Most of us have heard people talking about having their glands removed as part of surgery for HS, but aren't sure what that means. When referring to glands and gland removal we are commonly discussing apocrine glands.
Hidradenitis Suppurativa can appear anywhere on the body there are hair follicles are found (not necessarily just where you have hair) which is anywhere on the body with the exception of the palms of your hands, soles of your feet and lips.
In humans the apocrine sweat glands are found only in certain locations of the body:
Areola of the nipple area
Perianal (anus area)
Wings of the nostril
Specialized types of apocrine sweat glands on the eyelids are called Moll's glands
If hidradenitis is only an apocrine gland disease, then you would only get HS in these areas, correct? NOPE.
Apocrine glands form in utero (fetus stage), but don't go into action until puberty when they receive cues from the hormonal stimulation taking place and we know that you can develop hidradenitis at any age, even before puberty.
Eccrine and sebaceous glands are found throughout our entire body, as are hair follicles. Sebaceous glands are impossible to remove as they consist of 2,500 to 6,000 glands per square inch and are microscopic.
If you are having sweat glands removed for other reasons or complications i.e., excessive sweating or hyperhidrosis it may help with that particular situation, trigger or aggravation. Removal of sweat glands will not directly address HS and is an additional and unnecessary surgery. Many people have had their glands removed and have shown no improvement initially or their Hidradenitis Suppurativa later returned as there is no way to remove all of the glands involved.
Gland removal is no different than regular wide excision surgery meaning that we have the same success, if not better, with a wide excision surgery without specific gland removal.
In some cases glands can become involved if tunneling is deep and extensive. Your specialist or surgeon will do imaging if necessary and then it can be determined if it's best to remove the affected glands.
Why Gland Removal is Now Considered Outdated
Over the past several years, long-standing and robust studies support Hidradenitis Suppurativa as an inflammatory illness follicular occlusion, also referred to as an immune-mediated inflammatory illness. If glands are affected they would be secondary, depending on severity.
In the past HS was identified as only an apocrine disease, which has now been proven untrue, especially since you can get hidradenitis anywhere on the body, including places where apocrine glands do not exist (see above for list of where apocrine glands are found).
The Apocrine Hidradenitis Suppurativa History
Originally Hidradenitis Suppurativa was thought to be a disease of the apocrine glands because it most commonly occurs in apocrine gland-rich intertriginous areas, however, Hidradenitis Suppurativa has been shown to be a disease that centers on the hair follicular unit, eccrine and sebaceous gland involvement, resulting in follicular occlusion and inflammation.
The central pathogenic event in HS is believed to be the occlusion of the upper part of the folliculopilosebaceous unit by increased outer root sheath keratinocyte proliferation leading to the rupture of the sebofollicular canal and extrusion of contents, including corneocytes, bacteria, yeast, sebum, and pilar residua ruptured hair follicles into the surrounding dermis, with the consequent development of perifollicular lymphohistiocytic inflammation [3,15,33,34,35,36]. The basis for follicular occlusion in HS has yet to be fully defined. However, impaired notch signaling has been proposed as the major pathogenic mechanism of HS. Appropriate notch signaling is of pivotal importance for maintaining the inner and outer root sheath of the hair follicle and skin appendages [37,38,39]. Indeed, Melnik and Plewig eloquently described the concept of HS as an autoinflammatory disease with dysregulation of the γ-secretase/notch pathway . Particularly, mutations of the γ-secretase-notch pathway have already been shown to be involved in the molecular pathogenesis of familial HS among Chinese, British, Japanese, and French families [30,31]. Moreover, deficient notch signaling is able to switch the fate of outer root sheath cells, resulting in the conversion of hair follicles to keratin-enriched epidermal cysts, and compromise apocrine gland homoeostasis also leading to stimulation of toll-like receptor (TLR)-mediated innate immunity by damage-associated molecular pattern molecules released by either ruptured epidermal cysts exposing keratin fibers or altered structural components of less maintained apocrine glands, supporting and maintaining chronic inflammation. Particularly, it is believed that stimulation of TLRs on macrophages and dendritic cells (DCs), the most abundant cells in HS lesions, leads to increased amounts of proinflammatory cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1β) and activation of DCs, which secrete IL-23 promoting Th17 cell polarization (IL-17-producing T helper cells were found to infiltrate the dermis in chronic HS lesions) [40,41,42,43,44,45,46]. Due to deficient notch signaling, impaired notch-mediated feedback inhibition of innate immunity by reduced activation of MAPK phosphatase-1 may result in chronic inflammation and Th17-driven auto-inflammation leading to progressive tissue destruction and IL-17-mediated neutrophil attraction in HS [40,41].
Therefore, as shown above, deficient notch signaling seems to be implicated in the genesis of established HS lesions and their peculiar features (follicular plugging, follicular cysts, reduced volume of the Eccrine and sebaceous glands, sinus tracts lined by a stratified epithelium, and neutrophilic abscesses) . Therefore, inappropriate notch signaling may not only initiate inflammation in HS but may lead to insufficient feedback inhibition of overstimulated innate immunity. In this context, TNF-α is considered as one of the major actors in TLR-activated innate immunity in HS. Indeed, its overexpression has been observed in lesional and perilesional skin of HS together with a positive correlation with disease severity, providing a rationale for HS treatment with biologic drugs such as inhibitors of TNF-α [48,49] whose use, particularly adalimumab, has been shown to suppress the overexpression of most of the upregulated cytokines in HS such as IL-1β, CXCL9, B-lymphocyte chemoattractant, as well as the number of inflammatory CD11c+ DCs in HS lesional skin . Hence, it is clear that HS is a follicular disease showing some defect in keratin clearance with resultant follicular occlusion, where defective innate cellular immunity plays an important role [24,44]. This fact is also highlighted by the increased expression of antimicrobial peptides (AMPs) such as cathelicidin (LL-37), psoriasin and human β-defensin (HBD)-2 and HBD-3 observed in HS skin [50,51,52]. Particularly, AMPs can activate the adaptive immune system inducing keratinocyte migration and proliferation, providing a basis for the development of follicular occlusion . Moreover, AMPs are part of a complex production network of cytokines and chemokines (notably HBD-2 and HBD-3 expression are under control of IL-1β and TNF-α)  and their presence, absence, or abnormality of one of any of the AMPs could explain the inflammatory features of HS, being directly involved in its pathophysiology. As a result of increased AMPs in HS skin, HS is not a classic skin disease, with strong evidence of innate immunity and follicular occlusion inflammation .
Please refer to our Inflammatory/Follicular Occlusion article for more information on this subject.
Watch an interview with Dr. Barry Resnik covering this topic below.
Content in this article is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay seeking treatment because of something you have read on this website.
Written by Denise Panter-Fixsen
Edited by Brindley Brooks