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PubMedDate not supplied

Primary testicular abnormalities causing precocious puberty Leydig cell tumor, Leydig cell hyperplasia, and adrenal rest tumor.

The child with testicular enlargement in the absence of gonadotrophin stimulation presents a difficult diagnostic dilemma. Leydig cell tumors, Leydig cell hyperplasia, and tumors of adrenal rest tissue are the primary etiologic considerations. Because of considerable overlap in clinical presentation, careful biochemical and histologic evaluations are necessary to make the diagnosis. These should include serum levels of testosterone, dehydroepiandosterone, androstenedione, 17-hydroxyprogesterone, and 11-desoxycortisol, as well as urinary levels of 17-ketosteroids. If diagnostic changes in the biochemical profile are not present, then testicular biopsy is indicated. Encapsulation, presence or absence of the crystalloids of Reinke, degree of seminiferous tubule maturation, and the site of any abnormal tissue are important observations in the examination of the tissue specimen. Once the diagnosis has been established, then appropriate and specific medical or surgical therapy can be instituted. With appropriate treatment, the long-term prognosis in each condition is good.

Adolescent↗
PubMed1980

[Androgen-producing hilus cell tumor (Leydig cell tumor) of the ovary: case contribution to the differential diagnosis of virilization in the adult woman].

Severe hirsutism, deepening of the voice and enlargement of the clitoris developed in the course of two years in a 55-year old hysterectomized woman. Laboratory examinations showed markedly elevated plasma concentrations of testosterone and androstenedione and a moderately increased urinary excretion of 17-ketosteroids. Gaschromatographic analysis of the urinary steroids, revealed that she mainly excreted etiocholanolone, androsterone and pregnanetriol. Plasma androgens and urinary 17-ketosteroids were not suppressed by dexamethasone treatment. During catheterization of the vena cava blood samples were selectively taken from the ovarian veins. Androgen concentrations were the highest in the plasma from the right ovarian vein. However, phlebography as well as adrenal scanning with 131I-adosterol indicated a tumor of the right adrenal gland. During laparoscopy the right ovary was found to be enlarged, and it was subsequently removed. It contained a tumor 2.5 cm in diameter which had the histological features of a hilus cell tumor (Leydig cell adenoma). Two years later, the patient underwent surgery for suspected tumor of the left kidney. A functionless atrophic left kidney was removed. There was a complete thrombosis of the left renal and ovarian veins. Possibly, this severe lesion of the two vessels had been caused by their previous catheterization.

Androgens↗
PubMed1995

Virilizing stromal Leydig cell tumor (Leydig cell-containing thecoma) of the ovary in pregnancy. A case report with extensive immunohistochemical investigation of the tumor cells.

The rare case of a stromal Leydig cell tumor of the ovary occurring in a 21-year-old woman who developed signs of virilization during pregnancy is reported. Serum androgen levels were markedly elevated. At cesarean section, a slightly hypotrophic, but otherwise normal, female infant was delivered and a tumor of the right ovary measuring 12 cm in maximum diameter was resected. Histologic examination revealed a sex cord-stromal tumor consisting of spindle-shaped, thecomatous cells and a large number of loosely scattered clusters of large polygonal cells with abundant eosinophilic cytoplasm. Both types of tumor cells were strongly immunoreactive for vimentin, but exhibited no proliferative activity and no overexpression of p53 protein. A few of the polygonal cells contained typical crystalloids of Reinke. Cellular atypia was not a prominent feature, and a diagnosis of benign stromal Leydig cell tumor was established. As expected, 20 months after diagnosis the patient exhibits no signs of recurrence or dissemination. To the best of our knowledge this is only the second case of a stromal Leydig cell tumor occurring in pregnancy to be described.

Adult↗
PubMed1995

Case report: congenital adrenal hyperplasia and malignant Leydig cell tumor.

Leydig cell tumors are very rarely seen testicular tumors and can be difficult to distinguish from testicular tumors of the adrenogenital syndrome. Testicular tumors of the adrenogenital syndrome are confined to patients with congenital adrenal hyperplasia. The authors report a case of a patient with malignant Leydig cell tumor and a history of congenital adrenal hyperplasia (adrenogenital syndrome). To the authors' knowledge, this has not been reported previously.

Adrenal Hyperplasia, Congenital↗
PubMed1987

Biological and biochemical characterization of estrogen-dependent mouse Leydig cell tumors.

Leydig cell tumors formed in BALB/c mice were found to be able to be transplanted subcutaneously in the same strain. One of the sublines, called T 22137, showed growth inhibition in response to estrogenization of host mice. The other subline (T 124958-O), which was originally classified as an estrogen-independent line, was observed to contain the low-affinity estradiol binding component in the cytosol fraction. At a later stage of transplantation, however, the growth of this subline was modestly but significantly enhanced by estrogenic stimuli. This alteration was accompanied by appearance of an estrogen receptor-like molecule which was associated with chromatin even in the absence of estrogen stimuli. In the presence of estrogen selection pressure, a new tumor line, designated as T 124958-R, was established, which showed marked estrogen-dependent growth. T 124958-R was found to contain the cytosolic estrogen receptor. The additional difference was that the annulate lamellae were identified only in T 124958-R, but not in T 124958, by electron microscopic studies. The estrogen dependency of T 124958-R was further substantiated by demonstration of an estrogen secretory protein as well as the estrogen-enhanced formation of 5 alpha-steroids. T 22137 showed growth inhibition in tamoxifen-treated mice. The growth of T 124958-R was enhanced by the administration of tamoxifen to mice. This tamoxifen-induced tumor growth was further stimulated by the simultaneous administration of estrogen. These observations would suggest that mouse Leydig cell tumor systems provide us with a valuable model to investigate the influence of estrogen as well as antiestrogen on malignant cells.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1993

Metachronous germ cell and Leydig cell tumors of the testis. Do testicular germ cell tumors and Leydig cell tumors share common etiologic factors?

BACKGROUND: Testicular germ cell neoplasms occur bilaterally in approximately 2-5% of patients. Bilateral testicular tumors of different histogenesis are extremely rare, and the study of such cases may offer clues to the pathogenesis of both tumor entities. METHODS: A report of a case and review of the literature are presented. RESULTS: A 33-year-old man had a right-sided testicular neoplasm consisting of teratoma, embryonal carcinoma, and yolk sac tumor. Retroperitoneal lymph node metastases were excised, and, subsequently, adjuvant abdominal radiation therapy was administered. The patient later received six cycles of cisplatin-based chemotherapy for pulmonary relapse. When he was 40 years of age, a contralateral Leydig cell tumor (LCT) was treated by testis-sparing excision. This is the first observation of testicular germ cell tumor (GCT) and contralateral LCT. Three cases of germ cell neoplasm and concurrent ipsilateral LCT have been reported previously. CONCLUSIONS: The association of GCT and LCT in one patient is quite unusual because both entities are rare. Sharing of common etiologic factors by both entities is a possible explanation.

Adult↗
PubMed1997

Metachronous development of malignant Leydig cell tumor.

Leydig cell tumor (LCT), a rare testicular tumor, is malignant in only about 10% of the cases. We report the case of a patient with bilateral malignant LCTs that developed metachronously. After undergoing a right inguinal orchiectomy for a malignant LCT at the age of 43 years, the patient was given cisplatin-based chemotherapy for suspected para-aortic lymph node metastasis. Eighteen months after the right orchiectomy, examination of a left testicular biopsy specimen showed a malignant LCT and a left inguinal orchiectomy was performed. Histologically, the initial malignant LCT exhibited a highly pleomorphic appearance with mitotic figures (58/10 HPF), whereas the second malignant LCT showed fewer mitoses (2/10 HPF). The proliferating cell nuclear antigen (PCNA)-labelling index in these tumors also differed (right-sided tumor, 50%; left-sided tumor, 28%). These findings suggest that the malignant LCT in the left testis developed as a second primary rather than as a metastatic tumor. There have been no known similar cases, although three cases of malignant LCT with contralateral metastasis have been reported.

Adult↗
PubMed1984

Evidence for the synthesis of multiple pro-opiomelanocortin-like precursors in murine Leydig tumor cells.

The opiate peptide beta-endorphin has recently been localized in extrapituitary tissues and cells, including the Leydig cells of the testis, by immunohistochemical techniques. An intriguing question is whether this localization reflects an accumulation of the peptide through a specific uptake mechanism or is the result of synthesis within the cell in a large precursor form similar to pro-opiomelanocortin synthesized in the pituitary. Evidence is presented herein that specific antibodies against beta-endorphin and adrenocorticotrophic hormone precipitate identical precursor molecules from total cellular mRNA translation products of M5480A Leydig tumor cells. In addition, mRNA from these cells cross-hybridizes under stringent conditions with a cDNA coding for the rat pituitary pro-opiomelanocortin sequence. These data demonstrate the synthesis of a pro-opiomelanocortin-like mRNA in this Leydig cell tumor and strongly implicate biosynthesis within these cells.

Animals↗
PubMed2005

Imatinib mesylate inhibits Leydig cell tumor growth: evidence for in vitro and in vivo activity.

Leydig cell tumors are usually benign tumors of the male gonad. However, if the tumor is malignant, no effective treatments are currently available. Leydig cell tumors express platelet-derived growth factor (PDGF), kit ligand and their respective receptors, PDGFR and c-kit. We therefore evaluated the effects of imatinib mesylate (imatinib), a selective inhibitor of the c-kit and PDGFR tyrosine kinases, on the growth of rodent Leydig tumor cell lines in vivo and in vitro, and examined, in human Leydig cell tumor samples, the expression of activated PDGFR and c-kit and the mutations in exons of the c-kit gene commonly associated with solid tumors. Imatinib caused concentration-dependent decreases in the viability of Leydig tumor cell lines, which coincided with apoptosis and inhibition of proliferation and ligand-stimulated phosphorylation of c-kit and PDGFRs. Mice bearing s.c. allografts of a Leydig tumor cell line treated with imatinib p.o., had an almost complete inhibition of tumor growth, less tumor cell proliferation, increased apoptosis, and a lesser amount of tumor-associated mean vessel density compared with controls. No drug-resistant tumors appeared during imatinib treatment but tumors regrew after drug withdrawal. Human Leydig cell tumors showed an intense expression of the phosphorylated form of c-kit and a less intense expression of phosphorylated PDGFRs. No activating mutations in common regions of mutation of the c-kit gene were found. Our studies suggest that Leydig cell tumors might be a potential target for imatinib therapy.

Animals↗
PubMed1998

Leydig cell tumor of the testis: a clinicopathologic, DNA content, and MIB-1 comparison of nonmetastasizing and metastasizing tumors.

Leydig cell tumors of the testis are rare and account for a small proportion of testicular neoplasms. The objective of this study was to identify clinical and morphologic features predictive of metastasis in a large series of Leydig cell tumors, and to determine whether ploidy or proliferative activity were predictive of malignancy. Thirty cases of Leydig cell tumor of the testis (23 tumors that had not metastasized and 7 that had metastasized) were studied. Clinical history and follow-up were collected in all cases. The morphologic features examined included tumor size, mitotic index (mitotic figures/10 high-power fields), necrosis, angiolymphatic invasion, cell type, tumor-testicle interface, presence of extension beyond the testicular parenchyma, and presence of lipochrome and Reinke crystals. Most patients (93%) had a testicular mass. Patients with Leydig cell tumors that metastasized were diagnosed at a mean age of 62 years (range, 39-70 years) compared with 48 years (range, 9-79 years) in patients with nonmetastasizing tumors (p = 0.25). Leydig cell tumors that metastasized were significantly larger than nonmetastasizing tumors (mean, 4.7 versus 2.6 cm, respectively; p = 0.008), and had a significantly higher mitotic index (mean, 13.9 versus 1.9, respectively; p < 0.0001). Metastasizing Leydig cell tumors were significantly associated with atypical mitotic figures (p < 0.0001), nuclear variation (p = 0.0025), necrosis (p < 0.0001), angiolymphatic invasion (p = 0.009), infiltrative margins (p < 0.0001), high grade (p = 0.0004), and invasion into rete testis, epididymis, or tunica (p = 0.001) when compared with nonmetastasizing tumors. There was no significant difference between metastasizing and nonmetastasizing tumors in regard to cell type, lipochrome content, presence of Reinke crystals, or nuclear inclusions. All Leydig cell tumors that metastasized and 7 of 18 (38.9%) nonmetastasizing tumors were DNA aneuploid by static image analysis (p = 0.02). Metastasizing Leydig cell tumors had a significantly higher mean MIB-1 activity of 18.6% (range, 5.8-33.6) compared with 1.2% (range, 0.04-8.2) in nonmetastasizing tumors (p = 0.001). In this study, the presence of cytologic atypia, necrosis, angiolymphatic invasion, increased mitotic activity, atypical mitotic figures, infiltrative margins, extension beyond the testicular parenchyma, DNA aneuploidy, and increased MIB-1 activity were significantly associated with metastatic behavior in Leydig cell tumors.

Adolescent↗
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↗
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↗