Symposium on Hidradenitis Suppurativa Advances 2025 Proceedings

Introduction

The 10th Annual Symposium on Hidradenitis Suppurativa Advances (SHSA) was held in Nashville, TN, USA, from 31 October to 2 November 2025. The symposium was jointly hosted by the US Hidradenitis Suppurativa Foundation (HSF) and the Canadian HS Foundation (CHSF), with Dr. Vincent Piguet serving as the 2025 SHSA Planning Chair and Dr. Martina Porter serving as Vice Chair. The conference featured presentations from experts in hidradenitis suppurativa (HS) across multiple disciplines, coming together to discuss the recent scientific, pharmaceutical, and technological advancements in our understanding and management of HS. Panelists and presenters discussed new perspectives on HS pathogenesis, management of complex medical cases, procedural interventions, and novel biologic and small-molecule therapeutic agents in the pipeline, among several other topics. SHSA is the largest research-focused HS conference in North America, with 537 attendees from 18 countries, and over 30 individuals living with HS in attendance at the 10th annual meeting. The symposium featured five plenary talks, four expert panel discussions, procedural and ultrasound workshops, and selected oral abstract presentations, including a late breaking abstract session that included top-line data from phase 3 clinical trials being presented at a conference for the first time. The following proceedings are a summary of highlights from the plenary sessions, panels, and select late-breaking abstracts presented at the conference. The complete anthology of abstracts presented at SHSA 2025 has been published [1]. This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.

Plenary Talk 1: Pathogenesis

Dr. James Krueger (The Rockefeller University) delivered the first plenary talk on pathogenesis of HS. He provided a comprehensive update on recent proteomic and transcriptomic developments in HS, which, in addition to characterizing the inflammasome profile, have expanded the understanding of HS pathogenesis beyond the limited landscape of psoriasis (PsO) immunotherapy targets. HS and PsO demonstrate elevated T-helper (Th)17/interleukin (IL)-17 signatures; however, this pathway is more intensely upregulated in HS, with Th17 cells enriched more than 26-fold in HS than PsO lesional skin [2]. Additionally, the predominance of the varied pathways upstream of IL-17 may differ; this is reflected by the limited clinical efficacy of IL-23 inhibitors in HS, despite being considered a key driver of IL-17 production in PsO [2]. IL-23 inhibitors, including guselkumab and risankizumab, are effective in PsO, but neither antibody has met Hidradenitis Suppurativa Clinical Response (HiSCR)50 in phase 2 clinical trials in patients with moderate-to-severe HS, suggesting that in HS, IL-17 production may predominantly occur independently of IL-23 activity [2]. Therefore, targeting IL-17 directly may offer a superior approach for HS. Dr. Kreuger described a previous HS study published in 2020 (n = 10), which reported that 100% of subjects on brodalumab achieved HiSCR50 by week 2, sustained through week 24, with 100% reaching HiSCR75, and 40% achieving complete clearance at week 24 [3]. These early findings illustrated the need for disease-specific immunotherapy targets; subsequent phase 3 trials for secukinumab, bimekizumab, and sonelokimab have further defined IL-17 as an effective immunotherapy target for HS.

Next, Dr. Krueger addressed the need to characterize dermal tunnels in greater depth. Tunnels represent a distinct lesion type that is unique to HS, which differ from other inflammatory lesions in both clinical morphology and immunological composition. They exhibit pseudo-psoriasiform epidermal changes and are now understood to be neo-epithelialized, IL-17-responsive, and immunologically active structures that sustain chronic inflammation and drive disease persistence [4, 5]. A key mechanism in HS tunnel pathogenesis involves a paracrine feedback loop in which IL-1β, activated by the inflammasome, triggers IL-6 production from regulatory T cells and Th17 cells, further amplifying IL-6 release by surrounding dendritic cells, keratinocytes, and fibroblasts [6]. There may also be molecular predispositions for dermal tunneling. When HS samples, independent of disease severity and lesion type, are clustered on the basis of lipocalin-2 (LCN2) expression, the LCN2-high subtype correlated with presence of tunnels and upregulation of genes involved in keratinocyte differentiation and cornification, similar to psoriasiform epidermal remodeling [7]. Comparatively, HS samples identified as the LCN2-low subtype demonstrated lower serum IL-17A expression and decreased tumor necrosis factor (TNF) and markers of neutrophilic inflammation, possibly representative of a less aggressive or earlier disease phenotype, which may be more fibroblast- than neutrophil-dominant [7]. Another tunnel-associated marker, hepatocyte growth factor (HGF), is particularly elevated within HS tunnels, with studies showing that HGF is predominantly produced by fibroblasts, while its receptor is expressed abundantly in keratinocytes, likely functioning to upregulate epithelial–mesenchymal transition and sustaining tunnel chronicity [8].

In conclusion, Dr. Krueger emphasized unresolved gaps in pathogenesis. For example, it remains unclear whether keratinocyte hyperplasia induces the inflammatory cascade or results from it, though the latter seems increasingly likely given the significant preclinical inflammation detected in nonlesional HS skin, preceding signs and symptoms of follicular occlusion [9]. Further study is needed to investigate dermal tunneling as a dysregulated wound-healing process, given the high levels of matrix metalloproteinases and epithelial mesenchymal transition-like keratinocyte changes [9]. Lastly, as molecular targets expand, combination immunotherapy to target multiple axes simultaneously may offer a robust strategy for recalcitrant HS, drawing from fields such as oncology and rheumatology where multi-axis treatment is often standard of care for achieving meaningful remission [10].

Plenary Talk 2: Pediatric HS: A Deeper Dive

Dr. Colleen Cotton (Children’s National Hospital and George Washington School of Medicine and Health Sciences) opened the second plenary session with an overview of the pediatric HS research landscape, noting that recent years have seen a surge in systematic reviews and meta-analyses, with comparatively fewer primary studies. However, the data available collectively reaffirms that the pediatric HS comorbidity burden is similar to that of adult HS populations. One observational study compared the comorbidity prevalence of 304 pediatric patients with HS with those without HS at an urban safety-net hospital [11]. While the study was limited by a lack of age, sex, or ethnicity matching of controls, they found that obesity, acne vulgaris, depression, anxiety, and polycystic ovary syndrome were among the most common comorbidities (p < 0.0001) [11]. This supports the use of multidisciplinary care in pediatric HS. Quality-of-life (QoL) impairment is also significant in this population. Higher Hurley stage and pain correlate with lower QoL scores and educational attainment; however, patients with Hurley stage I disease can also be significantly affected [12, 13]. Clinicians can provide relief through a 504 plan (in the USA) and/or accommodation requests that allow for greater privacy in educational settings. Such accommodations include access to private bathrooms, use of elevator where feasible, and the ability to be excused from class or physical exercise without having to explain why in front of the class.

Next, select medical and procedural therapies in pediatric HS were presented. Progestin-only pills have classically been known to worsen HS; however, this is in reference to older-generation progestins. Third‑generation (desogestrel/norgestimate) and particularly fourth‑generation (drospirenone) progestins are more antiandrogenic and are unlikely to cause HS flares. Combined oral contraceptive pills (OCPs) are potential adjuncts in HS management. For female patients with HS who experience menstrual flares, Dr. Cotton recommended continuous cycling of monophasic combined OCPs (with a minimum of 30–35 mcg ethinyl estradiol for bone health), as there is no medical benefit of inducing withdrawal bleeding. Higher‑estrogen formulations may be required to reduce breakthrough bleeding. Data on biologics in pediatric HS are dominated by adalimumab, which appears to be effective and well tolerated in this population. In a multicenter cohort study involving 294 patients, 47% of those who started on adalimumab improved on their original dose, 12% after dose escalation, and 31% failed and transitioned to a different biologic. Adverse events were uncommon (the most common being injection‑site reactions in 4%), and serious adverse events were extremely rare (single cases of sepsis and tumor necrosis factor [TNF]-induced lupus). Clinical trials including adolescent patients are ongoing. Deroofing procedures are also well tolerated, but setting expectations around postprocedural pain, cosmesis, and return to full activities (approximately 6 weeks) is important [14, 15]. Dr. Cotton recommended the use of lacrimal probes for small, targeted deroofings, and to schedule follow up appointments 2–3 weeks post-procedure to identify and treat early formation of hypergranulation tissue.

She ended the session by reviewing mimickers of HS, including inborn errors of immunity. Female carriers of chronic granulomatous disease may present with “HS‑like” tunnels in adolescence due to skewed lyonization, requiring antimicrobial therapy rather than immunosuppression. Red-flag features include early onset disease (< 10 years), recurrent fevers, painless purulent abscesses, unusual pathogens, refractory disease, family history of early deaths or immunodeficiency, or frequent sinopulmonary infections. These characteristics should prompt an immune workup or immunology referral.

Plenary Talk 3: Hamzavi Lectureship: Managing HS—Where Have We Come from, Where Are We Going?

The third plenary talk was the Hamzavi Lectureship, delivered by Dr. Michelle Lowes (Montefiore Medical Center). The Hamzavi Lectureship is a named lectureship in honor of Dr. Iltefat Hamzavi, former president of the HSF and a tremendous leader in the field of HS. The Hamzavi Lectureship seeks to shed light on the advancements in translational research alongside the practical applications of these discoveries in patient care, with the goal of improving the lives of individuals with HS and their caregivers. The lectureship seeks to foster a sense of community and shared purpose while advancing the HSF’s mission to deepen understanding of and ultimately overcome the complexities of HS.

Dr. Lowes offered a comprehensive overview of the evolution of HS research and management. She began by reviewing the historical understanding of HS, once regarded as an inflammatory or infectious disorder of the apocrine glands. Prior to 2015, there were no US Food and Drug Administration (FDA)-approved therapies, and National Institutes of Health (NIH) funding for HS totaled only $270,000 in 2014. Management relied heavily on repeated courses of antibiotics and surgery. Genetic research focused largely on γ-secretase mutations. Patients with HS faced stigma, limited treatment options, and diagnostic delays averaging a decade. Dr. Lowes discussed that the establishment and growth of the HS Foundation created the groundwork for coordinated research, education, and patient advocacy efforts.

Dr. Lowes examined major advances in the last decade from 2015 to 2025, including publication of the North American clinical management guidelines in 2019 and continued guideline efforts, which standardized care and emphasized comorbidity screening. She noted that consensus documents addressing HS morphology, surgery, biomarkers, and registry design strengthened consistency in clinical practice and research studies. Expansion of HS societies and increased NIH funding over the past decade ($51 million) supported endeavors with multicenter collaboration. Over the past decade, the FDA has approved three biologics: adalimumab, secukinumab, and bimekizumab.

Progress has also been made in HS pathogenesis. Dr. Lowes reviewed IL-17’s role in HS inflammation, with disease drivers differing from those observed in psoriasis, where IL-23 predominates. She also discussed genome-wide association studies identifying susceptibility loci (SOX9, CXCR4, CD74, HLA-DRB1, and KLF5) linked to immune dysregulation. Dr. Lowes examined infection and immunity, noting that inflammation may arise from both noncommensal and commensal microbes. She added that certain monogenic traits represent inborn errors of immunity that can heighten or mitigate infectious responses, illustrating how genetic variation may shape HS susceptibility. Antibacterial therapy, including short-term ertapenem, was cited as effective in severe cases, and early results from the minimally invasive tunnel (MINT) procedure showed promising outcomes with antimicrobial gel application within tunnels.

Dr. Lowes further reviewed data demonstrating broad immune dysregulation in HS lesions, characterized by mixed cellular infiltrates and overlapping autoimmune and autoinflammatory features. She noted emerging evidence of antinuclear antibodies and the potential role of Fc glycoproteins in modulating inflammatory pathways. She described how neutrophil extracellular traps (NETs) are abundant in HS and activate adaptive immune cells, dendritic cells, and fibroblasts. Recent transcriptome studies have demonstrated B cell signatures, suggesting that B cells may play a role in autoantibody production, antigen presentation, and modulation of inflammatory responses. Dr. Lowes also identified LCN2 as a potential biomarker for HS, with elevated levels correlating positively with disease severity.

In closing, Dr. Lowes reflected on improvements in HS care, highlighting reduced diagnostic delays and expanding clinical expertise, with multimodal management including biologics, small molecule inhibitors, hormonal and metabolic agents, antibiotics, laser hair removal, and surgery. She discussed the HS PROGRESS registry, a multicenter longitudinal study clarifying disease course, with early findings showing shorter diagnostic delays (4.5 years) and increased biologic use (nearly 50%). Dr. Lowes concluded with a vision for 2035, centered on early diagnosis, biomarker-guided therapy, and timely intervention within the window of opportunity to prevent scarring and improve outcomes.

Plenary Talk 4: The Microbial Landscape of HS: What We Know and What Is on the Horizon

In the fourth plenary session, Dr. Amanda Nelson (Pennsylvania State University College of Medicine) provided a comprehensive overview of the evolving understanding of the HS microbiome and its implications for disease pathogenesis and management. Framed as a “perfect storm” of genetics, follicular occlusion, dysbiosis, and hormonal influence, HS was emphasized to be a chronic inflammatory condition rather than a primary infectious disease. Antibiotics remain a mainstay of treatment; however, their effectiveness likely reflects modulation of microbial communities and inflammation rather than direct antimicrobial activity.

Over 50 studies have now characterized the HS microbiome, collectively pointing toward an overabundance of anaerobic pathogens and a loss of commensal skin bacteria. Both alpha and beta diversity metrics demonstrate consistent dysbiosis compared with healthy controls, though the magnitude and direction of changes vary by lesion type, site, and sampling method. Dr. Nelson underscored the importance of standardizing clinical collection and analytical pipelines to improve reproducibility and cross-study comparison. Emerging data highlight enrichment of anaerobes such as Porphyromonas and Fusibacterium, and depletion of protective commensals such as Staphylococcus epidermidis. Beyond bacteria, the virome and mycobiome remain poorly characterized, representing key areas for future investigation. The gut microbiome may also contribute to systemic inflammation. Dr. Nelson discussed smaller pilot studies showing reduced alpha diversity and altered metabolic potential, including enrichment of Ruminococcus gnavus, a species associated with proinflammatory metabolic activity and disordered glucose metabolism [16]. However, larger cohorts are needed to validate these findings and disentangle these relationships.

Biofilms are multispecies bacterial communities that adopt distinct phenotypes and have been identified in some HS lesions, but not universally. No studies have yet definitively demonstrated intact biofilm structures in vivo, leaving their contribution to chronic inflammation an open question. Dr. Nelson called for standardized imaging and molecular criteria for biofilm identification and emphasized that future studies must move beyond compositional analyses toward understanding functional capacity, virulence gene expression, and metabolite production within the HS microenvironment.

The host response to the microbial community remains a critical but underexplored dimension. Keratinocytes in HS are increasingly recognized as immune-active cells capable of sensing microbial metabolites and triggering cytokine cascades. Citing work from Dr. James Krueger and others, Dr. Nelson discussed how commensal or pathogenic metabolites can differentially induce keratinocyte inflammatory pathways or antimicrobial peptide production. Transcriptomic analyses reveal overlapping inflammatory signatures between HS lesions enriched for Prevotella species and other inflammatory dermatoses, whereas S. epidermidis-dominated environments exhibit distinct, less inflammatory profiles [17]. These insights suggest that microbial context may shape disease heterogeneity.

The lecture concluded with a call to unify methodological standards, integrate robust metadata, and employ multiomic approaches to capture microbial, immunologic, and clinical dimensions of HS. Understanding the functional consequences of dysbiosis could enable microbe-targeted interventions designed to restore microbial equilibrium while preserving beneficial commensals. Dr. Nelson proposed that strategies such as combining probiotics, postbiotics, or narrow-spectrum antimicrobials could prevent collateral damage and promote durable disease control. Overall, this session highlighted that while dysbiosis in HS is well established, the field now stands poised to define its mechanistic and therapeutic relevance through rigorous, standardized, and functionally informed investigation.

Plenary Talk 5: Procedural Interventions across the Spectrum of HS

Dr. Ralph George (University of Toronto/CIBC Breast Centre at St. Michael’s Hospital) gave the fifth plenary lecture on procedural interventions in HS. Over the past decade, the management of HS has experienced a substantial paradigm shift, attributable to significant advancements in both medical and surgical modalities. Historically, surgical intervention for HS was typified by extensive resections, high recurrence rates, and protracted recoveries. Patients frequently underwent radical procedures associated with considerable morbidity, as surgical approaches alone were insufficient to address the underlying inflammatory pathophysiology of the disease.

The advent of biologic therapies, coupled with the development of standardized treatment guidelines, has fundamentally transformed the therapeutic landscape. Biologics, through modulation of systemic inflammation, have facilitated preoperative disease control and enhanced postoperative healing, thereby enabling the adoption of less invasive surgical techniques without compromising clinical efficacy. The integration of medical and surgical management is now central to contemporary HS care, with multidisciplinary collaboration between dermatologists and surgeons yielding improved outcomes and reduced recurrence rates.

Among the most notable advances is the increased utilization of healing by secondary intention. Previously underutilized in North America, this approach is now favored owing to its association with lower rates of infection and dehiscence, enhanced patient mobility, and superior overall healing. Surgical techniques such as deroofing and tissue-sparing excision, including electrosurgical peeling, prioritize the preservation of healthy skin and minimize the extent of excision. These innovations have contributed to greater patient satisfaction, reduced contracture, and expedited recovery.

The expansion of office-based interventions has further diversified procedural options. Fractional carbon dioxide (CO₂) lasers and radiofrequency devices are increasingly employed in the management of early stage disease, thereby reducing the necessity for major operative interventions. These energy-based modalities afford precision and minimal downtime, facilitating targeted excisions within clinic settings.

Current surgical management strategies for HS can be tailored according to extent of tissue destruction, as delineated by Hurley staging. For individuals with Hurley stage I disease, optimal medical management is emphasized, including early initiation of biologic agents and adjunctive therapies such as laser hair removal. Hurley stage II disease is typically managed with a combination of medical therapy and targeted excisions, frequently performed in the outpatient setting utilizing advanced energy devices to minimize invasiveness and recovery time. Fractional CO₂ may be utilized for the treatment of scarring. Even in advanced stage III disease, biologic therapies enable less aggressive surgical approaches that may be performed outside of the operating room and support improved healing, culminating in superior patient outcomes and enhanced quality of life.

The procedural management of HS now reflects a nuanced understanding of disease complexity, leveraging both medical and surgical innovations to optimize patient outcomes. Ongoing research and continued multidisciplinary collaboration promise further improvements in the quality of life for those affected by HS.

Tackling the Pain of HS Panel: A Multidisciplinary Approach

Patient and advocate, Ashley Dalton, opened this session, describing her journey of first developing symptoms of HS at 13 years old, to now working as a patient advocate with HS Connect. It took her years to find a regimen that manages her HS pain, which consists of a wide range of medications and lifestyle adjustments.

Next, Dr. Vivian Shi (University of Washington) presented on integrative approaches to pain management for HS with two clinical cases [18]. The first described a patient with Hurley stage III HS experiencing debilitating chronic joint pain. Dr. Shi emphasized that pain is positively correlated with HS severity, and treating HS tends to improve associated pain. Therapeutic data on current biologic options such as secukinumab and bimekizumab were discussed. She outlined key distinctions between acute and chronic pain and discussed nociceptive, neuropathic, and nociplastic mechanisms, underscoring the need for multidisciplinary collaboration in chronic pain management [19]. Frequently used pain strategies were reviewed, including warm compresses, over-the-counter analgesics, and bathing additives, with the most helpful patient-reported intervention being cannabis-based products. Additional treatments discussed included acupressure and experimental green light therapy.

The second case discussed pre- and postoperative pain considerations for a patient with Hurley stage II HS with a painful abscess requiring incision and drainage (I&D) with subsequent deroofing. Recommendations for pre- and periprocedural pain control consisted of topical analgesia containing benzocaine, lidocaine, and tetracaine; tumescent analgesia; and intralesional triamcinolone placed at the wound base. Postoperative pain is typically managed with alternating acetaminophen and ibuprofen, but for larger and deeper wounds, a short course of opioids such as tramadol, hydrocodone/acetaminophen, codeine/acetaminophen, or oxycodone may be appropriate. Applying topical lidocaine–pramoxine to the wound base during dressing changes is also helpful. Dr. Shi also reviewed the proper technique for intralesional corticosteroid injections for different lesion types as well as the use of intralesional therapy during punch deroofing and I&D procedures.

Dr. Kimberly Curseen (Emory Healthcare), a geriatric and palliative care physician, then discussed integrating palliative care principles into management of chronic HS pain. She noted that traditional dermatologic care, which focuses on HS lesions, may not sufficiently address the physical, psychological, social, and spiritual distress experienced by patients living with HS. Findings from ambulatory palliative care studies in patients with HS demonstrated high baseline pain scores, significant emotional burden, frustration or anger toward their bodies, and reports of invalidation and stigma when seeking pain treatment [20, 21]. Patient-centered care, including comprehensive pain assessment, multimodal analgesic planning, mental health support, engagement of social work resources, and empathetic communication were shown to help address unmet needs across multiple domains. Palliative care provides a supportive framework to help patients construct adaptive coping strategies and improve overall quality of life. Dr. Tammy Gonzales moderated the concluding discussion, where helpful resources, including the HS Papaya app and GetPalliativeCare.org website, were recommended.

Complex HS Medical Management Panel

This session focused on advanced therapeutic decision-making in HS through a panel discussion of complex, real-world clinical cases presented by Dr. Martina Porter (Beth Israel Deaconess Medical Center), Dr. Jennifer Hsiao (University of Southern California), and Dr. John Frew (University of New South Wales).

Case 1 described a woman with an extensive history of HS with multiple prior surgeries and inadequate responses to adalimumab and secukinumab who presented with large ulcerated axillary plaques. Discussion centered on whether monotherapy could be effective after prior partial responses and subsequent loss of response (LOR). The definitions of primary and secondary nonresponse were reviewed, referencing criteria used in rheumatology. Primary nonresponse is a lack of adequate therapeutic benefit from baseline. Secondary LOR is characterized by a pattern of initial response that diminishes over time. Proposed mechanisms underlying secondary LOR include antidrug antibodies (ADA), subtherapeutic drug levels, inadequate peak levels, and immunologic pathway shifts. Therapeutic drug monitoring can help guide next steps: For example, high drug levels without ADA may prompt a switch to a drug with a different mechanism of action instead of dose escalation. Comorbidities such as coexisting inflammatory bowel disease (IBD) or arthritis also inform biologic choice.

Case 2 involved a man with HS and psoriatic arthritis (PsA) who was an adalimumab primary nonresponder with hypersensitivity to infliximab, presenting with extensive dermatitis, maceration, and drainage beneath the pannus, and requiring inpatient hospitalization. Dr. Frew and Dr. Hsiao commented on the importance of recognizing when a patient’s care may need escalation to hospitalization, such as when home self-care is unrealistic, pain cannot be adequately controlled in an outpatient setting, or the patient is experiencing serious complications (e.g., Fournier’s gangrene or sepsis). Inpatient care should be multidisciplinary, encompassing wound care, pain control, infection treatment, and systemic therapy for HS. Because many biologics are not on formulary, “meds-to-beds” workflows, in which a licensed pharmacist delivers medications and instructions to patients prior to discharge, help ensure access to medications after patients leave the hospital. Dual immunomodulator therapy, such as with both a Janus kinase (JAK) inhibitor and a biologic, may be useful in refractory cases, though safety and access require careful consideration.

Case 3 focused on a patient with rapid-onset, refractory HS and secondary LOR to adalimumab. Secukinumab titration raised concern for psoriasiform dermatitis and possible Crohn’s disease. The patient was referred to gastroenterology, who ultimately did not find evidence of IBD; however, the patient was still switched to an IL-23 inhibitor, risankizumab, with improvement in the rash and HS. Addition of upadacitinib led to disease quiescence after 13 months. Patients with concurrent HS and Crohn’s disease are limited in biologic options, as IL-17 inhibitors are contraindicated in patients with active IBD [22]. Dr. Frew explained that despite phase 2 trial data for risankizumab in HS not meeting primary endpoint [23], some patients did experience improvement, particularly subgroups of patients with inguinal/gluteal disease and young, lean male patients. Because IL-23 inhibitors have a slower onset of action, expectation-setting is essential when counseling patients. The panelists also discussed that with dual immunomodulator therapy, gradual tapering of the less effective agent should be considered when possible.

Addressing the Comorbidities of HS Panel

HS is a disease that is not only limited to the skin; many patients experience comorbidities that increase morbidity and significantly impact quality of life. This panel discussion by Dr. Raed Alhusayen (University of Toronto), Dr. Afsaneh Alavi (Mayo Clinic), Dr. Reza Mirza (McMaster University), Dr. Baldeep Pabla (Vanderbilt University Medical Center), and Dr. Simon (Se Mang) Wong (University of British Columbia) explored the full spectrum of HS-related comorbidities and strategies for comprehensive, multidisciplinary care.

Dr. Simon Wong opened the session with an overview of psychiatric comorbidities in HS. Anxiety and depression affects 15–30% of patients with HS [24], with other concurrent psychiatric disorders, including obsessive–compulsive disorder [25]. Contrary to the traditional view that psychiatric comorbidities only stem from the psychological impact of skin disease, emerging evidence suggests that cytokine dysregulation may play a pathogenic role [26]. Elevated levels of IL-23 and IL-17A have been reported in patients with depression [27]; however, a significant correlation between change in cytokine level and corresponding clinical improvement of depression has not been demonstrated [28]. Similar modulation has been observed in generalized anxiety disorder, with selective serotonin reuptake inhibitors reducing levels of baseline proinflammatory cytokines [29, 30]. For comprehensive care, the use of screening tools such as the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder 7-item scale (GAD-7), and supportive, open-ended questions about mood were recommended. When appropriate, interdisciplinary collaboration and psychotropic therapy may be considered.

Dr. Reza Mirza discussed inflammatory arthritis, which affects 7–14% of patients with HS; there are threefold increased odds of peripheral arthritis in patients with HS compared with controls [31, 32]. Inflammatory arthritis subtypes may include rheumatoid arthritis; spondyloarthritis; seronegative arthritis; IBD-associated arthritis; syndromic forms including synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome; and others [31, 32]. Commonly affected sites include the back, sacroiliac joints, and large joints [31–33]. Approximately half of patients with HS also experience peri-flare arthralgias in the absence of established musculoskeletal comorbidities, which may indicate early inflammatory arthritis [33]. HS-associated arthritis may be an underrecognized entity, as immunosuppressive therapy can mask clinical and radiographic features, and serology may deviate from conventional patterns. Both HS and its associated arthritis are driven by Th17-mediated inflammation, triggered by skin and gut dysbiosis. This may support an emerging mucocutaneous, seronegative phenotype of inflammatory arthritis in HS that preferentially affects large joints.

From a gastroenterology perspective, Dr. Baldeep Pabla addressed the association between HS and IBD. Differentiating pelvic HS from fistulizing IBD requires detailed history-taking on smoking, obesity, and affected sites, as well as imaging to characterize luminal involvement. Accurate diagnosis is crucial as IL-17 inhibition can exacerbate IBD [22], with one analysis of adverse event databases demonstrating 2.1 and 2.8 times increased odds for gastrointestinal toxicity with secukinumab and ixekizumab, respectively [22]. Notably, this signal was not observed with brodalumab, an IL-17A receptor antagonist. Medications such as JAK inhibitors have shown dual efficacy in patients with HS and comorbid IBD [34]. Combination therapies may be warranted in refractory cases.

Dr. Afsaneh Alavi addressed the diagnostic challenges in distinguishing perianal HS from IBD, particularly in patients presenting with isolated pelvic HS, or those classified as having IBD without luminal involvement who then subsequently develop it. A large retrospective review highlighted key differentiating features in HS and IBD. Clinically, knife-cut lesions, fistulae, perianal skin tags, genital edema, and digestive symptoms were more characteristic of IBD, whereas involvement of other typical body sites such as the axillae favored HS [35]. Magnetic resonance imaging (MRI) findings further supported differentiation. Cutaneous and subcutaneous inflammation and inguinal lymphadenopathy were more consistent with HS, while inter-sphincteric fistulae and mesorectal lymphadenopathy were more suggestive of IBD [35]. Investigations, including colonoscopy, anemia workup, and monocyte-to-lymphocyte ratio, can provide further diagnostic clarity [35]. The study’s scoring system, which incorporated these parameters, demonstrated 77% sensitivity and 80% specificity and may aid in clinical decision-making [35]. Ongoing research is required to determine whether perianal fistulizing disease represents a clinical entity distinct from HS and IBD.

Late-Breaking Abstracts

Several phase 2 and phase 3 trials in moderate-to-severe HS were presented at the SHSA 2025, including the first presentation of the pivotal phase 3 data from the sonelokimab trials and the 4-year efficacy and safety data from the secukinumab long-term extension trials.

In patients with moderate-to-severe HS, sonelokimab, an IL-17A/F nanobody, reported consistent HiSCR75 (34.8–35.9%) and HiSCR50 (51.6–58.7%) responses at week 16 in both phase 3 VELA-1 and VELA-2 trials. However, in VELA-2, the primary endpoint of HiSCR75 at week 16 just missed statistical significance, potentially impacted by a higher placebo response rate of 24.9% (p = 0.053) in VELA-2; placebo response rate was 17.5% (p < 0.025) for VELA-1 [1]. There was a rapid onset of pain improvement by week 1, HiSCR75 responses as early as week 4, and a favorable safety profile [1].

Povorcitinib, an oral selective JAK1 inhibitor, met both primary endpoints at week 12 in its phase 3 STOP-HS1 and STOP-HS2 trials, with HiSCR50 rates of about 40.2–42.3% for both 45 mg and 75 mg doses of the drug versus 28.6–29.7% on placebo [1]. Moreover, both dose groups showed greater responses in HiSCR75, ≥ 3-point skin pain numerical rating scale (NRS) reduction, fewer flares, and decreases in draining tunnels, with continued improvements in HiSCR50, HiSCR75, HiSCR90, and HiSCR100 through week 24 and a low frequency of clinically relevant hematologic abnormalities [1].

Long-term IL-17 pathway inhibition also demonstrated durable responses. In pooled BE HEARD I/II and BE HEARD EXTENSION trials, bimekizumab produced week 48 HiSCR50/75/90/100 rates of 79.9%/64.0%/42.3%/30.2%, which were maintained at 90.2%/81.2%/64.3%/50.1% at week 148. The studies also showed sustained reductions in draining tunnels and greater proportions of patients achieving a Dermatology Life Quality Index (DLQI) score of 0 or 1, with no new safety concerns [1].

A post hoc analysis of continuous secukinumab therapy in the SUNSHINE/SUNRISE core and extension trials showed maintenance of HiSCR50, HiSCR75, HiSCR90, and HiSCR100 responses through week 204 in a HiSCR responder cohort, with HiSCR50 achieved by 83.2%, a 68.5% reduction in mean draining tunnel count, and favorable tolerability at week 204 [1].

In a phase 2 trial, brivekimig, a dual TNF/OX40L nanobody biologic, achieved HiSCR50 in 67% of biologic-naïve patients versus 37% with placebo at week 16, with higher HiSCR75 (54% versus 22%) and HiSCR90 (31% versus 9%) rates. Patients on brivekimig experienced a mean 56.0% reduction in draining tunnels compared with a 10.9% increase in draining tunnels with placebo. Brivekimig was generally well tolerated, with no new safety signals and no serious adverse events [1].

In another phase 2 trial, upadacitinib 30 mg demonstrated HiSCR50/75/90 responses of 38.3%/21.3%/8.5% versus placebo with 23.8% HiSCR50 at week 12 [5]. In addition, upadacitinib responders had HiSCR50/75/90 of 72.2%/70.0%/50.0% at week 12 and maintained the response through week 40 [1]. Patients who switched from placebo to upadacitinib 15 mg also demonstrated maintained responses [1].

In a phase 2 trial, among patients with moderate-to-severe HS who failed or demonstrated intolerance to anti-TNF therapy, lutikizumab demonstrated higher achievement of composite outcomes compared with patients. A greater proportion of patients treated with lutikizumab 300 mg (every week or every other week) achieved concomitant improvements in quality of life (as measured by the achievement of the minimal clinically important difference in DLQI [DLQI-MCID]) and objective clinical response (as measured by HiSCR50) by week 16—DLQI-MCID + HiSCR50: 35.1% and 33.3% versus 13.5% placebo; DLQI-MCID + HiSCR75: 29.7% and 27.3% versus 5.4% placebo. Higher proportions of patients also achieved concomitant improvements in pain (as measured by ≥ 30% and ≥ 2-point reduction in skin pain [NRS30]) and objective clinical response (as measured by HiSCR75)—NRS30 + HiSCR50: 26.1% and 31% versus 6.5% placebo; NRS30 + HiSCR75: 17.4% and 24.1% versus 0% [1].

Achievements and Initiatives by the HS Foundations of the USA and Canada

The presidents of the US HSF and the CHSF, Dr. Hadar Lev-Tov and Dr. Helene Veillette, respectively, highlighted major achievements and strategic initiatives for their respective organizations over the past year. Presentations emphasized advances in research funding, education, access to specialized care, patient engagement, and international collaboration.

Dr. Lev-Tov and Dr. Veillette described patient-centric initiatives by the HSF and CHSF that bridge the gap between patients and healthcare access. The HSF expanded its digital resources for patients to include over 70 accessible research summaries and the HSF clinic finder (https://www.hs-foundation.org/hs-specialty-clinics) [36]. The foundation also launched a new tool to help patients locate wound care clinics, further improving access to specialized services. Furthermore, the HS Buddy Program assists patients in navigating the complexities of clinical trial enrollment. The CHSF focused on community mobilization through a Social Media Ambassador Program led by dermatology residents and the planning of a coordinated 2025 HS Awareness Week across Canada.

Research funding and the evolution of clinical guidelines remain at the forefront of both foundations’ agendas. The HSF demonstrated a significant commitment to scientific advancement, with research investments projected to reach $495,000 by 2026. Dr. Lev-Tov also announced the new HS-specific Career Development Award established in partnership with the Dermatology Foundation. Dr. Veillette highlighted CHSF leadership in supporting the HS Living Guidelines, a concept initiated in 2023 by Dr. Raed Alhusayen. This initiative introduces a dynamic, continuously updated approach to clinical guidelines, with modular, online publication of recommendations that incorporate new evidence as it becomes available. Although initiated in Canada, the HS Living Guidelines are supported by contributors worldwide, reflecting a global collaborative effort.

In terms of physician education, both organizations have invested heavily in the HS HCP pipeline. The HSF’s annual HS Academy that focuses on dermatology resident education has seen rapid growth, with participation increasing from 69 trainees at its launch in 2021 to 135 participants in 2025. The HSF has also updated over 25 prior authorization templates to reduce physician administrative burden. The CHSF has made progress with an HS Surgical Initiative to help standardize surgical care.

Both Dr. Lev-Tov and Dr. Veillette concluded with a look toward the future, with continued efforts to streamline research into clinical practice recommendations and to utilize technology to make healthcare more accessible to patients.

Conclusion

SHSA 2025 featured cutting-edge HS research, plenary sessions covering hot topics in HS, and expert panels discussing best-practice strategies. Future directions of the US and Canadian HS Foundations bring further hope for increased funding, educational opportunities, and innovative progress in HS research.

Author Contributions

Dr. Jennifer Hsiao contributed to concept and design, as well as supervision. Claire Chung, Kenan Kherallah, Nazrin Ashina, Gabriela Beraja, Anuj Budhiraja, Serena Dienes, Mollye Goldberg, Grace Xiong, and Tammy Gonzalez contributed to the preparation of the original draft. Dr. Raed Alhusayen, Dr. Stephanie Goldberg, Dr. Jennifer Hsiao, Dr. Hadar Lev-Tov, Dr. Cathryn Sibbald, Dr. Vincent Piguet, and Dr. Martina Porter reviewed and edited the manuscript. All authors read and approved the final manuscript.

Funding

No funding or sponsorship was received for this study or publication of this article.

Data Availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Declarations

Conflicts of Interest

Dr. Raed Alhusayen is on the advisory board or has received honorarium from AbbVie, Bausch Health, Bio Jamp, Boehringer Ingelheim, Fresenius Kabi, Galderma, Incyte, Janssen, Novartis, Pfizer, Sandoz, Sanofi, and UCB, and has received investigator fees from AbbVie, Bausch Health, Incyte, Janssen, and Novartis. Dr. Stephanie Goldberg is on the advisory board for UCB and board of directors for the HS Foundation and HS Connect, and is president of the HS Coalition. Dr. Jennifer Hsiao is an editor-in-chief of Dermatology and Therapy, serves on the board of directors for the HS Foundation, and has served as an advisor, investigator, and/or speaker for AbbVie, Amgen, Aclaris, AstraZeneca, Boehringer Ingelheim, Galderma, Incyte, Insmed, Moonlake, Navigator Medicines, Novartis, Oruka Therapeutics, Pfizer, Sanofi, Regeneron, and UCB; Dr. Jennifer Hsiao was not involved in the selection of peer reviewers of the manuscript or any of the subsequent editorial decisions. Dr. Hadar Lev-Tov has served as advisor, investigator, and/or speaker for Incyte, Insmed, Moonlake, Novartis, and UCB. Dr. Cathryn Sibbald has received honorarium from Abbvie, Incyte, Leo Pharma, Novartis, Pfizer, Sanofi, UCB Pharma, and Sun Pharma; has participated in advisory boards with Arcutis, Sanofi, Pfizer, Sun Pharma, Incyte, and Eli Lily; and has participated in clinical trials with Bristol Myers Squibb, Incyte, Pfizer, and Sun Pharma. Dr. Vincent Piguet has received grants from AbbVie, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Incyte, Janssen, LEO Pharma, L’Oréal, Novartis, Organon, Pfizer, Sandoz, and Sanofi; received payment or honoraria for speaking engagement from Sanofi; participated on an advisory board for LEO Pharma, Novartis, Sanofi, Union Therapeutics, Abbvie, and UCB; and received equipment donation from L’Oréal. Dr. Martina Porter has served as consultant and investigator for AbbVie, Avalo Therapeutics, Arcutis, Aristea Therapeutics, Eli Lilly and Company, Incyte, Janssen, Merck, MoonLake Immunotherapeutics, Navigator Biosciences, Novartis, Pfizer, Prometheus, Sanofi, Sonoma Biotherapeutics, UCB, Ventyx, and Zura Bio; consultant for Almiral, FIDE, Otsuka, Propeller Biosciences, and Trifecta Clinical/WCG; investigator for AnaptysBio, Bayer, Bristol Myers Squibb, OASIS Pharmaceuticals, and Regeneron; received royalties from Beth Israel Deaconess Medical Center; and received fellowship funding to institution from AbbVie. Claire S. Chung, Kenan Kherallah, Nazrin Ashina, Gabriela E. Beraja, Anuj Budhiraja, Serena Dienes, Mollye Goldberg, Grace Xiong, and Tammy Gonzalez have nothing to disclose.

Ethical Approval

This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.