Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 60-year-old postmenopausal woman presented with evidence of hirsutism, alopecia and mild virilization. Clinical examination and biochemical abnormalities suggested that the source of androgen excess was ovarian, and an ovarian tumor was confirmed and removed at laparotomy followed by normal endocrine profile in the postoperative period.
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PMID:Virilization due to a rare ovarian tumor in a postmenopausal woman. 290 13

The clinical and pathologic features of 13 cases of juvenile granulosa cell tumor were studied. Patients' ages ranged from 6 months to 56 years (median age, 17 years). Only one patient was postmenopausal. Three premenarchal patients had isosexual development. Five of seven postmenarchal patients had menstrual abnormalities, and two patients demonstrated virilization. Ascites was present in two patients. All patients had unilateral stage I tumors, ranging from 2.5 to 24.5 cm in greatest dimension (mean greatest dimension, 12.2 cm). Characteristic histologic features included nodular architecture, follicle formation, abundant interstitial and intrafollicular acid mucopolysaccharide-rich fluid, irregular microcysts, individual cell necrosis, and high mitotic activity (mean activity, 11 mitotic figures per ten high-power fields). The interstitial mucinous fluid consisted predominantly of hyaluronic acid. Immunohistochemical staining in five cases showed prominent positivity for vimentin (four cases), isolated cytokeratin AE1/3-positive cells (two cases), and nonreactivity for carcinoembryonic antigen and milk fat globule-2. Ultrastructurally, epithelial cells that resembled granulosa cells of the nonneoplastic preovulatory follicle and occasional cells with steroidogenic organelles were also found. Follow-up of ten patients revealed no tumor recurrences from six months to 33 years (mean, 9.5 years) after operation.
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PMID:Juvenile granulosa cell tumors of the ovary. 291 Feb 25

Partial virilization at birth of a genotypic female resulting in varying degrees of posterior labial fusion and clitoral enlargement is most commonly due to excess androgen production from congenital adrenal hyperplasia. Rarely, labial fusion arises secondary to maternal androgen ingestion or an androgen-secreting tumor during pregnancy. We report a case of posterior labial fusion without clitorimegaly in a 12-year-old girl in which there was no evidence of androgen excess. The family history was remarkable for a similar congenital defect in two aunts and their daughters, suggesting an autosomal dominant trait with incomplete penetrance.
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PMID:Familial posterior labial fusion. 291 82

A 71-year-old woman, 26 years post-menopause, presented with virilization. Facial hirsuties, non-hereditary frontal balding, voice changes, male escutcheon, and mild clitorimegaly accompanied a right adnexal mass. Blood hormone studies showed testosterone 430 ng/dL, FSH 118 mIU/mL, and LH 210 mIU/mL. By ultrasound examination, the cystic adnexal mass involved the right ovary. An 18-cm, 1300-g, unicameral mass with 1200 mL of clear serous fluid and with smooth inner and outer surfaces was removed from the right broad ligament. Intraoperative testosterone levels were as follows: peripheral vein 285 ng/dL, left ovarian vein 301 ng/dL, and right ovarian vein 1635 ng/dL; tumor cystic fluid was 3032 ng/dL. Peripheral vein testosterone was 15 ng/dL 3 days postoperatively. Histopathologically, the tumor was a serous cystadenoma. No evidence of stromal luteinization, hyperplasia, or inflammation was found, and other virilizing lesions were not encountered in either ovary or in other tissues. Epithelial cells constituting the tumor may have been the source of the excess testosterone in this unique case of virilizing serous cystadenoma.
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PMID:Virilizing serous cystadenoma. 291 83

A premenopausal woman with a mucinous carcinoma of one ovary, and a mucinous adenoma of the other, together with secondary virilization, is reported. Preoperative levels of androstenedione, testosterone and dehydroepiandrosterone sulphate were high, suggesting the presence of a virilizing tumor. Preoperative plasma estrone (E1), but not estradiol (E2), was elevated along with inversion of the E2/E1 ratio, suggesting a peripheral origin of the estrogens. FSH and LH plasma concentrations were low. After bilateral ovariectomy, levels of all steroids measured significantly decreased and gonadotropins rose to the postmenopausal range.
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PMID:A case of mucinous cystadenocarcinoma of the ovary associated with virilization: pre and post-operative steroid plasma levels. 293 45

A case of hyperandrogenism and virilization is described in an elderly female. She had elevated testosterone levels, but normal DHEAS and 24-h urinary 17-oxosteroid excretion, suggesting an ovarian tumor. Stimulation and suppression tests, and radioisotopic and radiological scans proved unhelpful in the diagnosis although hyperthecosis of the ovary was later suggested by ultrasound. Testosterone and gonadotropin levels fell during therapy with cyproterone acetate and subsequently ethinyl estradiol. Because of side effects encountered on these drugs, she was treated with a synthetic, slow-release preparation of an LHRH agonist, D-TRP-6-LHRH (Decapeptyl), with symptomatic and biochemical improvement. Long term LHRH agonists might be a valuable treatment for hyperandrogenic states in elderly patients.
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PMID:The treatment of a hyperandrogenic and virilizing state in an elderly female with a synthetic LHRH agonist. 297 52

The novel association of virilization and placental-site trophoblastic tumor, an uncommon form of gestational trophoblastic disease (formerly called "trophoblastic pseudotumor"), is described in a 32-year old woman. Multiple agent chemotherapy lowered serum concentrations of chorionic gonadotropin (hCG) (8.7 to 2.1 ng/mL), pregnancy-specific beta 1-glycoprotein (32 to 3.9 ng/mL), and testosterone (400 to 74 ng/dL). Subsequent hysterectomy revealed a 2-cm tumor nodule within the myometrium, and one week postoperatively serum concentrations of hCG (0.5 ng/mL), pregnancy-specific beta 1-glycoprotein (1.3 ng/mL), and testosterone (20 ng/dL) had all returned to normal. Percutaneous catheterization of the ovarian veins before chemotherapy demonstrated a 50-fold elevation of ovarian vein testosterone concentrations compared with normal women, whereas ovarian vein 17 beta-estradiol concentrations were only twofold higher than normal. Direct sampling of the uterine veins at the time of hysterectomy documented testosterone and estradiol production, presumably by the placental-site trophoblastic tumor. Ovarian vein testosterone concentrations at this time were only fourfold above normal, probably the result of falling serum concentrations of hCG. Wedge biopsy of the ovaries disclosed minimal histologic changes (thecal cell luteinization, focal thecosis) compatible with hCG stimulation. Failure of the placental-site trophoblastic tumor to produce large amounts of estrogen, in contrast to normal pregnancy and hydatidiform mole, resulted in marked androgen/estrogen imbalance, high circulating concentrations of free testosterone, and virilization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and laboratory investigation of a virilized woman with placental-site trophoblastic tumor. 298 18

During a 5-year study period 18 women with a serum testosterone concentrations of greater than 2 ng/ml were evaluated for a possible androgen-producing tumor. All subjects were hirsute and had menstrual irregularities, with the exception of one postmenopausal woman. The majority of the women were obese and 72% were greater than 50% over ideal body weight. Only two of 11 women undergoing operative and histologic evaluation of the ovaries were found to have an androgen-producing neoplasm. Seven additional women with serum testosterone concentration of greater than 2 ng/ml have been followed for over 1 year with no additional evidence of an androgen-producing neoplasm. The poor predictive value of a serum concentration of greater than 2 ng/ml in identification of an androgen-producing neoplasm is partially explained by the apparent prevalence of high testosterone concentrations in chronically anovulatory, hyperandrogenic obese women and by the large coefficient of variation observed in this study when analyzing testosterone concentrations were analyzed over an 8-hour interval (range, 3% to 42%). In the absence of an adnexal mass or rapidly progressive virilization, it is suggested that the use of venography or operative exploration to diagnose an androgen-producing neoplasm be reserved for women with a mean testosterone concentration derived from three daily samples that is at least 2.5 times greater than the upper range of normal in the given laboratory.
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PMID:Serum testosterone concentrations in the evaluation of androgen-producing tumors. 299 79

Hepatoblastoma is a rare hepatic tumor generally presenting during the first three years of life as an enlarging abdominal mass. Other symptoms are nonspecific; however, it may be associated with hemihypertrophy, virilization, and osteoporosis. The serum bilirubin infrequently is elevated, but up to 2/3's will have elevated serum alpha fetoprotein as a tumor marker. The overall survival rate is 35% in survivors who underwent a complete resection.
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PMID:Hepatoblastoma. 302 88

The ultrasound appearances of three children presenting with virilization are described. All cases were also examined by computed tomography. The value of ultrasound in the initial detection of virilizing neoplasm and in follow-up studies for localization of tumor recurrence following initial surgery are outlined. The advantages of ultrasound include confirmation of extrarenal and extrahepatic location in longitudinal sections, and clear demonstration of invasion of hepatic veins, the inferior vena cava (IVC), and the right atrium on real-time scanning. Computed tomography is also useful, particularly in the localization of small lesions and the detection of pulmonary metastases.
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PMID:Adrenocortical neoplasm in children. Ultrasound appearance. 303 58


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