[A case of testicular Leydig cell tumor with gynecomastia].
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Gynecomastia
Leydig Cell Tumor
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Summary OBJECTIVE We examined the gonadotrophin secretion in patients with increased plasma concentrations of testosterone and oestradiol due to hCG‐producing tumours. DESIGN Comparison of plasma gonadotrophin concentrations before and after stimulation by GnRH, in eight men with hCG‐producing tumours resulting in Increased testosterone and oestradiol plasma levels, and In 29 men with Leydig cell tumours resulting in increased oestradiol and normal to low testosterone plasma levels. PATIENTS Eight men with hCG‐producing tumours (six with testicular tumours, two with extratesticular tumours), 29 men with Leydig cell tumours and 15 normal men. The six men with germinal cell tumours of the testis were studied before and after unilateral orchidectomy. MEASUREMENTS Plasma concentrations of hCG, testosterone and oestradiol were measured before and after intramuscular injection of hCG. LH and FSH were measured before and after intravenous Injection of 100 μg GnRH. RESULTS Plasma LH and FSH concentrations were low In patients with germ cell tumours, who exhibited increased plasma testosterone and oestradiol concentrations, and were normal in patients with Leydig cell tumours, in whom oestradiol only was increased. Plasma LH and FSH were normalized in the five patients with successful (e.g. normal hCG, testosterone and oestradiol) unilateral orchldectomy. Basal plasma testosterone concentrations correlated positively ( P <001) with plasma oestradiol concentrations in patients with germ cell tumours and negatively ( P <0 01) in patients with Leydig cell tumours. CONCLUSIONS In patients with hCG‐secreting germ cell tumours complete suppression of plasma LH and FSH with increased plasma concentrations of both testosterone and oestradiol are often discovered. No such gonadotrophin suppression is found In patients with Leydig cell tumours, but the negative correlation observed between plasma testosterone and oestradiol in these patients suggests a weak negative feedback effect of oestradiol on LH secretion, which cannot be demonstrated by basal LH measurements in plasma.
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SUMMARY Gynaecomastia caused by Leydig cell tumours (LCT) in adult men may appear a long time before clinical evidence of testicular swelling. To evaluate the diagnostic criteria for LCT, hormonal status was studied in 14 cases and compared with results of a control group (CG) and 10 men with idiopathic gynaecomastia (IG). The mean plasma T level was significantly ( P < 0.005) lower in LCT (16.7 ± 1.7 SEM nmol/l) than in CG (23.0 ± 1.3 nmol/l). However, individual plasma T levels were in the normal range in 9/14 LCT. The mean plasma E 2 level was significantly ( P < 0.001) higher in LCT (204.9 ± 27‐6 pmol/1) than in CG (87.9 ± 7.7 pmol/l). However, individual plasma E 2 levels were in the normal range in 5/14 LCT. In LCT, neither means of basal gonadotrophin levels nor the gonadotrophin responses to LHRH were different from CG. The mean of the plasma T responses to hCG did not differ between LTC, CG and IG. However the mean of E 2 peak responses appeared significantly ( P < 0.005) higher in LCT (735.3 ± 103.4 pmol/l) than in CG (420.5 ± 40.4 pmol/l). The mean of the E 2 peak responses was significantly ( P < 0.001) lower in IG (196.5 ± 33.4 pmol/l) than in CG. Likewise the mean of plasma E 2 levels, measured on day three following hCG administration, remained significantly ( P < 0.001) higher in LCT (662 ± 94 pmol/l) than either in CG (228 ± 14 pmol/l) or in IG (158 ± 25 pmol/l). On day 3 following hCG administration, there was no overlap in individual plasma E 2 levels between either LCT and CG or LCT and IG. In all LCT, plasma β‐hCG levels were in the normal range. A testicular echogram, performed in 12 LCT, confirmed the presence of a palpable tumour in 10 and revealed an occult tumour in two cases. We conclude that normal plasma β‐hCG levels, a prolonged plasma E 2 response to hCG and testicular echogram appear to be the best criteria for early diagnosis of LCT responsible for gynaecomastia in adult men.
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Gonadotropin
Leydig Cell Tumor
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CHORIONIC gonadotropin is known to stimulate growth and endocrine function of the immature human testis. When administered to cryptorchid boys, it can produce enlargement and descent of the testis and, with sufficient amounts, sexual development. In hypogonadotropic eunuchoids, it produces differentiation and growth of Leydig cells and secretion of androgen (1). Little information is available, however, regarding the effects of chorionic gonadotropin on the mature human testis. The purpose of this study has been to determine the effects of chorionic gonadotropin on the structure and function of the adult human testis. During the course of the investigation, an increase in estrogen excretion was regularly observed when the hormone was administered to men having functioning testes. The source of the estrogen, therefore, became one of the major problems of the study. Previous investigations have indicated that the testis is a major source of estrogen in men: castration results in a drop in urinary estrogen l...
Human chorionic gonadotropin
Gonadotropin
Gynecomastia
Equine chorionic gonadotropin
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This study was undertaken to investigate the endocrine changes that occur in male Tig:Wistar rats with Leydig cell tumors, with special reference to immunoreactive inhibin (ir-inhibin) and its dimeric forms. Adult male rats from 2 to 28 months of age were used. Blood samples were taken to measure plasma concentrations of ir-inhibin, inhibin-A, inhibin-B, 17beta-estradiol (E2), testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Inhibin bioactivity in both peripheral plasma and testicular extracts was also measured. Rats aged 18 months and older had testicular Leydig cell tumor. Testicular tissue sections from 27-month-old rats examined immunohistochemically showed strong positive staining for all 3 inhibin subunits, in particular inhibin alpha and betaA subunits, in the tumor cells. Plasma concentrations of ir-inhibin began to rise significantly (P < .05) at 18 months of age. High bioactivity of inhibin was detected not only in testicular extracts but also in peripheral plasma of aged rats. Thus, plasma concentrations of bioactive inhibin-A, but not inhibin-B, were significantly elevated with increasing age. The concentrations were significantly higher than those in normal male (P < .01) or normal female (P < .05) rats. Plasma concentrations of E2 were significantly (P < .05) elevated only at 23-24 months of age. A marked reduction (P < .05 to .001) in plasma LH and FSH concentrations was observed at 18 months of age and older. Plasma concentrations of testosterone were highest at 2 months of age and then decreased gradually and significantly (P < .05 to .001) afterward. Significant (P < .05 to .001) positive (testosterone vs LH) and negative (ir-inhibin vs FSH, ir-inhibin vs LH, and E2 vs FSH) correlations were observed. It is suggested that plasma inhibin-A levels are elevated in male Tig:Wistar rats with Leydig cell tumor, and thus inhibin-A may be used as a specific marker of testicular Leydig cell tumors. The present results also suggest that the age-related decline in plasma gonadotropins and thus testosterone levels in Tig:Wistar rats may be due to the development of tumors of the Leydig cells rather than to aging per se.
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The Rice-500 Leydig cell tumor of Fischer rats is associated with humoral hypercalcemia in vivo and produces a factor that stimulates cAMP formation in cultured rat osteosarcoma cells. We found that cultured human skin fibroblasts respond to both human PTH-(1-34) and the factor produced by cultured rat Leydig tumor cells with a dose-dependent rise in cAMP formation. The time courses for stimulation of the two agents were similar, and stimulation by both was blocked by the competitive PTH antagonist [8,18-norleucine,34-tyrosine]bovine PTH-(3-34) amide. These data suggest that PTH-like factors secreted by a murine tumor are capable of interacting with the human PTH receptor.
Cyclic adenosine monophosphate
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We tested the effects of thyroid hormone on Leydig cell (LC) regeneration in the adult rat testis after ethane dimethyl sulphonate (EDS) treatment. Ninety-day-old, thyroid-intact (n = 96) and thyroidectomized (n = 5) male Sprague-Dawley rats were injected intraperitoneally (single injection) with EDS (75 mg/kg) to destroy LC. Thyroid-intact, EDS-treated rats were equally divided into three groups (n = 32 per group) and treated as follows: control (saline-injected), hypothyroid (provided 0.1% propyl thiouracil in drinking water), and hyperthyroid (received daily subcutaneous injections of tri-iodothyronine, 100 microg/kg). Testing was done at Days 2, 7, 14, and 21 for thyroid-intact rats and at Day 21 for thyroidectomized rats after the EDS treatment. Leydig cells were absent in control and hyperthyroid rats at Days 2, 7, and 14; in hypothyroid rats at all ages; and in thyroidectomized rats at Day 21. The LC number per testis in hyperthyroid rats was twice as those of controls at Day 21. 3beta-Hydroxysteroid dehydrogenase (LC marker) immunocytochemistry results agreed with these findings. Mesenchymal cell number per testis was similar in the three treatment groups of thyroid-intact rats on Days 2 and 7, but it was different on Days 14 and 21. The highest number was in the hypothyroid rats, and the lowest was in the hyperthyroid rats. Serum testosterone levels could be measured in control rats only on Day 21, were undetectable in hypothyroid rats at all stages, and were detected in hyperthyroid rats on Days 14 and 21. These levels in hyperthyroid rats were twofold greater than those of controls on Day 21. Serum androstenedione levels could be measured only in the hyperthyroid rats on Day 21. Testosterone and androstenedione levels in the incubation media showed similar patterns to those in serum, but with larger values. These findings indicate that hypothyroidism inhibits LC regeneration and hyperthyroidism results in accelerated differentiation of more mesenchymal cells into LC following the EDS treatment. The observations of the EDS-treated, thyroidectomized rats confirmed that the findings in hypothyroid rats were, indeed, due to the deficiency of thyroid hormone.
Thiouracil
Leydig Cell Tumor
Testicle
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LH (50 μg) given sc to normal mice and Leydig cell tumor bearing mice promoted a decrease in the content of esterified cholesterol in the testes of normal mice and in the tumor. The observation that LH promoted a change in the tumor ester cholesterol levels was interpreted to mean that its action on testicular ester levels was probably on the interstitial cells. (Endocrinology91: 323, 1972
Leydig Cell Tumor
Interstitial cell
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Anorexia occurs in male rats bearing transplantable.TW(m) Leydig cell tumors. Previous studies had shown that i his tumor caused decreased food consumption and weight loss vithin 2 weeks of implantation. Additional studies reported here demonstrate that this tumor had little anorectic effect in female rats, and that male rats with LTW(m) tumors had eleva,ed concentrations of circulating estradiol and low levels of testosterone. The tumor was also anorexigenic in castrated male rats. Exogenous estrogen given in the form of sc implanted pellet 8 of estradiol reduced weight gain in male rats in proportion to ths dose of estradiol. Weight gain was reduced when the plasma estradiol concentration was as low as 49 ± 3 pg/ml; control estradiol levels were 25 ± 4 pg/ml. Similar effects were observed in male Zucker fatty rats. It was further demonstrated that the tumor is anorexigenic in ventromedial hypothalamuslesioned rats, an effect previously observed in ventromedial hypothalamus-lesioned rats given exogenous estradiol. Carcass analysis revealed that tumor-bearing rats used a metabolic fuel mixture containing a higher percentage of fat-derived substrates compared to nonimplanted controls, suggesting that altered fuel utilization may contribute to the decreased weight gain of tumorbearing rats. We conclude that the circulating substance responsible for LTW(m) tumor-induced anorexia in male rats is likely to be an estrogenic steroid. (Endocrinology115: 167–173,1984)
Anorectic
Anorexia
Leydig Cell Tumor
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A 14-yr-old boy developed spectacular gynecomastia in association with pubescent growth and rapid sexual maturation. Histologic examination of the testis disclosed plump active Leydig cells and accompanying spermatogenesis. Breast tissue was like that usually seen in gynecomastia and did not contain detectable quantities of the specific 8S estradiol binding protein and also failed to convert testosterone to dihydrotestosterone. The plasma concentration of testosterone was consistently above the range observed in normal men and other pubertal boys. The plasma estradiol concentration was proportionately elevated. Adrenocortical steroids were present in normal amounts. Plasma FSH and LH concentrations were also within the normal range. Testosterone and estradiol concentrations rose with chorionic gonadotropin therapy, but the testosterone level was not suppressed by treatment with prednisone or fluoxymesterone. It was concluded that the gynecomastia was the result of elevated levels of testicular sex hormones. This hyperleydigism was explained on the basis of a failure of the negative hypothalamic-pituitary feedback system to respond appropriately to circulating testosterone and estradiol.
Gynecomastia
Dihydrotestosterone
Gonadotropin
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An 18-yr-old eunuchoidal male complained of gynecomastia and galactorrhea of 8 yr duration. Clinical studies excluded the gross lesions generally associated with these findings. The testostei'one excretion rate was low and showed a subnormal rise during acute stimulation with human chorionic gonadotropin despite a 3-fold increase in 17-ketosteroids. The control excretion of luteinizing hormone was normal. Spermatic vein analysis of steroids demonstrated secretion of dehydroepiandrosterone but not of testosterone or androstenedione. The conversion rate of androstenedione to urinary testosterone glucuronoside was reduced. The reduced testosterone excretion rate is best explained by a testicular defect in testosterone synthesis and in addition a diminished ability to convert precursors peripherally to testosterone glucuronoside.
Gynecomastia
Galactorrhea
Human chorionic gonadotropin
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