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Endocrinology 12 Michel Faure, Evelyne Drapier-Faure Chapter 12 Endocrinology 12 Michel Faure, Evelyne Drapier-Faure Key points 12.1 Introduction Q HS does not generally appear to be In 1986 Mortimer et al. [14] reported that hi- associated with signs of hyperan- dradenitis suppurativa (HS) responded to treat- drogenism ment with the potent antiandrogen cyproterone acetate. They suggested that the disease could Q Sex hormones may affect the course of be androgen-dependent [8]. This hypothesis HS indirectly through, for example, was also upheld by occasional reports of women their effects on inflammation with HS under antiandrogen therapy [18]. Actu- ally, the androgen dependence of HS (similarly Q The role of end-organ sensitivity to acne) is only poorly substantiated. cannot be excluded at the time of writing 12.2 Hyperandrogenism and the Skin Q The prevalence of polycystic ovary syndrome in HS has not been system- Androgen-dependent disorders encompass a atically investigated broad spectrum of overlapping entities that may be related in women to the clinical consequenc- es of the effects of androgens on target tissues and of associated endocrine and metabolic dys- functions, when present. #ONTENTS 12.1 Introduction ...........................95 12.2.1 Androgenization 12.2 Hyperandrogenism and the Skin .........95 12.2.1 Androgenization .......................95 One of the less sex-specific effects of androgens 12.2.2 Androgen Metabolism ..................96 12.2.3 Causes of Hyperandrogenism ...........96 is that on the skin and its appendages, and in particular their action on the pilosebaceous 12.3 Lack of Association between HS unit. Hirsutism is the major symptom of hyper- and Endocrinopathies ..................97 androgenism in women. Other dermatological 12.4 HS and Biological Hyperandrogenism ...97 conditions include acne and the chronic hair 12.5 End-Organ Androgen Sensitivity? .......98 loss usually termed androgenic alopecia (AGA). References .............................98 Whereas acne, hirsutism and chronic hair loss may coexist in the same patient, it is not unusu- al to find only one of these androgenic manifes- tations [16]. Depending on the presence of ovarian dys- function, extracutaneous manifestations may include abnormalities of menstruation with 96 Michel Faure, Evelyne Drapier-Faure anovulatory patterns, oligomenorrhoea, fertili- Sebaceous glands, but also keratinocytes ty problems, android obesity and risks for from the acroinfundibulum and dermal papilla metabolic complications, such as hyperinsulin- cells, can synthesize androgens de novo from ism, insulin resistance, diabetes mellitus, and cholesterol or by locally converting weaker an- dyslipidaemia, and for cardiovascular diseases drogens (64A and DHEA) to testosterone and [6, 16]. DHT. As in other classic steroidogenic organs, the pilosebaceous unit expresses the major en- zymes involved in androgen metabolism, name- 12.2.2 Androgen Metabolism ly steroid sulfatase, 3`-, 3_- and 17`-hydroxys- teroid dehydrogenases, and 5_-reductase, which The causes of hyperandrogenism are multiple converts testosterone into DHT. Furthermore (Table 12.1). Skin androgenization in women aromatase, which converts testosterone into may be due to abnormal production of andro- oestradiol, is localized to sebaceous glands and gens by the ovaries and/or the adrenal glands, to both outer and inner root sheath cells of ana- and/or to an excessive response of target cells gen terminal hair follicles. This hormone may in the pilosebaceous unit (peripheral androgen- play a “detoxifying” role by removing excess an- ism) [6]. drogens [5]. Androgens [testosterone and the less po- tent androgens in women 64-androstenedione (64A) and dehydroepiandrosterone (DHEA)] 12.2.3 Causes of Hyperandrogenism are synthesized by the adrenals (mostly DHEA and its sulfate – SDHEA) and the ovaries (most- As far as hyperandrogenisms due to an excess of ly 64A) and may be subsequently transformed androgen production are concerned, tumoral into oestrogens through the aromatization of causes and Cushing’s syndrome are rare. The the molecules. Sex hormone binding globulin most common endocrine disorders are polycys- (SHBG) synthesized in the liver is the major tic ovary syndrome (PCOS) and non-classic ad- carrier protein for androgens and oestradiol. renal hyperplasia (NCAH) with 21-hydroxylase Only free androgens, unbound to SHBG, are di- deficiency. Hyperandrogenism is associated rectly active on target cells. In tissues, andro- with high levels of circulating androgens and 12 gens are first metabolically transformed into decreased SHBG levels. PCOS also requires mor- the active form dihydrotestosterone (DHT), phological and ultrasound criteria: an increased which then binds to androgen receptors (AR) number of subcapsular follicles and stromal [16]. hyperplasia. Plasma levels of 17-hydroxyproges- terone (17-HP) are increased in NCAH. If NCAH is only suspected with moderately increased Table 12.1. Causes of hyperandrogenism 17-HP, an adrenocorticotropic hormone (ACTH) test must be performed [1, 6, 7]. 1. Polycystic ovary syndrome (PCOS) On the other hand, hyperandrogenic skin 2. Non-classic adrenal hyperplasia changes (“idiopathic” hirsutism, hypertrichosis with 21-hydroxylase deficiency in men, most cases of acne, AGA in women but 3. Skin hypersensitivity = also in men) mostly occur in fact in patients peripheral hyperandrogenism: with normal androgen levels. Increased enzyme – with hirsutism (idiopathic) activities in the peripheral metabolism of ste- – and/or acne or androgenic alopecia roids, and/or increased sensitivity of AR, both 4. Drugs presumed to be subjected to genetic polymor- – androgenic progestins phisms, might account for abnormal responses – OP contraception with androgenic progestins to androgens. The first possibility in patients 5. Others (rare): with androgen-dependent skin manifestations – adrenal and ovarian tumours corresponds to increased metabolic pathways – Cushing’s syndrome that lead to the transformation of weaker an- Endocrinology Chapter 12 97 drogens to testosterone, increased 5_ reduction lapse after pregnancy, as well as premenstrual to DHT and lower aromatase activity [16]. and menstrual exacerbations are usually noted, The second possibility (the two not being suggesting that hormones, at least oestrogens, mutually exclusive) is directly linked to AR sen- may influence the course of the disease. Oestro- sitivity. AR is a structurally conserved member gens in fact are known to interfere with inflam- of the nuclear receptor superfamily. The amino- matory processes, independently of a direct ge- terminal domain is required for transcriptional nomic action of the steroids. This could account activation and contains a region of polygluta- for their influence on the natural course of in- mine encoded by CAG trinucleotide repeats. In flammatory diseases, such as acne, but also HS. humans the number of CAG repeats is polymor- Other observations in HS in terms of premen- phic. Longer repeat lengths are associated with strual and/or menstrual exacerbations may be androgen-insensitivity syndromes. It has been unrelated to the oestrogen or androgen depen- suggested that AR polymorphisms (CAG-repeat dency of the disease. lengths) account for AGA, hirsutism and acne, Although HS may be associated in some since shorter repeat lengths may be associated women with classic signs of skin androgeniza- with the development of androgen-mediated tion such as acne and/or hirsutism, no real as- skin disorders in men and women [17]. sociation of HS with hirsutism (the major symp- tom of hyperandrogenism) has ever been reported. In a series of 70 women with HS, acne 12.3 Lack of Association between HS was not more frequent than in controls [10]. The and Endocrinopathies incidence of patients with signs of androgeniza- tion did not differ significantly between the two Although HS has been reported in two men groups. Only a shorter menstrual cycle and a with acromegaly [4], which is very likely due to longer duration of menses in patients with HS a direct effect not of androgens but of growth were noted. Although there was no evidence in hormone on apocrine glands, HS was not found favour of or against an association with PCOS to be associated with endocrine disorders. or with NCAH, these data indicate that HS is In women HS has not been reported in asso- not accompanied by the usual clinical signs of ciation with ovarian or adrenal tumours, Cush- androgenization. ing’ syndrome, PCOS or NCAH, all known causes of hyperandrogenism with increased or abnormal androgen production. In fact, a pos- 12.4 HS and Biological sible association of HS with functional hyperan- Hyperandrogenism drogenism (ovarian or adrenal dysfunction) merits investigation with modern biological and Furthermore, as far as serum levels of andro- ultrasound markers [7]. gens and SHBG are concerned, there is no clear HS usually begins after puberty when the evidence for biochemical hyperandrogenism. apocrine glands are fully developed. A few cases On average, androgen levels (total plasma tes- have been reported in children, as clinical man- tosterone and free testosterone index due to a ifestations of premature adrenarche or early pu- low SHBG) were increased, but were normal in berty [11, 12, 15]. This represents in fact the many individual patients, and no significant de- strongest evidence for an influence of andro- crease of SHBG could be detected [13]. In fact, gens on HS. However, HS is more common in SHBG is known to be regulated by factors that women and usually
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