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PubMed1991

Effect of 4-hydroxyandrostenedione on murine Leydig tumor cell steroidogenesis.

The murine Leydig cell tumor (M5480A) possesses high levels of estrogen receptor and is known to produce estrogens. In these studies we examined the effects of the potent aromatase inhibitor 4-hydroxyandrostenedione (4-OHA) on Leydig tumor cell steroidogenesis both in vitro and in vivo. The addition of 4-OHA to Leydig tumor cells in primary culture resulted in a dose- and a time-dependent decrease in media progesterone levels. The observed decrease was most likely due to impaired synthesis of progesterone, inasmuch as no alteration in progesterone metabolism was seen when progesterone levels were diminishing. However, 4-OHA inhibited progesterone conversion to testosterone following 1 h of incubation, but this effect disappeared coincident with 4-OHA metabolism. Analysis of pregnenolone production revealed a biphasic dose-dependent effect of 4-OHA. At low doses (0.01-0.1 microM), 4-OHA was found to decrease pregnenolone concentrations, while at higher doses (1-10 microM) pregnenolone levels were elevated. Therefore, the actions of 4-OHA on Leydig cell steroidogenesis in vitro appear to be multifocal. Other experiments were performed to evaluate the effects of 4-OHA on tumor-bearing male mice in vivo. In these studies, the predominant effects of 4-OHA were to act as an aromatase inhibitor and to inhibit progesterone production. Thus, while 4-OHA is a potent aromatase inhibitor, we have found that this compound may alter steroidogenesis in Leydig tumor cells at several sites prior to aromatization.

Androstenedione↗
PubMedDate not supplied

Absence of activating mutations in the hot spots of the LH receptor and Gs-alpha genes in Leydig cell tumors.

Leydig-cell tumors are functioning endocrine tumors that produce T autonomously leading to isosexual precocity in boys and virilization in female patients. Molecular abnormalities such as activating mutations of the luteinizing hormone receptor (LHR), a G protein-coupled receptor, and of the Gs-alpha subunit of G protein have recently been described in these tumors. Both mutations cause continuous activation of the cAMP signaling cascade, autonomous production of T and cell proliferation. We searched for activating mutations in exon 11 of the LHR gene and in exons 8 and 9 of the Gs-a gene, which contain all hot spots for those mutations, in 4 Leydig cell tumors obtained from 4 patients (one boy with LH-independent precocious puberty and 3 women with virilization). DNA was extracted from paraffin-embedded neoplastic and non-neoplastic tissues and from peripheral lymphocytes. Hot spot regions of exons 11 of LHR and exons 8 and 9 of Gs-alpha genes were amplified by PCR and the purified PCR products were directly sequenced. No LHR or Gs-alpha gene mutations were found in the 4 tumors studied. Considering the previously reported mutations found in Leydig cell tumors, the absence of activating mutations in the hot spot regions for activating mutations in these tumors indicate molecular heterogeneity among Leydig cell tumors.

Aged↗
PubMed2006

Enucleation for prepubertal leydig cell tumor.

PURPOSE: Leydig cell tumors in children are rare, comprising only 4% to 9% of all primary testis tumors in prepubertal males. Almost all of these boys present with isosexual precocious pseudopuberty associated with increased testosterone, low gonadotropin levels and a testis mass. We present our experience with testis sparing enucleation of Leydig cell tumor in prepubertal boys. MATERIALS AND METHODS: Two patients presented with isosexual precocious puberty at ages 6 and 9 years. Each patient had a well circumscribed, painless testicular mass, increased serum testosterone (101 and 444 ng/dl [normal 0 to 25]), normal gonadotropins and negative alpha-fetoprotein levels. Both patients underwent successful enucleation of the testis mass following proper testis oncological surgical principles. RESULTS: Both patients had normalization of the serum testosterone following enucleation of the Leydig cell tumor. At 9 and 44 months of followup they have maintained normal ipsilateral testicular volume compared to the contralateral gonad, and 1 patient entered puberty spontaneously at 1 year postoperatively. Neither patient suffered any morbidity, and both have presumably benefited from preservation of the involved gonad with preserved testicular volume. CONCLUSIONS: Prepubertal boys with isosexual precocious pseudopuberty, an isolated testis mass, increased testosterone and low or normal gonadotropin levels can reliably be diagnosed with Leydig cell tumors. Based on the ability to establish the diagnosis preoperatively and the universal benign behavior of unilateral, prepubertal Leydig cell tumor, we believe these patients are best treated with testis sparing enucleation of the tumor. In view of the high likelihood that this tumor in prepubertal boys is benign, a transscrotal surgical approach should be considered.

Child↗
PubMed1999

Inhibition of hCG-stimulated steroidogenesis in cultured mouse Leydig tumor cells by bisphenol A and octylphenols.

Some environmental chemicals exhibit estrogenic or antiandrogenic activity. Some of these, such as bisphenol A (bis A) and octylphenols, are used in large amounts in many applications. We have analyzed the effects of bis A and octylphenols on steroidogenesis in Leydig cells by measuring the LH receptor-mediated cAMP and progesterone (P) production in cultured mouse Leydig tumor cells (mLTC-1 cells). After preincubation of mLTC-1 cells for 48 h in the presence of bis A or one of the octylphenols in micromolar concentration, the hCG-stimulated cAMP and P formation in these cells was inhibited. Bis A or octylphenols could neither inhibit cAMP nor P formation stimulated by forskolin (Fk) or cholera toxin (CT) nor steroidogenesis stimulated by 8-Br-cAMP. The preincubation of mLTC-1 cells with estradiol or diethylstilbesterol (DES) at the concentration of 10(-8) mol/liter had no inhibitory effect on cAMP formation stimulated by hCG or Fk but P production was inhibited. Similarly, both estrogens inhibited P production stimulated by 8-Br-cAMP. Bis A or octylphenols had no effect on 125I-hCG binding to Leydig cell LH-receptors. Thus, these environmental chemicals appear to inhibit cAMP formation and steroidogenesis in mLTC-1 Leydig tumor cells by preventing the coupling between LH receptor and the adenylate cyclase. Since, estradiol did not inhibit hCG-stimulated cAMP production, the effects of bis A and octylphenols may not be estrogen related. This emphasizes the complexity of endocrine disruption: chemicals show multiple endocrine activities that may disturb several organs in distinct ways.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Effect of different steroidogenic stimuli on protein phosphorylation and steroidogenesis in MA-10 mouse Leydig tumor cells.

Numerous studies have indicated that treatment of Leydig cells with gonadotropin results in increased levels of intracellular cAMP, binding of cAMP to and activation of protein kinase A, phosphorylation of proteins, synthesis of new proteins and eventually, stimulation of steroidogenesis. In addition, recent studies have indicated that protein phosphorylation is an indispensable event in the production of steroids in response to hormone stimulation in adrenal cells. Because of the important role of phosphorylation in steroidogenic regulation, we investigated the effects of human chorionic gonadotropin (hCG), dibutyryl cyclic AMP (dbcAMP), forskolin and the phorbol ester, phorbol-12-myristate 13-acetate (PMA) on protein phosphorylation in MA-10 mouse Leydig tumor cells. Cells were stimulated with different steroidogenic compounds in the presence of [32P]orthophosphoric acid for 2 h and phosphoproteins analyzed by two-dimensional polyacrylamide gel-electrophoresis (PAGE). Results demonstrated an increase in the phosphorylation of four proteins (22 kDa, pI 5.9; 24 kDa, pI 6.7 and 30 kDa, pI 6.3 and 6.5) in response to 34 ng/ml hCG, 1 mM dbcAMP and 100 microM forskolin. Conversely, treatment of cells with PMA increased the phosphorylation of only one of these proteins (30 kDa, pI 6.3). At least two of these proteins (30 kDa, pI 6.5 and 6.3) appear to be identical to proteins which we and others have shown to be synthesized in response to trophic hormone stimulation in adrenal, luteal and Leydig cells. In addition, they also appear to be identical to adrenal cell mitochondrial proteins demonstrated to be phosphorylated in response to ACTH. These data indicate that proteins similar to those phosphorylated in adrenal cells in response to ACTH are phosphorylated in hormone stimulated testicular Leydig cells and that these proteins may be involved in steroidogenic regulation.

Animals↗
PubMedDate not supplied

Effect of mono-ethylhexyl phthalate on MA-10 Leydig tumor cells.

We examined the effect of mono-ethylhexyl phthalate (MEHP) on MA-10 Leydig tumor cell structure and function. Cells were exposed to various concentrations of MEHP for 24 h and then stimulated with saturating concentrations of hCG for 2.5 h. Progesterone production, cell viability, and protein content were moderately inhibited by low concentrations and severely inhibited by high concentrations of MEHP. Electron microscopy showed a variety of alterations in the MEHP-treated cells, increasing in severity with increasing concentrations of MEHP. Lipid droplets were profoundly affected in the cells treated with MEHP and morphologic evidence that metabolism of lipid storage droplets ceases at approximately the same time progesterone synthesis stops was seen. Morphometric studies indicated that the number of lipid droplets appeared to be increased 2.5-fold over control levels at MEHP concentrations of 10(-6) to 10(-3) M whereas mitochondrial volume fraction decreased. These results suggest that MEHP in Leydig cells may act as a mitochondrial toxicant and lipid metabolism disrupter.

Animals↗
PubMed1993

Cytotoxic activity of lutropin-gelonin conjugate in mouse Leydig tumor cells: potentiation of the hormonotoxin activity by different drugs.

A hormonotoxin preparation composed of gelonin, a basic protein of 30,000 Da isolated from the plant Gelonium multiflorum and the luteinizing hormone (LH, lutropin) isolated from the sheep pituitary has been studied for its cytotoxic action on mouse testicular Leydig tumor cells (MA-10 cells). Gelonin modified with 2-iminothiolane and conjugated with hormone modified by N-succinimidyl-3-2-pyridyl dithiopropionate was able to inhibit protein synthesis in Leydig tumor cells. An enhancement of the cytotoxicity of the hormonotoxin was obtained in the presence of drugs like quinacrine, chloroquine, verapamil and monensin. We report that the cytotoxicity of hormonotoxin was enhanced 10-15 times with quinacrine (7.6 microM), chloroquine (29 microM), verapamil (40 microM) and monensin (0.29 microM). While quinacrine, chloroquine and verapamil were not cytotoxic to MA-10 cells for up to 48 h, monensin alone reduced protein synthesis significantly in 48 h. All the drugs studied here inhibited steroidogenic action of the native hormone even at concentrations which were not detrimental to protein synthesis. On the basis of the above studies, we suggest that it may be feasible to develop combination strategies to destroy gonadal cells bearing gonadotropin (LH) receptors. In cells not bearing LH receptors (COS-7 cell line) there was no cytotoxicity either with hormonotoxin alone or in combination with the drugs, suggesting specificity of action.

Animals↗
PubMed1989

Effects of hormones and intracellular mediators on differentiated functions of cultured Leydig tumor cells.

Cellular regulation by hormones that utilize a myriad of intracellular signaling pathways is recognized to be quite complex. To investigate some of these effects in an established cell line, we tested a panel of hormones and modulators for their effects on cyclic AMP (cAMP) and progesterone production, both alone and in combination with human chorionic gonadotropin (hCG), using the MA-10 cultured Leydig tumor cell line. None significantly affected intracellular levels of cAMP, and only epidermal growth factor (EGF) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) stimulated progesterone production. While EGF, basic fibroblast growth factor, insulin, insulin-like growth factor-1, and transforming growth factor beta all decreased cAMP production only, TPA decreased hCG-stimulated cAMP and progesterone production. Those factors that stimulated progesterone production also induced a characteristic morphological change ("rounding") of these cells. In addition, EGF, insulin, and TPA, like hCG, elevated mRNA levels of competence oncogenes (c-fos and c-myc), albeit to different extents. These data demonstrate the wide range of hormones to which the cultured Leydig tumor cell will respond, as well as the varying degree of responses observed in the intracellular signaling pathways that we examined.

Animals↗
PubMed2001

7,12-Dimethylbenz[a]anthracene inhibition of steroid production in MA-10 mouse Leydig tumor cells is not directly linked to induction of CYP1B1.

Testosterone, which is essential for spermatogenesis, is synthesized in the Leydig cells of the testis. This study addresses whether male reproductive toxicity from exposure to polycyclic or polychlorinated aromatic hydrocarbons, such as 7,12-dimethylbenz[a]anthracene (DMBA) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), may be due to direct effects on Leydig cell function. Using a cell-based assay, the effects of TCDD, benz[a]anthracene (BA), and DMBA on steroid production and cytochrome P4501B1 (CYP1B1) expression in treated MA-10 mouse Leydig tumor cells or primary cultures of rat Leydig cells was determined. (Bu)(2)cAMP-stimulated steroid production was inhibited approximately 25% and approximately 80% by DMBA treatment of MA-10 cells and rat Leydig cells, respectively, while BA or TCDD were without effect. Conversely, male Sprague-Dawley rats treated with TCDD displayed a 75% decrease in serum testosterone levels, while DMBA-treated rats had circulating testosterone levels comparable to control rats. Injection of human chorionic gonadotropin (hCG) 1 h prior to euthanasia restored testosterone levels in TCDD-treated rats to 79% of the hCG-stimulated levels in control rats. Steady-state levels of CYP1B1 mRNA, as detected by RT-PCR, are present in the MA-10 cells and treatment with TCDD, BA, DMBA, or the cAMP analog (Bu)(2)cAMP induced CYP1B1 mRNA expression levels. CYP1B1 was constitutively expressed in rat testis, adrenal, liver, and kidney tissues while CYP1A1 was undetectable. TCDD treatment induced CYP1B1 expression in the adrenal and liver and CYP1A1 in the kidney and liver. DMBA treatment induced only CYP1A1 levels in kidney and liver. In sum, DMBA or a reactive DMBA metabolite, but not TCDD, has a direct effect on steroidogenesis in isolated Leydig cells. CYP1B1 expression levels, however, cannot be directly correlated to potential in vitro or in vivo toxic effects of TCDD or DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Expression of aromatase cytochrome P450 in rat H540 Leydig tumor cells.

The rat H540 Leydig cell tumor has been shown to express cholesterol side-chain cleavage and 17alpha-hydroxylase cytochrome P450s, 3beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase, and steroid 5alpha-reductase, making it a useful model in which to study steroidogenesis. In the current studies, we report that cultured H540 cells express high levels of aromatase cytochrome P450 (P450arom), which converts androgens to estrogens. Levels of aromatase activity varied from 9.4 to 51.7 pmol/h/mg protein and inhibition of 5alpha-reductase with finasteride did not significantly effect aromatase measurements, indicating that 5alpha-reductase is not competing for the substrate used in the aromatase assays. Aromatase activity was decreased 95% by preincubating the cells with 4-hydroxyandrostenedione, an aromatase inhibitor. Characterization of the aromatase mRNA expressed in the H540 cell line demonstrates that, like R2C cells and rat ovarian tissue, three distinct P450arom mRNA species are detected by Northern analysis, and that these transcripts are derived from the same site of transcription initiation. Despite these similarities, the regulation of aromatase activity by 8-bromo-cAMP in H540 cells differs from both R2C cells and rat ovarian tissue. As the H540 and R2C cell lines appear to have distinct origins, H540 is the second rat Leydig tumor cell line characterized that constitutively expresses high levels of aromatase.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

[Gynecomastia and Leydig cell tumor].

INTRODUCTION: Leydig cell tumors may generate estrogen production and gynecomastia. CASE PRESENTED: A 32-year man asked for medical advice due to gynecomastia. He had raised estrogen levels and diminished testosterone/estradiol index. A testicular echogram showed a nodular image in the right testis. Orchidectomy was performed and the diagnosis of a Leydig cell tumor was confirmed. The gynecomastia diminished, and estradiol remained lightly elevated, with little response to HCG. DISCUSSION: The more frequent hormonal manifestations of these tumors are high plasmatic and urinary estrogen levels, low serum testosterone, low testosterone/estradiol index, and FSH or LH low levels as well. The low response to HCG, the absence of metastasis and the good clinical evolution suggested the tumor was benign. Testicular echography is useful in the diagnosis of these tumors.

Adult↗
PubMed1978

Gonadotropin binding and stimulation of steroidogenesis in Leydig tumor cells.

Testicular tumors are generally characterized by a loss of responsiveness to gonadotropins. The M5480 Leydig cell tumor is unusual, if not unique, in that it responds to human choriogonadotropin and to lutropin via increased steroidogenesis. This report describes the identification of two variants of the original M5480 tumor that have altered steroid output both in the basal state and in response to human choriogonadotropin. One of the tumors produces mainly progesterone, which is stimulated by the choriogonadotropin; the other tumor produces about equal amounts of progesterone and testosterone, and the secretion of both is stimulated by the choriogonadotropin. The dissociation constant describing the interaction between Leydig tumor cells and (125)I-labeled human choriogonadotropin is between 3 and 5x10(-11) M. This agrees with values reported for normal Leydig cells, although the tumor cells appear to have fewer receptors. The differences noted in the two tumors and normal Leydig cells may have arisen from alterations in gene regulation, or in mutations, involving one or more enzymes in the pathway in which progesterone is converted to testosterone. Under the experimental conditions used, all the tumors studied (seven generations) responded to the choriogonadotropin both in binding and in the resultant stimulation of steroidogenesis. This property, together with the characteristic that a homogeneous cell population can be obtained without enzymatic treatment, should qualify the M5480 Leydig cell tumor(s) as a model system for further studies on the mechanism of action of gonadotropin, on hormone receptors, and on hormonally responsive tumors.

Animals↗
PubMed1996

Regulation of function of the murine luteinizing hormone receptor promoter by cis- and trans-acting elements in mouse Leydig tumor cells.

The transcriptional activity of various lengths of the 5'-untranslated region (UTR) of the murine LH receptor (R) gene were studied using the luciferase reporter gene in transiently transfected mouse Leydig tumor cells (mLTC-1). Chinese hamster ovarian (CHO) and HeLa cells were used as controls. The basal transcriptional promoter activity in mLTC-1 cells resided within the first 173 base pairs (bp) of the 5'-UTR. Placing an LHR promoter fragment (bases -715/ -56) in front of the Herpes simplex virus thymidine kinase (TK) minimal promoter resulted in a 7-fold increase in luciferase activity. Deletion of bases -56 to -173 of the above construct totally abolished the increased luciferase activity, brought about by the LHR promoter sequences. Basically similar results on LHR promoter function were observed using CHO cells. In contrast, no LHR promoter activity was detected in HeLa cells, indicating a cell specific nature of its function. The first 173 bp promoter domain is GC-rich, with several SP-1 binding domains, and it bound specifically nuclear proteins isolated from mLTC-1 and HeLa cells. RNAse protection assays reconfirmed the presence of several transcription initiation sites within the first 310 bp of the 5'-UTR, also in the absence of the cognate LHR coding sequences. The most distal site at bp -310 did not function in the absence of the first 173 bp of the 5'-UTR. Other transcription initiation sites were identified closer to the translation initiation site. hCG (50 micrograms/l), 8-bromo (Br)-cAMP (100 mumol/l) and cholera toxin (100 microgram/l) displayed qualitatively similar negative effects on the LHR promoter activity in the transfected mLTC-1 cells when the constructs containing at least the first 565 bp of the LHR 5'-UTR were used, but the inhibitory effects were greatly decreased in constructs containing < or = 304 bp of the promoter region. Hence, the hCG/cAMP associated inhibitory effects interact with region(s) located mainly between bp -565 and -305 of the LHR promoter. The inhibitory role of cAMP on LHR gene expression was also confirmed at the level of hCO-binding and hCG stimulated cAMP production of mLTC-1 cells. In conclusion, the current results elucidate the cis- and trans-acting elements in the regulation of expression of the murine LHR gene in cultured mouse Leydig cells. The minimal basal promoter activity is within the first 173 nucleotides of the 5'-UTR and the structural elements of the negative LHR regulation by the cognate hormone and elevated cAMP levels are mainly located within nucleotides -305 to -565 of the 5'-UTR. The function of the murine LHR promoter is similar to, though not identical with that of the rat, but at variance with that of the human LHR gene.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

Regulation of parathyroid hormone-related peptide production in vitro by the rat hypercalcemic Leydig cell tumor H-500.

The transplantable rat Leydig cell tumor H-500 is known to cause hypercalcemia in vivo by the release of abundant PTH-related peptide (PTHRP) and to closely reproduce the human syndrome of malignancy-associated hypercalcemia. In the rat only a single messenger RNA species of 1.4 kilobases is expressed which encodes a peptide of 141 amino acid as the sole molecular form. We have examined in cultured rat Leydig tumor cells H-500, the capacity of multiple factors to regulate PTHRP messenger RNA expression and secretion. Both fetal bovine serum and epidermal growth factor stimulated PTHRP gene expression and secretion into conditioned culture medium. Dexamethasone and 1,25-dihydroxyvitamin D3 produced inhibition of PTHRP gene expression and secretion. Furthermore, in these testicular cells, after 12 h or more of incubation, testosterone produced a dose-dependent (10(-9)-10(-7) M) inhibition of PTHRP production. No significant difference in this inhibitory response was seen between testosterone and its 5 alpha-reduced metabolite dihydrotestosterone whereas 17 beta-estradiol, progesterone, LH, FSH, and PRL were ineffective. An androgen receptor antagonist Win 49596 blocked the androgen-mediated inhibition of PTHRP gene expression and secretion, but not that due to dexamethasone. Epidermal growth factor caused an increase, whereas androgen caused a decrease in PTHRP gene transcription. These studies demonstrated that growth factors, dexamethasone, and 1,25-dihydroxyvitamin D3 are broadly active regulatory agents of PTHRP production which cross species and tissue barriers. Testosterone may be a more selective modulator which can regulate PTHRP in tissues such as Leydig cell neoplasms which express the androgen receptor.

Androgen Receptor Antagonists↗
PubMedDate not supplied

[Ovarian Leydig cell tumor].

INTRODUCTION: Leydig cell tumors are sex cord-stromal tumors with sexual steroid production (predominantly testosterone). They account for less than 0.6% of ovarian neoplasms and mostly appear at the age of 28. HISTOPATHOLOGY: It is a solid yellowish nodular tumor, less than 5 cm in diameter. It consists of polygonal Leydig cells, eosinophillic cytoplasm with lipid vacuole and lipochrome pigments. Nuclei are oval, pleomorphic with rare nucleoli. Hyperthecosis is around the tumor. CASE DESCRIPTION: Signs and symptoms depend on age of women and testosterone levels. Women complain about hirsutism, hoarseness, muscular hypertrophy, increased libido, clitoromegaly, temporal hair loss and menstrual disturbances. DIAGNOSIS: Basal hormone analysis reveals extremely high testosterone levels, mildly high androstenedione and 17 OH progesterone, and suppressed follicle stimulating hormone and luteinizing hormone. Estradiol, dehydroepiandrosterone sulfate and other hormones are normal. Dexamethasone screening test decreases dehydroepioandrosterone sulfate and androstenedion, whereas testosterone levels are only partly suppressed. Human choriogonadotropin test is clearly stimulatory for testosterone. Suppressed gonadotropin levels do not respond to luteinizing hormone releasing hormone stimulation. Ultrasonography, nuclear magnetic imaging, Doppler sonography, ovarian vein catheterization can be used for visualization. The removal of tumor is followed by normalization of testosterone levels, increase of gonadotropins and gradual disappearance of all symptoms and signs. THERAPY: The only effective therapy is operative.

Child↗
PubMed1991

Treatment of malignant Leydig cell tumor.

Malignant Leydig cell tumors (LCT) are rare. Only 32 cases of malignant LCT (as evidenced by metastatic spread) were reported. Generally metastatic spread occurs within 2 years of the primary LCT, and the patient dies within 2 years of the discovery of metastatic disease. The tumor is highly resistant to both radiation and chemotherapy. It also has a great propensity for recurring after surgical resection. A case is reported of a patient whose metastatic disease occurred 8 years after his primary LCT had been resected. He was treated with doxorubicin and mitotane without response. The clinical features of this case are highlighted, and a review of the literature describing treatment of this rare disease is presented.

Doxorubicin↗
PubMed1985

[Leydig cell tumors in adults. Value of ultrasonic diagnosis. Apropos of 7 tumors].

Leydig cell tumors arise from the gonadal stroma and represent two or three per cent of all testicular tumors. They may occur at any age in contrast with germinal tumor. In adults, about 20 per cent occur with endocrine disturbance: gynecomastia or impotence. Ten per cent are malignant and few cases are bilateral. They are small, yellow, brown tumor. Reinke's crystals are observed in 50 per cent and are pathognomonic. They present no necrosis no hemorrhage, no cyst. A benign tumor is difficult to distinguish from a malignant tumor. A vascular and capsular invasion, an infiltrative margin, a bilateral or multiple tumors must evoke a malignant case. Cryptorchidism, even corrected seems to be partly responsible in tumor induction. Ultrasonography can help for a precocious and reliable diagnosis of tumors, specially in case of occult tumors (2 cases). It also helps to survey the controlateral testis (bilateral tumor: 1 case).

Adult↗