Cases reported "Hirsutism"

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1/2. Recurrent severe hyperandrogenism during pregnancy: a case report.

    This report describes the case of a 28 year old woman with virilisation occurring in two successive pregnancies. Recurrent maternal virilisation is rare (seven previous reports) and this case is unique in its severity. Differential diagnoses include ovarian disease and fetal aromatase deficiency. New techniques to exclude a fetal cause were used in this case. This patient presented during the third trimester of her first pregnancy with rapid onset of hirsuitism, increased musculature, and deepening voice. A blood hormone profile revealed significant hyperandrogenism (testosterone, 72.4 nmol/litre; normal range, 0.5-3.0). She delivered a normal boy and maternal androgen concentrations returned rapidly to normal (testosterone, 0.8 nmol/litre). She presented two years later, during her second pregnancy, with similar symptoms and biochemistry (testosterone, 47.5 nmol/litre). Again, she delivered a healthy normal boy and androgens returned immediately to normal (serum testosterone, 2.0 nmol/litre). ultrasonography revealed no evidence of ovarian (or adrenal) masses in either pregnancy. umbilical cord venous blood sampling and placental assays revealed no evidence of fetal aromatase deficiency. Recurrent hyperandrogenism during pregnancy is rare. Ovarian luteoma rarely recurs and hyperreactio luteinalis does not lead to such pronounced androgen concentrations. Therefore, this patient has a unique ovarian condition that could be harmful to offspring and mother.
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2/2. Adrenocortical 11 beta-hydroxylation defect in adult women with postmenarchial onset of symptoms.

    Four cases in adults of a deficiency in the 11 beta-hydroxylation of corticosteroids were investigated by both basal and dynamic biological studies. Symptoms varied from patient to patient; hirsutism, menstrual disturbance, acne, deepening of the voice, and arterial hypertension appeared post puberty. Basal testing demonstrated elevated levels of plasma androgens. These include delta 4-androstenedione (patients, 3.80-6.43 ng/ml; normal, 1.33 /- 0.33 ng/ml), urinary 17-ketosteroids (patients, 11.8-16.7 mg/24 h; normal, 5-10 mg/24 h), and urinary dehydroepiandrosterone. The basal tests were often insufficient to show the accumulation of the precursors (especially 17-hydroxyprogesterone) which are often given as evidence for an increase in ACTH stimulation. In studying the levels of the mineralocorticoids, there was shown to be an increased basal level of tetrahydrodeoxycorticosterone (patients, 142-317 microgram/24 h; normal, 60-80 microgram/24 h) which was raised by ACTH stimulation. These results, therefore, confirm the characteristic partial enzyme defect and give evidence for the heterogeneity of this syndrome. Based on the above observations, we believe it is appropriate to rename this condition adult adrenocortical 11 beta-hydroxylation defect rather than late-onset congenital adrenal hyperplasia.
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