Advancing Our Understanding of Hidradenitis Suppurativa: A Comprehensive Guide for Clinicians Designed to Improve Therapeutic Outcomes for Patients—Part 1

J Clin Aesthet Dermatol. 2026;19(8):20–29.

James Q. Del Rosso, DO; Lauren Lam, BScH, MD, FRCPC; Diego Ruiz Dasilva, MD; Joshua Burshtein, MD; Graham Litchman, DO, MS, FAAD; Christopher G. Bunick, MD; Lara Shqair, BA; Andrea Murina, MD; Tiffany Mayo, MD; Katrina H. Lee, MD; Jennifer Hsiao, MD; Andrew Ferrier, MD, PhD, FRCPC, DABD; Michael Payette, MD; Steve Daveluy, MD; Victoria Farley, MD; and Vivian Shi, MD

Dr. Del Rosso is with JDR Dermatology Research, Las Vegas, Nevada. Dr. Lam is the Vice President of the Canadian Hidradenitis Suppurativa Foundation, Calgary, Canada. Dr. Dasilva is with Eastern Virginia Medical School, Norfolk, Virginia. Dr. Burshtein is with the Department of Dermatology, University of Illinois Chicago, Chicago, Illinois. Dr. Litchman and Dr. Farley are with Vivida Dermatology, Las Vegas, Nevada. Dr. Bunick is with the Department of Dermatology, Yale School of Medicine, New Haven, Connecticut. Ms. Shqair is with the Icahn School of Medicine at Mount Sinai, New York, New York. Dr. Murina is with the Tulane University School of Medicine, New Orleans, Louisiana. Dr. Mayo is with the University of Alabama at Birmingham, Birmingham, Alabama. Dr. Lee and Dr. Hsiao are with the Department of Dermatology, Keck School of Medicine of USC, Los Angeles, California. Dr. Ferrier is with the Division of Dermatology, Department of Medicine, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Canada. Dr. Payette is with Central Connecticut Dermatology, Cromwell, Connecticut. Dr. Daveluy is with the Department of Dermatology, Wayne State University, Detroit, Michigan. Dr. Shi is with the Department of Dermatology, University of Washington, Seattle, Washington.

FUNDING: No funding was provided for this article.

Introduction

Among the many chronic inflammatory cutaneous diseases that clinicians encounter, hidradenitis suppurativa (HS) is one of the most physically and psychologically devastating to those who are affected by it. HS usually starts in the second or third decade of life.¹ The visible and symptomatic characteristics of HS lesions, the multiple anatomic locations affected, and the chronicity and frequent progression of this unrelenting disease state represent just the tip of the iceberg of what comprises HS.¹

Epidemiology. Historically, epidemiologic studies of HS have shown variations in prevalence rates that are likely influenced by both regional geographic differences and data collection methods, the latter including the use of diagnosis codes and self-reporting.¹ An age- and gender-adjusted population analysis of HS noted a variable global prevalence of 0.00033% to 4.1%, with an estimated prevalence of 0.1% in the United States (US) that is 2-fold greater in men than women and 3-fold greater in Blacks patients compared to White patients.^2,3 As more research attention is given to HS as a disease state, approaches to assess prevalence have improved; HS is no longer considered a rare disease and more precise data on epidemiology, demographics, and burden of disease are emerging.^1,4

Clinical characteristics and early recognition. Many cases of HS are recognized clinically, especially when encountering the frequently observed “textbook presentation” of skin lesions that includes abscesses, nodules, sinus tracts with or without purulent drainage, scarring deformity, and dyspigmentation involving predominantly axillary, inframammary, inguinal, perianal, and other anatomic sites. Unfortunately, early recognition has often been challenging, especially when the course of disease progression is slower and evaluations occur intermittently and primarily during “flares” by different clinicians or by those who are not as familiar or experienced with HS. In addition, prior to the availability of the first systemic agent approved by the United States Food and Drug Administration (FDA) for HS in 2015 (adalimumab), there was a conspicuous absence of emerging research on the pathophysiology of and therapeutic approaches for managing HS, especially with individualized approaches.¹ Collectively, these and other factors resulted in an average diagnostic delay of 7 years with HS.⁵ Slow development of therapies directed at the pathophysiologic targets observed in HS has also limited the effective management of this progressive inflammatory and cicatricial skin disorder.^1,3,6,7 Physical scarring as a common eventual sequelae of HS lesions is a major factor that differentiates HS from several other common chronic inflammatory skin conditions, such as cutaneous psoriasis and atopic dermatitis.

Mental and social impact. Beyond the recurrent and persistent physical and markedly symptomatic characteristics of HS and the relentless cycle of unpredictable flares, the adverse mental health and social aspects of the disease significantly impair quality of life (QoL) and are among the most challenging for patients and their family, partners, cohabitants, and clinicians.^1,4,8 Consistent concerns about an inability to participate in social or professional activities, the presence of draining and foul-smelling lesions, the embarrassment related to appearance and poor self-image, and the associated pain and frictional discomfort are all common examples of real-life factors that have marked impact on overall mental and physical health. Multiple reports support that depression, generalized anxiety disorder, substance use disorder, and suicidal ideation/behavior are all adverse psychological disorders with an increased risk in patients with HS.^8,9 The common presence of physical and symptomatic scarring and the markedly adverse psychosocial burden with HS underscore the need for an early, correct diagnosis and the use of an advanced comprehensive and individualized approach to achieve optimal disease control and to significantly halt disease progression.

About This Article Series

This 4-part article series on HS has been organized and structured a bit differently than most manuscripts. Multiple authors have separately contributed individual sections, inclusive of supporting references. These authors were primarily responsible for their individual sections but also participated in the review and finalization of the complete series of articles. The article sections in this series include the disease state overview of HS; an overview of the pathophysiology, physical examination, laboratory evaluation, comorbidities, therapeutic management, topical therapies, antibiotic management, adalimumab, infliximab, secukinumab, bimekizumab, systemic Janus kinase (JAK) inhibitors, glucagon-like peptide-1 receptor agonists, office-based procedures, patient support programs; and putting it all together in managing HS.

This article series reflects what information is believed to be understood about HS to date, with an emphasis on clinical management and colored throughout with the perspectives of several dermatologists who are highly dedicated to this subject area and experienced in managing patients with HS. The order of the authors in the article heading reflects the order of appearance of their sections in the article series. This series is designed to be comprehensive and clinically useful but does not include all potential subsections related to HS. It is also important to note that, as the lead author, Dr. Del Rosso tried to maintain some consistency in flow and writing style, but there was no intent to soften or remove the perspectives of any of the authors or remove areas of content repetition discussed in separate sections. The reader is encouraged to use this article as a “guidance tool” to assist them in clinical practice but to always expand their knowledge through other educational resources, especially as new data are constantly emerging from basic science, translational, and clinical research.

Overview of Pathophysiology and Etiology

James Q. Del Rosso, DO

The pathophysiology and development of HS is complex, multifactorial, not fully understood, and a “moving target” that continues to evolve.^1,10–17 Genetic, epigenetic, and exogenous lifestyle factors appear to be contributory, with the interactions of multiple potential genes involved in many cases, and some cases of syndromic HS identified.^1,16,17

Several cascades, structural changes, pathways, signals, contributory cytokines, and comorbid factors have been described as components of the pathophysiology of HS, with the diversity and variable progression of tissue alterations confounding the ability to develop a centrally cohesive model of pathogenesis. An in-depth review of HS pathophysiology is beyond the scope of this manuscript; however, some key features of how the pathophysiology of HS has emerged over time are discussed.

Follicular occlusion and autoinflammatory paradigms. The historical belief that the evolution of HS centered around apocrine gland inflammation has been refuted, with perifollicular and follicular infundibular inflammation and occlusion recognized as primary drivers of HS, occurring as a precedent to or nearly concurrent with other auto-inflammatory processes.^1,11–14 Perifollicular inflammation is present and associated with follicular hyperkeratosis, comedogenesis, and expansion of the hair follicle lumen. Skin occlusive changes promote increased local pH and alterations in cutaneous microbiota.^1,14 Additional immune responses that appear to be associated with development of HS, including earlier skin alterations, include neutrophil and macrophage infiltration, interleukin (IL)-1α, IL-1β, tumor necrosis factor-α (TNF-α), T lymphocyte (T1, T17) immune reactions, promotion of specific chemokines (ie, CCL20), and follicular dysbiosis; later, more advanced folliculocentric skin alterations include epithelial strand formation, sometimes with formation of tunnels that recapitulate the overlying epidermal structure, and formation of lower follicular inflammatory nodules.^1,14 Adipose tissue can also produce a signature of pro-inflammatory cytokines (including TNF-α, IL-1β, IL-6, and IL-17) with adipokines capable of mediating inflammation and insulin resistance.¹⁴

Selected important observations. A few other important observations become apparent after assessing the collective body of data on HS pathophysiology and its multiple associations:

Infundibular keratinocyte dysregulation, follicular/perifollicular inflammation with structural changes, and systemic subclinical inflammation are potential contributory factors to HS, with the important consideration that some factors may be more involved in the initiation of HS development while others may contribute more to perpetuation of the disease.^12,14,18

Inflammatory signatures obtained from lesional HS tissues demonstrate multiple cytokines and chemokines, with many of the same cytokines also upregulated in nonlesional tissue.^14,19

Although both helper T (Th) 17 cells and Th1 cells are the predominant cell types that comprise HS lesions, along with the marked presence of IL-17 cytokines (ie, IL-17A, IL-17F) and interferon (INF)-γ, self-perpetuation of clinically established HS is strongly associated with Th17 inflammation.^1,14 Similar to psoriasis, IL-17 induced “feed forward” loops with further production of certain cytokines (IL-1β, IL-6, TNF-α) may be present in HS; in contrast to psoriasis, CD4+ Th17 cells in HS are predominantly supported by IL-1β and not by IL-23.¹⁴

Histologic and transcriptomic studies support a definite presence of B cells and plasma cells often present in dermal tertiary lymphoid structures; these may be reflective of more long-standing disease, possibly suggestive of an antibody-mediated or autoimmune component in more severe HS.^1,14

Dermal tunnels may contribute to keratinocyte-induced inflammatory cell recruitment and further inflammation of dermal stroma and potential scar formation; this observation supports the integration when needed of physical procedures such as deroofing and/or excision.^1,14

Currently available histologic and molecular evidence support both follicular occlusion and multiple sources of inflammation as important contributory components of HS, with little benefit in holding up therapeutic progress while debating which is primary and which is secondary. Suggested principles on therapeutic management are discussed in the second article in this series. The reader is also referred to a helpful evidence-based approach that correlates the pathophysiologic changes with disease progression and the timing of therapeutic interventions that are most likely to reduce current disease activity and suppress progression of HS.¹

Clinical challenges related to pathophysiology and disease progression. What is both unique and challenging with HS is the variability and magnitude of responses that occur throughout the full thickness of the skin. These responses are inclusive of marked epidermal, superficial dermal, and deep dermal alterations coupled with both reversible inflammatory and irreversible cicatricial lesions of HS. What is further difficult for clinicians is that clinical evaluation is confounded by the actual severity of disease being affected both by what is visible and what lies beneath that is not directly visible, as well as fluctuations in clinical disease activity that can influence what is observed during the office visit. This underscores the importance of thorough documentation of the history, careful clinical observation, and gentle palpation during the physical examination.\

Physical Examination

Lauren Lam, BScH, MD, FRCPC

As HS is a clinical diagnosis, physical examination is crucial in optimizing the accuracy of diagnosis, assessing disease severity, and determining and adjusting management strategies for HS. The histology of HS is nonspecific and highly variable, thus the diagnosis cannot be anchored on this alone. Given that it is a waxing-and-waning disease, it is critical to consider that the physical examination on a particular day may not reflect the worst severity the patient has experienced, and what appears to be nonexistent disease activity can be astonishingly different in photographs obtained during flares. Examining photographs can often appropriately raise the stage at which the patient is classified, thus escalating treatment accordingly. It is also prudent to note that the presence of sinus tract scarring may not be detectable with visual examination or palpation alone but may be detected with use of ultrasound.²⁰

Clinical definition and clinical characteristics. HS is defined as having 2 or more lesions in at least 2 typical body sites for at least 6 months. The classic morphology is described as tender nodules, abscesses, sinus tracts, and double comedones, which are sinus tracts on histopathologic examination and have been considered pathognomonic. Nodules differ from furuncles as they can recur or create interconnecting sinus tracts as a result of the follicular occlusion and aberrant inflammatory response to this, as discussed in the Pathogenesis section. Fibrotic and atrophic scarring and fibrotic nondraining sinus tracts reflect irreversible sequelae resulting from the chronic inflammatory cascade and are persistent and independent of the presence or absence of inflammatory HS lesions.^1,21 Figure 1, Figure 2, and Figure 3 depict a variety of clinical presentations of HS reflecting lesion types occurring at various stages of their development and that have an impact on treatment selection, with clinical relevance explained later in this article series in the Therapeutic Management Principles section.

Less common clinical presentations. It is important for clinicians to consider that other less common morphologies are also seen in HS, including folliculocentric acneiform papules, erosions, and pyogenic granuloma-like lesions.²² The classically involved areas are described as intertriginous locations, such as axillae, inframammary folds, inguinal folds, and inner thighs as well as pubic, vulvar, scrotal, perineal, gluteal, and perianal areas.²¹ Nevertheless, HS can also involve other less classic areas such as the retro-auricular areas, scalp, and trunk.²¹ Indeed, HS can be observed in nearly all body sites. Although axillae are often thought to be the most common site involved among all ages, this is more reflective of patients younger than 18 years.¹ In fact, the groin is more often involved in adult women (~87% in women vs ~61% in men), whereas adult men have axillary involvement more often (~48% in women vs ~70% in men).¹

Consequences of chronic disease. Secondary consequences of chronic HS can also form because of persistent inflammation, including strictures, fistulas, lymphedema, elephantiasis, interstitial keratitis, and squamous cell carcinomas (SCC).²³ The latter is associated with chronic scarring and can be fatal if undetected and progresses without intervention. However, SCCs can be difficult to distinguish since chronic HS can often result in nonhealing lesions.

Although there is no universally accepted subtype classification system, there are several that have been described in multiple publications from various groups. It is important to note that there are several subtypes that do not reflect what is often considered the classic archetype of HS and could lead to misdiagnosis if not recognized on physical examination.

Disease assessment and phenotype classifications. Hurley staging, developed initially for presurgical clinical staging of the disease, has conventionally been the most common staging system used in clinical research for determining the overall stage of HS.¹ The 3 Hurley stages are based primarily on the presence or absence of sinus tracts (tunnels) and/or scarring (Table 1). As such, Hurley staging may be helpful in the initial determination of disease severity and correlation with selection of therapy. However, this staging method has proven to be inadequate in assessment of disease severity and is not suitable for detection of progressive disease worsening or response to treatment.¹ The clinical application of staging systems and correlation with appropriate aggressiveness of treatment selection are discussed in more detail in the Therapeutic Management section in the second article of this series.

The commonly described classifications include follicular vs inflammatory and phenotypes such as classic, frictional furunculoid, and conglobata.²⁰ The follicular classification is characterized by comedones and nodules as the predominant morphology, tends to have a younger age of onset (~18 years), and is more common in women. In contrast, the inflammatory classification is characterized predominantly by draining tunnels and abscesses, is more common in men, and may be more aggressive and progressive.

The hallmark characteristics of conglobata phenotype are acneiform lesions, cysts, and comedones, especially on the back, face, and ears. Conglobata is more prevalent in men. Scarring folliculitis phenotype is consistent with icepick scarring, papules, and pustules, especially in the pubic and gluteal areas. Lastly, frictional furunculoid phenotype involves nodules and abscesses in the frictional surfaces, especially the inner thighs and the mammary and abdominal folds.

As a known component of the follicular occlusion tetrad, it is also worth examining for evidence of dissecting cellulitis of the scalp, acne, and pilonidal cysts. This can help raise suspicion for HS if the physical examination findings are not diagnostic on the day of examination. In addition, it may alter the treatment plan based on the existence of these comorbid dermatologic conditions.

Comorbid conditions. Noting other nondermatologic comorbid diseases on physical examination may be prudent, since suggestive findings can alter treatment decisions. Management of these conditions may be beyond the scope of the dermatologist and warrant involvement of other specialists. The more common inflammatory comorbidities include Crohn’s disease and spondyloarthropathy (SpA).²⁰ Thus, consider noting knife-like fissures suggestive of cutaneous Crohn’s disease and inflamed joints on examination. Rarer syndromes involving HS, such as PAPASH (pyogenic arthritis, pyoderma gangrenosum, acne, suppurative hidradenitis) and PASH (pyoderma gangrenosum, acne, suppurative hidradenitis), may result in comorbid pyoderma gangrenosum on examination.²⁰

Ultrasound and staging of disease. Ultrasound is a growing and evolving field in the detection, diagnosis, pre-operative planning, and postoperative/medical assessment of HS. Factors that support the integration of ultrasound in HS management are: (1) it can noninvasively visualize subclinical lesions, especially sinus tracts, and (2) it can assist in determining a more accurate severity stage for the patient, typically a higher stage, by objectively confirming and documenting subclinical changes that cannot be observed during external visual examination.^20,23 Thus, earlier escalation of treatment and disease stabilization is more likely to be achieved with the use of ultrasound, when reasonably accessible, to further support physical examination, which ultimately may prevent disease progression and associated morbidity.

A study assessing patients with HS with ultrasonography using the Sonographic Scoring System for HS (Table 1) demonstrated a change in medical management in approximately 84% of cases and a pivot to include surgical management in 24% of cases.²⁰ Findings of HS on ultrasound include thickened dermis, widened hair follicles, retained hair tracts, hypoechoic fluid pockets, interconnected sinus tracts, and decreased echogenicity of surrounding tissues.^20,23 Sinus tracts can be further classified into subtypes that correlate with distinct pathogenesis and treatment response. The reader is referred to reference 20 and reference 23 if interested in seeing photographs demonstrating ultrasound findings from patients with HS.

Using physical and ultrasound examination findings, patients can be staged based on the classification system of choice and treatments can be initiated based on severity. Each staging system has its strengths and weaknesses, which have been summarized in the Table 2. If ultrasound is integrated into the assessment of the patient, the clinician can adjust the severity staging of HS accordingly. Limitations of ultrasound are that it is not usually directly accessible within dermatology offices or other primary ambulatory practices where patients with HS are routinely cared for, thus requiring referral to a radiology facility, which is not often convenient logistically and/or financially. It is also important that the clinician caring for the patient have a good working relationship with the radiologist evaluating HS by ultrasonography, as familiarity with this approach in HS is still evolving as part of the care of patients.

Fundamental Laboratory Evaluation of HS

Diego Ruiz Dasilva, MD

As with many other chronic inflammatory skin diseases, HS is increasingly recognized as a systemic condition with a broad spectrum of potential comorbidities. A structured, evidence-based approach to core baseline laboratory evaluation and comorbidity screening is essential to delivering comprehensive care, particularly in patients with moderate-to-severe disease and/or clinically apparent disease progression.^24,25

Fundamental laboratory testing. A complete blood count (CBC) is a fundamental baseline recommendation to evaluate for anemia of chronic disease, leukocytosis, and other potential abnormalities. Inflammatory markers such as C-reactive protein and erythrocyte sedimentation rate may be useful in correlating with disease activity and severity.²⁵ A comprehensive metabolic panel is also important, especially for assessment of hepatic and renal function and for potential detection of diabetes that is unknown to the patient. A core laboratory evaluation workup may not seem necessary for many patients with HS but is especially critical prior to initiating systemic treatments such as biologics, oral antibiotics, immunosuppressants, or other off-label agents.²⁴

Comorbidities, concomitant therapies, and laboratory testing. Metabolic comorbidities are highly prevalent in HS. Fasting glucose or hemoglobin A1C can be obtained to screen for insulin resistance and type 2 diabetes, which affects over 20% of patients with moderate-to-severe HS.^26,27 A lipid panel is also important, as dyslipidemia and increased cardiovascular risk are well documented in this population.²⁶ While much of this may be monitored by the primary care clinician, dermatologists are well-prepared to do so for our patients who do not have routine primary care or when communication of information between clinicians is suboptimal logistically.

Before initiating immunosuppressive therapies, serologic screening for HIV, hepatitis B, and hepatitis C are recommended in accordance with established clinical guidelines.^24,25 For female patients, clinicians can consider screening for polyendocrine metabolic ovarian syndrome (PMOS), formerly referred to as polycystic ovarian syndrome (PCOS), or other causes of androgen excess when clinical signs such as menstrual irregularity, hirsutism, and/or obesity are present. Evaluation may include serum androgen levels, pelvic ultrasound, and referral to gynecology or endocrinology when additional expertise is deemed to be necessary.²⁶

There is a well-established association between HS and inflammatory bowel disease (IBD), particularly Crohn’s disease.²⁶ Clinicians can inquire about gastrointestinal symptoms and consider fecal calprotectin testing and/or referral to gastroenterology. Similarly, musculoskeletal symptoms such as axial pain, enthesitis, or morning stiffness may signal a seronegative inflammatory arthritis. In such cases, HLA-B27 testing and referral to rheumatology may be considered.²⁸

Dermatologists as “the ringleaders” of care. A comprehensive, structured evaluation enables clinicians to assess systemic involvement, stratify risk, and tailor treatment strategies effectively (Table 3). A multidisciplinary approach in select patients with HS, including collaboration with endocrinologists, gastroenterologists, psychiatrists, and rheumatologists, can significantly improve outcomes for those with more complicated and/or severe disease. It is important that the dermatologist maintain their role as the central “ringleader” of care for the patient so that the patient can feel comfortable that their care remains well coordinated and that they have an anchoring physician to depend upon with management of their HS. As HS research, awareness, and advocacy continue to grow, these recommendations are very likely to evolve to reflect ongoing insights that will further support the care of patients with HS and their families and caretakers.^24,25

Comorbidities of HS

Joshua Burshtein, MD

There are a variety of conditions and comorbid diseases that have been associated with HS. Smoking and obesity are commonly noted in patients with HS and have been directly correlated with severity and progression of HS.^1,29 Both of these factors are modifiable, especially with good support provided to the patient. Common concomitant diseases include depression/anxiety, insulin resistance, type 2 diabetes, metabolic syndrome, arteriosclerosis, inflammatory bowel disease (IBD), metabolic dysfunction-associated steatotic liver disease (MASLD), formerly referred to as nonalcoholic fatty liver disease (NAFLD), inflammatory arthritis, sexual impairment, and PMOS (Table 4).¹ It is vital for clinicians to be aware of these potential associated conditions and comorbid disease states associated with HS.

Rational timing and implementation of individualized comorbidity screening. As patients affected by HS are at risk for the current presence and/or eventual development of multiple comorbidities that can significantly impact their overall health and QoL, it is important for clinicians to prioritize how and when they address specific factors so that the patient and their caretakers are not overwhelmed, confused, and/or frustrated by “being hit with too much too soon”. This practical consideration is important to address upfront for each patient with HS so that the overall quality of care for each individual is not lost. Vigilance by clinicians and their staff in determining if any of their patients with HS exhibit signs, symptoms, or risk factors for any clinically relevant comorbidities can markedly expedite early detection and effective management. Therapeutically addressing many of these comorbid disorders with a well-designed and properly measured approach for the individual patient and caretaker(s), especially for those factors that are modifiable and of personal significance to the patient, often provides dual benefit by improving both the HS and the comorbid condition(s). For additional support, suggested screening recommendations are available from the United States HS Foundation and from the Canadian HS Foundation.²⁹

Untangling the plethora of potential comorbid conditions affecting patients with HS. The group of conditions classified as metabolic syndrome, including obesity, hypertriglyceridemia, hypertension, and hyperglycemia, has been reported in up to 50% of patients with HS.^27,30 These patients exhibit 2.7-fold increased odds of developing metabolic syndrome compared to control populations.^27,30 Patients with HS also demonstrate 2× higher odds of developing metabolic syndrome compared to those without HS.³¹ In addition, patients with HS have been associated with greater odds of diabetes (almost 3× higher), arteriosclerosis, myocardial infarction, and stroke.^31–36 One study found that those with HS had a 23% higher risk of myocardial infarction and stroke, and another reported 1.7× higher odds of stroke compared to controls.^35,37 Another retrospective population-based study found that patients with HS have up to 1.5× risk of major adverse cardiac events compared to controls.^35,36

HS has been associated with a variety of gastrointestinal diseases, including Crohn’s disease, ulcerative colitis (UC), and liver diseases. HS and IBD share common features in pathogenesis, clinical presentations, and response to advanced targeted therapeutics.^38,39 In patients with IBD, there is a 9× higher relative risk of HS than control populations.⁴⁰ About 2% of patients with HS have Crohn’s disease and 1.3% have UC.^41–43 Further, there is a 2.1× and 1.5× higher odds of Crohn’s disease and UC among patients with HS, respectively.^41–43 Notably, patients who have both IBD and HS have more severe disease compared to controls.⁴⁴ Another common comorbid disease with HS is MASLD, which is the leading cause of cirrhosis. Greater than 50% of patients with HS were found to have MASLD, and there is a 2.8× greater odds of developing MASLD compared to controls.⁴⁵ HS also confers a greater risk of hepatitis B.⁴⁶

Other systemic inflammatory conditions have also been associated with HS, including axial SpA and autoinflammatory syndromes. Large cohort studies have reported the prevalence of inflammatory arthritis to be between 0.8% to 5.2% in patients with HS.^28,47 Specifically, there is a 2.1× and 2× greater odds for SpA and rheumatoid arthritis in these patients, respectively.^28,47 Several studies report a wide range of prevalence rates for SpA in patients with HS, likely due to differences in study design and assessment criteria. A large European prospective study found a prevalence rate of 3.7%.²⁸

Due to the clinical symptoms of HS, including nodules, abscesses, malodorous drainage, and scarring, this disease has a substantial impact on QoL and mental health. Patients with HS have been shown to be at a higher risk for social stigmatization, low self-esteem, depression, anxiety, psychosis, personality disorders, adjustment disorders, and developmental disorders.^48,49 Prevalence rates of depression in patients with HS are up to 30% in adults and 16% in children, with adults having a 2 to 2.5× higher odds compared to controls.^50–52 Women and those with obesity are associated with higher rates of depression in patients with HS.⁵³ Furthermore, 20% of patients with HS are found to have anxiety (2.0× higher risk).^51,52 They also have been linked to greater use of antidepressants and 2× to 3× risk of completed suicides.⁵⁴

Another comorbidity of HS that can cause substantial psychological burden is sexual impairment, present in up to 60% of patients with HS.⁵⁵ Both the physical and mental effects of HS can negatively impact the sexual activity of those with HS and their partners. A cross-sectional analysis found that 63.3% of men with HS experienced erectile dysfunction and 40.6% of women had sexual dysfunction.⁵⁶ The severity of sexual impairment is independent of HS severity and has been reported to be more pronounced in women.^57,58 Stable partnership has been described as a protective factor that may mitigate the risk of sexual dysfunction, stress, and fear or rejection.⁵⁶

Additionally, PMOS has also been reported in up to 12% of patients with HS. There was about a 2.6× higher odds than the control populations, with greater odds in patients with concomitant obesity and/or diabetes and among children and adolescent patients.^59–62

Due to the shared pathogenesis of chronic inflammation of the folliculopilosebaceous units, other dermatologic diseases including acne vulgaris/conglobata, pilonidal disease, and dissecting cellulitis have been associated with HS. One study found that acne vulgaris was present in 15.2% of patients with HS, and another reported that pilonidal cyst disease was 8× more prevalent with mild HS and 35× more prevalent with severe HS.^63,64 Further, pyogenic granulomas can coexist with HS, with one study reporting a prevalence of 0.18% (vs 0.01% in controls), as well as acne (PASH) and pyogenic arthritis (PAPASH).^65,66

Practical application of putting it all together in caring for each individual patient. Several additional observations are noted for the clinician about HS, as it is a complex disease state associated with several characteristics that adversely affect patients physically, psychosocially, and medically. With the high burden of comorbidities associated with HS, screening patients with a rational approach tailored to their individual needs is vital to provide comprehensive care. Dermatologists are uniquely positioned to identify conditions in both younger and older patients that may have been previously undiagnosed or undertreated by incorporating age-appropriate comorbidity assessments into routine practice. Optimized screening is best individualized, including a thorough cutaneous examination along with a focused review of systems addressing both cutaneous and extracutaneous comorbidities. Based on findings, dermatologists can coordinate care by directing patients to their primary care provider or referring them to appropriate specialists as needed. Additionally, in patients with HS who require systemic therapy and have comorbid conditions such as IBD that also necessitate systemic treatment, interdisciplinary coordination is often essential. Collaborative decision-making can facilitate the selection of an agent with efficacy for both conditions and/or avoid unanticipated adverse effects, thereby optimizing therapeutic outcomes and minimizing treatment burdens.

What is Coming Up Next?

In the second article of this series, topics to be discussed include therapeutic management principles, topical therapies, antibiotic management, adalimumab, and infliximab.

Disclosures

Dr. Del Rosso is a consultant/advisor, research investigator, and/or speaker for AbbVie, Almirall, Alumis, Amgen, Apogee, Arcutis, Bausch Health/OrthoDermatologics, Beiersdorf, Biofrontera, Bluefin, Blueprint Medicines, Botanix, Bristol Myers Squibb, Cara, Celgene, Ferndale, Galderma, Incyte, Janssen, Johnson & Johnson, La Roche-Posay, LEO Pharma, Lilly, L’Oréal, MC2 Therapeutics, MoonLake, Novan, Oruka, Pelthos Therapeutics, Pfizer, Regeneron, Sanofi, Sun Pharma, Takeda, Trevi, UCB, and Verrica. Dr. Dasilva reports being an investigator for Galderma and Novartis; consultant/promotional speaker for AbbVie, Arcutis, Castle Biosciences, Dermavant/Organon, Galderma, Incyte, Johnson & Johnson, LEO Pharma, Lilly, Novartis, Pfizer, Sanofi/Regeneron, UCB, Takeda, Vanta Diagnostic, and Verrica; a board member and associate editor for the Journal of Clinical and Aesthetic Dermatology and ReachRx. Dr. Litchman has served as a consultant, investigator, and/or speaker for AbbVie, Almirall, Arcutis, Bristol Myers Squibb, Castle Biosciences, Galderma, Incyte, Janssen, Johnson & Johnson, LEO Pharma, Novartis, Organon, Pfizer, Regeneron, Sanofi-Genzyme, Sun Pharma, Takeda, UCB, and Veradermics. Dr. Bunick has served as an investigator and/or consultant for AbbVie, AbSci, Almirall, Alumis, Amgen, Apogee, Arcutis, AvantGuard, Avene, Botanix, Castle Biosciences, Connect BioPharma, Daiichi Sankyo, Dermavant, Disc Medicine, EPI Health/Novan, Galderma, Highlight Therapeutics, Incyte, LEO Pharma, Lilly, Novartis, Ortho Dermatologics, Palvella, Pfizer, Primus, Priovant, Regeneron, Sanofi, South Beach Symposium, Sun Pharma, Takeda, Timber, Teladoc, Triveni, UCB, Veradermics, and ZenZema. Dr. Murina is a speaker for AbbVie, Amgen, Botanix, Galderma, Johnson & Johnson, Ortho Dermatologics Pfizer, and UCB and has served as a consultant for Johnson & Johnson, LEO Pharma, Lilly, Novartis, Ortho Dermatologics, Sun Pharma, Takeda, UCB, and Veradermics. Dr. Mayo has served as an investigator or consultant for AbbVie, Acelyrin, Arcutis, BMS, Boehringer Ingelheim, Galderma, Janssen, ITB, Incyte, LaRoche Posay, LEO Pharma, L’Oréal, Lilly, Merck, Novartis, Oruka, Pfizer, Procter & Gamble, Sanofi, Takeda, UCB. Dr. Lee has served as an advisory board member and/or investigator for Incyte and Novartis. Dr. Hsiao has served as an advisor, investigator, and/or speaker for AbbVie, Amgen, Aclaris, Arcutis, AstraZeneca, Boehringer Ingelheim, Galderma, Incyte, Insmed, LEO Pharma, Moonlake, Navigator Medicines, Novartis, Oruka Therapeutics, Pfizer, Sanofi, Spyre, Regeneron, and UCB. Dr. Ferrier reports consulting fees and/or serving on an advisory board for AbbVie, Arcutis, Bausch Health, Bristol Myers Squibb, CeraVe, Galderma, Janssen, Johnson & Johnson, LEO Pharma, Lilly, L’Oréal, Novartis, Sanofi, Sun Pharma, and UCB; speakers bureau/honoraria from AbbVie, Arcutis, Bausch Health, Galderma, Incyte, L’Oréal, Novartis, Sanofi, and Sun Pharma; and clinical trial/research participation as a Principal Investigator in clinical trials sponsored by AbbVie, Amgen, Avalo Therapeutics, Bristol Myers Squibb, Celldex Therapeutics, Insmed, Sanofi, and Sun Pharma. Dr. Payette is a speaker for AbbVie, Amgen, Arcutis, Botanix, Galderma, Incyte, Johnson & Johnson, Lilly, Novartis, Organon, Pfizer, Sanofi-Genzyme, Regeneron, Sun Pharma, and UCB; a consultant for AbbVie, Amgen, Apogee Therapeutics, Arcutis, Boehringer Ingelheim, Botanix, Bristol Meyers Squibb, Castle Biosciences, Disc Medicine, FIDE, Galderma, Incyte, Johnson & Johnson, LEO Pharma, Lilly, Nielson Bio, Novartis, ONVIV, Ortho Dermatologics, Pfizer, Sanofi-Genzyme, Regeneron, Sun Pharma, Takeda, UCB, and VeraDermics; and an investigator for AbbVie, Botanix, Cara Therapeutics, CorEvitas (Atopic Dermatitis, Psoriasis and Generalized Pustular Psoriasis registries), Dermavant, Incyte, LEO Pharma, Lilly, Mindera Health, Novartis, and Oruka. Dr. Daveluy is a speaker and consultant for AbbVie, Incyte, Novartis, and UCB; a speaker for LEO Pharma​​​; and an investigator for AbbVie, Incyte, Insmed, Moonlake, Novartis, Pfizer, Regeneron, Sanofi, and UCB. Dr. Farley is a clinical investigator with AbbVie, Amgen, Janssen, Moonlake, Novartis, Sun Pharma, and Takeda and on advisory boards for AbbVie, Galderma, Incyte, LEO Pharma, and Pfizer. Dr. Shi is on the board of directors for the Hidradenitis Suppurativa Foundation, an advisor for the National Eczema Association, and a stock shareholder of Learn Health and has served as an advisory board member, investigator, speaker, and/or received research funding from AbbVie, Almirall, Altus Lab/cQuell, Alumis, Apogee, Arcutis, Aristea Therapeutics, ASLAN, Avalo, Bain Capital, Boehringer Ingelheim, Burt’s Bees, Castle Biosciences, Ceraclere, Dermavant, Dermira, Galderma, Genentech, GpSkin, Incyte, Insmed, Kiniksa, LEO Pharma, Lilly, Menlo Therapeutics, Moonlake, MYOR, Navigator Medicine, Novartis, Oruka, Pfizer, Polyfins Technology, Sanofi/Regeneron, Skin Actives Scientific, Sun Pharma, Takeda, Target-PharmaSolutions, UCB, Veradermics, and ZuraBio. The remaining authors have no relevant conflicts of interest.

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