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Onl Er Exd 712 1..18 DOI:10.1111/j.1600-0625.2008.0712.x www.blackwellpublishing.com/EXD Controversies in Experimental Dermatology Section Editor: Ralf Paus, Lu¨ beck What causes hidradenitis suppurativa? H. Kurzen, I. Kurokawa, G. B. E. Jemec, L. Emtestam, K. Sellheyer, E. J. Giamarellos-Bourboulis, I. Nagy, F. G. Bechara, K. Sartorius, J. Lapins, D. Krahl, P. Altmeyer, J. Revuz and C. C. Zouboulis Abstract: Hidradenitis suppurativa (HS) – a rather common, very traces of terminological bickering remain visible, it does the HS chronic and debilitating inflammatory skin appendage disorder experts in our virtual debate room credit that they engage in a with a notoriously underestimated burden of disease – has long constructive and comprehensive dissection of potential been a playground for the high priests of nomenclature: Ask a pathogenesis pathways that may culminate in the clinical picture bunch of eminent dermatologists and skin pathologists to publicly we know under the competing terms HS or acne inversa. These share their thoughts on what causes HS, and they will soon get experts sketch more often complementary than mutually exclusive entrenched in a heated debate on whether this historical term is pathogenesis scenarios, and the outlines of a conceivable a despicable misnomer. Fortunately, the recently founded consensus on the many open pathobiology questions begin to Hidradenitis Suppurativa Foundation (HSF; http://www. emerge in these CONTROVERSIES. Hopefully, this heralds a hs-foundation.org), to which EXP DERMATOL serves as home welcome new tradition: to get to the molecular heart of HS journal, has broken with this unproductive tradition and has pathogenesis, which can only be achieved by a renaissance of solid encouraged publication of the current CONTROVERSIES feature. basic HS research, as the key to developing more effective HS This is exclusively devoted to discussing the pathobiology of this therapy. chronic neutrophilic folliculitis of unknown origin. Although Please cite this paper as: What causes hidradenitis suppurativa?. Experimental Dermatology 2008. Prelude as corticosteroids, immunosuppressive drugs and ⁄ or anti- TNF agents, may improve the disease Apocrine or not, that is the question… YET In the context of HS, it has become foolhardy to speak of One of the most useful drug regimens in cases of active apocrine sweat glands ever since pathologists have demon- inflammatory lesions is a combination of two antibiotics: strated that the primary histological event was in the follic- rifadin and clindamycin (1). ular duct, like in acne. It was then simple, if not to say simplistic, for many dermatologists to forget any major dif- Paradoxon 1 ferences between acne and HS, and to rename the disease The topography of involvement may be explained by two – ‘acne inversa’, thus replacing one possible misnomer (HS) not mutually exclusive – hypotheses: (a) the distribution of with another – and leading investigators to a dead end, apocrine glands; and (b) shearing forces, which originate in and practitioners to use ineffective treatments. large skin folds, especially of overweight patients. Any hypothesis about HS must take two paradoxons into Obesity and overweight are frequent in HS and could be account: a risk factor (2). However, HS is not infrequent in inter- 1 Hidradenitis suppurativa lesions have a very specific mammary folds and on the buttocks, where such shearing topography which is a copy of the anatomical distribution forces are absent. Moreover, individuals with low or nor- of apocrine sweat glands: axillae and groin as the main mal body mass index also do develop HS. Thus, while areas; breast, perineum and buttocks as accessory regions. obesity and overweight are strongly associated with severity YET in HS, they are insufficient to explain the specific topogra- Apocrine glands are not the primary target of the patholog- phy of the disease. ical process. So, what about apocrine sweat glands? The rejection of 2 Hidradenitis suppurativa is not primarily an infectious apocrine glands as a main factor in the pathogenesis of HS disease, and yet drugs that are conducive to infection, such originates in the clear demonstration that they are spared ª 2008 The Authors Journal compilation ª 2008 Blackwell Munksgaard, Experimental Dermatology 1 Kurzen et al. by the initial inflammatory and destructive process. The New ones, psoriasin (7), are under consideration. Some of primary event is a follicular hyperkeratosis with plugging these peptides are produced by mature keratinocytes and dilatation of the hair follicle ensuing in inflammation, spontaneously or after stimulation, some are produced by abscess and sinus tract formation. Apocrine involvement eccrine sweat glands, and some are prominently subject to appears as a secondary phenomenon resulting from the modulation by antibiotics (7–9). diffusion of the granulomatous inflammation in deep However, until now, nothing is known about anti-micro- structures of the skin. bial peptides that are specifically produced in apocrine The mechanism by which follicular plugging occurs in sweat glands. This is where we need to search. acne is not known; various candidates are hypersecretion of sebum, proliferation of P. Acnes favoured by an alteration Conclusion of innate immunity and ⁄ or of inflammatory reactions, and Hidradenitis suppurativa is as multifactorial as any chronic possibly several others. disease and probably heterogeneous. Here, I have only con- Here, the specific anatomical relationship of the apocrine sidered the role that apocrine glands may have, a role that gland with the follicular canal has to be taken into account: might well be central – no matter, how much this gland In contrast to eccrine glands, whose ducts open onto the has fallen out of fashion in HS research. The role of other skin surface, apocrine glands empty their content into the factors – e.g. hair follicle anatomical ⁄ structural abnormali- follicular canal, just above the sebaceous gland duct. In HS, ties (highly probable at least in a subset of HS patients), hyperseborrhoea is definitely absent but the other factors the role of obesity, the role of cigarette smoking – all may be at work: deserve careful exploration. Any pathogenesis scenario, An abnormal secretion – excess or absence – of a sub- however, that completely discards apocrine glands and their stance that is present in apocrine gland secretion under specific distribution as key elements in the development of physiological conditions may therefore, after all, be the HS may soon turn out to have to be discarded itself! triggering factor of HS! Its morphologically recognizable effect could be in the acro infundibulum of the follicle, Jean Revuz with the responsible gland disguising itself as an innocent Department of Dermatology, Henri Mondor Hospital, bystander upon histology – a perfectly masked ‘criminal’. 94000 Creteil, France; E-mail: [email protected] Paradoxon 2 Hidradenitis suppurativa is a disease in which numerous References bacteria are present and active (3), and in which various 1 Mendonc¸a C O, Griffiths C E M. Br J Dermatol 2006: 154: 977–978. 2 Naldi L. Epidemiology. In: Jemec G, Revuz J, Leyden J, eds. Hidrade- antibiotic regimens have definitely improved the condition nitis suppurativa, Chap. 8. Springer Verlag, 2006: 58–64. in patients with severe inflammatory involvement (2). Sur- 3 Faye O, Poli F, Gabison G, Pouget F, Wolkenstein P, Revuz J. Associa- prisingly, numerous pro-infectious drugs have also been tion rifampicine ⁄ clindamycine dans l’hidrade´ nite suppure´ e. Ann Der- used with good results: corticosteroids, immunosuppressive matol Venereol 2005: 132: 68–69. drugs, anti-tumour necrosis factor (4,5). The coexistence of 4 Oprica C, Nord C E. Bacteriology of hidradenitis suppurative. In: Jemec G, Revuz J, Leyden J, eds. Hidradenitis suppurativa, Chap. 11. these two seemingly contradictory phenomena calls for a Berlin: Springer Verlag, 2006: 86–94. closer look at the properties of anti bacterial molecules 5 Nybaek H, Jemec G B E. Immunosuppressive therapy. In: Jemec G, which play a key role in innate and acquired immunity: the Revuz J, Leyden J, eds. Hidradenitis Suppurativa, Chap. 18. Berlin: so-called anti-microbial peptides (6). Springer Verlag, 2006: 136–140. They are known to exert both pro- and anti-inflamma- 6 Jacob S E, Kerdel F A. Biologic for hidradenitis suppurativa (Verneuil’s disease in the Era of biologics). In: Jemec G, Revuz J, Leyden J, eds. tory functions; they alarm and activate the adaptive Hidradenitis suppurativa, Chap. 20. Berlin: Springer Verlag, 2006: immune system and the keratinocytes that produce them. 145–149. They induce keratinocytes migration, proliferation – a role 7 Schauber J, Gallo R L. Expanding the roles of antimicrobial peptides in follicular occlusion? They are part of a complex network in skin: alarming and arming keratinocytes. J Invest Dermatol 2007: of cytokine and chemokine production. The absence or 127: 510–512. 8 Gla¨ ser R et al. Antimicrobial psoriasin (S100A7) protects human skin abnormality of one of these anti-microbial peptides would from Escherichia coli infection. Nat Immunol 2005: 6: 1–57. be a good candidate for explaining the infectious and 9 Tokura Y et al. Epidermal chemokines and modulation by antihista- inflammatory features of HS. Cathelicidins and defensins mines, antibiotics and antifungals. Exp Dermatol 2007: November 22 are the main representatives of this family identified today. [Epub ahead of print]. ª 2008 The Authors 2 Journal compilation ª 2008 Blackwell
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