Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042755 (masculinization)
 2,562 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pregnancy luteoma represents an unusual response of ovarian stromal cells to the altered hormonal levels of pregnancy. It is a distinctive non-neoplastic lesion characterized by solid proliferations of luteinized cells resulting in a tumor-like ovarian enlargement. Most patients are asymptomatic; the ovarian enlargement is usually discovered incidentally at cesarean section or during postpartum tubal ligation. We report a typical case that we found at cesarean section to be associated with a virilized infant who manifested clitoromegaly and labial fusion. We detected an increased level of testosterone in the maternal patient. We concluded that the ovarian luteoma induced the fetal virilization.
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PMID:Luteoma-induced fetal virilization. 2014 54

Hyperandrogenic states in pregnancy are almost always the result of a condition that arises during pregnancy. The onset of virilization symptoms is often very fast. The mother is protected against hyperandrogenism by a high level of SHBG, by placental aromatase and a high level of progesterone. The fetus is protected from the mother's hyperandrogenism partly by the placental aromatase, that transforms the androgens into estrogens, and partly by SHGB. Nevertheless there is a significant risk of virilization of the female fetus if the mother's hyperandrogenic state is serious. The most frequent cause of hyperandrogenic states during pregnancy are pregnancy luteoma and hyperreactio luteinalis. Hormonal production is evident in a third of all luteomas, which corresponds to virilization in 25-35 % of mothers with luteoma. The female fetus is afflicted with virilization with two thirds of virilized mothers. Hyperreactio luteinalis is created in connection with a high level of hCG, e.g. during multi-fetus pregnancies. This condition most frequently arises in the third trimester, virilization of the mother occurs in a third of cases. Virilization of the fetus has not yet been described. The most serious cause of hyperandrogenism is represented by ovarian tumors, which are fortunately rare.
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PMID:Hyperandrogenic states in pregnancy. 2111 72

This paper describes the case of a 25-year-old woman with virilisation occurring during pregnancy in the presence of metastatic colorectal cancer. Virilisation during pregnancy is rare. The potential causes include adrenal, foetal, or ovarian pathologies. The most common causes during pregnancy are pregnancy luteoma and hyperreactio luteinalis. The incidence of cancer during pregnancy is rare and the incidence of colorectal cancer (CRC) in pregnancy is even rarer. The presenting signs and symptoms of CRC can be confused with symptoms commonly encountered during pregnancy, thereby delaying diagnosis and commencement of treatment. Diagnosis and staging also proves more problematic in the pregnant patient as the usual modalities of colonoscopy with biopsy and imaging with CT are relatively contraindicated. Treatment is dependent on gestational age of the foetus. There is currently no agreed best practice as to the role of prophylactic oophorectomy in the prevention of metachronous ovarian metastases. Surgical and adjuvant treatments have implications for females of child-bearing age.
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PMID:Virilisation during Pregnancy in a Patient with Metastatic Colorectal Cancer. 2309 39

Virilising ovarian tumours are a rare cause of hyperandrogenism in women, accounting for less than 5% of all ovarian neoplasms. It occurs most often in - and postmenopausal women. We report a case of a 64 year-old woman with signs of virilisation that had started 3 years before. Blood hormone analysis revealed increased levels of testosterone, and 17-hydroxyprogesterone. The tetracosactin test revealed 21-hydroxylase deficiency. Radiological imaging demonstrated a nodule in her left ovary. The patient was submitted to bilateral laparoscopic oophorectomy, and histopathological examination revealed a luteoma of the left ovary. Postoperative serum testosterone level and 17-hydroxyprogesterone returned to normal levels in one month. Virilism regressed within six months. Our patient also showed an elevation in 17-OHP serum levels. Normalization of 17-OHP after oophorectomy suggests a case of intratumoral 21-hydroxylase deficiency. To our knowledge, this is the first description of ovarian intratumoral 21-hydroxylase deficiency in a postmenopausal woman.
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PMID:Ovarian intratumoral 21-hydroxylase deficiency in a postmenopausal hirsute woman. 2332 92

Maternal virilization in pregnancy with or without fetal female pseudohermaphroditism has several etiologies. Of these, pregnancy luteoma is the most common cause of maternal virilization during pregnancy, and approximately 20 cases have been reported in recent years. Moreover, four cases of pregnancy luteomas with female pseudohermaphroditism have been reported. However, the extremely rare steroid cell tumor, not otherwise specified (NOS), has been reported only once as a cause for maternal virilization. Herein, the authors report the first case of maternal virilization with female pseudohermaphroditism associated with steroid cell tumor-NOS along with the clinical course, pathological features, and a review of the literature.
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PMID:Female pseudohermaphroditism associated with maternal steroid cell tumor, not otherwise specified of the ovary: a case report and literature review. 2459 65

Pregnancy luteomas are rare, nonneoplastic lesions of the ovary thought to be caused by the hormonal effects of pregnancy. Most of these patients are asymptomatic with the ovarian enlargement being incidentally discovered during imaging or surgery. Some patients develop hirsutism or virilization during late pregnancy. Luteomas spontaneously regress postpartum. It may be a diagnostic and management challenge as it can mimic the presentation of malignant ovarian tumors. We present a 33-year-old female with an enlarged ovary discovered incidentally at the time of cesarean section.
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PMID:Pregnancy luteoma: A rare case report. 2785 98


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