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Query: UMLS:C0042755 (masculinization)
 2,562 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of maternal virilization associated with bilateral luteomas of pregnancy is described. Urinary 17-ketosteroids and plasma testosterone fell from markedly abnormal values to normal limits within 2 weeks of delivery. However, symptoms of virilization persisted in the postpartum state. A possible relation between polycystic ovarian syndrome in the nonpregnant state and luteoma of pregnancy is proposed.
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PMID:Virilization associated with bilateral luteomas of pregnancy. 16 43

The clinical course of a 26-year-old primigravid woman with a virilizing luteoma of pregnancy is described. It was demonstrated by endocrine studies that the tumor secreted an excessive amount of testosterone. After removal of the luteoma in week 32 of pregnancy, the virilizing symptoms of the mother completely regressed. A normal male infant was delivered in week 39. From 100 luteomas of pregnancy described in the literature, 26 cases have been cited to elicit endocrine virilizing activity. An evaluative synopsis indicates that including the case described in this paper only 13 can be regarded as a clinical, morphologic, and functional entity. This entity should be differentiated from the inhomogeneous group of luteomas as the "androluteoma syndrome of pregnancy." It is characterized by the following major criteria: virilization, beginning with the second trimester of pregnancy; histologic criteria of a luteoma of pregnancy; production of testosterone, leading to excessive plasma levels (exceeding the concentration of androstenedione), and masculinization of female fetuses.
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PMID:Androluteoma syndrome of pregnancy. 20 61

Lacl of masculinization in female infants whose virilized mothers have h. luteinalis is in contrast to the common finding of fetal masculinization when maternal virilization occurs with luteoma of pregnancy. From the data at hand, this variation in fetal response cannot be explained by differences in the quantity of androgen production nor by the stage of pregnancy when maternal virilization becomes evident. Steroid analysis from cases of h. luteinalis suggests that the placenta may serve as an androgen barrier by aromatizing steroids before they reach the fetus. Testosterone conversion by the placenta of an anencephalic fetus confirms that conversion to estrogens occurs even without significant fetal adrenal activity. Understanding of the breakdown of this mechanism, with resultant fetal masculinization, will require careful evaluation of the steroid milieu in conditions like luteoma in which fetal masculinization often occurs. Both cystic and solid ovarian hyperplasia are recognized as are complications of pregnancy which require proper identification and conservative management. The significant difference in patients at risk for luteoma and h. luteinalis and the pathological and hormonal differences clearly indicate that these are distinct and separate entities.
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PMID:Differential maternal-fetal response to androgenizing luteoma or hyperreactio luteinalis. 20 19

Multiple lutein cyst (MLC) and luteoma are two aspects of ovarian hyperplasia induced by high levels of human chorionic gonadotrophin (HCG). Using a case report of MLC, the authors compare it with luteoma (the anatomoclinical and pathogenic data). Luteoma are more frequent with multipara, whereas MLC are more often seen with paucipara. Maternal virilization can occur in both cases but MLC does not seem to be responsible for fetal virilization. The fetus could be protected by the placenta, thanks to increased aromatase activity and sex binding globulin production. MLC and luteoma are usually found by chance. The pathology must be known, because of their spontaneous regression after delivery. So, the attitude will be conservative under the control of biopsies.
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PMID:[Luteinized cystic hyperplasia of the ovaries during pregnancy. A case report]. 132 53

Benign causes of maternal virilization in pregnancy, such as luteoma of pregnancy and hyperreactio luteinalis, are generally believed to resolve completely post partum and not to recur. We present the fifth case in the literature of recurrent maternal virilization in pregnancy. These lesions should be viewed as potentially recurrent and cases should be managed accordingly.
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PMID:Recurrent maternal virilization during pregnancy caused by benign androgen-producing ovarian lesions. 133 77

Postmenopausal hyperandrogenism with overt clinical effects is rare and often related to ovarian stromal disorders. We present a clinicopathologic study of 4 cases. The patients (age range 41-75 years; mean 62 years) had evidence of hirsutism or frank virilization. Their serum testosterone was elevated with or without increases in their serum androstenedione and DHEA levels. There were two right-ovarian hilus cell tumors, one associated with left-ovarian stromal hyperplasia and the other with bilateral hyperthecosis and nodular hilus cell hyperplasia. The other tumor was a small corticomedullary stromal luteoma with bilateral hyperthecosis and nodular hilus cell hyperplasia. The fourth patient had bilateral hilus cell hyperplasia with mild cortical-stromal hyperplasia. All these patients had rapid normalization of androgen levels after surgery without recurrence after a 2- to 10-year follow-up.
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PMID:Postmenopausal hyperandrogenism of ovarian origin. A clinicopathologic study of four cases. 152 32

Maternal virilization association with the birth of a virilized female infant has been reported in gravidas with luteoma. We describe a similar case with ambiguous genitalia (type Prader III). The only pathological finding was an elevated postpartum maternal serum testosterone (4.11 ng/ml). Excluding all differential diagnosis we conclude, that the only possibility for the virilization of the newborn female was a luteoma.
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PMID:[Luteoma of the mother as a possible cause of external female pseudohermaphroditism]. 215 16

A case of hyperreactio luteinalis in a patient with normal singleton pregnancy is reported. The course of pregnancy had been normal until the 24th week of gestation, when the mother developed lower abdominal pain and signs of virilization. She delivered of a normal female infant at 39 weeks' gestation. The baby did not show any signs of masculinization. Serum testosterone, delta 4-androstene-dione, and 5 alpha-dihydrotestosterone of the mother were markedly elevated. They remained high after the delivery but returned to the normal ranges soon after the partial resection of the enlarged ovaries. Reported causes of hyperreactio luteinalis are reviewed. Their maternal serum androgen levels were compared with cases of luteoma of pregnancy.
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PMID:Hyperreactio luteinalis in normal singleton pregnancy. 257 38

A masculinized female infant was born to a mother who had virilizing signs dating from the fourth month of pregnancy. Serum 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, and testosterone levels were all normal in the infant. Maternal testosterone level was markedly elevated one week post partum. Dexamethasone phosphate suppression was normal. Human chorionic gonadotropin stimulation five weeks post partum revealed further elevation of high baseline free and total testosterone levels. Free and total testosterone levels 30 weeks post partum were normal, and all maternal virilizing signs had regressed with the exception of her deepened voice. The child has had no progression of masculinization. The mother is believed to have had a luteoma of pregnancy.
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PMID:Fetal and maternal virilization associated with pregnancy. A case report and review of the literature. 628 Apr 91

The patient was born with ambiguous genitalia (stade III of Prader). The karyotype revealed a normal female genotype. A defect in 21-hydroxylase, at first suspected, was denied by the hormonal studies. Indeed, extremely high levels of pregnenolone, pregnenolone sulfate, progesterone were found in association with low plasma levels of delta 4-androstenedione, testosterone, dehydroepiandrosterone and its sulfate, while cortisol 17OH-progesterone and ACTH levels and plasma renin activity were normal. The hormonal pattern was thus consistent with 17,20-desmolase deficiency. The dynamic studies further supported this contention: all the progestagens rose further after ACTH stimulation and were suppressed by dexamethasone. Meanwhile, all androgens failed to rise after ACTH: the responses of cortisol were normal. The in utero virilization of the female fetus was not understood until an history of virilization was allegedly found in the mother (luteoma of pregnancy). This is the first case of 17-20 desmolase defect recognized in a female newborn. This child, born with ambiguous genitalia had presented the concurrence of two very rare conditions. The in utero virilization of maternal origin enabled us to make the diagnosis of the 17-20 desmolase defect, which otherwise would have been ignored in a XX subject in the neonatal period because it would obviously be unsymptomatic at this age.
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PMID:17,20-desmolase deficiency in a female newborn, paradoxically virilized in utero. 632 71


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