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Review

Associations of Hidradenitis Suppurativa with Atopic Dermatitis: A Review of Shared Pathogenesis and Approach to Treatment of Concomitant Disease

by
Rayad B. Shams
1,2,*,
Hiral S. Patel
3 and
Christopher J. Sayed
2
1
School of Medicine, University of North Carolina Chapel Hill, Chapel Hill, NC 27599, USA
2
Department of Dermatology, University of North Carolina Chapel Hill, Chapel Hill, NC 27516, USA
3
School of Medicine, East Carolina University, Greenville, NC 27834, USA
*
Author to whom correspondence should be addressed.
Allergies 2025, 5(2), 20; https://doi.org/10.3390/allergies5020020
Submission received: 7 February 2025 / Revised: 21 May 2025 / Accepted: 5 June 2025 / Published: 13 June 2025
(This article belongs to the Section Dermatology)
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Abstract

Hidradenitis suppurativa (HS) and atopic dermatitis (AD) are both inflammatory dermatoses that can significantly impact patient quality of life, however, limited research exists regarding their association. The purpose of this comprehensive review is to compare the inflammatory pathogenesis of HS and AD, explore the associations between these diseases, and discuss standalone and concomitant disease treatment options. Although HS and AD are understood to be primarily driven by the Th1 and Th2 inflammation pathways, respectively, these conditions both utilize the Janus Kinase/Signal transducer and activator of transcription (JAK/STAT) pathway to promote inflammation. Newer research also suggests that IL-36 and IL-1 receptor-associated kinase 4 (IRAK4) may be two additional inflammatory signals shared between the HS and AD disease pathways. These shared mechanisms are reflected in patient presentations as HS and AD are often concomitantly present and demonstrate a bidirectional association in the current literature. Treatment options for concomitant disease are limited, but leverage the shared immune pathogenesis of both diseases. Dupilumab has been reported to improve both HS and AD symptoms in select patients. JAK inhibitors are currently FDA-approved for the treatment of AD, and early trials have suggested benefits from JAK inhibitors such as upadacitinib, povorcitinib, and topical ruxolitinib for HS. Possible future avenues for research on treating both HS and AD include IRAK-4 inhibitors such as zabedosertib and BAY1830839, and diet and gut microbiome modifications.

1. Introduction

Hidradenitis suppurativa (HS) is a debilitating chronic inflammatory condition characterized by recurrent abscesses, nodules, and tunnels in skinfold areas like the underarms, buttocks, and groin [1]. Atopic dermatitis (AD) is an inflammatory skin disease characterized by the presence of eczematous, dry, scaly, and pruritic skin patches [2]. Although prior literature has explored the pathogenesis of HS and AD, there is a paucity of information regarding the associations of HS with AD. Furthermore, although for some patients, HS is often comorbid with AD, suitable treatment approaches for patients with both remain unclear. The purpose of this review is to discuss the current state of the literature regarding the role of the immune system for HS and AD, explore their associations, and discuss management options for patients with concomitant disease.

2. The Role of the Immune System in Atopic Dermatitis and Hidradenitis Suppurativa

AD is understood to be caused by the combination of dysregulated immune response and skin barrier impairment [3,4,5,6]. AD is primarily understood to be a Th2-dominated inflammatory process with skin barrier defects, which allows infiltration of allergens and microbes, leading to Th2 cell sensitization that subsequently leads to cytokine release [7,8]. However, recent data suggests that chronic AD is more biphasic with an initial Th2 response in the acute phase, leading to lesion development via Th17 and Th22 responses in the chronic phase [8,9,10]. Some of the cytokines implicated in AD include IL-4, IL-5, and IL-13 [11,12,13,14]. IL-4 and IL-13 are both thought to bind to IL-4 receptor alpha (IL-4Ra). They are responsible for the production of the extracellular matrix and can cause skin micro-epidermal fissuring and epidermal water loss through kallikrein 7 production (Figure 1). IL-17, another proinflammatory cytokine, is also thought to play a role in AD pathogenesis. Damaged keratinocytes in AD produce IL-17E that subsequently stimulates IL-5 and IL-13 production while inhibiting the release of filaggrin, important for skin barrier maintenance [15] (Figure 1).
The pathogenesis of HS is incompletely understood; however, newer research suggests that the immune system plays a pivotal role. Th1/17 cells are important for HS pathogenesis, subsequently leading to the release of numerous proinflammatory cytokines. Key cytokines of interest include IL-17, IL-23, IL-1, Tumor Necrosis Factor-a (TNF-a), and IL-12, which are elevated in patient lesional HS skin [16,17]. TNF-α promoted T-cell proliferation and CD8+ cytotoxic T-cell stimulation and was expressed in higher levels in HS skin and positively correlated to increased disease severity [18,19]. IL-23 participates in the activation of TH17 cells, which induces the production of IL-17A, IL-17F, TNF-α, and IL-16 [15,20] (Figure 1).
The Janus Kinase/Signal transducer and activator of transcription (JAK/STAT) pathway presents perhaps the clearest overlap in inflammatory mechanisms between HS and AD and is currently an important target for therapeutics related to inflammatory or autoimmune dermatoses. The transmembrane receptor JAK, once activated, phosphorylates both itself and the cytoplasmic STAT. STAT subsequently travels to the nucleus as a transcription factor regulating gene expression [21]. Different inflammatory cytokines induce JAK expression, including IL-4, IL-5, and IL-31 [22,23,24]. Multiple components of the JAK/STAT pathway have been implicated in AD. In the IL-4 pathway, IL-4 binds to its corresponding receptor and induces phosphorylation of JAK1 and JAK3, which subsequently activate IL-4Ra and STAT6 [22]. Alternatively, IL-4 and IL-13 may also bind the IL-4 receptor and strongly phosphorylate JAK1 and TYK2. This causes downstream STAT3 and STAT6 phosphorylation that can lead to skin barrier dysfunction and increased accumulation of TSLP, IL-25, and IL-33 in keratinocytes [25]. Thymic stromal lymphopoietin (TSLP), a Th2-related immune factor associated with inflammatory diseases, also contributes to the JAK/STAT pathway by binding the TSLP receptor and IL-7 receptor alpha (IL-7Rα) and subsequently phosphorylating JAK1 and JAK2. IL-5 can also phosphorylate JAK1 and JAK2, resulting in the activation of STAT1, STAT3, and STAT5 [23] (Figure 1).
The JAK/STAT pathway is also closely involved with multiple inflammatory markers associated with HS, including TNF-α and IFN-γ [26]. This pathway may also contribute to inflammatory cytokine accumulation in HS lesions, as demonstrated by a quantitative analysis of JAK/STAT pathway signaling by Dermirci et al., who found an overexpression of all cytokines except STAT6 in HS skin compared to controls [27]. JAK1 inhibitors have been evaluated in HS with promising initial results [28].
IL-36 is a member of the IL-1 cytokine family whose role in inflammatory skin conditions has been explored in recent years (Figure 1). It is comprised of three agonists (IL-36α, IL-36β, and IL-36γ) and one antagonist (IL-36Ra). IL-36α and IL-36γ are proinflammatory. While IL-36Ra is understood to be anti-inflammatory, the role of IL-36β remains incompletely understood, but is thought to induce antimicrobial peptides, matrix metalloproteinases, and IL-8 expression in keratinocytes [29,30]. In allergic contact dermatitis, a disease that frequently co-occurs with AD, IL-36 promotes disease, with overexpression of IL-36α, IL-36β, and IL-36γ occurring in areas of active lesions and positive skin patch test results [30,31]. A study exploring lesional AD transcriptomics using RNA sequencing demonstrated increased expression of IL-36 cytokine in AD skin lesions compared to non-lesional skin [32]. Tsoi et al. also found a marked increase in IL-36 in chronic compared to acute AD lesions, suggesting its potential role in the progression from acute to chronic AD in humans. They postulate regarding the potential efficacy of anti-IL-36 treatments for AD but acknowledge that data supporting this hypothesis is lacking [33]. A phase IIa randomized, double-blind, placebo-controlled study of an anti-IL-36 antibody, Spesolimab, failed to produce statistically significant differences in Eczema Area and Severity Index (EASI) scores at Week 16 from baseline compared to placebo [34].
IL-36 expression is also pertinent to HS, with multiple studies demonstrating increased epidermal expression of all IL-36 cytokines in lesional compared to healthy skin [35,36,37]. In the immunohistochemistry and mRNA analysis of IL-36 in lesional HS versus healthy and psoriatic skin, Thomi et al. demonstrated that IL-36α was statistically significantly increased in HS skin versus healthy skin. However, although all IL-36 isomers were elevated in HS skin compared to healthy skin, expressions were significantly lower compared to psoriatic skin, raising questions about the significance of their role in HS and its viability as a therapeutic target [37] (Figure 1). A proof-of-concept, randomized double-blind, placebo-controlled study of Spesolimab for moderate-to-severe HS did not result in a significant difference in the primary endpoint of abscess and nodule (AN) count between Spesolimab treatment and placebo. However, Spesolimab did decrease overall disease severity as measured by other validated tools, including the International Hidradenitis Suppurativa Severity (IHS4), Hidradenitis Suppurativa Area and Severity Index (HASI-R), Hidradenitis Suppurativa Clinical Response (HiSCR50), and draining tunnel count, suggesting future therapeutic potential, especially for patients with multiple draining tunnels [38].
Finally, IL-1 receptor-associated kinase 4 (IRAK4) is also thought to contribute to the shared pathogenesis of HS and AD by acting as a key regulator of our innate immunity [39,40,41,42]. IRAK4 is a part of the complex called the myddosome, whose kinase functions enable the signaling of toll-like receptors (TLR) and interleukin-1 receptors (IL-1Rs), contributing to an inflammatory state [43,44] (Figure 1). Inhibition of IRAK4 has been shown to reverse pathogenic molecular signatures by affecting central mediators of atopic dermatitis, such as IL-4 and IL-13 [45].
Our current understanding of the pathogenesis of HS and AD suggests both are fundamentally inflammatory processes, albeit with distinct pathways. Nevertheless, a few common inflammatory cytokines are found to be pertinent to both diseases, leading to new potential targets for concomitant disease. These current and future therapeutic options are discussed in further detail below.

3. Associations of AD and HS

HS has long been associated with inflammatory pathways involving cytokines like IL-1β, TNFα, IFN-γ, and IL-17/22. However, a recent meta-analysis has challenged the clear distinction between HS and other conditions like atopic dermatitis, suggesting these diseases may share more in common than previously thought [46]. Furthermore, one study pointed to a potential relationship between increased apoptosis of TH1 cells, which are known for producing elevated levels of IFN-γ, and the dominant TH2 immune response typically seen in atopic disorders. This finding hints at overlapping immune mechanisms between these conditions, highlighting the possibility of shared pathways in their pathogenesis [47,48].
Moreover, a bidirectional association between HS and atopic dermatitis (AD) has been observed, suggesting that individuals with HS are at a higher risk of developing AD, and vice versa [49]. A study investigating this relationship found that patients with AD had a 5.57-fold increased odds ratio of having HS compared with those who did not have AD [50]. Another Mendelian randomization study exploring the relationship between AD and HS using genome-wide association data found a causal connection of AD on HS (OR: 1.78, p = 0.006) [51]. Rick et al. discuss their experience observing this trajectory of concomitant AD and HS, with uncontrolled AD featuring prominent xerosis and ichthyosis vulgaris presenting early in childhood and persisting as patients reach early adulthood and develop HS symptoms [52].
Such associations may extend to others in the atopic triad as well, with Kridin et al. reporting 1.4-fold greater odds of HS in patients with a history of asthma in their age, sex, and ethnicity-matched longitudinal study [53]. Interestingly, the inverse relationship of patients with HS developing new-onset asthma was not statistically significant. A case-control study using the All of Us Research Program by Chen et al. further supports such an association between HS and asthma and allergic rhinitis. In their multivariable analysis, HS was significantly associated with allergic rhinitis (OR: 1.68, 95%CI: 1.47–1.92, p < 0.001) and asthma (OR: 1.73, 95%CI: 1.52–1.97, p < 0.001) even after controlling for multiple patient characteristics, including BMI, smoking, eczema, and food allergy [54].
Several hypotheses have been proposed to explain the connection between HS and atopic diseases. One suggests that deficient notch signaling may lead to epidermal barrier defects, resulting in increased inflammation in both conditions, as a disrupted skin barrier can fuel ongoing inflammatory responses. Another theory points to the dysregulation of antimicrobial peptides (AMPs), which may enhance inflammatory activity in both HS and AD. Genetic susceptibility is another potential factor, with shared genetic predispositions potentially connecting the two diseases [50]. Coates et al. in their analysis of HS skin transcriptomics found S100A7A (also known as S100A15, Koebnerisin) to be the most significantly upregulated gene in HS lesional skin [55]. Interestingly, the S100A7A gene has also been found to be upregulated in other skin conditions, including psoriasis and, notably, atopic dermatitis [56,57]. Additionally, alterations in sphingolipid metabolism have been proposed as a mechanism contributing to immune dysregulation in HS [58]. These hypotheses suggest a complex interplay of immune dysregulation, genetic susceptibility, and barrier dysfunction that may underlie the co-occurrence of HS and atopic diseases [59,60,61,62]. However, multiple unanswered questions remain, including (1) if patients with concomitant AD and HS follow a similar disease trajectory as those with standalone disease; (2) if these patients are more likely to have other atopic and follicular diseases; and whether (3) immunomodulation to treat either HS or AD contributes to the pathogenesis of the other [52]. Therefore, further research is necessary to elucidate these shared pathways and to improve therapeutic approaches for individuals affected by these conditions.

4. Current Treatment Landscape of HS and AD

4.1. Atopic Dermatitis

Atopic dermatitis treatment strategies vary depending on the severity and location of the disease, but often start with regular emollients alongside topical treatments such as corticosteroids or calcineurin inhibitors. Recent approvals for topical formulations of the JAK inhibitor ruxolitinib, aryl hydrocarbon receptor agonist tapinarof, and phosphodiesterase-4 antagonist roflumilast have opened up a new variety of non-steroid topical treatment options. Lifestyle adjustments, such as regular bleach baths, may be necessary for moderate-to-severe cases, but are not recommended for mild disease. For widespread disease or topical treatment failures, systemic biologics such as dupilumab (dual inhibitor of IL-4 and IL-13) or tralokinumab (IL-13 inhibitor) should be added [63]. These biologics represented a major step forward in AD management and were followed by the FDA approval of Janus Kinase (JAK) inhibitors upadacitinib and abrocitinib, which are also highly efficacious [64,65]. The IL-31 antagonist nemolizumab was also recently approved for moderate-to-severe AD [66] (Table 1). The 2023 American Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force guidelines recommend against the use of prescription moisturizers or methotrexate/azathioprine, given lower levels of supporting evidence [63].

4.2. Hidradenitis Suppurativa

The current treatment landscape for HS involves a multidisciplinary approach aimed at managing symptoms and improving quality of life. Lifestyle modifications include weight loss, smoking cessation, and managing comorbidities. For mild-to-moderate cases, topical treatments, including antiseptics and antibiotics, are commonly used [67]. In more severe cases, systemic antibiotics are prescribed not only for their antimicrobial properties but also for their anti-inflammatory and immunomodulatory effects. Biologic therapies are increasingly employed for moderate-to-severe HS, targeting specific inflammatory pathways. In advanced cases, surgical interventions may be necessary to remove affected tissue and prevent further complications. This comprehensive approach allows for personalized treatment plans based on disease severity and patient needs [67] (Table 1).
Adalimumab was the first FDA-approved biologic for the treatment of moderate-to-severe HS. It is a fully humanized anti-TNF-α monoclonal antibody that has been shown to reduce the number of abscesses and inflammatory nodules in HS patients [68]. Secukinumab, an IL-17A antagonist, and bimekizumab, an IL-17A/F dual antagonist, were approved for the treatment of HS in 2023 and 2024, respectively [69,70,71,72]. Other biologics with potential benefits from HS treatment include infliximab (a chimeric anti-TNF-α monoclonal antibody), ustekinumab (interleukin-12/23 (IL) receptor antagonist), and anakinra (IL-1 receptor antagonist) [73,74,75] (Table 1).

5. Approach to Treatment of Overlapping HS and AD

For patients with both HS and AD, the goal of current therapeutic research is to identify treatments that may offer the greatest benefit for both conditions. However, it is important to note that comorbid HS and AD is relatively rare, and a single treatment alone may be insufficient to manage both diseases. Despite a paucity of data to support a specific treatment algorithm for concomitant HS and AD, some therapeutic suggestions based on the current literature are provided below.
Corticosteroids may be employed, given the inflammatory nature of both HS and AD; however, different delivery vehicles may have varying levels of efficacy. While topical corticosteroids are commonly used for mild-to-moderate AD, they seemingly have minimal efficacy for HS, likely due to inadequate lesion penetration. Intralesional steroids are commonly employed for HS instead; however, the data regarding their efficacy is mixed. While a few small studies have found intralesional triamcinolone (ILT) to improve patient symptoms and reduce lesion burden in HS, a double-blind, randomized, placebo-controlled trial by Fajgenbaum et al. found no statistically significant difference between varying concentrations of triamcinolone and placebo for the treatment of HS lesions [76,77,78]. Finally, systemic corticosteroids may be employed for recalcitrant HS or AD; however, alternative treatments are preferred given the low certainty of evidence for oral corticosteroid use for AD and concern for systemic side effects with prolonged exposure for HS [79] (Table 1).
Dupilumab, an IL-4/13 inhibitor primarily used for AD, has also shown success in treating HS in a few patients with concomitant HS and AD [48,58,80,81]. However, it is important to note that HS is primarily considered a T1/T17-mediated inflammatory disease, while dupilumab targets T2-mediated inflammation, suggesting dupilumab may not be a long-term treatment option for patients with severe HS and AD (Table 1).
Other small-molecule inhibitors commonly employed for AD, particularly Janus Kinase (JAK) inhibitors such as upadacitinib and abrocitinib, can also be therapeutic for HS and AD. In a randomized clinical trial, upadacitinib was found to be superior in improving AD compared to dupilumab in a head-to-head comparison [82]. The data on upadacitinib for the treatment of HS is less comprehensive, but initial results remain promising. Two open-label, phase II trials of upadacitinib 15/30/60/90 mg once daily versus placebo for HS found moderate efficacy, with an increasing proportion of HS patients achieving HiSCR 50 with increased dose (15 mg: 43%, 30 mg: 56%, 60 mg: 56%, 90 mg: 88%) [83]. However, concerns remain given the small sample size and high percentage of HS patients (70% and 81%) reporting at least one treatment-related adverse effect. A novel JAK inhibitor, povorcitinib, was recently evaluated in a Phase 2b study of 209 subjects with HS randomized to daily doses of 15 mg, 45 mg, 75 mg, or placebo. Treatment arms all showed improved efficacy relative to placebo, and phase 3 trials are currently underway for both povorcitinib and upadacitinib [84]. Smaller, single-center, real-world efficacy studies and case reports also found similar results, suggesting JAK inhibitors as potentially important therapeutic options for concomitant HS and AD [85,86,87,88]. The topical JAK inhibitor ruxolitinib has also been the subject of early clinical trials that suggest it may be effective for patients with mild-to-moderate HS [89] (Table 1).
IL-17 inhibitor biologics such as secukinumab, commonly used for moderate-to-severe HS, have also been minimally investigated for AD, albeit with poor results. A phase 2 randomized, double-blind study by Ungar et al. found minimal improvement with secukinumab, questioning the validity of IL-17 as a therapeutic target for AD [90]. Furthermore, a few case reports suggest IL-17 inhibitors may instead cause an AD-like reaction in some patients with psoriasis [91,92,93]. Hence, the authors recommend against using IL-17 inhibitors for concomitant HS and AD, although further research is needed to validate these findings (Table 1).

6. Future Directions

Multiple other avenues for HS and AD treatment are currently being explored. IRAK-4, important for toll-like receptor and IL-1 receptor signaling, has been implicated in multiple inflammatory conditions and is currently being explored as a therapeutic target with promising initial results. The oral IRAK4 inhibitors zabedosertib and BAY1830839 were found to significantly reduce inflammatory response via reduction in serum TNF-a, IL-6, and IL-8 [94]. An initial double-blind, placebo-controlled phase 1 trial by Ackerman et al. demonstrated excellent tolerability and improvement in skin lesions in both HS and AD, with minimal side effects, making it a future potential therapeutic target [95].
Modification of nutrition also continues to be a topic of interest for the treatment of inflammatory conditions such as AD and HS. The relationship between dietary restriction and AD improvement remains unclear, with data suggesting that severe dietary restrictions, often undertaken by patients with medical advice, do not work and instead may reduce growth in pediatric patients with AD [96]. However, a study by Finch et al. found the incidence of AD in pediatric patients dropped significantly if their mothers received prophylactic administration of prenatal Lactobacillus. Breastfeeding may also have a protective effect against AD [97].
Dietary modifications are also often undertaken by HS patients, although data regarding their efficacy remains limited. A cross-sectional study surveying more than 1400 HS patients found that a diet high in sugars, fat, and alcohol was reported as a common HS flare trigger [98]. Multiple dietary modifications have been proposed, including weight loss, a dairy and brewer’s yeast-free diet, and the addition of zinc and vitamin D supplementation [99]. However, very little evidence and no randomized control trials exist to support these findings; hence, nutrition poses a possible frontier for future personalized medicine research.
The role of gut microbiota in multiple systemic inflammatory conditions is already being evaluated and may present another avenue for future research regarding inflammatory dermatoses. The mechanism behind the gut’s influence on skin disease remains unclear; however, the common coexistence of other inflammatory GI disorders, such as inflammatory bowel disease, with inflammatory skin conditions may provide an initial clue. Furthermore, initial research postulates that high-fat diets may induce HS lesion development by increasing matrix metalloproteinase levels [100]. HS patients were found to have lower levels of Faecalibacterium prausnitzii and increased E. coli, although the effect of this difference on disease progression and severity remains unclear [101,102,103].
The influence of gut microbiome on AD has also been explored minimally, and multiple pathways have been proposed. Dysbiosis of a subspecies of Faecalibacterium prausnitzii was found in the fecal samples of patients with AD [104]. Short-chain fatty acids (SCFAs), thought to be important for epithelial barrier maintenance, were also found at lower levels in AD patient fecal samples. Overall, these dysbioses are thought to cause toxins and harmful gut microbiota to penetrate the epithelial barrier, causing significant Th2-type inflammation [105,106,107]. Regardless of the mechanism of action, personalized medicine focused on changing gut microbiota to address systemic inflammation continues to be an exciting area of future research.

7. Conclusions

In conclusion, HS and AD can be frequently concomitant in dermatology patients, with their associations highlighting shared mechanisms of immune dysregulation, barrier dysfunction, and genetic susceptibility. The overlap between Th1/Th17 inflammation in HS and Th2-driven responses in atopic conditions suggests a complex relationship. While multiple treatment options exist for both, modalities that treat both can be difficult to find but may include JAK inhibitors such as upadacitinib and abrocitinib, and IL-4/13 inhibitors such as dupilumab. The future landscape of treatment of concomitant HS and AD may include IRAK-4 degraders and personalized nutrition and gut microbiota therapy that reduce the inflammatory burden, although significant additional research is needed to validate these potential therapies.

Author Contributions

R.B.S.: Conceptualization, methodology, data curation, writing—original draft, writing—reviewing and editing. H.S.P.: Writing—original draft, writing—reviewing and editing. C.J.S.: Conceptualization, validation, writing—reviewing and editing, supervision, project administration. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

R.B.S. and H.S.P. report no conflicts of interest. C.J.S. reports being an investigator for AbbVie, Astrazeneca, ChemoCentryx, Incyte, InflaRx, Novartis, and UCB Pharma; receiving consultancy fees from AbbVie, Astrazeneca, Alumis, Astrazeneca, InflaRx, Sandoz, Sanofi, Incyte, Logical Images, Sonoma Biotherapeutics, and UCB Pharma; and serving as a speaker for AbbVie and Novartis.

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Figure 1. Key inflammatory cytokines involved in the pathogenesis of Hidradenitis suppurativa and atopic dermatitis with an emphasis on shared pathways.
Figure 1. Key inflammatory cytokines involved in the pathogenesis of Hidradenitis suppurativa and atopic dermatitis with an emphasis on shared pathways.
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Table 1. Available treatment modalities for Hidradenitis suppurativa, atopic dermatitis, and concomitant HS and AD.
Table 1. Available treatment modalities for Hidradenitis suppurativa, atopic dermatitis, and concomitant HS and AD.
TreatmentHidradenitis Suppurativa (HS)Atopic Dermatitis (AD)Both HS and AD
Topical Treatments
Topical corticosteroidsYesYes *Yes
Topical calcineurin inhibitorsNoYes *No
Topical Janus Kinase (JAK) inhibitorsNoYes *Yes
Topical PDE4 inhibitorsNoYes *No
Topical antibioticsYesNoNo
Topical antisepticsYesNoNo
Oral Treatments
Oral antibioticsYesNoNo
Oral JAK inhibitors (Upadacitinib, abrocitinib)YesYes *Yes
Oral corticosteroidsYesYesYes
Injectables and Infusions
Dupilumab (IL-4 and IL-13 antagonist)NoYes *Yes #
Tralokinumab (IL-13 antagonist)NoYes *No
Nemolizumab (IL-31 antagonist)NoYes *No
Adalimumab (anti-TNF-a)Yes *NoNo
Infliximab (anti-TNF-a chimeric antibody)YesNoNo
Secukinumab (IL-17A antagonist)Yes *NoNo
Bimekizumab (IL-17A/F dual antagonist)Yes *NoNo
Ustekinumab (IL-12/23 antagonist)YesNoNo
Anakinra (IL-1 receptor antagonist)YesNoNo
Other Treatments
Allergen ImmunotherapyNoYesNo
Bleach bathsNoYesNo
Surgical interventionYesNoNo
* FDA-approved treatments. # Treatment recommendations found to be efficacious for both HS and AD are primarily based on case reports, case series, or small studies. No established clinical guidelines exist for single modality treatments that can improve the treatment of both HS and AD simultaneously.
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Shams, R.B.; Patel, H.S.; Sayed, C.J. Associations of Hidradenitis Suppurativa with Atopic Dermatitis: A Review of Shared Pathogenesis and Approach to Treatment of Concomitant Disease. Allergies 2025, 5, 20. https://doi.org/10.3390/allergies5020020

AMA Style

Shams RB, Patel HS, Sayed CJ. Associations of Hidradenitis Suppurativa with Atopic Dermatitis: A Review of Shared Pathogenesis and Approach to Treatment of Concomitant Disease. Allergies. 2025; 5(2):20. https://doi.org/10.3390/allergies5020020

Chicago/Turabian Style

Shams, Rayad B., Hiral S. Patel, and Christopher J. Sayed. 2025. "Associations of Hidradenitis Suppurativa with Atopic Dermatitis: A Review of Shared Pathogenesis and Approach to Treatment of Concomitant Disease" Allergies 5, no. 2: 20. https://doi.org/10.3390/allergies5020020

APA Style

Shams, R. B., Patel, H. S., & Sayed, C. J. (2025). Associations of Hidradenitis Suppurativa with Atopic Dermatitis: A Review of Shared Pathogenesis and Approach to Treatment of Concomitant Disease. Allergies, 5(2), 20. https://doi.org/10.3390/allergies5020020

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