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At least 19 recordsLinked to original sources
PubMed1976

[Integrated stimulation test with releasing hormones on healthy men and on patients with various forms of male hypogonadism].

Ninety subjects were examined; 20 healthy males, 20 patients with primary hypogonadism, 30 patients with Klinefelter's syndrome and 20 patients with secondary hypogonadism. The stimulating test with 200 mug LH-RH and 200 mug TTH was carried out tp all subjects examined, applied in two successive o.v. injections. The plasma as regards the levels of TTH, prolactin, FSH, LH, ACTH and STH is investigated every 0,20, 30, 60 and 90 minutes. The levels of tbe mentioned hormones were determined as well as the normal respond reaction. The basic LH and FSH levels are considerabty elevated in patients with primary hypogonadism and Klinefelter's syndrome and the respond reaction to stimulation is normal or diminished. A strict correlation between the number of X chromosomes and the level of FSH and LH was established in the patients with Klinefelter's syndrome. With respect to TTH, the basic, level in patients with primary hypogonadism in normal in 13 patients and pathological deviations were found in 7 patients. A strict correlation between TTH level and the number of X-chromosomes exists, Prolactin level in both groups is decreased. In patients with secondary hypogonadism the basic level of LH and ESH is decreased or at the lower limits of the norm. The respond reaction is absent. Both TTH and prolactin levels are pathologically changed as well as the respond reactions to stimulation depending on the etiology of the primary endocrine distrubance that had led to hypoginadism development.

Adult↗
PubMed1975

Neuroichthyosis with hypogonadism (Rud's syndrome).

Rud's syndrome is a neuroichthyosis with hypogonadism, associated with mental deficiency and epilepsy. Short stature is a frequent component of the syndrome. The primary genetic defect and the pattern of inheritance have not yet been determined. A typical patient is presented, with mental deficiency, short stature, pypoacusia, muscular atrophy, tylosis, pseudoacanthosis nigricans and endocrine disturbances. The neuroichthyosis with hypogonadism must be considered Rud's syndrome. A classification of neuroichthyosis is proposed. In a first group is neuroichthyosis with hypogonadism, in the second group is neuroichthyosis with spasticity and in the third group, neuroichthyosis without hypogonadism or spasticity.

Adolescent↗
PubMed1978

The effect of LH-RH infusion on serum LH, FSH and testosterone in boys with advanced puberty, delayed puberty and hypogonadotrophic hypogonadism.

LH-RH injection and infusion studies were performed in advanced puberty, delayed puberty and hypogonadotrophic hypogonadism. No differential diagnosis could be made between delayed puberty and hypogonadotrophic hypogonadism using LH-RH injection. In the LH-RH infusion studies evidence was obtained that stimulation of the pituitary during 4 h results in continuously rising LH levels in advanced puberty and in delayed puberty while in hypogonadotrophic hypogonadism the secretory capacity of the pituitary is gradually exhausted. This phenomenon can be used in the differential diagnosis between delayed puberty and hypogonadotrophic hypogonadism. Though the FSH data point in the same direction they are not useful in this connection as the overlap between the different categories was considerable.

Adolescent↗
PubMed1978

Prolactin-secreting tumors and hypogonadism in 22 men.

We studied 22 men with prolactin-secreting pituitary tumors and hypogonadism. Twenty complained of impotence, nine had visual impairment, and three experienced galactorrhea. None of the 17 patients undergoing operation or radiotherapy, or both, were subsequently normoprolactinemic. In all 13 patients treated with bromocryptine major clinical improvement was associated with a decrease in serum prolactin levels and in nine with an increase in serum testosterone. Two patients receiving testosterone replacement therapy showed improved potency only after bromocryptine was administered. The results indicate that hyperprolactinemia frequently induces hypogonadism in men, that bromocryptine ameliorates symptoms of disease previously unchanged by operation or radiotherapy, and that the impotence observed may not be solely the result of hypogonadism.

Adenoma, Acidophil↗
PubMed1979

Effects of androgen on sexual behavior in hypogonadal men.

Despite the widespread use of androgen in the treatment of hypogonadal men, its efficacy in restoring sexual behavior to hypogonadal patients has not been established in appropriately controlled behavioral studies. Accordingly, testosterone enanthate or vehicle was injected once every 4 weeks im in a double blind experiment. The subjects were six adult males, aged 32-65 yr, two with gonadal failure and four with secondary hypogonadism. Two doses of testosterone (100 and 400 mg) were administered for approximately 5 months, with the treatments varied at random within and among subjects. Details of sexual activity and experience were followed by the use of daily logs. Frequencies of erections, including nocturnal erections and coitus, showed significant dose-related responses to androgen treatment which closely followed the fluctuations in the circulating testosterone level. As indicated by the Profile of Mood States test, behavioral responses did not appear to be mediated by changes in mood. We concluded that the stimulatory effects of testosterone on sexual activity are rapid, reliable, and not due to a placebo effect. To maintain plasma testosterone and adequate sexual function within normal levels, even high doses of testosterone enanthate should be given no less frequency than once every 3 weeks.

Adult↗
PubMed1979

Gonadotropin-releasing hormone test for hypogonadic men.

Gonadotropin patterns before and after stimulation with gonadotropin-releasing hormone (GnRH) have been studied in 69 hypogonadic men of various types: patients with expansive hypothalamus--pituitary disorders before and after surgery, patients with hypogonadotropic hypogonadism, and patients with oligozoospermia or azoospermia who have primary partial or total testicular deficiency. Three characteristic gonadotropin patterns were found: (a) low basal values of LH and FSH with either absent or decreased and delayed responses; (b) normal basal values and pituitary responses above the normal range; or (c) high basal values and pituitary responses above the normal range. These gonadotropin patterns were correlated with disorders of the hypothalamus--pituitary--testis axis. The advantages and disadvantages of the GnRH test for the clinical evaluation of male hypogonadism are discussed.

Adolescent↗
PubMed1979

[Pathomorphological studies of the testes in various forms of hypogonadism in young men].

The authors studied 32 biopsies of testes of patients, aged 18 to 26 with various forms of male hypogonadism: Klinefelter's syndrome--16, primary hypotrophy pogonadism with other known and unknown etiology--6, cryptorchism--1, secondary hypogonadism--4, later puberty--3. The materials were studied by the standard histological techniques. The authors report about definite structural changes with the various forms of hypogonadism, manifested in the elements of seminal tubules, Sertoli's cells, basal membrane of the ducts and Leydig's cells, situated in the interstitial spaces.

Adolescent↗
PubMed1978

Moebius syndrome, peripheral neuropathy and hypogonadotrophic hypogonadism.

The association of congenital ophthalmoplegia and facial paresis (Moebius syndrome) with a variety of other developmental somatic defects has been widely recognised. Its co-existence with hypogonadism of hypothalamic/pituitary origin and subclinical peripheral neuropathy has been reported and in this paper we describe the second case of the Moebius syndrome in association with hypogonadotrophic hypogonadism and a progressive peripheral neuropathy of mixed axonal and demyelinating type.

Adolescent↗
PubMed1979

Effect of D-leucine-6-luteinizing hormone-releasing hormone ethylamide in patients with hypogonadotropic hypogonadism with anosmia.

Four men with hypogonadotropic hypogonadism and anosmia were tested with acute intravenous injections of luteinizing hormone-releasing hormone (LH-RH) and D-leucine-6-LH-RH-ethylamide (D-L eu-6-LH-RH-EA) with a 1-week interval. Each patient was then treated with this drug for 60 days and tested again after this period with an intravenous injection of D-L eu-6-LH-RH-EA. The administration of LH-RH resulted in a significant increase in the LH level in only one patient and in follicle-stimulating hormone (FSH) and testosterone increases in none. The analog D-Leu-6-LH-RH-EA resulted in significant increases in LH levels in two patients, in FSH levels in three, and in testosterone levels in one. Results obtained after treatment were closely similar to those observed before treatment. Clinical improvement in terms of increased libido, erection, pubic hair growth, and testicular size was observed. D-Leu-6-LH-RH-EA could be useful in the treatment of patients with hypogonadotropic hypogonadism, a possibility deserving further studies.

Adult↗
PubMed1978

Effects of oral testosterone undecanoate in hypogonadal male patients.

Effects on plasma T, DHT, A, FSH, LH and PRL concentrations and the pituitary responsiveness to the LHRH/TRH stimulation, as well as on libido and sexual, mental and physical activities were studied in ten hypogonadal male patients undergoing therapy with oral testosterone undecanoate (TU) for 9 weeks. The daily dose of TU needed for satisfactory clinical effect was 120 mg (6 cases) and 240 mg (4 cases). There was a significant rise in circulation androgen concentrations in all patients. Mean plasma T, DHT and A increased at 9 weeks from 1.20, 0.12 and 0.36 ng/ml to 4.34 (P less than 0.0004), 0.39 (P less than 0.0004) and 1.24 ng/ml (P less than 0.005), respectively. In hypergonadotrophic patients (N = 6) plasma FSH and LH fell progressively (P less than 0.05), while in hypogonadotrophic patients (N = 4) a marked rise in plasma FSH (P less than 0.05) was found, while LH tended to rise as well. Base-line plasma PRL remained unchanged. In three out of four patients with poor PRL response to TRH, normal responses were established after TU therapy. Increase in libido and sexual activity was reported by nine patients. An increase in mental and physical activity was found in seven and two patients, respectively. Tolerance was excellent. It was concluded that oral TU is an effective form of substitution therapy in male hypogonadal patients.

Adolescent↗
PubMed1979

Metoclopramide induced growth hormone release in hypogonadal males.

The growth hormone (GH) response to 10 mg intravenous metoclopramide (MCP) ('Maxolon'--Beecham Laboratories) was determined in ten hypogonadal adult males. All the subjects responded with a peak growth hormone level greater than 14 mU/l within 1 hour of administration of MCP. Seven normal adult males did not respond to MCP administration. It is concluded that MCP stimulation may be a useful test for both prolactin and growth hormone reserve in hypogonadal males.

Adolescent↗
PubMed1979

Hyperprolactinaemia and hypogonadism in men: response to exogenous gonadotrophins.

Three male patients with pituitary tumours and marked hyperprolactinaemia were investigated. Their prolactin (PRL) levels ranged from 210 to 2500 ng/ml. The subjects had clinical and laboratory characteristics of hypogonadotrophic hypogonadism. All were treated with human chorionic gonadotrophin (HCG) and in one subject human menopausal gonadotrophin (HMG) was given in addition. In all three patients, despite the persistence of hyperprolactinaemia, serum testosterone had risen to normal levels within 4--17 days after starting HCG. Despite the normal testosterone level, impotence persisted in two patients and the third had persistently decreased libido. The hypogonadism in these patients may be related to an absolute reduction in gonadotroph number secondary to destruction by tumour mass. Alternatively, hyperprolactinaemia may inhibit the synthesis or release of the gonadotrophins or LHRH. Despite hyperprolactinaemia, pharmacological doses of HCG induced testosterone secretion in all these three subjects.

Adult↗
PubMed1978

Endocrine studies in primary hypogonadism.

Two 15-year-old boys with primary hypogonadism had evaluation of their hypothalamic-pituitary-gonadal axis. Testicular biopsies and chromsomal studies were also performed. Both patients presented with delayed puberty and short stature and had prepubertal LH, FSH and testosterone concentrations. Serial 24-hour frequent-interval blood studies over a 2-year period in one patient (R.F.) showed a gradual progression from a normal early pubertal LH secretory pattern to one characteristic of 'primary' testicular failure. The testicular biopsies showed prepubertal tests with no significant germinal cell maturation. Although both patients had some somatic stigmata of Noonan's syndrome, they had different karyotypes (XY and xyq-). These studies show that elevated levels of LH and FSH in primary hypogonadism syndrome may not become apparent until after the onset of CNS puberty.

Adolescent↗
PubMedDate not supplied

Congenital anosmia: detection thresholds for seven odorant classes in hypogonadal and eugonadal patients.

Detection thresholds for a representative from each of seven odorant classes (putrid, pepperminty, ethereal, camphoraceous, pungent, musky, floral) were determined by double-blind smell testing of seven normal males, six normal females, 6 patients with uncomplicated congenital anosmia and 13 patients with the syndrome of congenital anosmia and hypogonadotropic hypogonadism (the Kallmann syndrome, olfactogenital dysplasia). The median detection thresholds did not differ significantly between hypogonadal and eugonadal anosmics for any of the odorants, suggesting that the endocrine deficit does not result from inadequate rhinencephalic input to brain centers controlling gonadotropin release. Phenylethylmethylethylcarbinol (PEMEC), a stable chemical of the floral class, was detecred at very low concentrations (10(-6) to 10(-8) M in water) by all normals tested. Since no patient with congenital anosmia was able to distinguish even undiluted PEMEC from water, we suggest that this compound is the material of choice for convenient, rapid and objective testing of the sense of smell (cranial nerve I).

Adolescent↗
PubMed1977

Differential response of serum LH in hypogonadotropic hypogonadism and delayed puberty to LH-RH stimulation before and after clomiphene citrate administration.

The differential diagnosis between hypogonadotropic hypogonadism and delayed puberty is facilitated by comparing the response of gonadotropins to LH-RH stimulation before and after administration of clomiphene citrate 200 mg daily during 7 days. Premedication of clomiphene citrate depresses peak values of LH and FSH on LH-RH in delayed puberty. In hypogonadotropic hypogonadism clomiphene citrate raises LH-RH induced peak LH while FSH does not change.

Adolescent↗
PubMed1979

Repetitive infusion of gonadotropin-releasing hormone distinguishes hypothalamic from pituitary hypogonadism.

Patients who have severe hypogonadotropic hypogonadism caused by presumed hypothalamic disease often have a subnormal LH response to a bolus dose of gonadotropin-releasing hormone (GnRH). To determine if this subnormal response is the result of lack of exposure of the pituitary gonadotroph cells to GnRH, five such men were given daily infusions of 500 microgram GnRH, for 7 days. A standard 250-microgram bolus test dose of GnRH was administered before and again immediately after the week of GnRH infusions. Five men who had severe hypogonadotropic hypogonadism as a result of presumed pituitary disease also received daily GnRH infusions for 1 week. The mean incremental LH responses (+/- SE) to GnRH of the men with presumed hypothalamic disease were 5.0 +/- 1.9 mIU/ml before and 56.9 mIU/ml after the week of infusions. The mean incremental LH responses of the men with presumed pituitary disease were 2.4 +/- 0.7 mIU/ml before and 3.7 +/- 2.9 mIU/ml after the week of infusions. These data suggest that the normal gonadotroph requires prolonged exposure to GnRH for LH responsiveness to become normal, but that the severely damaged gonadotroph cannot be stimulated to release LH normally even by the same prolonged stimulation with GnRH.

Adolescent↗
PubMed1977

Familial idiopathic hypogonadotrophic hypogonadism.

A new case of familial idiopathic hypogonadotrophic hypogonadism is presented: 3 males and 2 females among 9 siblings are affected. Very low to non-detectable levels of plasma LH and FSH levels were found in each patient. LH-RH stimulation test gave in one male a slight increase in plasma LH levels while no change was observed in the others. Prolonged treatment with gonadotrophins or testosterone gave poor results in the males while evidence of ovulation was obtained in the two females during a unique induced artificial cycle with combined HMG and HCG treatment; rapid feminization was also obtained in the females with oestrogen therapy. The striking difference in the results of the substitution treatments between males and females suggest that some degree of acquired insensitivity of the testes to gonadotrophins and of peripheral tissues to male sex hormones are present in male hypogonadotrophic hypogonadism. This may be the consequence of a lack of hormonal stimulation or impregnation during infancy and childhood

Adult↗