Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated plasma testosterone levels were found in 8 women with Cushing's disease and oligo-or amenorrhea and/or hirsutism. In 4 men with Cushing's syndrome either due to adrenal hyperplasia or adenoma, plasma testosterone levels were lowered. Three of these 4 men complained of impotence or loss of libodo. Evidence for a major adrenal origin of the elevated testosterone values in the women with Cushing's disease was derived from the parallel suppression of cortisol and testosterone during dexamethasone administration, the testosterone responsiveness to ACTH and its dramatic fall after adrenalectomy. In the men with Cushing's syndrome the lowered plasma testosterone values were further suppressed by high doses of dexamethasone irrespective of concomitant cortisol suppression. Adrenalectomy or adenotomy restored the decreased plasma testosterone levels to normal. In women with Cushing's syndrome adrenal hyperandrogenism may account for the sexual and gonadal disturbances, in men glucocorticoid induced suppression of Leydig cell function may be responsible.
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PMID:Plasma testosterone profiles in Cushing's syndrome. 19 73

In a boxer dog aged 12 years who had deceased from circulatory insufficiency due to purulent endomyocarditis, there occurred a Leydig cell adenoma of the testis and multiple cutaneous naevi (haemangioma, pigmented naevus and various cutanous organ naevi). The findings have been discussed with reference to the race disposal to neoplastic growth.
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PMID:[Simultaneous occurrence of structurally variegated cutaneous nevi in the dog]. 61 29

Six lines of transgenic mice harboring the cDNA for polyomavirus large-T antigen (PVLT) linked to the mouse metallothionein-1 promoter were isolated. The transgene was expressed in testes in all lines isolated and in testes and seminal vesicles in two lines. Three lines developed enlarged testes and seminal vesicles. Development of the phenotype was divided into three stages separable by age and pathology. In stage 1, birth to 6 mo, PVLT was expressed in testes but no pathology was noted; in stage 2, 6-10 mo, PVLT was expressed solely in testes and not in seminal vesicles, yet the seminal vesicles were enlarged; and in stage 3, 10 mo and older, both testes and seminal vesicles expressed PVLT and both were enlarged. Testes were up to sevenfold heavier and increased up to fourfold to fivefold in each dimension. Seminal vesicles were enlarged up to 20-fold as the result of an accumulation of seminal vesicle fluid. In addition to the four major proteins of seminal vesicle fluid, extra proteins, initially found in stage 2, were increased in stage 3 seminal vesicle fluid. The Leydig cell was the dominant cell type in affected testes; there were few or no normal Sertoli cells or seminiferous tubules remaining by stage 3. The Leydig cells were physiologically active, as indicated by a 8.5-fold higher testosterone level in sera from stage 3 affected mice compared with sera from age-matched normal males. PVLT was present in the nuclei of the Leydig cells and was able to confer an immortal phenotype in vitro. Formation of the Leydig cell adenoma was dependent on PVLT expression, but since PVLT expression occurred much earlier than did pathology, additional secondary factors must determine the delay in phenotype development.
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PMID:Testicular adenoma and seminal vesicle engorgement in polyomavirus large-T antigen transgenic mice. 137 29

Proliferative Leydig cell (LC) alterations (hyperplasia, adenoma) of laboratory rats often pose diagnostic problems because the progression from normal to hyperplasia to neoplasia is continuous. The LC compartments of 130 Wistar rats (kfm: WIST strain) of approximately 2 years of age were examined. Ten typical cases conventionally classified as being normal or as showing diffuse or focal hyperplasia or small or large adenomata were investigated in more detail. In large adenomata, areas with large and small LC nuclei were identified. Immunohistochemical characterization, EM examination, as well as stereologic and planimetric investigations were performed. Hyperplastic and neoplastic LC essentially retained their normal appearance and immunohistochemical characteristics, but were found to contain more lipid droplets, fibroblast-like cells and patches of collagen than normal LC at the EM level. LC proliferation was accompanied by significant LC hypertrophy. LC nuclei of hyperplastic LC compartments were slightly larger while those of LC adenoma were markedly larger than nuclei of normal LC. The values for circle-related and ellipticity factors indicated that the nuclei of normal and hyperplastic LC were more markedly oval than nuclei of neoplastic LC. Concavity factor and bending energy measurements revealed that the small and oval nuclei of normal and hyperplastic LC had significantly more and deeper indentations than the larger and somewhat rounder nuclei of neoplastic LC. It is concluded that LC proliferations conventionally diagnosed as hyperplasia or adenoma on the basis of their size were composed of cytologically different LC populations.
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PMID:Morphological, immunohistochemical, stereological and nuclear shape characteristics of proliferative Leydig cell alterations in rats. 140 4

Wyeth-14,643 (WY) belongs to a diverse class of compounds which have been shown to produce hepatic peroxisome proliferation and hepatocellular carcinoma in rodents. Based on a review of bioassay data, a relationship appears to exist between peroxisome proliferating compounds and Leydig cell adenoma formation. Most rat bioassays with peroxisome proliferators have been conducted in the Fisher-344 (F344) rat, which has a high spontaneous incidence of Leydig cell adenomas. Thus, it was necessary to use an alternative animal model to investigate this relationship further. Therefore the Crl:CD BR (CD) rat, which has a low spontaneous Leydig cell adenoma incidence, was chosen for a 2-year feeding study with WY. Before initiating this 2-year feeding study, it was necessary to investigate whether any strain differences existed between CD and F344 rats with respect to WY-induced peroxisome and cell proliferation. In this study, male CD and F344 rats were fed diets containing 0, 50, or 1000 ppm WY for 21 days. Peroxisome proliferation in the liver and testis was determined biochemically by measuring beta-oxidation activity and was confirmed ultrastructurally. Serum hormone levels and cell proliferation rates in the liver and testis were also measured. In addition, basal beta-oxidation activity and cell proliferation rates were compared between the CD and F344 rats. A significant decrease in final body weight was observed in the 1000 ppm WY groups for both CD and F344 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the effects of Wyeth-14,643 in Crl:CD BR and Fisher-344 rats. 142 18

1,3-butadiene (BD) is present in synthetic rubber and motor fuels (gasoline). BD is shown to cause lymphocytic lymphomas, heart hemangiosarcomas, lung alveolar bronchiolar cancers, forestomach-squamous cell cancers, harderian gland neoplasms, preputial gland adenoma or carcinoma, liver-hepatocellular cancers, mammary gland acinar cell carcinomas, ovary-glanulosa cell carcinoma, brain cancers, pancreas adenoma and carcinoma, testis-Leydig cell tumors, thyroid follicular adenoma and carcinoma, and zymbal gland carcinoma in rodents and to date no exposure level has been established at which this chemical does not cause cancers. In humans BD causes increase in lymphomas, leukemias, and other cancers of hematopoietic systems and organs. BD is also a potent alkylating agent, directly toxic to developing embryos and damages progeny after parental exposure.
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PMID:Dangerous and cancer-causing properties of products and chemicals in the oil refining and petrochemical industry--Part II: Carcinogenicity, mutagenicity, and developmental toxicity of 1,3-butadiene. 194 58

Virilizing adrenal adenomas are rare, and Leydig cell adenomas of the adrenal rarer still. Our patient, a 60-year-old virilized woman, was found to have a Leydig cell adenoma. Virilization associated with normal 17-ketosteroid and elevated testosterone levels necessitates excluding an adrenal cause. Although one might expect high testosterone levels to suppress gonadotropins, this is not the case. In addition to other studies recommended for assessing the incidentally discovered adrenal mass, we would add a testosterone assay.
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PMID:Virilization due to a Leydig cell adrenal adenoma. 283 7

A 49-year-old woman with virilization demonstrated biochemical features traditionally ascribed to virilizing ovarian tumors: marked elevation of serum testosterone level with normal urinary excretion of 17-ketosteroids and normal serum dehydroepiandrosterone level. An adrenal cortical adenoma containing neoplastic cells indistinguishable from Leydig cells, including the demonstration of characteristic crystalloids of Reinke, was shown to be the source of the elevated testosterone level. A review of the literature revealed 13 cases with a similar biochemical profile, and of these, two were reported to contain crystalloids of Reinke. Taking cognizance of the fact that these characteristic crystalloids are only found in 40 percent of Leydig cell tumors of the testis, it is concluded that Leydig cells may be present in, and may be active participants in, the pathophysiology of a number of testosterone-secreting adrenal tumors.
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PMID:Testosterone-secreting adrenal adenoma containing crystalloids characteristic of Leydig cells. 300 Jan 78

We describe the third report testosterone-producing, virilizing, adrenal Leydig cell adenoma, which was identified in a oophorectomized postmenopausal female patient. Light- and electron-microscopy demonstrated typical Leydig cell differentiation, including numerous intracytoplasmic and intranuclear Reinke crystals and rice-like bodies (elementary tubular inclusions). Testosterone production by the adenoma was demonstrated by the immunoperoxidase technique. We propose that adrenal Leydig cell adenomas arise as a result of ovarian gonadal stromal metaplasia associated with elevated follicle-stimulating hormone and luteinizing hormone in the postmenopausal female patient. Adrenal Leydig cell lesions must be considered in the virilized woman with elevated testosterone levels and normal levels of the adrenal androgens and their 17-ketosteroid metabolites.
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PMID:Virilizing Leydig cell adenoma of adrenal gland. 302 13

The effects of hyperprolactinemia on testicular structure and pituitary-gonadal function were investigated in male rats. Hyperprolactinemia was induced in the Wistar-Furth rat by implantation of tissue fragments of a prolactin-secreting MtTW15 pituitary adenoma. The MtTW15 tissue was maintained in one animal group for 27 days (group A) and in another group for 37 days (group B). Appropriate age-matched controls were utilized in each study. Serum prolactin was significantly elevated (P less than 0.001) in both groups of MtTW15-bearing rats compared with their controls. The degree of hyperprolactinemia was more severe in rats of group B (2842 +/- 546 ng/ml) than in rats of group A (367 +/- 38 ng/ml). Accessory sex organ weights in group B rats were significantly lower than in controls, but were apparently unaffected in group A rats. Hyperprolactinemia induced definite but variable testicular alterations in both animal groups that presented as seminiferous epithelial disorganization, germ cell exfoliation, increased tubule wall thickness, and abnormal Leydig cell lipid content. Electron microscopy revealed structural disruption of Sertoli-germ cell junctional complexes and apical Sertoli cell cytoplasmic degeneration. The hyperprolactinemic rat exhibited significant reductions in serum luteinizing hormone (LH), testosterone (T), and androgen binding protein (ABP) when compared with controls. Eighty-six days following surgical removal of the MtTW15 tissue in a subgroup of group B rats, serum levels of prolactin and LH returned to normal, as did weights of accessory sex organs and testicular morphology. These results indicate that exposure to the MtTW15 adenoma and its later removal in the rat provides a workable model for studying the effects of hyperprolactinemia on testicular structure and function, and for identifying events involved in the subsequent recovery of spermatogenic disruption.
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PMID:Alterations of testicular function induced by hyperprolactinemia in the rat. 403 18


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