty at that time versus those in which puberty was being delayed. Neonates treated with Ant either alone or with androgen replacement had higher leptin levels than controls throughout development. While leptin exhibited no significant changes during the peripubertal period, T4 values increased and declined in parallel with the peripubertal changes in hypothalamic-pituitary-testicular activity. CONCLUSIONS: These data do not support the concept that a transient rise in leptin triggers the onset of puberty in male monkeys. However, the disruption of neonatal activity of the pituitary-testicular axis alters the developmental pattern of leptin. The changes in T4 levels during the peripubertal period suggest that thyroid status may be a significant contributor to the process of sexual development in the male monkey and that peripubertal changes in secretion of this hormone may serve as an effective physiological response during a critical period of elevated energy expenditure.
Aging↗