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University of Groningen Hidradenitis Suppurativa Dickinson-Blok, Janine

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University of Groningen Hidradenitis Suppurativa Dickinson-Blok, Janine University of Groningen Hidradenitis suppurativa Dickinson-Blok, Janine Louise IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2015 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Dickinson-Blok, J. L. (2015). Hidradenitis suppurativa: From pathogenesis to emerging treatment options. University of Groningen. Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license. More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne- amendment. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 07-10-2021 HIDRADENITIS SUPPURATIVA FROM PATHOGENESIS TO EMERGING TREATMENT STRATEGIES Janine Louise Dickinson-Blok ISBN: 978-90-367-8142-8 ISBN: 978-90-367-8141-1 (e-version) © 2015 by J.L. Dickinson-Blok, Groningen, The Netherlands Financial support for the publication of this thesis was provided by: AbbVie BV, ALK-Abelló BV, Almirall, Celgene BV, Fagron BV, Flen Pharma, Galderma Benelux BV, Janssen-Cilag BV, La Roche-Posay, Leo Pharma BV, Molnlycke Health Care, Rijksuniversiteit Groningen, Studiefonds Dermatologie, Universitair Medisch Centrum Groningen, Will Pharma. Design and layout: Arjan Veening, Id Graficus, Assen, The Netherlands Printing: GVO drukkers & vormgevers B.V., Ede, The Netherland HIDRADENITIS SUPPURATIVA FROM PATHOGENESIS TO EMERGING TREATMENT STRATEGIES PROEFSCHRIFT ter verkrijging van de graad van doctor aan de Rijksuniversiteit Groningen op gezag van de rector magnificus prof. dr. E. Sterken en volgens besluit van het College voor Promoties. De openbare verdediging zal plaatsvinden op woensdag 30 september 2015 om 11.00 uur door Janine Louise Blok geboren op 11 juli 1984 te Deventer Promotor Prof. dr. M.F. Jonkman Copromotor Dr. B. Horváth Beoordelingscommissie Prof. dr. B. van der Lei Prof. dr. E.P. Prens Prof. dr. G.B.E. Jemec Paranimfen Katarzyna Gostyńska Ineke Janse CONTENTS List of abbreviations 7 Chapter 1. Introduction 9 Chapter 2. Increased expression of integrin α6β4 at the basement membrane 23 zone lining the sebaceous glands in hidradenitis suppurativa Chapter 3. The possible association of hidradenitis suppurativa and Down 37 syndrome: are impaired Notch signaling and immunological abnormalities the missing links? Chapter 4. Gene expression profiling in skin and blood in hidradenitis 45 suppurativa Chapter 5. Systemic therapy with immunosuppressive agents and retinoids 51 in hidradenitis suppurativa: a systematic review Chapter 6. Ustekinumab in hidradenitis suppurativa: a clinical open label 79 study with analyses of the protein expression profile in serum Chapter 7. Skin-tissue-sparing excision with electrosurgical peeling (STEEP): 97 a surgical treatment option for severe hidradenitis suppurativa Hurley stage II/III Chapter 8. Surgery under general anesthesia in severe hidradenitis 107 suppurativa: a study of 363 primary operations in 113 patients Chapter 9. General discussion and future perspectives 125 Chapter 10. Dutch summary / Nederlandse samenvatting 137 Appendices List of publications 145 Dankwoord Curriculum vitae LIST OF abbreviatiONS AE adverse event BMZ basement membrane zone DLQI daily life quality index FPSU folliculopilosebaceous unit HiSCR hidradenitis suppurativa clinical response HS hidadenitis suppurativa IF immunofluorescence IFE interfollicular epidermis IL interleukine m-HSLASI modified hidradenitis suppurativa-lesion area and severity index mSS modified Sartorius scale PAS periodic acid–schiff PGA physician’s global assessment SFJ sebofollicular junction STEEP skin tissue sparing excision with electrosurgical peeling Th-cells T-helper cells TNF-α tumor-necrosis-factor-α VAS visual analogue scale 1 INTRODUCTION J.L. Dickinson-Blok 9 Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease affecting approximately 1-4% of the general population.1 The disease is characterized by painful deep-seated nodules and abscesses. In a later stage, epitheliazed sinus tracts are formed in the dermis and subcutaneous fat. The lesions seen in HS are mainly restricted to the body folds, like the axillary, inguinal and anogenital regions.2 These locations have several characteristics in common: 1) the skin contains apocrine glands, 2) a predisposition to mechanical friction and 3) humid conditions. Lesions commonly heal with hypertrophic fibrous scarring resulting in complete architectural loss, cosmetic disfigurement and in some cases even movement impairment.3 Not surprisingly, patient’s quality of life is impaired to a great extent.4 In fact, it has been found that quality of life scores are worse in HS compared to other distressing chronic dermatoses like atopic dermatitis, psoriasis, Darier’s disease and Hailey-Hailey disease.5 In addition to their professional career, patient’s intimate, sexual and social relationships are adversely affected by the disease. HS has also an impact on society, as it is associated with frequent and/or long-term sick leaves.6 Due to embarrassment, ignorance and neglect of the patient, as well as a lack of knowledge of regarding HS under certain medical specialists, diagnostic delays of several years are not uncommon.7,8 Pathogenesis The pathogenesis of HS is still largely unknown. The term hidradenitis suppurativa dates back to a time where it was assumed to be primarily a disease of the apocrine sweat glands.3 Although, it is now generally accepted that the hair follicle is primarily involved while the associated apocrine gland is affected in only the minority of patients as a secondary event (figure 1).9 The role of bacteria in this inflammatory process remains elusive. Fulminant discharge suggests bacterial involvement but cultures in microbiological studies have been shown to be negative or mainly revealed commensal bacteria of the skin or intestine, dependent on the investigated body location.10-12 Psoriasiform hyperplasia, follicular hyperkeratosis and occlusion are early events in the disease process.13-15 It has been suggested that these histopathological changes result from subclinical inflammation initiated by keratinocytes reacting to commensal skin bacteria.16 Additionally, a recent study suggested that fragility of the sebofollicular junction (SFJ) as part of the folliculopilosebaceous unit (FPSU) could contribute to the inflammatory activity by a defect in the follicular basement membrane zone (BMZ) that allows the release of follicular content into the surrounding dermis.17 Massive inflammation as a result of immune system activation occurs upon complete rupturing of the occluded hair follicle. 10 Epidermis Sebaceous gland Dermis Apocrine gland FPSU Hair follicle Subcutaneous fat Figure 1. The folliculopilosebaceous unit (FPSU) in the skin. * sebofollicular junction (SFJ) In addition, overproduction of interleukin (IL)-1β and tumor necrosis factor (TNF)-α from the innate immune system as well as IL-10, IL-12, IL-17 and IL-23 from the adaptive immune system have been demonstrated in HS skin.18,19 Epithelialized sinus tracts may be formed from epithelial strands in the dermis in response to these cytokines. This may facilitate access for (commensal) bacteria, leading to repetitive inflammation, further extension of the disease, and subsequently a vicious circle is made with ever increasing architectural destruction. Unraveling what cytokines are predominant in the inflammatory cascade is an important step for a better understanding of the HS pathogenesis and for identifying therapeutic targets. Epidemiology The prevalence of HS varies between studies and is estimated to be 1-4% in Europe, these numbers are mostly derived from population based questionnaires.20,21 Substantial lower prevalence rates were found in the United States, varying from 0.053 to 0.078%.22,23 Females are three times more often affected than men.1,20,24 First symptoms typically occur in the second or third decades of life but disease onset during childhood is not exceptional.25-27 11 About 80% of HS patients has a history of smoking, making it a well-known risk factor for HS.20,24,28,29 The exact pathogenic mechanism remains unclear, however, tobacco smoking may induce HS by promoting follicular occlusion, augmenting the innate immune system and triggering pro-inflammatory cytokine release.30 The association between obesity and HS has also widely been recognized and may result from increased mechanical friction of the skin and inducing a pro-inflammatory state.20,29,31 Both smoking and obesity are associated with higher disease severity.31 The role of hormones in HS remains controversial, especially regarding androgens. Studies have shown that HS improves
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