Hirsutism in the Adolescent Female

Bailey-Pridham, Dwight D.; Sanfilippo, Joseph S.

doi:10.1016/s0031-3955(16)36687-1

Cited by 14 publications

(7 citation statements)

References 41 publications

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“…Hirsutism was clinically assessed by the Ferriman-Gallwey method [12], in which hair growth in nine androgen-sensitive body areas is graded from 0 (no hirsutism) to 4 (severe), with normal value below 8 [2]. Acne was assessed according to the clinical scoring system, in which lesions were graded from 0 (no acne or microcomedones) to 5 (cystic) [13].…”

Section: Methodsmentioning

confidence: 99%

“…In many cases hirsutism is not related to a specific disease, and it is associated with normal circulating androgen levels (the so-called ''idiopathic hirsutism'') [1,2]. This condition is related to an increased sensitivity of the pilo-sebaceous unit in androgen dependent skin areas to normal sex steroid levels [3].…”

mentioning

confidence: 99%

“…In skin, the action of testosterone is mediated by dihydrotestosterone (DHT) formed in the target organ itself by the action of 5␣-reductase enzyme [4]. Increased activity of 5␣-reductase has been suggested to explain the occurrence of hirsutism in women with normal circulating androgens, but androgen hypersensitivity may be also mediated by receptor or postreceptor mechanisms [2,3]. In these cases, therapeutic intervention may be conducted with drugs that prevent the interaction of androgens with their receptor (antiandrogens) [1,5].…”

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confidence: 99%

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Androgen-Receptor Blockade Does Not Impair Bone Mineral Density in Adolescent Females

et al. 1997

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The effect of peripheral androgen hypersensitivity on bone mineral density (BMD) was investigated in a group of adolescent women with idiopathic hirsutism (n = 17; mean age 17.0 +/- 1.7 years). The effect of long-term androgen-receptor blockade with flutamide (500 mg daily in two divided doses for 12 months) on BMD was assessed too. BMD was measured at lumbar spine (L2-L4) by a dual energy X-ray densitometer. Before flutamide treatment, patient BMD (1.14 +/- 0.07 g/cm2) was not significantly different from that of the control group (1.16 +/- 0.12 g/cm2, n = 22), and was normal for age and sex (BMD 0.14 +/- 0.69 SDS, P = NS vs. 0). After 12 months of treatment, absolute BMD in patients increased (1.18 +/- 0.08 g/cm2, P < 0.002), but SDS BMD did not change (0.21 +/- 0.72, P = NS vs. baseline). Flutamide treatment determined a clinical, marked improvement of androgen hypersensitivity (Ferriman-Gallwey score: before 22.0 +/- 6.2; 6 months: 13.2 +/- 6.4, P < 0.003; 12 months; 7.6 +/- 4.1, P < 0. 001; acne score: before 3.8 +/- 0.8; 3 months 0.8 +/- 0.5, P < 0. 001; later disappeared). The serum levels of 3alpha-androstenediol-glucoronide decreased (before: 8.6 +/- 1.1 microg/liter; 12 months: 7.2 +/- 1.0 microg/liter, P < 0.02), whereas the other endocrinological parameters did not change. No relationship was found between BMD and clinical or biochemical parameters of hyperandrogenism. We concluded that in adolescent women, peripheral hyperandrogenism is not associated with abnormal BMD; long-term treatment with flutamide, which blocks the androgen receptor, does not alter their BMD.

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Section: Methodsmentioning

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Androgen-Receptor Blockade Does Not Impair Bone Mineral Density in Adolescent Females

et al. 1997

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“…Las concentraciones altas de DHEA-S indican aumento de la actividad suprarrenal 21 ' 22 , pero no su etiologia, que puede ser el estres de un paciente infertil 17 , alteraciones del metabolismo de la prolactina y bloqueos enzimaticos parciales 17 ' 19 ' 23) 24 . La mejoria clinica del hirsutismo en las pacientes tratadas con dexametasona debe ser interpretada con cautela, pues si bien parece tentador atribuir la disminucion del vello a una deficiencia enzimatica suprarrenal parcial, la dexametasona ejerce tambien acciones en otros niveles, ya que eleva el nivel de la globulina transportadora de hormonas sexuales (SHBG) 24 a la que 80% de la testosterona circulaunida, en circunstancias que solo las fracciones libre y unida a albumina son biologicamente activas, pudiendo, por lo tanto, un aumento de la SHBG provocar disminucion del hirsutismo.…”

Section: Comentariounclassified

Hirsutismo en niñas adolescentes: Estudio clínico y de laboratorio

S²,

F³

et al. 1992

Rev. chil. pediatr.

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Fourteen girls with hirsutisn, aged 12.5 to 16 years, were prospective!-/ studied. Patients with adrenal tumors, pnmary ovary disease or classical congenital adrenal hyperplasia were excluded from this study. Hirsutism was evaluated by the Ferriman score. All patients had normal weight and blood pressure. Urinary 17 hydroxicorticosteroids, pregnanetriol and dehydroepiandrosterone were measured in 24 hour urine samples. Lh, FSH, cortisoi, 1 7-hidroxyprogesterone (17-OhP), dehydroepiandrosterone sulfate (DHEAS) and testosterone in plasms were also measured Defore and 60 min after .ntravenous injection of rapidly acting ACTH (0.25 mg). Ultrasonography of the ovary was also done to each patient. Two patients were probably heterozygotus for 21-hydroxylase deficiency, nine other girls showed high blood levels of DHtAS (average 8289 ng/ml) but in three cases no apparent cause was detected and they were labeled as idiopatic hirsutism. The two patients with evidence of heterozygosity for 21-hidroxylase deficiency and b patients with high DHEAS improved after dexametasone treatment and normalization of their olood ievels of 1 7-OHP and DHEA-S respectively.

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“…Idiopathic hirsutism is defined as hirsutism in the absence of any identifiable ovarian or adrenal dysfunc tion [10]. It represents the prototypical form at androgen hypersensitivity and results from excessive activity of the enzyme 5a-reductase which further amplifies the message of testosterone.…”

Section: Idiopathic Hirsutismmentioning

confidence: 99%

Management of Hyperandrogenism in Adolescent Girls

et al. 1991

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Hyperandrogenism in adolescent girls can be a troubling problem because of the difficulty in establishing a diagnosis and in prescribing appropriate therapy. Androgen excess in adolescent patients encompasses a spectrum of clinical presentations, including acne, hirsutism, oligomenorrhea, amenorrhea, virilism, and ovarian cysts. Androgen excess is a clinical and chemical feature of idiopathic hirsutism, late-onset forms of congenital adrenal hyperplasia, and polycystic ovarian disease; in some cases, functional hyperandrogenism is discussed. We recommend screening for hyperandrogenism by measuring blood levels of testosterone, dehydroepiandrosterone sulfate, and Δ4-androstenedione, while others propose a first dexamethasone suppression test for evaluation of free testosterone, dehydroepiandrosterone sulfate, and cortisol. Treatment will be chosen according to particular symptoms such as acne, hirsutism, obesity, or oligomenorrhea.

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Hirsutism in the Adolescent Female

Cited by 14 publications

References 41 publications

Androgen-Receptor Blockade Does Not Impair Bone Mineral Density in Adolescent Females

Androgen-Receptor Blockade Does Not Impair Bone Mineral Density in Adolescent Females

Hirsutismo en niñas adolescentes: Estudio clínico y de laboratorio

Management of Hyperandrogenism in Adolescent Girls

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