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PubMed2000

Delayed puberty associated with hyperprolactinemia caused by pituitary microadenoma.

Primary amenorrhea caused by the hyperprolactinemia is a rare condition characterized by the onset of thelarche and pubarche at appropriate ages but arrest of pubertal development before menarche. Hyperprolactinemia might be found in a few women with primary amenorrhea, yet relevant experience has apparently not been reported. We report a 16-year-old patient with hyperprolactinemia caused by a pituitary microadenoma. Her only symptom was delayed puberty without galactorrhea. Bromocriptine therapy was useful in order to induce the ovulation and cause the menarche.

Adenoma↗
PubMed1984

Dietary arginine deprivation and delayed puberty in the female rat.

Dietary arginine deprivation was found to delay puberty in the female rat. Physiological pinealectomy by exposing to constant light suggests this gland is not involved in this delay. Compensatory ovarian hypertrophy (COH) was used to test the hypothalamic sensitivity to negative steroid feedback. COH occurred in hemiovariectomized immature rats ad libitum fed the control or arginine-deficient diet but failed to occur in hemiovariectomized, underfed, growth-matched control rats, which suggests that feed restriction and arginine deficiency do not exert identical effects on the hypothalamic-pituitary-gonadal axis. Puberty, as defined by vaginal opening, first ovulation and the initiation of estrous cycles, was advanced by a week in the immature female rat fed a control diet after treatment with estradiol benzoate, 0.05 microgram/(100 g body weight X day) starting at 26 days of age. The time of first estrus and the first ovulation was not advanced in arginine-deficient rats by the same dosage of estrogen when administration began at 26 days of age. Treatment at an older age (40 or 54 days) or with a higher dosage [0.25 microgram/(100 g body weight X day)] at 26 days of age did advance puberty. The failure of estrogen to induce a vaginal cyclicity suggests an insufficient amount of endogenous estrogen to trigger a gonadotropin surge to cause the onset of puberty in the rat fed an arginine-deficient diet.

Animals↗
PubMed1996

Macroprolactinomas as cause of delayed puberty. A report of two cases and effects of medical therapy.

About 3-5% of pituitary tumors occur in pediatric patients, often showing a considerable severity during childhood and puberty and major difficulties in their therapeutic management. As far as macroprolactinomas are concerned, surgery is often not resolutive, so that the need for postoperative treatment, consisting of either radiotherapy or bromocriptine, is the rule for tumors with extrasellar extension. In the present manuscript we report two cases of macroprolactinomas in adolescent patients suffering from delayed puberty, short stature and ocular symptoms together with hormonal levels indicating the presence of hypopituitarism. In both patients bromocriptine therapy showed a particular efficacy both in controlling tumor size and growth and in reducing clinical signs and symptoms. We conclude proposing DA-therapy as a first line of management in adolescents affected by macroprolactinomas, even in the presence of neurological symptoms.

Adolescent↗
PubMed2002

Delayed puberty.

Puberty is the acquisition of secondary sexual characteristics associated with a growth spurt and resulting in the attainment of reproductive function. Delayed puberty is diagnosed when there is no breast development by 13.4 years of age in a girl and no testicular enlargement by 14.0 years in a boy. The aetiologies are: (i) pubertal delay, either with constitutional delay of growth and puberty or secondary to chronic illness, and (ii) pubertal failure, with hypogonadotrophic (defect in the hypothalamo-pituitary region) or hypergonadotrophic (secondary to gonadal failure) hypogonadism, or both (secondary to radio/chemotherapy). The investigation includes: history, auxological data and pubertal development examination. Boys usually require treatment and, if they do not respond, investigation. In girls it is appropriate to measure the thyroid function and karyotype first and, if necessary, to offer treatment. If they present with dysmorphic features, or positive familial history, an assessment is required before treatment.

Adolescent↗
PubMed1989

The production of and sensitivity to cues that delay puberty and prolong subsequent oestrous cycles in female mice are influenced by prior intrauterine position.

Four experiments were conducted with CF-1 house mice (Mus domesticus) to examine the relationship between a female's prior intrauterine position (2M = between 2 male fetuses, 1M = next to one male fetus, 0M = not next to a male fetus) and the timing of puberty and length of subsequent oestrous cycles under a variety of housing conditions. The results of Exp. 1 confirmed that the presence of males was required for females to enter puberty and exhibit regular oestrous cycles, regardless of prior intrauterine position. When housed individually after weaning either with a male in the cage or separated by a wire mesh partition, 0M-females ovulated and mated at a younger age and had shorter post-pubertal oestrous cycles than did 2M-females (1M-females were intermediate between 0M- and 2M-females). Other females were also housed after weaning with a male or separated by a wire mesh partition from a male in a variety of social environments (4 0M-females and 1 2M-female, 4 2M-females and 1 0M-female, 5 1M-females, 3 0M-females and 3 2M-females). The objective of these different housing conditions was to determine whether prior intrauterine position influenced the transmission of and/or sensitivity to cues that delay puberty and prolong subsequent oestrous cycles. Relative to 2M-females, 0M-females both produced more potent cues and were more sensitive to the cues (again, 1M-females were intermediate between 0M- and 2M-females). Specifically, in the presence of other females, puberty was delayed and post-pubertal oestrous cycles were prolonged to the greatest extent in 0M-females. Prior intrauterine position is therefore a source of individual variation in the production of and sensitivity to cues that modulate the timing of puberty and the length of subsequent oestrous cycles in female mice. The findings suggest that prenatally-androgenized 2M-females may have a reproductive advantage over other females at high population densities.

Androgens↗
PubMed1993

Successful treatment of short stature and delayed puberty in congenital magnesium-losing kidney.

Bartter's syndrome is a well described but uncommon disease characterized by hypokalaemia and hyperplasia of the juxtaglomerular apparatus of the kidney. It may present in infancy with failure to thrive and muscle weakness; it commonly causes short stature. Lesions at different sites within the renal tubule have been proposed as the cause of the syndrome. However, the biochemical abnormalities in many cases can be explained by defective reabsorption of chloride in the ascending loop of Henle, with loss of sodium and water and a secondary increase in renin and aldosterone concentrations. Less severe cases have been described which present in adolescence and have tetany as a prominent feature. Primary renal loss of magnesium associated with potassium wasting has been described in such cases and it has been suggested that these can be distinguished from classical Bartter's syndrome by hypocalciuria. This less well characterized disease has been named Welt, Gitelman-Welt or Gitelman syndrome and may include deficient tubular reabsorption of chloride, but the sites of magnesium and potassium loss in the kidney are uncertain. We describe a patient with this syndrome who presented with short stature, delayed puberty and tetany and responded well to magnesium replacement.

Adolescent↗
PubMed1985

Delayed puberty and hypoplastic uterus associated with hyperprolactinemia: successful treatment with bromocriptine.

A 15-year-old girl referred because of primary amenorrhea was found to have a hypoplastic uterus and persistent hyperprolactinemia (72-110 ng/ml). The gonadotrophin-dependent pubertal signs, i.e. breast and vulvar development, were significantly retarded (Tanner stage 2-3) while sexual hair was well developed; bone age was 13 years. The endocrinological evaluation revealed gonadotrophin secretion (LH-basal: 0.85-1.25; peak after LH-RH: 10.4 mIU/ml; FSH-basal: 1.63-2.5; peak: 8.2 mIU/ml) and E2 levels (26-68 pg/ml) which were appropriate for Tanner stage 3. The high basal levels of PRL were nonresponsive to either stimulatory (TRH) or inhibitory (nomifensine) agents. CT scan of the brain suggested the presence of a pituitary microadenoma. Following therapy with bromocriptine (2.5 mg/day) plasma PRL levels dropped to normal (5-6.8 ng/ml) with an accompanying catch-up of pubertal development and linear growth and a marked increase in size of the uterus as documented by repeated ultrasonographic examinations. Menarche occurred 5 months after initiation of therapy, followed by regular menses thereafter. Repeated CT scan of the brain showed a decrease in the density and size of the still persisting lesion. This patient demonstrates that hyperprolactinemia can cause delayed puberty with a particular inhibitory effect on uterine growth and development.

Adenoma↗
PubMed1982

Hypopituitarism and idiopathic delayed puberty: a longitudinal study in an attempt to diagnose gonadotropin deficiency before puberty.

Fifty-five hypopituitary patients (43 boys and 12 girls) treated with human GH were studied longitudinally before and during puberty, occurring either spontaneously or induced with testosterone enanthate (100 mg/month, im) in boys and ethinylestradiol (10 micrograms/day, orally) in girls. In addition, 53 boys with idiopathic delayed puberty (IDP) were studied. Gonadotropin integrated responses (IRs) during 90 min after the iv injection of 25 micrograms/m2 LRH, bone ages (BA), and plasma levels of dehydroepiandrosterone sulfate and testosterone were determined at least yearly. Prepubertal hypopituitary patients with gonadotropin deficiency were characterized by: 1) a lowered FSH IR to LRH in most boys and in all girls; 2) a low LH IR for BA; 3) adrenarche either absent or delayed BA; 4) height age close to BA; and 5) the presence of several pituitary deficiencies. In contrast, most prepubertal hypopituitary patients without gonadotropin deficiency showed: 1) a normal FSH IR to LRH; 2) a normal or intermediate (greater than or equal to 75 mIU/ml . 90 min) LH IR for BA; 3) a normal adrenarche for BA; 4) a height age below BA; and 5) isolated GH or GH plus TSH deficiencies. A significant linear correlation was found between LH IR and the logarithm of plasma testosterone. The slopes and levels were similar in controls and hypopituitary boy without gonadotropin deficiency. In IDP, the level was significantly higher. All data obtained in these patients show that the increase in plasma testosterone and the clinical onset of puberty are delayed for the observed pubertal pattern of LH responsiveness. It is concluded that the study of several clinical and biological features, especially the gonadotropin IR to LRH, are of predictive value for the diagnosis of normal or deficient gonadotropic function in prepubertal patients with IDP and hypopituitarism.

Adolescent↗
PubMed1984

Testosterone treatment and arginine-induced growth hormone stimulation in male delayed puberty: effects on serum calcium, phosphate and vitamin D metabolites.

Hormonal changes after arginine-induced growth hormone stimulation and subsequent testosterone treatment were examined in 5 patients classified as having male delayed puberty. All the patients responded well to growth hormone stimulation and a significant negative correlation was found between the delay in height age and the maximal growth hormone response, r = 0.80, P less than 0.05. The testosterone treatment did not alter this pattern. Changes in PTH, 25OHD, 24.25(OH)2D, and 1.25(OH)2D were examined at 24 h after the infusion. The results showed significant reductions in PTH (P less than 0.05) and 24.25 (OH)2D (P less than 0.05) and a possible increase in 1.25(OH)2D, whereas 25OHD remained unchanged. These results may support the conception of growth hormone as a common denominator of growth and bone metabolism.

Adolescent↗
PubMed2002

Delayed puberty.

Normal puberty is a time of life and a process of development that results in full adult maturity of growth, sexual development, and psychosocial achievement. Delayed puberty describes the clinical condition in which the pubertal events start late (usually > +2.5 SD later than the mean) or are attenuated in progression. The differential diagnosis includes syndromes of low gonadotropin production, usually constitutional delay of growth and maturation associated with chronic disease, but also an array of gene-mediated disorders, and syndromes of primary gonadal dysfunction with hypergonadotropic hypogonadism, including Turner and Klinefelter syndromes, and a group of acquired and genetic abnormalities. Diagnostic assessment and varied therapeutic modalities are discussed. The issues of androgen or estrogen therapy are important to assess, and growth hormone treatment remains a difficult dilemma.

Adolescent↗
PubMed1981

Activation of growth hormone short loop negative feedback delays puberty in the female rat.

Implantation of GH in the median eminence of the hypothalamus of 23-day-old female rats tonically inhibited serum GH levels throughout prepubertal development (days 23-36) and depressed GH diurnal pulsatile release. Puberty was significantly delayed in GH-deficient animals, a delay associated with a blunted in vitro ovarian steroidal responsiveness to gonadotropins (particularly estradiol) and a marked decrease in prepubertal uterine weight, as evaluated 4, 7, and 13 days after GH implantation. The prepubertal body weight increase was also depressed. Neither ovarian weight nor serum levels of LH, FSH, PRL, or TSH were consistently altered by the GH implant. In addition, evaluation of pulsatile PRL release in 33-day-old rats revealed no difference between control and GH-deficient animals. Ovarian LH receptor content was lower in GH-implanted rats than in controls, suggesting that a decrease in LH receptors may be one of the mechanisms by which a chronic decrease in serum gH depressed the prepubertal ovarian estradiol and, to a lesser extent, the progesterone response to gonadotropins. A direct ovarian site of action for GH was indicated by the results of experiments in which GH was administered to immature hypophysectomized estrogen-treated rats. The in vitro ovarian progesterone response of the GH-treated animals to both hCG and human FSH was distinctly increased by prior in vivo GH treatment. This effect of GH was not reproduced either by the in vivo administration of LH at a dose calculated by RIA to be contaminating the GH preparation or by FSH at a dose that induced a marked increase in aromatase activity in the same ovaries. GH treatment of hypophysectomized rats failed to affect either aromatase activity or hCG-induced estradiol release, indicating that GH does not directly facilitate the production of estradiol by the ovary. The fact that intact rats with GH implants did not actually show a decrease in the ovarian estradiol response to hCG but, rather, failed to show an increased response at the same time as control animals strongly suggests that ovarian maturation was delayed in GH-deficient rats. It is suggested that, in addition to PRL, GH may also play a role in the process of prepubertal reproductive development by enhancing the steroidal response of the ovary to gonadotropins.

Animals↗
PubMed1977

Hyperprolactinemia as a cause of delayed puberty: successful treatment with bromocriptine.

An 18-year-old male patient was referred because of galactorrhea and delayed puberty. There was no gynecomastia, but a white milky secretion could easily be expressed from each breast. The chest and skull X-rays were normal. The plasma prolactin was increased to 58 ng/ml and rose to 97 ng/ml after 200 microgram TRF iv. The patient was treated for one year with testosterone; his voice deepened, body hair developed, libido and sexual function became overt, and bone age advanced from 14 1/2 to 17 years, but the galactorrhea increased. After a satisfactory stage of pubertal development was reached, the testosterone was stopped. tthe galactorrhea then decreased to its pretreatment intensity; however, sexual potency diminished, sexual hair growth decreased, and the plasma prolactin levels rose to 246 ng/ml. After a 5-month interval without treatment, bromocriptine was given and brought about an impressive improvement. Virilization and general well being were superior to that during testosterone treatment, the galactorrhea vanished, plasma prolactin decreased, testosterone rose to normal values, and a normal semen analysis was recorded.

Adolescent↗
PubMed1983

[Hypogonadotropic hypogonadism and delayed puberty: differential diagnosis using the LH-RH-infusion test].

Serum concentrations of LH and FSH were determined during an intravenous infusion of LH-RH (200 micrograms, t = 4 hours) in 8 patients (age: 15 to 20 years) with delayed sexual maturation and retarded bone age. Four patients who by clinical criteria were later recognized as suffering from hypogonadotropic hypogonadism (HH) presented during the infusion of LH-RH with only a small response of LH (and, in three cases, of FSH). In 3 patients with HH a deficiency of endogenous LH-RH due to a hypothalamic defect was suggested by an enhanced secretion of LH and FSH during a second LH-RH infusion test performed after priming of the pituitary by pulsatile, subcutaneous infusions of LH-RH (50 micrograms/night for 9 consecutive nights). The fourth patient with HH, who suffered from a pituitary adenoma, failed to display this enhanced secretion of gonadotropins following pituitary priming by intermittent administration of LH-RH. As compared with the patients with HH, 4 patients in whom puberty, although delayed, later occurred spontaneously (pubertas tarda, PT), presented with a considerably more pronounced secretion of LH and FSH during the infusion of LH-RH, and priming by intermittent subcutaneous LH-RH failed to achieve further enhancement of the secretion of LH and FSH during a second infusion test in these patients. The intravenous infusion of LH-RH in combination with a protocol of pituitary priming offers a possibility of distinguishing patients with delayed puberty from those with various forms of hypogonadotropic hypogonadism.

Adolescent↗
PubMed2004

Longitudinal monitoring of bone accretion measured by quantitative multi-site ultrasound (QUS) of bones in patients with delayed puberty (a pilot study).

OBJECTIVE: to compare the effect of anabolic agents on bone accretion in boys with constitutional delay of puberty (CGDP). RATIONALE: it has been suggested that an appropriate timing of puberty is necessary for normal bone mineral density (BMD) acquisition. Proper bone development during childhood is the key factor in achieving higher peak bone mass during middle age, which may not be achievable in CGDP children, and thereby osteoporosis may appear at an earlier age then expected. PATIENTS AND METHODS: 45 boys with CGDP aged 14-16 years were monitored longitudinally, every 3 months over 12 months with Sunlight Omnisense, a quantitative ultrasound device (Tel Aviv, Israel). The apparatus is a multi-site bone sonometer that obtains axial Speed of Sound (SOS). Based on a reference database obtained on n=1,085 (490 boys) 0-18 years, a normative curve was determined. Fifteen (14-16 years old) of the CGDP patients were treated with I.M. testovirone depot 100 mg monthly for 6 months, 15 (14-16 years old) were treated with oxandrolone 5 mg/m(2) daily for 6 months, and 15 (14-16 years old) were in an observation group. RESULTS: whereas the quantitative ultrasound (QUS) Z-score had shown some increase over time in CGDP-treated patients, an increase was found in tibia Z-score from -0.5(-0.64, -0.36) to -0.4(-0.54, -0.26) and from -0.52(-0.67, -0.38) to -0.31(-0.44, -0.11) in the testosterone and oxandrolone-treated groups, respectively, [median (25%, 75%)]. An increase in radius Z-score from -0.52(-0.65, -0.25) to -0.4(-0.54, -0.15) and from -0.51(-0.61, -0.21) to -0.37(-0.47, -0.07) in the testosterone- and oxandrolone-treated groups respectively [median (25%,75%)]. Z-score SOS decreased in the observation group -0.5(-0.66, -0.3) to -0.69(-0.85, -0.54) and -0.5(-0.59, -0.41) to -0.81(-0.95, -0.55) in tibia (P = 0.032) and radius (P = 0.029), respectively. Despite the fact that QUS remained in the normative range in all patients, a clear deterioration was demonstrated in untreated CGDP patients. CONCLUSION: longitudinal follow-up of patients with CGDP may detect an early pattern of deterioration of bone mass.

Adolescent↗
PubMed2002

Neonatal PACAP administration in rats delays puberty through the influence of the LHRH neuronal system.

The onset of puberty is a concerted action of many factors which leads to cyclic LHRH release in rats. It has been demonstrated that; in common with vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase activating polypeptide (PACAP) is also involved in the differentiation of the central nervous system. In our previous work, it was shown that a single PACAP injection into neonatal female rats delayed puberty. In the present work, neonatal administration of PACAP delayed the vaginal opening and decreased the weight of anterior pituitaries, the number of expelled ova at the first ovulation and the intensity of LHRH immunostaining in the septo-preoptico-infundibular system. PACAP antiserum had a reverse effect on LHRH immunoreactivity. The other studied parameters in the latter group remained unchanged compared to control rats. It was concluded that neonatal PACAP administration delayed the onset of puberty through the influence of the LHRH neuronal system.

Animals↗
PubMed2002

A possible association between dietary intake of copper, zinc and phosphate and delayed puberty in heifers in Sudan.

Zinc and copper deficiencies have been reported in heifers of various breeds at four different locations in Sudan. These were Kuku (5 km north of Khartoum), Seleit (20 km northwest of Khartoum), Medani (180 km south of Khartoum) and El Obeid (600 km west of Khartoum). Phosphorus deficiency was only observed in the serum of heifers at El Obeid. The heifers at all locations showed delayed puberty, stunted growth and infertility. The heifers of the local breeds at El Obeid only attained puberty by 1530 days of age compared with 840 days for the pure Friesian heifers at Seleit. The crossbred animals at Kuku and Medani attained puberty at 1440 and 1020 days of age, respectively. The marginal or low zinc and copper contents in pasture, soil or animal feed may have been predisposing factors for the observed deficiencies and might have been responsible for the delayed age of puberty.

Animal Feed↗
PubMed1995

[Delayed constitutional puberty or hypogonadotrophic hypogonadism?].

This review is focused on the diagnosis, clinical and general therapeutic approach of constitutional growth and puberty delay and hypogonadotrophic hypogonadism in males, two entities that are difficult to distinguish. Clinical history and physical examination must be carefully performed. Delayed puberty is due to constitutional growth and puberty delay in the vast majority of children. These must be distinguished from a small fraction of boys with hypogonadism, a pathological condition. A number of laboratory test allow the prediction of puberty onset and progression. Nevertheless, the advent of highly sensitive immunoassay and radiometric immunoassay systems for LH, FSH and testosterone has not entirely solved the problems, since their values may overlap between normal and pathological conditions.

Adolescent↗