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Pathology of Hidradenitis Suppurativa 4 Alison Layton Chapter 4 Pathology of Hidradenitis Suppurativa 4 Alison Layton 4.7 Conclusions ...........................32 Key points Acknowledgements ....................33 Q HS is a follicular disease References .............................33 Q Apocrine gland involvement appears to be secondary to follicular events 4.1 Introduction Q A lymphocytic infiltrate predominates There has been significant debate around the in early lesions pathological features of hidradenitis suppurati- va (HS) over the years. This debate focuses on Q Keratin expression suggests that sinus whether the primary event relates to an inflam- tracts are fragile matory process of the apocrine duct or whether follicular occlusion is integral to the initiating Q Keratin expression suggests that the process. outer root sheet may be involved HS was first described as a distinct clinical in HS lesions entity in 1839 by Velpeau [1]. In 1854 Verneuil suggested that the inflammatory changes which affected skin of the axillae, sub-mammary/ mammary regions (Fig. 4.1) and perianal areas #ONTENTS were linked directly to a disease of the sweat 4.1 Introduction ..........................25 glands [2]. In 1922 a direct association was made between HS and the apocrine glands [3]. As a 4.2 Glandular Elements of the Skin ..........26 result of the anatomical distribution and the 4.2.1 Sebaceous Glands and the Pilosebaceous Unit .............26 inflammatory changes noted, the term “apo- 4.2.2 Apocrine Glands . .27 crinitis” was used as a synonym for HS. This 4.2.3 Eccrine Glands ........................27 terminology was supported when Brunsting 4.2.4 Apoeccrine Glands .....................27 demonstrated the presence of distended apo- 4.3 HistologicalAppearanceofHS ..........27 crine glands containing polymorph neutrophils 4.3.1 Early Lesions .....................27 in the subcutis sections from 16 cases of estab- 4.3.2 Established Hidradenitis Suppurativa ..28 lished HS. He concluded that the disease was an 4.4 Immunohistochemistry infection that entered the hair follicle duct and of Hidradenitis Suppurativa ............30 expressed its full inflammatory effect within 4.5 Cytokeratin Expression in HS ...........30 apocrine glands, with further progression oc- curring via the subcutaneous lymphatic chan- 4.6 Comparison with Other Disorders .......31 nels [4]. This explanation of pathogenesis was 4.6.1 Fox–Fordyce Disease ...................31 4.6.2 Acne ..................................31 considered the explanation for the increased 4.6.3 Follicular Occlusion Triad ..............31 frequency of HS in African Americans, who 4.6.4 Pilonidal Sinus ........................31 have more apocrine glands per unit area of 4.6.5 Crohn’s Disease ........................32 skin. 26 Alison Layton was evident in all of the specimens regardless of disease duration, which ranged from 1 month to 18 years. In contrast, control specimens from axillary and inguinal regions did not demon- strate any follicular occlusion [7]. In the same study, active folliculitis was associated with apocrinitis and apocrine destruction whereas apoeccrine glands, which drain directly onto the epidermal surface, remained intact and 4 showed no evidence of inflammation. This work provided clear evidence that follicular occlusion by keratinous material, with subsequent active folliculitis and secondary destruction of the skin adnexae and subcutis, occurs as an integral step in the pathogenesis of HS. A further study examining early lesions has confirmed that keratin plugging of follicles and sinuses and inflammation around the hair fol- licle are frequent features in HS [8]. Clinical support for follicular occlusion includes typical, large, multiple and grouped comedones evident Fig. 4.1. Chronic hidradenitis suppurativa of the axilla in HS in apocrine sites [9, 10]. Hence, it is now believed that HS conforms to a disorder of terminal follicular epithelium However, in 1955 Shelley and Cahn applied within apocrine-gland-bearing skin but that belladonna-impregnated occlusive tape to de- apocrine involvement does not appear to be a pilated axillary skin in 12 healthy male volun- primary event in the majority of cases [11]. teers. They produced typical lesions of HS in 3 out of the 12 cases at the sites of application of the adhesive tape. The histological inflamma- 4.2 Glandular Elements of the Skin tion was confined to the apocrine glands [5]. This work introduced the concept that the initi- The cutaneous glands in humans include holo- ating event in HS relates to follicular occlusion crine or sebaceous glands and merocrine or followed by involvement of the apocrine gland. sweat glands. Merocrine glands are subdivided In 1990, Yu and Cook retrospectively examined into apocrine and eccrine glands. axillary skin from 12 patients with established HS [6]. Of the 12 cases, 10 showed squamous- epithelium-lined cysts or sinuses in the dermis 4.2.1 Sebaceous Glands all containing keratin and half contained hair and the Pilosebaceous Unit shafts, suggesting they were derived from hair follicles. Only 4 of the cases had apocrine in- The sebaceous glands are an integral part of the flammation and when apparent this was evident pilosebaceous unit and are found over the entire around eccrine glands, hair follicles and epithe- body surface with the exception of the palms lium-lined structures. This work suggested that and soles. The gland itself is made up of several follicular occlusion was a more constant diag- lobules, which are separated by vascular con- nostic feature than inflammation around the nective tissue. These lobules all empty into a apocrine glands. short duct which then empties into the upper A further retrospective pathological study of part of a hair follicle at the level of the infun- 118 skin specimens from 110 patients suffering dibulum. More than one sebaceous duct may from HS demonstrated that follicular occlusion drain into the upper part of the hair follicle. Pathology of Hidradenitis Suppurativa Chapter 4 27 4.2.3 Eccrine Glands Eccrine glands are derived from a specialized down-growth of the epidermis in utero. They represent small tubular structures that drain di- rectly onto the skin surface. They exhibit ther- moregulatory control when the body is exposed to a warm environment or during heavy exer- cise. They are found in all sites of the skin ex- cluding mucous membranes. The sites of maxi- mum concentration are the palms, soles, axillae and forehead. 4.2.4 Apoeccrine Glands These represent axillary glands in adults and combine morphological features of both eccrine Fig. 4.2. Diagrammatic representation of the piloseba- and apocrine glands. A straight intradermal ceous unit duct opens directly onto the skin surface. The deep secretory component conforms to a dilated The hair follicle, the hair, the sebaceous gland apocrine segment whilst proximally the epithe- and arrectores pilorum muscle and (in certain lium is compatible with an eccrine derivation. regions) the apocrine glands make up the pilo- sebaceous unit (Fig. 4.2). 4.3 Histological Appearance of HS 4.2.2 Apocrine Glands 4.3.1 Early Lesions (Fig. 4.3a–d) Apocrine glands are found predominantly in Follicular hyperkeratosis with plugging and the axillary and anogenital regions, although dilatation of the hair follicle is seen as an early they are also found in the ear canal (ceruminal event in HS. The follicular epithelium may pro- glands) and eyelids (Moll’s glands). They are liferate or may be destroyed. Inflammation is derived from epidermis and develop as an out- frequently not apparent in early lesions but peri- growth of follicular epithelium. They represent folliculitis will ensue and the inflammatory in- compound sweat glands with a secretory coil filtrate embraces neutrophils, lymphocytes and that extends deep through the dermis into sub- histiocytes. Early lesions may show acute in- cutaneous tissue and drains via a long straight flammation involving the apocrine gland and secretory duct, usually into a hair follicle. The duct but this is not always apparent and would function of apocrine glands in humans is not appear to be a rare primary event [7]. In a study altogether clear but in other mammals they are of 36 patients apocrinitis was present in only 5% responsible for sexual attraction, and scent pro- [11]. duction is responsible for axillary and inguinal Rupture of the follicle spills its contents, in- odour. They become functionally active and cluding keratin and bacteria, into the surround- larger at puberty. The secretion is opalescent ing dermis [12]. and malodorous. 28 Alison Layton 4 Fig. 4.3a–d. Early lesions in hidradenitis suppurativa. a Acute HS – lower power. b Follicular plugging. c Folliculitis – dense collection of neutrophils around hair follicle. d Acute folliculitis in HS 4.3.2 Established Hidradenitis histiocytes and giant cells that may be related to Suppurativa (Fig. 4.4a–e) keratin fragments. Granulation tissue with in- flammatory cells and occasional foreign body Biopsy samples from established HS lesions giant cells is present in 25% of biopsy specimens show sinus tracts with marked suppuration and [13]. Apocrine glands are generally absent in the frank abscess formation. The sinuses are lined affected area but may appear quite normal in by stratified epithelium and are surrounded by adjacent tissue. Extensive fibrosis is frequently fibrosis and inflammation. The squamous epi- seen as a late result in the disease course [14]. thelium extends from the associated follicular Hence it would appear that the involvement
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