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hypertrichosis/progesterone

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[Progesterone metabolism in women with so-called essential hypertrichosis].

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[Hirsutism and hypertrichosis in adults: investigations and treatment].

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Hypertrichosis, characterized by increased hair growth located in non-androgen-dependent areas, does not justify the monitoring of hormone levels, conversely to hirsutism, with increased hair growth in androgen-dependent areas of the female genitals. Adult hypertrichosis is iatrogenic (minoxidil,

Obesity, Hypertrichosis and Sex Steroids: Are these Factors Related to the Pilonidal Sinus Disease?

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Pilonidal sinus disease causes chronic inflammation of the skin and subcutaneous fatty tissue, and it commonly localises in the sacrococcygeal region. This study evaluated the effects of hypertrichosis, family history, obesity and sex steroids in 298 patients with pilonidal sinus

Hormonal profile and androgen receptor study in prepubertal girls with hypertrichosis.

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BACKGROUND Prepubertal hypertrichosis is a reportedly benign condition characterized by an excessive growth of vellous hair in non-androgen dependent areas of the body compared to the amount usually present in normal subjects of the same age, race and sex. Although this condition is usually

Unusual heterozygotes of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

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Three otherwise healthy relatives of patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency and salt-wasting presented with clinical and/or biochemical findings, which exceeded those usually seen in heterozygotes: Two females (1 mother and 1 prepubertal sister of a
BACKGROUND Steroid 11beta-hydroxylase deficiency (11beta-OHD), an autosomal recessive inherited disease, accounts for 5% - 8% of congenital adrenal hyperplasia. It was scarcely reported in China. This article reports two Chinese girls with 11beta-OHD. METHODS The two patients were sisters and
Congenital adrenal hyperplasia (CAH) is most commonly due to 21-hydroxylase deficiency and presents a wide spectrum of clinical manifestations from a severe classical form to a milder late-onset form with a variable severity of hyperandrogenic symptoms. A limited number of mutations account for the
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