Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association between testicular tumors/nodules and congenital adrenal hyperplasia (CAH) has been previously reported. From 1960 to 1989, three patients (13 to 18 years old) with long-standing CAH developed testicular masses. Two patients with 21-hydroxylase deficiency were diagnosed in the neonatal period while one other with 11-hydroxylase deficiency was diagnosed at 3 years of age when he presented with sexual precocity. In all three patients, medical compliance was poor. The testicular masses were bilateral in two patients and unilateral in one, measured 1 to 2 cm, and occupied only the upper half of the testicle. Testicular biopsy specimens were obtained after at least 6 months of evidence of compliance with the adrenocorticotrophic hormone (ACTH) suppressive medication and failure of the nodules to regress. On gross examination the masses appeared to be firm yellow brown nodules. Light microscopy showed interlacing strands, cords, and rests of cells resembling interstitial (Leydig) cells but with no Reinke crystalloids. Electronmicroscopy in all patients showed variable amounts of both smooth and rough endoplasmic reticulum, the later with occasional dilated cisternae. Follow-up ranged from 6 months to 6 years. No further surgical treatment has been necessary. There has been no evidence of recurrence, distant metastases, or secondary malignancies during the time of follow-up. These findings suggest that testicular tumors may develop from chronic excessive ACTH stimulation of a putative pluripotential testicular cell, a Leydig cell, or an adrenal cortical rest. Unlike other testicular tumors these do not require orchiectomy as the initial form of therapy.
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PMID:Benign testicular tumors in children with congenital adrenal hyperplasia. 132 Jun 75

Leydig cell tumors represent about 3% of all testicular neoplasms. Actually no specific pathologic criteria has really distinguished the benign from the malignant tumors which represent about 11% of the cases. The presence of metastases is the only unequivocal criteria of malignancy. Authors present a rare Leydigoma case with gynecomastia. Clinical, diagnostical and most of all therapeutical aspects are discussed reconfirming the role of the orchifuniculectomy in T1 N0 M0 stage.
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PMID:[A case of Leydig cell tumor of the testis]. 149 76

Fertility and Leydig cell function were investigated in 31 patients previously treated for nonseminomatous testicular cancer. Twenty-two patients with metastatic cancer had received cisplatin-based chemotherapy, and the median follow-up was 64 months (range, 42 to 100 months). Nine patients without metastases were treated with orchiectomy alone, and follow-up in this group was a median of 61 months (range, 40 to 77 months). None of the patients have relapsed and retroperitoneal lymph node dissection was not performed in any patient. Both the concentration of spermatozoa and the volume of the remaining testis are significantly reduced in patients who had previously received chemotherapy when compared with patients treated with orchiectomy alone (P less than .05). There were no significant differences between groups when comparing morphology, motility, and penetration of the spermatozoa. Subclinical Leydig cell dysfunction with normal testosterone and elevated luteinizing hormone (LH) was observed in one patient (11%) treated with orchiectomy alone, while 59% of the patients who had received chemotherapy had elevated LH (P less than .05). We conclude that cisplatin-based chemotherapy leads to a persistent impairment of fertility and Leydig cell function in the majority of patients with testicular cancer.
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PMID:Long-term fertility and Leydig cell function in patients treated for germ cell cancer with cisplatin, vinblastine, and bleomycin versus surveillance. 169 35

During a routine long-term drug safety study, lasting approximately 2 1/2 yr, male Wistar rats, treated with a prolactin-inhibiting compound, developed an excess of Leydig cell tumors (LCTs). Most tumors were typical for the rat but a small number showed an unusual variation and some appeared malignant. The variation consisted of glandular and/or tubular structures within the tumor mass which occasionally anastomosed and contained an eosinophilic periodic-acid Schiff (PAS) positive material. In a few of these variants, malignant features such as cellular atypia, capsular, and lymphatic invasion and necrosis were seen. No metastases were detected. Detailed morphological and immunohistochemical investigations were conducted in order to establish the cell of origin of these variants. Glandular/tubular structures were found to stain with varying intensity for vimentin and cytokeratin, but were always negative for beta-tubulin. The results indicated that the cell of origin of these LCT variants was indeed the Leydig cell and that glandular and/or tubular structures within LCTs represented a form of Leydig cell metaplasia.
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PMID:Morphologic and immunohistochemical characterization of Leydig cell tumor variants in Wistar rats. 172 33

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.
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PMID:Treatment of malignant Leydig cell tumor. 191 69

Serum concentrations of testosterone, luteinizing hormone and follicle-stimulating hormone were measured before, and at 1, 12 and 24 months after cessation of long-term estrogen treatment (mean 8.7 years, range 4.3 to 13.1 years) in 14 patients with prostatic carcinoma but without metastases. In addition, the same hormones were measured before and up to 24 months after orchiectomy in 14 age-matched, previously untreated patients also without metastases. In long-term estrogen-treated patients serum concentrations of testosterone found at 1, 12 and 24 months after cessation of estrogen did not differ significantly either from the value before estrogen withdrawal or from the corresponding values found in age-matched patients after orchiectomy. The concentrations of luteinizing and follicle-stimulating hormones increased significantly in the estrogen-treated patients after cessation of estrogen and in the age-matched patients after orchiectomy. However, luteinizing and follicle-stimulating hormones were significantly lower in the patients after estrogen treatment than in the age-matched patients after orchiectomy. During the study period only 1 patient from the estrogen-treated group had clinical progression and he died of prostatic carcinoma. We conclude that long-term estrogen treatment causes impairment of Leydig cell function in patients with prostatic carcinoma and, as a result, the serum testosterone concentrations do not increase when that treatment is discontinued.
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PMID:Hormonal effects of cessation of estrogen treatment for prostatic carcinoma. 311 81

Between 1983 and 1986 179 inguinal testicular explorations were performed. Testicular palpation and sonograms were carried out. 163 patients (91%) had malignant testicular tumours. 16 patients (9%) were found to have benign, nongerminal testicular tumours. When intraoperative frozen section diagnosed epidermoid cysts, the majority of these were enucleated, while the dermoid cysts and Leydig cell tumours were removed together with the testicle. The postoperative follow-up on all patients showed no evidence of local recurrence or metastases.
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PMID:[Nongerminal, benign testicular tumors--report of experiences]. 328 40

Metastatic Leydig cell carcinomas account for less than 0.2% of all testicular cancers, and may be associated with sex hormone production. Leydig cell carcinoma is relatively refractory to radiotherapy and chemotherapy, and median survival of patients with metastatic disease is less than 2 years. Presented are three cases of metastatic Leydig cell cancer, and a review of the literature pertaining to this rare tumor.
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PMID:Metastatic Leydig cell tumor of the testis. Report of three cases and review of the literature. 375 26

This report analyzes six ovarian Sertoli-Leydig cell tumors that showed retiform differentiation. The patients were young (6-29 years; average age, 17). The tumors were all limited to one ovary, and the patients have remained disease-free, with one exception, a patient who died of recurrent neoplasm 3.5 years after operation. On microscopic examination, the retiform areas were predominant in three cases and focal in the other three. The retiform areas consisted of an irregular anastomosing network of spaces lined by cuboidal cells, often with papillary formations and sometimes with tubules compressed to form slit-like spaces. In three cases the retiform areas appeared mature, and in three they were less differentiated. All tumors also had areas of typical Sertoli-Leydig cell tumor of either poor or intermediate differentiation. In the patient with metastatic disease, the metastases had a pure sarcomatoid pattern without any retiform areas.
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PMID:Retiform differentiation in ovarian Sertoli-Leydig cell tumors. A clinicopathologic study of six cases from a Gynecologic Oncology Group study. 396 93

Tumours of the testis are common in dogs, uncommon in other domestic animals. Leydig cell tumours, Sertoli cell tumours, and seminomas occur with similar frequencies and not uncommonly in the same testis. Dogs with Sertoli cell tumours may develop female characteristics and become sexually attractive to other males. It is unusual for testicular tumours in dogs to metastasize. Various histological types within the three main categories are described.
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PMID:Tumours of the testis. 454 53


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