JAK Inhibitors in Hidradenitis Suppurativa: A Systematic Review 

Hidradenitis suppurativa (HS) is a chronic, disfiguring, debilitating, inflammatory disorder that is characterized by inflammatory nodules, abscesses, fistulae/sinus tracts, and scarring to the axilla, inframammary folds, and groin.¹ The typical onset of HS is around puberty with recurrence of the disease that is lifelong. There are multiple long-term effects of HS, including contractures, increased risk of squamous cell carcinoma, and significant scarring.² The pathogenesis has yet to be completely elucidated but is centered around the apocrine glands and pilosebaceous units with follicular occlusion and dilation, rupture of the hair follicle with formation of nodules and abscesses, and chronic state with sinus tract formation and scarring.³

In spite of topical washes/antibiotics, systemic antibiotics, biologics, hormonal therapies, surgery, and lifestyle modifications, effective treatment of HS continues to prove difficult among practitioners. Most treatments remain anecdotal, based on expert consensus, or derived from limited case reports/series.³ Current evidence suggests altered levels of pro-inflammatory cytokines—specifically, tumor necrosis factor (TNF)-α, interleukin (IL)-17, IL-12, IL-23, and IL-36—play an important role in the disease process.^1,4 Adalimumab and secukinumab are FDA-approved biologics for HS and offered great strides in an exciting direction. Unfortunately, their effectiveness varies as many patients require additional or alternative treatments. This variability stresses the need for innovative therapies that can more effectively manage HS. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway offers a prime therapeutic target as it plays a pivotal role in cytokine signaling and immune response regulation. JAK inhibitors modulate this pathway, offering a seminal approach to disrupting the HS pathophysiology. This review examines the efficacy and safety of JAK inhibitors in HS treatment, exploring their role as a potential transformative therapy for this challenging condition.

Literature Search Strategy

This systematic review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.⁵ and was registered with the PROSPERO registry. We conducted a comprehensive search for articles on JAK inhibitors in HS across PubMed, Ovid, Cochrane Library, and Google Scholar databases from inception to May 2024. The search terms included combinations of “hidradenitis suppurativa,” “acne inversa,” “JAK inhibitors,” “Janus kinase inhibitors,” “tofacitinib,” “ruxolitinib,” “upadacitinib,” “abrocitinib,” “baricitinib,” “filgotinib,” and “povorcitinib.” 

Two independent reviewers (NC, TH) performed screening, citation searching, and data extraction. Items extracted included: first author’s name; year of study; study type; Hurley stage; number of patients; evaluation of the progression of HS symptoms; JAK inhibitor used; dosage of JAK inhibitor; time between the initiation of JAK inhibitor therapy and clinical improvement; duration of JAK inhibitor therapy; all adverse events; treatment groups; and clinically relevant patient history. Missing or incomplete values were excluded from the qualitative analysis. Studies were included if they met the following criteria: (1) evaluated the use of JAK inhibitors in patients diagnosed with HS; (2) were classified as case reports, clinical trials, proof-of-concept studies, or cohort studies (both retrospective and prospective). Exclusion criteria were: (1) articles not published in English; (2) editorials and opinion pieces; and (3) studies that did not focus on HS or did not assess the outcomes of JAK inhibitor treatment. Discrepancies were resolved by the senior author (CH). Publications were graded according to the Oxford Centre for Evidence-Based Medicine 2009 Levels of Evidence: (A) randomized controlled trials or retrospective studies and (B) case reports or case series.⁶ Rayyan (Boston, MA) was used for screening and deduplication.⁷

Literature Analysis Results

The systematic search yielded a total of 10 publications, involving 344 patients treated with JAK inhibitors, all of which were included in this systematic review after full-text screening (Figure). The study selection comprised 4 case reports, 2 case series, 2 clinical trials, 2 proof-of-concept studies, and 1 retrospective cohort study focusing on the use of various JAK inhibitors in the treatment of HS.

Figure. PRISMA flow diagram.

The breakdown of studies by therapeutic agent is as follows—abrocitinib: 1 case report; baricitinib: 1 case report; tofacitinib: 1 case report, 2 case series; upadacitinib: 1 retrospective cohort analysis, 1 clinical trial, 1 case report; and povorcitinib: 2 proof-of-concept studies, 1 clinical trial.

The primary endpoint utilized in the assessment of these studies was clinical improvement in HS symptomology. The studies involving povorcitinib and upadacitinib were objectively measured with the Hidradenitis Suppurativa Clinical Response (HiSCR). HiSCR is a widely accepted clinical endpoint in HS trials, requiring at least a 50% reduction in the total abscess and inflammatory nodule (AN) count with no increase in the number of abscesses or draining fistulas.

Among the combined 344 total patients treated with JAK inhibitors across all studies included in this review, symptom alleviation was reported in 48% of patients (n = 165/344), treatment emergent adverse events were observed in 43% of patients (n = 150/344), and serious adverse events were described in 2.6% of patients (n = 9/344). Adverse events varied among patients receiving different JAK inhibitors and are discussed in their respective sections below. 

Abrocitinib

Abrocitinib (Cibinqo) is an oral selective JAK1 inhibitor recently approved by the US Food and Drug Administration (FDA) for treating atopic dermatitis (AD) in patients 12 years and older.⁸ It has shown promise in off-label treatments for other dermatologic conditions, such as alopecia areata (AA) and lichen sclerosis.^9,10

There is currently only one case report documenting the use of abrocitinib for refractory HS. This case involved a 17-year-old male with a multi-year history of recurrent axillary abscesses, unresponsive to various treatments, including glucocorticoids, doxycycline, retinoic acid, cyclosporine, and methotrexate. Surgical intervention was initially recommended but failed to prevent lesion recurrence. Histopathological examination confirmed the diagnosis of HS. The patient was subsequently treated with abrocitinib 100 mg daily, in combination with doxycycline 100 mg twice daily. After 2 weeks, significant reductions in pain and lesion size were observed, allowing for the discontinuation of doxycycline. Continued improvement was noted over the following weeks, with near-complete clearance of lesions at 6 weeks. The dosage of abrocitinib was then reduced to 100 mg every 2 days, maintaining lesion-free status within 10 weeks.¹¹ 

This single case report suggests that abrocitinib may be beneficial in managing refractory HS. However, the evidence is limited to one patient, and the improvement observed might be attributed partially to the initial combination therapy with doxycycline. More extensive longitudinal studies are required to confirm the efficacy and safety of abrocitinib in HS. Additionally, it is essential to consider whether the observed remission could be a temporary response to the concurrent doxycycline treatment rather than solely due to abrocitinib. Future research should focus on larger cohorts and lengthier follow-up periods to ascertain the long-term outcomes and potential adverse effects of abrocitinib in HS patients. Exploration of the underlying mechanisms by which abrocitinib exerts its effects on HS is vital to better understand its role in the therapy of this difficult-to-treat condition.

Baricitinib

Baricitinib (Olumiant) is an oral, selective, reversible inhibitor of JAK1 and JAK2, with a high affinity for these kinases, over 100-fold greater than for JAK3.¹² It is FDA-approved for the treatment of rheumatoid arthritis and AA.^12,13 Current off-label uses include psoriatic arthritis, vitiligo, and severe AD.¹² During the COVID-19 pandemic, it received emergency use authorization for combination therapy with remdesivir. It was then reauthorized to become the first solitary approved treatment for COVID-19.^14,15

There is currently one case report by Olbrich et al. documenting the treatment of HS with baricitinib. In this case, a patient with an autosomal dominant gain-of-function (GOF) mutation in the signal transducer and activator of transcription 1 (STAT1) with HS was treated with baricitinib after failure of treatment with immunosuppressant agents including infliximab, adalimumab, and azathioprine, among others. The patient also had chronic mucocutaneous candidiasis (CMC) and oral ulcers associated with the STAT1 mutation. Following the discovery of the mutation, treatment was initiated with baricitinib 2 mg daily in combination with itraconazole. The dose was subsequently increased to baricitinib 4 mg due to persistent symptoms. This regimen led to a decrease in the frequency of CMC, resolution of oral ulcers, and cessation of HS episodes. Upon discontinuation of baricitinib, both oral candidiasis and HS symptoms reappeared within 1 month. These pathologies resolved once again following the resumption of baricitinib.¹⁶

This case report suggests that baricitinib may be effective for HS, particularly in patients with specific genetic mutations similar to STAT1 GOF as this may influence their response to treatment. The unique genetic background of the patient could have played a substantial role in the treatment outcome, restricting the application of these results to a broader population. The co-administration of itraconazole likely addressed the fungal component of the patient’s condition, but the sustained remission of HS symptoms implies a potential role for baricitinib in the management of HS. As the data are limited to a single case report, these findings cannot be generalized without further research. Future studies should investigate the efficacy of baricitinib in a larger cohort of HS patients controlled for genetic mutations to better understand its potential benefits and risks. The potential interactions between baricitinib and other concomitant treatments (ie, itraconazole) need further exploration to delineate their individual contributions to the clinical outcome observed. Management of HS with baricitinib should be approached with caution, and patients should be monitored closely for any adverse effects or recurrence of symptoms upon discontinuation.

Tofacitinib

Tofacitinib (Xeljanz) is an oral immunosuppressant that is a specific inhibitor of the JAK pathway. This synthetic small molecule therapeutic agent displays high selectivity for JAK3 and also interacts with JAK1 and JAK2, though to a lesser extent.¹⁷ Tofacitinib is approved for the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis, and polyarticular juvenile idiopathic arthritis.¹⁸ Tofacitinib has additionally demonstrated efficacy in treating several dermatologic conditions off-label. There are no published controlled trials evaluating the use of tofacitinib for HS. The available data are currently limited to the following case reports.

The first case involves a 40-year-old male with an extensive history of HS unresponsive to adalimumab and systemic antibiotics who was treated with tofacitinib 5 mg twice daily. His comorbidities included tobacco use and obesity. He exhibited clinically stable disease with reduced inflammation, pain, and discharge after 36 weeks of treatment, but upon contracting COVID-19 and temporarily discontinuing tofacitinib, the patient was unable to recapture the initial therapeutic effect after resuming the medication. No side effects, aside from the COVID-19 infection, were reported.¹⁹

A second case describes a 16-year-old male with Hurley stage III axillary disease unresponsive to systemic antibiotics for 2 years who was started on tofacitinib 5 mg twice daily in combination with finasteride 1 mg daily. He showed a 90% improvement in signs and symptoms by the third month. Of note, elevated AST and ALT on liver function tests (LFTs) necessitated dose adjustments. His dose was initially decreased to 5 mg daily but the transaminitis remained unresolved. Dose adjustments eventually stabilized at 5 mg every other day, resulting in normalization of LFTs and maintained clinical improvement of HS symptomology at 6 months.¹⁹

In a third case, a 26-year-old male with a decade-long history of Hurley stage III HS initially treated with infliximab and amoxicillin was transitioned to tofacitinib 5 mg twice daily, cyclosporine at ~5 mg/kg, and amoxicillin 500 mg twice daily. At 4-month follow-up, he reported healing lesions, decreased pain, and drainage. His continued improvement at 8-month follow-up resulted in the decision to taper off cyclosporine. After 11 months of therapy, the patient achieved remission. Self-discontinuation at 12 months precipitated modest disease recurrence, but subsequent re-initiation of tofacitinib once again resulted in remission. No adverse effects were reported.²⁰

The fourth case involves a 23-year-old female with morbid obesity and a several-year history of HS that required multiple hospitalizations who was started on tofacitinib 5 mg twice daily alongside mycophenolate mofetil 1250 mg daily, topical triamcinolone ointment, and antibiotic cycles of amoxicillin-clavulanate and azithromycin. Over 3 years, she showed gradual disease improvement and normalization of hematologic abnormalities—specifically leukocytosis, thrombocytosis, and anemia. She experienced a localized herpes zoster infection after 3 years of treatment that required inpatient care.²⁰

Paradoxical development of HS has been reported, particularly with TNF-α inhibitors.²¹ Emerging evidence also suggests that IL-17 inhibitors such as secukinumab and IL-12/23 inhibitors such as ustekinumab may induce paradoxical HS.^22,23 Notably, one case has demonstrated paradoxical development of HS with tofacitinib. A 52-year-old woman with juvenile rheumatoid arthritis in which treatment with etanercept failed was administered tofacitinib. She subsequently developed axillary nodules and abscesses consistent with HS on biopsy. The HS resolved upon discontinuation of tofacitinib and did not recur after re-initiation.²⁴

An ongoing clinical trial is evaluating the use of tofacitinib in patients with Down syndrome as this genetic condition often manifests with several immune-related skin conditions secondary to inherent immune dysregulation. This study aims to assess the safety and efficacy of tofacitinib in inhibiting interferon signaling in various dermatologic conditions, including moderate-to-severe HS. The results of this trial have not yet been posted.²⁵

These reports highlight the potential of tofacitinib in safely managing refractory HS, though the efficacy seen in these cases may be influenced by the use of concomitant therapies such as finasteride, antibiotics, and cyclosporine. The observed adverse effects—particularly, elevated LFTs and hematologic abnormalities—underscore the necessity of monitoring lab work in patients taking tofacitinib. The transient loss of efficacy post-COVID-19 infection in one patient suggests the need for further investigation into the stability of the therapeutic effects tofacitinib exhibits under different clinical conditions. The single instances of a COVID-19 and a herpes zoster infection reported emphasize the importance of attentiveness for opportunistic infections during prolonged therapy. A potential risk of paradoxical HS likely connected to altered cytokine levels exists with tofacitinib and clinicians should exercise caution and monitor for worsening HS in patients utilizing this medication. The data on tofacitinib for HS are limited to case reports, only one of which follows the patient for 3 years. Controlled clinical trials to definitively establish both efficacy and a safety profile are a required next step. Further research should aim to isolate the effects of tofacitinib from other treatments and explore its long-term safety in larger patient cohorts. An additional understanding of the mechanisms underlying the clinical improvements observed in HS symptoms could help refine patient selection and optimize treatment protocols.

Upadacitinib

Upadacitinib (Rinvoq) is a second-generation JAK inhibitor that is most selective for JAK1 but also exhibits a weaker influence on JAK2, JAK3, and tyrosine kinase 2 (TYK2).^26,27 It is FDA-approved for a variety of indications such as atopic dermatitis, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis, Crohn’s disease, and non-radiographic axial spondyloarthritis. This medication is available as an extended-release tablet in 15-mg, 30-mg, and 45-mg dosages.^28,29 Building upon the hypothesized role of upadacitinib in HS therapy outlined in previous case reports, recent retrospective analyses and clinical trials offer a more powerful investigation.

In a retrospective cohort analysis of patients with moderate to severe HS, 20 patients were treated with upadacitinib monotherapy. Patients initially received 15 mg daily and were escalated to 30 mg daily at Week 4 in non-responders. HiSCR50 was achieved by 75% of patients by Week 4 and 100% of patients by Week 12, with continued maintenance at 100% through Week 24. HiSCR75 and HiSCR90 rates also improved over time. HiSCR75 was achieved in six patients at Week 4 and 19 at Week 12. HiSCR90 was achieved in four patients at Week 4 and in six patients at Week 12. These results were maintained at Week 24. Pain rating, severity scores, and quality of life indices all showed significant reductions during therapy. Adverse events included flares in 20%, VZV reactivation in 5%, transient transaminitis in 10%, and elevated creatine kinase (CK) levels in 80%, though none exhibited musculoskeletal symptoms or myoglobinuria. The relatively small sample size limits the generalizability of these findings.³⁰

A Phase 2 randomized, placebo-controlled study evaluated the efficacy and safety of upadacitinib in moderate-to-severe HS. Patients were randomized 2:1 to receive 30 mg once daily or placebo for 12 weeks. Placebo patients were then switched to 15 mg until Week 48. At Week 12, 38.3% of upadacitinib-treated patients achieved a ≥50% reduction in abscess and nodule count compared to 25% in the placebo group. 36.4% of patients treated with upadacitinib achieved a reduction of at least 30% and a reduction of at least one unit in the Patient’s Global Assessment of Skin Pain compared to 22.5% from the historical placebo rates derived from adalimumab studies. The long-term efficacy of upadacitinib was demonstrated through maintenance of HiSCR evaluations and pain reduction, measured via the Numeric Rating Scale (NRS30), through 40 weeks. Of note, upadacitinib was particularly effective among patients unresponsive to treatment with TNF-α inhibitors. The medication was well tolerated, with no MACE, VTE, or lab abnormalities reported and only one adverse event of worsening HS that led to discontinuation. One prostate cancer case was reported, although causality with upadacitinib is questionable.³¹ AbbVie has initiated Phase 3 trials for upadacitinib in HS patients aged 12 years and older, specifically targeting those who have failed anti-TNF therapy. The “Step-Up HS” trial is a double-blind, randomized, placebo-controlled study evaluating safety and efficacy. Results are anticipated by 2027.³²

A 2023 case report showcases the first instance of a severe adverse event related to upadacitinib use. A 34-year-old male with Crohn’s disease, rheumatoid arthritis, and Hurley stage III HS refractory to antibiotics, steroids, adalimumab, infliximab, anakinra, ustekinumab, and certolizumab pegol was started on upadacitinib 30 mg daily. Five weeks later, he developed a severe varicella zoster infection, sepsis, pneumonia, and generalized seizures. Further work-up and imaging revealed hyperferritinemia, splenomegaly, and hemophagocytosis in the bone marrow, leading to a diagnosis of secondary hemophagocytic lymphohistiocytosis (HLH) associated with his VZV infection. The condition improved with the discontinuation of upadacitinib, antivirals, IV immunoglobulins, and high-dose steroids. It was suspected that upadacitinib-induced immunosuppression predisposed the patient to the VZV infection, which led to VZV encephalitis, pneumonia, and secondary HLH.³³

The retrospective cohort study demonstrated that upadacitinib monotherapy with doses up to 30 mg safely induces clinical improvement in HS patients with Hurley Stage III disease. Although elevated CK levels were noted, all patients remained asymptomatic, suggesting minimal clinical significance. The Phase 2 trial supports the efficacy of upadacitinib in safely reducing HS symptoms. The favorable results showcase an improved patient quality of life in addition to a novel approach to ameliorate the suffering of patients unresponsive to TNF-α inhibitors. Despite mostly promising results, the case report highlights the risk of severe infections and HLH with upadacitinib, particularly in immunocompromised patients. The development of such complications emphasizes the need for careful patient selection and monitoring for herpes zoster complications following the initiation of upadacitinib.

Upadacitinib shows great potential as an effective treatment for HS, with multiple studies demonstrating significant improvements in clinical outcomes and quality of life. Although rare, regular monitoring and patient education about potential risks are warranted. Further outcomes on long-term safety and efficacy will soon be available through current ongoing clinical trials. Future studies should be dedicated to more prominent and more representative populations to confirm these findings and better define dosing strategies. Understanding the mechanisms of the effects that upadacitinib exerts to alleviate disease in HS will also offer crucial insight into optimizing treatment strategies and reducing adverse outcomes.

Povorcitinib

Povorcitinib is an oral, small-molecule JAK inhibitor. It has an approximately 52-fold greater selectivity for JAK1 over JAK2.³⁴ This medication is currently undergoing clinical trials for the treatment of HS in patients with moderate-to-severe disease and vitiligo.^34,35 Two proof-of-concept studies in Phase 2 were conducted in which patients were given either medication or placebo for 8 weeks and then followed for 4 weeks afterward for safety monitoring. HiSCR, a reduction in inflammatory lesion counts, safety, and patient-reported outcomes were the endpoints utilized in these studies.³⁴

In the first proof-of-concept study, 10 patients received povorcitinib 15 mg once daily. By week 8, three patients achieved HiSCR and 43% of patients experienced a ≥50% reduction in inflammatory lesion count. This increased to 57% by the end of follow-up 4 weeks later. No serious treatment-emergent adverse effects were reported, but 70% of the patients had at least one treatment emergent-adverse effect—most commonly an upper respiratory infection. Laboratory values remained within normal limits, and patients reported improvement in skin condition from baseline.³⁴

The second proof-of-concept study involved 35 patients randomized to receive a placebo or povorcitinib at doses of 30 mg, 60 mg, or 90 mg. By Week 8, 17 patients receiving povorcitinib achieved HiSCR compared to four patients receiving a placebo. Roughly half of the patients treated with povorcitinib experienced a ≥50% reduction in inflammatory lesions at Week 8, compared to 28% in the placebo group. A dose-dependent improvement in lesion counts was observed within the treatment group. During follow-up, there was a trend back towards baseline for some patients. 81% of the patients had at least one treatment-emergent adverse effect with the most common being fatigue and headache. Of note, only the 90-mg dose was correlated with thrombocytopenia. However, these patients had lower platelet counts at baseline in comparison to the other patients in this study. Echoing the results of the first study, patients in the treatment group of this study also reported improvement in their skin condition from baseline.³⁴ 

A Phase 2 randomized, double-blind, dose-ranging, placebo-controlled study evaluated the efficacy and safety of povorcitinib at doses of 15 mg, 45 mg, and 75 mg over 16 weeks. Prior treatment in these patients included oral antibiotics, adalimumab, and other biologics. Of the 209 randomized patients, 207 were treated and 174 completed the trial. Significant reductions in abscess and inflammatory nodule counts were observed, with the greatest improvement at the 45-mg dose. Greater HiSCR achievement was found in the povorcitinib groups compared to placebo, with higher doses offering a superior benefit. Patients also reported improvements in skin pain and quality of life, especially at higher doses. Common adverse effects included fatigue, headache, diarrhea, nausea, and upper respiratory infections, which were comparable to placebo. Acne was more frequent in povorcitinib-treated patients. Elevated CK was a noted laboratory abnormality, but no myositis or rhabdomyolysis symptoms were observed. Other lab abnormalities were extremely rare in the study but included elevations in AST/ALT, decreased platelet counts <100x109/L, and decreased neutrophil counts. Five serious adverse effects occurred in these patients: one patient on 15 mg suffered from a fall with rib fracture, another on 15 mg developed a pulmonary embolus and pneumonia—though pre-existing risk factors are thought to have contributed—and one patient on 45 mg developed a herniated disc.³⁶ 

Both proof-of-concept studies demonstrated the efficacy of povorcitinib in reducing HS symptoms, with significant improvements in lesion counts and patient-reported outcomes. The safety profile was generally favorable, with no serious adverse effects reported. However, the studies were limited by small sample sizes and short treatment durations, underscoring the need for larger, longer-term studies to confirm these findings. Notably, proteomic analysis showed little to no changes in TNF-α but did show decreases in IL-2 receptor alpha. The Phase 2 trial further supports the use of povorcitinib in treating HS, with significant and rapid clinical improvements observed in pruritis and skin pain—most prominent in the 45-mg and 75-mg dosages. It was generally well tolerated across all doses with no apparent relationship between adverse effects and increased dosages.  

Povorcitinib shows promise as a treatment for moderate-to-severe HS, with multiple studies indicating its potential to quickly reduce inflammatory lesion counts and improve patient-reported outcomes. The adverse effects observed were generally manageable, but further research is needed to establish long-term safety and efficacy. Larger, more diverse patient populations and extended follow-up periods are essential to validate these preliminary findings and refine the therapeutic protocols for povorcitinib in HS. Future studies on this medication should also explore the underlying mechanism contributing most directly to HS alleviation to better understand its role in the disease’s pathophysiology and optimize its use in clinical practice.

Conclusions

In conclusion, our review supports the auspicious emergence of JAK inhibitors as a viable treatment option for HS, particularly in patients who are refractory to conventional therapies. As with all pharmacologic therapies, it remains crucial to acknowledge that these medications come with their associated risks. With the exception of the singular instance of a pulmonary embolism in a patient with pre-existing risk factors in the povorcitinib trial, it is noteworthy that no venous thromboembolism (VTE) or major adverse cardiovascular events (MACE) were reported in the reviewed studies. Despite this, careful observance remains necessary in the exploration of any novel therapeutic agent. 

Due to the limitations of study design and publication bias, controlled clinical trials with larger sample sizes are a necessary next step in validating these preliminary findings and establishing the long-term safety and efficacy of JAK inhibitors in HS. Investigations should also focus on understanding the mechanisms these inhibitors use to control HS as this could help refine patient selection criteria and optimize treatment protocols. If established as a standard-of-care therapy, clinical trials that directly compare these medications would offer immense insight into HS management.

JAK inhibitors offer a promising new therapeutic avenue for HS and the potential to significantly improve patient outcomes, but their use must be guided by rigorous clinical evidence and close monitoring to ensure patient safety and maximize therapeutic benefits. As research progresses, these agents may become integral components of HS management, offering amelioration to patients suffering from this challenging condition. 

Disclosure: The authors declare that there is no conflict of interest regarding the publication of this paper. No funding was received to assist with the preparation of this manuscript.

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Nicholas J. Culotta, MD

• Department of Dermatology, Louisiana State University Health Sciences Center, New Orleans

Tyler D. Hernandez, BS

• Department of Dermatology, Louisiana State University Health Sciences Center, New Orleans

Christopher J. Haas, MD

• Department of Dermatology, Louisiana State University