Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve adult males with documented active Cushing's disease were studied. Mean plasma testosterone (T) was significantly decreased: 1.8 +/- 0.3 (SEM) ng/ml (N=6.8 +/- 0.5); gonadotropin measurements in 8 patients, in basal conditions and under LH-RH iv, showed a significant decrease in both FSH and LH. A further study of 11 patients in remission of Cushing's disease indicated a significant increase in plasma T and gonadotropins up to the normal range. One patient with an initial low T value had a normalized T while in remission, then a dramatic decrease when the disease relapsed. We conclude: a hypogonadotropic hypogonadism is found in male Cushing's disease; it disappears as early as hypercortisolism is suppressed. Some possible mechanisms are discussed.
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PMID:Reversible gonadotropin deficiency in male Cushing's disease. 19 24

The short-term metabolic effects of testosterone treatment on circulating levels of 1,25-dihydroxyvitamin D and insulin-like growth factor-I (IGF-I) were studied in 13 hypogonadal men. The study group included 11 men with Klinefelter's syndrome, with varying degree of androgen deficiency, and two men with secondary hypogonadism. Pretreatment levels of 1,25-dihydroxyvitamin D, vitamin D-binding protein and IGF-binding protein-I were all within the normal range. The levels of IGF-I were lower than normal in 5/11 of the Klinefelter patients and in one patient with GH-deficiency. Testosterone treatment increased circulating total 1,25-dihydroxyvitamin D significantly from 75 +/- 4 pmol l-1 (mean +/- SEM) to 86 +/- 4 (P less than 0.01) and the free 1,25-dihydroxyvitamin D-index from 1.95 +/- 0.11 to 2.39 +/- 0.12 (P less than 0.01). Serum levels of IGF-I increased from 117 +/- 22 micrograms/l to 143 +/- 23 (P less than 0.01) during androgen treatment. No significant effects on levels of IGF-binding protein-I were seen. It is concluded that androgen therapy increases the availability of 1,25-dihydroxyvitamin D and the level of IGF-I, which may be important links in the action of testosterone.
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PMID:Testosterone increases serum 1,25-dihydroxyvitamin D and insulin-like growth factor-I in hypogonadal men. 157 32

Although TRH stimulates the release of uncombined alpha-subunit into the circulation in patients with primary hypothyroidism, it is not clear whether alpha-subunit is released from the thyrotrophs in euthyroid subjects. We hypothesized that spontaneous fluctuations in circulating alpha-subunit released from gonadotrophs by GnRH in normal adults could obscure the detection of small changes in alpha-subunit after TRH administration. We, therefore, examined alpha-subunit responses to TRH in five euthyroid men with idiopathic hypogonadotropic hypogonadism (IHH), who produce little or no GnRH, five normal men, and four postmenopausal women. Mean (+/- SEM) basal serum alpha-subunit levels were significantly (P less than 0.05) less in men with IHH (0.26 +/- 0.07 microgram/L) than in the normal men (0.80 +/- 0.20 microgram/L) or postmenopausal women (3.54 +/- 0.60 microgram/L). alpha-Subunit levels rose after TRH administration in all men with IHH to a peak level of 0.86 +/- 0.25 ng/ml; TSH levels also increased from 1.9 +/- 0.4 to 13.0 +/- 5.6 mU/L. The increment in TSH and alpha-subunit levels was highly positively correlated (r = 0.96). alpha-Subunit levels also increased 2-fold in normal men given TRH, whereas alpha-subunit levels in postmenopausal women were unchanged. We conclude that thyrotrophs release alpha-subunit into the circulation in normal men and euthyroid men with IHH. Thus, both thyrotrophs and gonadotrophs appear to contribute to circulating alpha-subunit in men with IHH; however, most of the uncombined alpha-subunit in normal men appears to be from gonadotrophs.
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PMID:Pituitary glycoprotein hormone alpha-subunit secretion after thyrotropin-releasing hormone stimulation in normal men and men with idiopathic hypogonadotropic hypogonadism. 168 69

To study the ontogeny of spontaneous pulsatile LH and FSH secretion before the onset of puberty, plasma LH and FSH were measured by an ultrasensitive time-resolved immunoflurometric assay in 16 boys and 6 girls, aged 6.5 +/- 0.2 yr (+/- SEM; range, 4.4-8.0) with short stature. Eight male patients with idiopathic hypogonadotropic hypogonadism (Kallmann's syndrome), aged 24.1 +/- 3.4 yr, were also investigated. Blood samples were withdrawn at 10- to 20-min intervals for 12 h from 2000-0800 h. Pituitary responsiveness was assessed by a standard iv LHRH challenge test. LH and/or FSH pulses were detectable in all but two prepubertal subjects. In boys, low amplitude LH (0.16 +/- 0.06 U/L) and FSH (0.19 +/- 0.03 U/L) pulses were detectable at mean frequencies of 2.19 +/- 0.37 and 2.13 +/- 0.46 pulses/12 h, respectively. In girls, low amplitude LH (0.29 +/- 0.18 U/L) pulses, but higher (P less than 0.05 compared to boys) amplitude FSH (1.62 +/- 1.05 U/L) pulses were observed at frequencies of 1.71 +/- 0.56 and 1.67 +/- 0.53 pulses/12 h, respectively. Mean FSH in prepubertal girls (1.95 +/- 0.88 U/L) was significantly (P less than 0.05) higher than that in boys (0.46 +/- 0.07 U/L), but mean LH was not different at 0.17 +/- 0.07 and 0.10 +/- 0.03 U/L, respectively. Patients with Kallmann's syndrome had mean LH and FSH levels indistinguishable from those of prepubertal boys. Nocturnal augmentation of pulsatile LH or FSH secretion was observed in 74% of children (71% in girls and 75% in boys), but in none of the eight patients with Kallmann's syndrome. A close temporal association was observed between sleep onset and the appearance of nocturnal pulsatile gonadotropin secretion. The FSH response to exogenous LHRH in prepubertal girls was significantly greater than that in patients with Kallmann's syndrome and prepubertal boys, but LH responses were not different. Our results show that pulsatile LH and FSH secretion occurs in the majority of boys and girls in midchildhood, with a robust association with nocturnal sleep onset. Between the ages of 4-8 yr, these low amplitude and low frequency pulses are unable to activate gonadal function. The regulation of FSH secretion in prepubertal girls appears to be different from that in prepubertal boys.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Patterns of pulsatile luteinizing hormone and follicle-stimulating hormone secretion in prepubertal (midchildhood) boys and girls and patients with idiopathic hypogonadotropic hypogonadism (Kallmann's syndrome): a study using an ultrasensitive time-resolved immunofluorometric assay. 190 43

The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.
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PMID:Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG. 195 14

Although pharmacological doses of GnRH and TRH stimulate free alpha-subunit (alpha-subunit) secretion from the pituitary, little is known about the pattern and control of alpha-subunit release under physiological circumstances. Euthyroid men with idiopathic hypogonadotropic hypogonadism, a condition of deficient GnRH release, provide a unique opportunity to study alpha-subunit secretion before and during administration of a physiological regimen of GnRH administration. Before GnRH therapy, six euthyroid IHH men with normal endogenous TSH secretion had circulating alpha-subunit levels close to or below assay detection limits, with a mean level less than 0.5 ng/ml. During 12-42 weeks of physiological GnRH replacement, serum alpha-subunit concentrations rose to a mean value of 2.07 +/- 0.3 (+/- SEM) ng/ml (P less than 0.01). After GnRH administration, alpha-subunit was released in a pulsatile pattern following each dose of GnRH and mirrored the secretory pattern of LH. Increases in serum alpha-subunit concentrations during GnRH administration were closely correlated with increases in LH (r = 0.91; P less than 0.01), but not FSH (r = 0.24; P = NS), levels. In addition, a situation in which LH secretion was clearly predominant and FSH levels were barely detectable was created by increasing the frequency of GnRH administration to every 30 min. In this circumstance, free alpha-subunit concentrations increased in conjunction with LH levels in the face of decreased FSH levels. We conclude that replacement of GnRH regulates both the level and pattern of alpha-subunit secretion in GnRH-deficient men, and that there is tight correlation of alpha-subunit with LH, but not with FSH, secretion.
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PMID:Administration of low dose pulsatile gonadotropin-releasing hormone (GnRH) to GnRH-deficient men regulates free alpha-subunit secretion. 241 48

The authors compared curvilinear velocity (Vc) and linearity (L) of sperm from fertile oligospermic men with isolated hypogonadotropic hypogonadism (IHH) to Vc and L of sperm from fertile normal men in order to determine if sperm motion analysis is better than sperm density as an indicator of fertility potential. Nine fertile men with IHH treated with exogenous gonadotropins and 20 fertile normal men were studied. Sperm density was significantly lower in the men with IHH compared with normal men (15.5 +/- 4.8 x 10(6)/ml versus 92.4 +/- 9.7 x 10(6)/ml; mean +/- standard error of the mean [SEM]; P less than 0.01) as was percent motility (51.4 +/- 4.7 versus 73.4 +/- 3.1; P less than 0.01). While a small but significant difference in Vc was noted between the groups at the 40 micron/second cumulative distribution point (P less than 0.01), no difference in L was found between the two groups. When the men with IHH were subgrouped according to sperm density (greater than 20 x 10(6)/ml versus less than or equal to 20 x 10(6)/ml, no differences in Vc were found between the subsets, but for L sperm were somewhat less directional for the subgroup with a density less than or equal to 20 x 10(6)/ml (P = 0.05). Coanalysis using both Vc and L parameters indicated that sperm from IHH patients were distributed similarly to sperm from normal men. However, sperm motion characteristics in men with unexplained infertility were different from values measured in normal men and IHH patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sperm motion characteristics in men with isolated hypogonadotropic hypogonadism treated with gonadotropin. 264 9

Several lines of evidence indicate that hypothalamic-pituitary-gonadal activity varies among men with idiopathic hypogonadotropic hypogonadism (IHH). To test the hypothesis that a spectrum of abnormalities of GnRH secretion underlies the syndrome of IHH, we characterized the patterns of GnRH-induced gonadotropin secretion during periods of frequent sampling in 50 consecutive men with IHH and contrasted them with those in 20 normal men. The largest group of IHH patients (n = 42) had no detectable LH or FSH pulsations and could be categorized into 2 subsets according to the presence or absence of evidence of spontaneous puberty. The most severely affected subset (n = 32), who recalled no history of puberty, had testes with a mean volume of 3.3 +/- 0.5 (+/- SEM) ml, with a prepubertal appearance on biopsy, and often were anosmic (n = 17). The second subset of apulsatile IHH men (n = 10) had histories of partial or complete spontaneous sexual development with subsequent isolated loss of sexual function, testes with a mean volume of 13.3 +/- 1.9 ml (P less than 0.01 compared to the first subset), a pubertal or adult appearance of the testes on biopsy, and an intact sense of smell. In a second group of IHH patients (n = 3), LH was secreted predominantly in a nighttime pattern similar to that of normal children during early puberty. These men were aged 18-24 yr, had a mean testicular volume of 10.5 +/- 2.3 ml, pubertal changes on testicular biopsy, and an intact sense of smell. A third group of IHH men (n = 4) had LH pulses of abnormally low amplitude. Only one patient in this group had a history of spontaneous sexual development. The mean testicular volume of these patients was 5.6 +/- 1.9 ml, and the testes appeared prepubertal (n = 3) or pubertal (n = 1) on biopsy. In addition to these groups, another patient had apparent LH pulsations and nearly normal amplitude, but the LH was bioinactive and appeared to consist chiefly of alpha-subunit. Testing of other anterior pituitary hormone functions did not distinguish IHH men from normal men. However, those IHH patients with some evidence of endogenous GnRH secretion had higher basal and stimulated serum PRL levels than IHH men without such evidence (P less than 0.05), suggesting an influence of GnRH on PRL secretion.
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PMID:The spectrum of abnormal patterns of gonadotropin-releasing hormone secretion in men with idiopathic hypogonadotropic hypogonadism: clinical and laboratory correlations. 309 71

To test the hypothesis that the frequency of pulsatile LHRH stimulation can differentially control LH and FSH secretion in man, we administered low doses of LHRH in pulsatile fashion in several different regimens to men with idiopathic hypogonadotropic hypogonadism (IHH) and presumed endogenous LHRH deficiency. In study 1, four men with IHH received a constant amount of LHRH per day in three different frequencies. After an initial 7-day period of LHRH (5.0 micrograms every 2 h), the men received 2.5 micrograms every 1 h and 7.5 micrograms every 3 h, each for 4 days, in varying order. Frequent blood samples were obtained before LHRH administration and at the end of each regimen. Before LHRH administration, mean serum FSH and LH levels were low [28 +/- 3 (+/- SEM) and 6 +/- 2 ng/mL, respectively], and they increased into the normal adult male range during LHRH treatment. As the frequency of LHRH administration decreased from every 1 to 2 to 3 h, serum FSH levels progressively increased from 99 +/- 33 to 133 +/- 34 to 181 +/- 58 ng/mL (P less than 0.05). Serum LH levels (34 +/- 6, 33 +/- 6, and 34 +/- 5 ng/mL) were significantly higher than those before LHRH administration and did not differ significantly among the three regimens. Total serum testosterone (T), estradiol, and free T levels were increased by LHRH, but were not significantly different during the three regions of LHRH administration. In study 2, three men with IHH received the same amount of LHRH per dose, given in two different pulse frequencies; 2.5 micrograms LHRH were administered in frequencies of every 0.5 h and every 1.5 h, each for 4 days, in varying order. During the 0.5 h frequency, the mean serum FSH level was 42 +/- 13 ng/mL, and it rose to 80 +/- 19 ng/mL during the 1.5 h frequency (P less than 0.05). Corresponding mean serum LH levels were 25 +/- 5 and 27 +/- 4 ng/mL. Serum T and estradiol levels were not significantly different during the two LHRH regimens. We conclude that the frequency of LHRH stimulation can differentially control FSH and LH secretion by the human pituitary gland, and the pattern of hormonal stimulation may be a determinant of target organ response.
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PMID:Differential control of luteinizing hormone and follicle-stimulating hormone secretion by luteinizing hormone-releasing hormone pulse frequency in man. 310 45

Plasma LH and FSH were measured every 20 min in a group of patients with Klinefelter's syndrome before and after placebo or naloxone administration (8 mg iv as a bolus followed by an infusion of 4 mg/h for 4 h) both in baseline conditions (N = 6) and during treatment with testosterone enanthate (200 mg im every two weeks; N = 4). The mean LH areas measured during saline infusion in baseline conditions (7888 +/- 758 IU/l per min mean +/- SEM) and during testosterone treatment (5042 +/- 2039 IU/l per min) were not significantly different from those measured during naloxone infusion (baseline 8317 +/- 818 IU/l per min; during testosterone treatment 5395 +/- 2007 IU/l per min). Similar results were obtained for FSH. These data suggest that in patients with Klinefelter's syndrome, the opioidergic inhibition of gonadotropin release is lacking and is not restored by testosterone replacement therapy.
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PMID:Naloxone administration does not affect gonadotropin secretion in patients with Klinefelter's syndrome. 311 47


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