The relationship of mild hirsutism or acne in women to androgens

Reingold, S. B.

doi:10.1001/archderm.123.2.209

Cited by 33 publications

(18 citation statements)

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“…Thigh hair growth rate in 52 hirsute women was significantly correlated with plasma androstenedione and Scc-dihydrotestosterone levels, but not with testosterone, oestradiol, SHBG or free testosterone as estimated by the testosterone: SHBG ratio (Ebling et a/., 1984); sebum secretion was weakly correlated only to Scc-dihydrotestosterone concentration, but the correlation was only on the edge of significance (n= 18). Ruutiainen et al (1985) obtained a significant correlation between androstenedione levels and hirsutism grade according to the Ferriman and Gallwey score (Ferriman & Gallwey, 1961), but the scores also correlated positively with free testosterone and negatively with SHBG levels unlike those of Reingold and Rosenfield (1987). Ruutiainen et al (1987) also found a correlation with salivary testosterone levels.…”

Section: Hirsutismmentioning

confidence: 99%

Androgens and human hair growth

Randall

1994

Clinical Endocrinology

158

112

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Section: Hirsutismmentioning

confidence: 99%

Androgens and human hair growth

Randall

1994

Clinical Endocrinology

158

112

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“…Seborrhoea is a result of hypersensitivity of the follicular target organ to androgens. Acne alone, even comedonal acne, may be induced due to androgen excess, thus, minor or mild acne can be the sole manifestation of peripheral hyperandrogenism [47]. In the bald scalp the sebaceous glands rapidly transform DHEA-s through the action of Δ 5 -3β-HSD into androstenedione which is rapidly transformed into testosterone due to an increased activity of 17β-HSD, a fact that does not occur in non-bald scalp [48].…”

Section: Cutaneous Changes Induced By Peripheral Hyperandrogenismmentioning

confidence: 99%

The SAHA Syndrome

Orfanos

Adler

Zouboulis³

2000

Horm Res Paediatr

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The presence of seborrhoea, acne, hirsutism and alopecia in women has first been summarized as SAHA syndrome in 1982 and can be associated with polycystic ovary syndrome, cystic mastitis, obesity and infertility. In 1994, the association of these androgen-dependent cutaneous signs, was classified according to their etiology into four types: (1) idiopathic, (2) ovarian, (3) adrenal, and (4) hyperprolactinemic SAHA. The HAIRAN syndrome has been currently described as a fifth variant with polyendocrinopathy. The SAHA syndrome generally occurs in young to middle-aged women and involves either the presence of elevated blood levels of androgens or increased androgen-driven peripheral response with normal circulating androgen levels. Peripheral metabolism of androgens takes place in various areas within the pilosebaceous unit, as indicated by local differences in the activities of aromatase, 5α-reductase as well as of the presence of the androgen receptors. In cases of SAHA syndrome, careful diagnostic and clinical evaluation has to be performed in order to identify the cause for peripheral hyperandrogenism and to exclude androgen-producing tumors. Treatment will target the etiology, whereas the management in idiopathic cases will aim to improve the clinical features of SAHA.

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“…35 However, this criterion is controversial because mild hirsutism is due to ethnic or familial factors rather than hyperandrogenemia half of the time, in contrast to moderate-severe hirsutism, which is usually due to hyperandrogenemia. 36 On the other hand, hyperandrogenemia is variably accompanied by hirsutism: little more than half of hyperandrogenemic PCOS patients are hirsute. 1 …”

Section: Clinical and Biochemical Evidence Of Hyperandrogenism In Adomentioning

confidence: 99%

“…Although dihydrotestosterone generated in target tissue mediates most testosterone effects, its serum level is of little diagnostic value. 36 However, accurate determinations of total and free testosterone concentrations are often problematic. Diurnal rhythm, phase of menstrual cycle, and SHBG concentrations are biological variables that influence total testosterone concentrations.…”

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confidence: 99%

The Diagnosis of Polycystic Ovary Syndrome in Adolescents

2015

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Consensus has recently been reached by international pediatric subspecialty societies that otherwise unexplained persistent hyperandrogenic anovulation using age-and stage-appropriate standards are appropriate diagnostic criteria for polycystic ovary syndrome (PCOS) in adolescents. The purpose of this review is to summarize these recommendations and discuss their basis and implications. Anovulation is indicated by abnormal uterine bleeding, which exists when menstrual cycle length is outside the normal range or bleeding is excessive: cycles outside 19 to 90 days are always abnormal, and most are 21 to 45 days even during the first postmenarcheal year. Continued menstrual abnormality in a hyperandrogenic adolescent for 1 year prognosticates at least 50% risk of persistence. Hyperandrogenism is best indicated by persistent elevation of serum testosterone above adult norms as determined in a reliable reference laboratory. Because hyperandrogenemia documentation can be problematic, moderate-severe hirsutism constitutes clinical evidence of hyperandrogenism. Moderate-severe inflammatory acne vulgaris unresponsive to topical treatment is an indication to test for hyperandrogenemia. Treatment of PCOS is symptom-directed. Cyclic estrogenprogestin oral contraceptives are ordinarily the preferred first-line medical treatment because they reliably improve both the menstrual abnormality and hyperandrogenism. First-line treatment of the comorbidities of obesity and insulin resistance is lifestyle modification with calorie restriction and increased exercise. Metformin in conjunction with behavior modification is indicated for glucose intolerance. Although persistence of hyperandrogenic anovulation for $2 years ensures the distinction of PCOS from physiologic anovulation, early workup is advisable to make a provisional diagnosis so that combined oral contraceptive treatment, which will mask diagnosis by suppressing hyperandrogenemia, is not unnecessarily delayed.Polycystic ovary syndrome (PCOS) is the most common cause of chronic hyperandrogenic anovulation and the single most common cause of infertility in young women. 1 It is also a risk factor for metabolic syndrome-related comorbidities and for impaired wellbeing and mortality. 2 Considerable evidence suggests that PCOS has diverse causes, arising as a complex trait with contributions from both heritable and environmental factors that affect ovarian steroidogenesis. 3,4 Insulinresistant hyperinsulinism, in part related to coexistent obesity, is the most common nonsteroidogenic factor. The complex interactions generally mimic an autosomal dominant trait with variable penetrance: the disorder is correlated in identical twins 5 ; about half of sisters are hyperandrogenic, and half of these also have oligo-amenorrhea and thus PCOS 6,7 ; and polycystic ovaries appear to be inherited as an autosomal dominant trait. 7,8 Three percent to 35% of mothers have PCOS, 9,10 and metabolic syndrome prevalence is high in parents and siblings. 11-13 The syndrome was first described...

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The relationship of mild hirsutism or acne in women to androgens

Cited by 33 publications

References 0 publications

Androgens and human hair growth

Androgens and human hair growth

The SAHA Syndrome

The Diagnosis of Polycystic Ovary Syndrome in Adolescents

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