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 Table of Contents  
Year : 2022  |  Volume : 6  |  Issue : 2  |  Page : 88-96

Hidradenitis suppurativa: A review of available immunotherapeutic agents and advancement in treatment

1 University of Alabama at Birmingham School of Medicine, Birmingham, USA
2 Department of Dermatology, School of Medicine, University of Alabama at Birmingham, AL, USA

Date of Submission05-Aug-2021
Date of Decision14-Jan-2022
Date of Acceptance26-Jan-2022
Date of Web Publication26-Aug-2022

Correspondence Address:
Nabiha Yusuf
1670, University Boulevard, VH 566A, Birmingham, Alabama
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cdr.cdr_53_21

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Hidradenitis suppurativa (HS) is a chronic, inflammatory skin condition that poses a significant diagnostic, as well as therapeutic, challenge for clinicians. The purpose of this review is to explore current treatment guidelines, as well as the newer, investigative immunotherapies, used in the management of HS. Through a detailed, albeit nonexhaustive, literature review, the most-recently published management guidelines and clinical trials concerning HS therapy were identified and their implication in current and future disease management was explored. An understanding of available treatment options, and what lies on the horizon, is important as researchers and clinicians work toward better understanding this unique disease.

Keywords: Hidradenitis suppurativa, immunotherapeutic, treatment

How to cite this article:
Preda-Naumescu A, Sowell J, Ahmed HN, Mayo TT, Yusuf N. Hidradenitis suppurativa: A review of available immunotherapeutic agents and advancement in treatment. Clin Dermatol Rev 2022;6:88-96

How to cite this URL:
Preda-Naumescu A, Sowell J, Ahmed HN, Mayo TT, Yusuf N. Hidradenitis suppurativa: A review of available immunotherapeutic agents and advancement in treatment. Clin Dermatol Rev [serial online] 2022 [cited 2023 Jan 30];6:88-96. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/2/88/354757

  Introduction Top

Hidradenitis suppurativa (HS) is a chronic, recurring inflammatory disorder of the skin that may present initially as subcutaneous nodules before progressing to nonhealing abscesses.[1] HS affects apocrine gland-bearing skin of the axillae, perineum, and inframammary regions.[1] Often, flares of HS are accompanied by severe pain and suppuration at intervals. These flares recur in cycles of remission and relapse, increasing in severity with continued lack of treatment.[1] With untreated progression of the disease, the abscesses and deep, painful lesions characteristic of HS often form into draining sinus tracts. These tracts, through dermal fibrosis and healing processes, lead to deformation and contracture of the overlying skin.[1]

Research shows that HS is more common than previously thought, with an estimated population prevalence ranging from 1% to 4%.[2] Misdiagnosis and lack of accurate population data further obfuscate the correct estimation of HS occurrence.[3]

HS often develops after puberty, with most patients first developing symptoms in their 20s and 30s. There exists a female predominance in distribution of cases.[4] HS was historically considered a bacterial or inflammatory process of the apocrine glands, but recent data have led to a better understanding of the pathogenesis of HS as arising from follicular occlusion.[1] Follicular occlusion leads to rupture of the hair follicles and dermal inflammation that serves as the basis of continued disease.[1] The draining sinus tracts resulting from rupture of the follicular infundibulum and subsequent dermal inflammation often lead to bacterial infiltration and infection secondary to the initial disease.[4]

Diagnosis of HS poses a clinical challenge, as there exists wide variation in clinical appearance of disease with variability in response to treatment. As a result, diagnostic criteria and various disease severity assessment tools were created to better inform management options. The first severity assessment tool, the Hurley scoring system [Table 1], was created in 1989 for surgical approaches to the disease.[5] By placing patients into three stages of disease severity based on the presence of sinus tracts and scarring, the Hurley system gives clinicians an appropriate understanding of disease management.[5] In general, Stage I patients are considered manageable with medical therapy while, classically, Stage II patients required local surgery, and Stage III patients were considered for wide surgical excision of the entire affected region.[5] Although simple and very commonly used, the Hurley scoring system is not quantitative and fails to evolve with the patient's disease. As such, other scoring systems have been developed. For the sake of this review, we will refer only to the Hurley system.
Table 1: Hurley classification system

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  Current Treatment Guidelines Top

Treatment for HS has long posed a challenge for clinicians due to the multifactorial and poorly understood pathogenesis of the disease. A current treatment guideline, the European S1 guideline, was established by a group of experts in 2015 in hopes of providing an adequate treatment algorithm for providers to follow.[6],[7] Per their recommendations, treatment should be aggressive, initiated early in the disease course, and include:

  • 1% topical clindamycin
  • Systemic antibiotics (including tetracycline or clindamycin and rifampicin combination)
  • Retinoids
  • Hormone therapy.

Since the publication of the 2015 guidelines, several other HS treatment guidelines have been developed. A 2019 review conducted by Hendricks et al. sought to combine the published guidelines for HS treatment and compare international management recommendations to see if providers were in agreement concerning first-line therapies.[8],[9] A 2021 review by Shi et al. sought to amalgamate and compare the recent international HS guidelines on treatment modalities to prevent confusion and overlap in treatment recommendations.[9] Findings showed that there was generally a consensus on the first-line treatment agents, with significant variability in the second- and third-line treatment agents.[8],[9] First-line treatment options recommended across guidelines are outlined in [Table 2]a.[7],[8],[9] An overview of available treatment options is found in [Table 2]b.[7],[8],[9]
Table 2:

Click here to view

While antibiotics are at the forefront of the recommendations, large-scale randomized controlled trials evaluating their efficacy are scarce.[9] On the other hand, considerable research has been, and is being, conducted concerning the use of biologics as treatment options. While these novel therapeutic agents were recommended by several guidelines Hendricks et al. reviewed, there remains a lack of consensus regarding their use. As the use of adalimumab (ADA), a biologic agent, as a first-line therapeutic agent in the treatment of HS is now widely adopted, the efficacy of other biologic agents in the treatment of HS has begun to be explored. This review seeks to explore the nonbiologic and biologic treatment options for HS in hopes of helping clinicians make informed decisions on available and efficacious treatment options.

  Nonbiologic Therapies Top

Clindamycin and rifampicin combination therapy

With the exception of topical clindamycin and systemic tetracyclines, the efficacy of nonbiologic treatment options for HS is largely derived from case reports or expert opinion, including the European S1 guidelines.[1] Evidence-based literature concerning antibiotic use in HS is mostly based on retrospective research, and in 2019, in order to develop international consensus guidelines for the treatment and management of these patients, the HS ALLIANCE working group screened over 5310 articles to derive treatment recommendations. Of these, 171 were included in data analysis and 65 were used to derive treatment recommendations.[10] In line with their systematic review, topical clindamycin 1%, a lincosamide antibiotic with broad-spectrum antibacterial coverage, was shown to be a viable therapy option for early-stage HS (Hurley Stage I) – especially in the absence of deep inflammatory abscesses.[10] However, the possibility of clindamycin resistance must be considered, and the efficacy has been called into question by physicians treating patients with Hurley Stage II disease [Table 1]. In addition to topical clindamycin and systemic tetracyclines, the most researched treatment for HS is a combination of systemic clindamycin and rifampicin.[10]

Rifampicin, a widely used antibiotic in the treatment of mycobacterial infections, derives its antibacterial activity from inhibition of bacterial RNA polymerase.[11] Bacterial resistance is common, and clindamycin is often used in conjunction to avoid perpetuating this pitfall.[11] In addition to antibacterial effects, both clindamycin and rifampicin exert immunomodulatory and anti-inflammatory effects. Rifampicin alters cytokine production in monocytes, effectively inhibiting the secretion of interleukin-1B (IL-1B), tumor necrosis factor alpha (TNF -α), IL-6, and IL-10. As these cytokines have been found to be elevated to varying degrees in HS lesional skin, the benefit of combination therapy with rifampicin and clindamycin has been subject of several studies as treatment for HS.[10],[11],[12],[13] In patients with severe active lesions and Hurley II/III disease, systemic clindamycin and rifampicin (dosage: 300 mg twice daily) may be administered for an average length of 10 weeks.[10],[11],[12],[13],[14]


Ertapenem, an intravenous beta-lactam antibiotic that treats complicated skin and soft-tissue infections, has been used as an off-label treatment option for refractory HS.[15] Its antimicrobial spectrum covers the complex microflora of HS lesions, including anaerobes and anaerobic actinomycetes.[15] In selected patients with severe HS, who have failed prior therapeutic options and who are not surgical candidates, a 6-week course of intravenous ertapenem (1 g daily) may be considered.[10],[15] A retrospective chart review seeking to evaluate the efficacy of ertapenem in HS has demonstrated dramatic improvement in both clinical and laboratory markers of HS disease severity, supporting the utility of IV ertapenem as a treatment option.[16] However, while ertapenem has been shown to dramatically improve severe HS, a retrospective chart review of patients at the Montefiore/Einstein HS Treatment Center showed rapid relapse of disease within 1 month of ertapenem withdraw.[10],[17] As such, consolidation therapy consisting of rifampicin/moxifloxacin/metronidazole is recommended.[10],[15],[17]


Apremilast is an orally administered small molecule that specifically inhibits phosphodiesterase-4 and modulates expression of pro-inflammatory and anti-inflammatory mediators.[18] As several inflammatory cell types are shown to be involved in HS, apremilast has theoretical benefit in managing the disease state.[18] Findings from a double-blind randomized placebo-controlled trial (RCT) including 21 patients, of whom 20 received at least 1 dose of study medication, demonstrated clinically meaningful improvement of moderate HS (Hurley Stage I/II) after a treatment dose of 30 mg twice daily for 16 weeks.[18] The primary outcome was the percentage of patients reaching the Hidradenitis Suppurativa Clinical Response (HiSCR) at week 16, which was defined as at least a 50% reduction in total abscess and inflammatory nodule count, with no increase in abscess count and no increase in draining sinus count relative to baseline.[18] The HS clinical response was met in 8 of 15 patients in the apremilast group (53.3%) and none of 5 patients in the placebo group (0%).[18]

Initial responders continued treatment following completion of the RCT and, at 2-year follow-up, all patients still receiving the medication (4/8) achieved HiSCR compared with baseline.[19] As such, apremilast is a potential long-term treatment option in HS, with prolonged clinical efficacy at 1 and 2 years.[19] Similar results have been demonstrated in a case report during 72 weeks of treatment, and a case series in which 6 out of 9 patients continued treatment for 5–9 months.[19],[20],[21] While apremilast has been shown to significantly decrease disease activity, and is well tolerated by patients with moderate HS, it is contraindicated in pregnancy due to risk of abortion and fetal death in animal studies.[19]

Rifampin, moxifloxacin, and metronidazole triple therapy

While antibiotics have been shown to improve HS, complete remission using antibiotics alone is difficult and rare.[22] It has been hypothesized that this may be due to inadequate antimicrobial coverage or poor penetration into HS lesional skin.[22] As numerous different skin floras are found in HS lesional skin, including Gram-negative and anaerobic species, the use of bactericidal antibiotics with wide spectrums of coverage and good diffusion properties has been suggested.[22] As such, combination therapy using rifampin and moxifloxacin, a fluoroquinolone antibiotic, with the addition of metronidazole, a potent anaerobic drug, has been explored. As reports have shown that some Gram-negative anaerobic species are either naturally resistant or incompletely susceptible to moxifloxacin, the addition of metronidazole to this therapy regimen is important.[22]

A retrospective chart review of 28 patients with long-lasting refractory disease (Hurley Stage I/II/III) treated with combination of rifampin (10 mg/kg once daily), moxifloxacin (400 mg daily), and metronidazole (500 mg three times daily) sought to better understand the efficacy of this triple therapy regimen.[22] The rifampin-moxifloxacin-metronidazole combination was given for 6 weeks, and metronidazole was stopped thereafter to avoid neurological complications. Rifampin-moxifloxacin combination therapy was reassessed every 6 weeks, and treatment was continued as long as the patient's clinical status continued to improve without serious side effects.[22] Once complete remission was achieved, the rifampin-moxifloxacin combination was continued for at least 6 weeks as consolidation treatment.[22] Complete remission, defined as the absence of any persisting active clinical lesions at two consecutive follow-up visits, was achieved in 57% of patients, and relapse was observed in all patients who stopped their antimicrobial treatment before complete remission.[22] Relapse was also observed in 14% of patients that discontinued metronidazole, with remission once more achieved after reintroduction – findings suggestive of the importance of prolonged, optimized anaerobic treatment for HS lesions.[22]

Similar findings were demonstrated using oral combination of rifampin (10 mg/kg once daily), moxifloxacin (400 mg once daily), and metronidazole (250–500 mg three times daily) in a recent prospective, open-label, noncomparative cohort study in 28 consecutive patients.[23] Results demonstrated complete and prolonged remission in patients with severe HS using this targeted antimicrobial regimen, although controlled trials are needed to confirm these results.[23]

Role of fumarates

Fumarates, or fumaric acid esters, currently used in the treatment of multiple sclerosis, have been shown to be effective in the treatment of patients with psoriasis.[24] Their efficacy in this patient population is likely secondary to their immunomodulatory and anti-inflammatory effects.[24] Dimethylfumarate (DMF) impairs the production of pro-inflammatory cytokines IL-12 and IL-23 – both of which are found to be elevated in HS lesional skin.[24] In addition, the metabolite of DMF, monoethylfumarate, has been shown to mitigate the production of IL-12p70, IL-10, and (TNF-α).[24] Further support for the use of this therapy in HS comes from evidence showing that DMF, in high enough concentrations, causes a significant reduction in nuclear factor kappa-beta-mediated transcription of cytokines IL-1, TNF-α, and IL-8.[24] As these cytokines are thought to be implicated in the pathogenesis of HS, the potential role in the treatment is a topic of discussion. In a prospective, open-label pilot study, the effectiveness and short-term tolerability of fumarates in patients with moderate-to-severe HS (Hurley II/III) were investigated in seven patients. Included patients had failed multiple therapies for HS, and oral fumarates were investigated as a last resort.[24] Patients were treated for 20 weeks using the dosage schematics proposed for psoriasis by the European S3-guidelines.[23] Study results demonstrated clinically significant improvement in three of the seven patients, suggesting a role in the management of patients with recalcitrant or refractory HS. The other four patients discontinued therapy due to lack of response.[24]

  Biologics Top

Biologics are a relatively new and promising systemic treatment option for patients suffering with HS. Wlodarek et al. published a recent 2019 review that assessed the efficacy of currently available biologic therapy for HS. As researchers and clinicians learn more about the pathogenesis of the disease, including cytokines that drive the inflammation characteristic of HS, novel treatment options continue to emerge.[7]

The role of immune dysregulation is now widely accepted as central to the pathogenesis of HS. Several cytokines, including TNF-α, IL-1β, IL-17, and IL-23, have been implicated in this dysregulation, as well as in perpetuating a constant state of inflammation that plagues those who suffer with HS.[6] Biologic therapy targeted toward these inflammatory markers is a promising therapeutic option for patients.[7] A brief summary of biologic treatment options is reflected in [Table 3].[7],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35]
Table 3: Summary of biologic therapeutic options for hidradenitis suppurativa

Click here to view

  Adalimumab Top

Currently, the only Food and Drug Administration-approved biologic for HS is ADA, a human monoclonal antibody against soluble and transmembrane TNF-α.[7] As TNF-α is found to be increased in expression in HS sufferers, there exists significant rationale for the use of biologics targeting this inflammatory marker. ADA is approved for treatment of moderate-to-severe HS in adults following failure of classic treatment options.[7] By blocking the biologic activity of TNF-α, ADA is able to augment the innate immune response by decreasing levels of pro-inflammatory cytokines and inflammatory leukocytes.[7] Several clinical trials have sought to evaluate the efficacy of ADA, the most recent and most significant of which was the Phase III PIONEER 1 and II trials.[7] In PIONEER II, ADA proved to be significantly more effective than placebo in pain reduction, disease severity, and the number/morphology of skin lesions.[7] Overall, ADA has shown promising results in efficacy as well as safety for HS patients, with current evidence showing an improvement in quality of life, severity of pain, and depressive symptoms.[7]

  Infliximab Top

While ADA is the only FDA biologic currently approved for treatment of moderate-to-severe HS, several off-label treatment options are being explored. Infliximab (IFX), much like ADA, is a monoclonal IgG1 class antibody against soluble and transmembrane TNF-α that has been found to be effective in improving the quality of life of patients with HS.[7] While only one randomized, double-blind, placebo-controlled study has been conducted to evaluate the efficacy and safety of IFX, the results were promising, with a significantly greater number of patients treated with the active drug achieving at least 50% improvement in skin lesions when compared to placebo.[7] A retrospective study to compare the effectiveness of IFX versus ADA in HS therapy was conducted by Van Rappard et al., with results showing a reduction in inflammation and improvement in skin lesions in both subject groups. While the mean decrease in Sartorius score from baseline was greater (66%) for the ADA group when compared to IFX (54%), the improvement seen in the IFX group was still significant after 1 year whereas this was not the case for the ADA group.[7],[9],[27] In addition, IFX was found to be more effective than ADA in decreasing overall disease severity and improving quality of life and the duration of remission.[7],[9],[25] These findings suggest a promising and significant role for IFX as a therapeutic option for patients suffering with HS.

Several other potential biologic therapies for the treatment of HS exist, including etanercept (ETA), anakinra (ANA), ustekinumab (UST), secukinumab (SEC), and IFX-1.[7] In contrast to ADA and IFX, variable results have been documented with these agents, suggesting the need for further research before these drugs can become established therapeutic options for HS.[7]

  Etanercept Top

ETA is a recombinant fusion protein that, much like ADA and IFX, functions to inhibit TNF-α.[7] However, in contrast to the aforementioned therapeutic options, ETA only inhibits the transmembrane form of TNF-α, as opposed to both soluble and transmembrane forms.[7] Only one randomized, double-blind, placebo-controlled trial has sought to assess the efficacy of ETA in the treatment of HS, the results of which did not show any significant difference in patient global assessment, physician global assessment, or quality of life between ETA and placebo.[7] The reports concerning the efficacy of ETA are variable, which, when compared to the evident efficacy of the other anti-TNF treatment options of ADA and IFX, makes its utility as an established HS therapeutic option dubious.

Wlodarek et al. summarized the results of published data concerning the efficacy of ADA, IFX, and ETA in treatment of HS. Through the analysis of 69 total papers, most of which were case reports and case series but also some randomized control trials, Wlodarek et al. found that the highest response rate was seen in patients treated with IFX (82%) when compared to ADA and ETA (54%). However, while the highest response rate may have been seen with IFX, Wlodarek et al. emphasized that the highest quality of evidence was published for ADA, with a much greater number of patients analyzed following its use. Ultimately, this makes the results concerning the efficacy of ADA more reliable than the data available for IFX or ETA, suggesting that more randomized controlled trials are necessary to estimate the effectiveness of these medications in comparison to each other.[7]

  Anakinra Top

ANA is a recombinant IL-1 receptor antagonist that competitively blocks the binding of both IL-1α and IL-1β.[7] As IL-1β is a well-established marker of inflammation in HS, the immunomodulatory effects of ANA make it a promising alternative therapeutic option for HS patients who have not responded well to TNF-α antagonists. Wlodarek et al. described several studies in which the efficacy of ANA appeared promising, including a prospective open-label study and a larger randomized double-blinded, placebo-controlled trial. In both studies, patients treated with ADA therapy showed clinical improvement and established ANA as a potentially efficacious treatment option.[7] While these results are promising, there have been other contradictory reports concerning the efficacy of ANA with a few cases showing no response to treatment and one study even describing a worsening of the skin lesions in one of two patients treated with ADA.[7]

  Ustekinumab Top

UST is another promising treatment option for HS patients. A human monoclonal IgG1 antibody directed against the p40 subunit of IL-12 and IL-23, UST, takes advantage of the hypothesis that HS inflammation may be related to aberrant Notch signaling.[28] As previously discussed, abnormal Notch signals are thought to lead to abnormal differentiation and increased destruction of outer hair root sheath cells leading to the release of keratins that have the propensity to trigger macrophage and dendritic cell activation through binding of toll-like receptors.[28] Activation of these cells consequently leads to the release of pro-inflammatory IL-23, as well as IL-12, to activate T-helper 17 cells which then release other cytokines and perpetuate the cycle of inflammation.[28] UST suppresses both IL-23 and IL-12, and anti-IL-23/12 therapy may serve to ameliorate this cycle of immune dysregulation. While only one open-label clinical trial to evaluate the efficacy of UST in HS therapy has been conducted to date, the results were promising with patients showing moderate to marked improvement in skin lesions as assessed by Sartorius score, as well as significant improvement in quality of life as assessed by DLQI.[7],[29] UST offers a unique mechanism of inhibition, and it may provide clinicians with a novel therapeutic approach for HS in patients who fail the already available anti-TNF therapy.

  Secukinumab Top

SEC is a fully monoclonal antibody that, like UST, has a target other than TNF-α. It is directed against IL-17A, a cytokine that has recently been described to be significantly elevated in the blood, as well as lesional skin, of HS patients.[30] As a pro-inflammatory cytokine, IL-17A has the ability to activate neutrophils and lymphocytes, as well as induce the expression of other pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α.[30] SEC binds to IL-17A and effectively inhibits this inflammatory cascade, which suggests a potential role as therapy for HS. However, data concerning its efficacy are limited with only three cases currently published detailing the use of SEC in HS treatment following failure of standard as well as biologic therapy.[7] Of the published research concerning SEC, the results are promising, with marked improvement in terms of pain, inflammatory nodules, and number of lesions being reported.[7] While data may be limited, SEC is currently being evaluated in a randomized placebo-controlled trial consisting of a group of 21 h patients, the results of which will hopefully provide clinicians with a better understanding of its therapeutic potential.[7]

  Vilobelimab (infliximab-1) Top

Another promising therapeutic agent for patients with HS who have failed conventional treatment and other biologics is an anti-complement factor C5a monoclonal antibody, IFX-1.[7] The first of its kind, IFX-1, is a monoclonal antibody against C5a, an activation product of the complement cascade that is also involved in neutrophil activation and production of pro-inflammatory cytokines such as TNF-α.[7] A recent study by Kanni et al. found elevated levels of C5a in the plasma of HS patients, although there was a negative correlation with circulating C5a and HS disease severity. Nonetheless, the study was significant for its findings that C5a levels in the plasma of HS patients were greater than that of patients with severe sepsis or organ failure, suggesting a potentially significant role complement.[31] The safety and efficacy of IFX-1 has been assessed in an open-label Phase II clinical trial with promising results.[32] Currently, a large randomized, double-blinded, placebo-controlled multicenter Phase II study on a group of 175 patients is under recruitment to determine the efficacy of IFX-1 as a potential target of therapy.[7] [Table 2] summarizes the biologic therapy either currently available or under investigation.

Treatment for HS remains challenging, and several other therapeutic trials are currently underway to investigate potential targets, including a recent Phase II trial looking at inhibition of the inflammatory pathways IL-1α, IL-17, and C5a.[7] Finally, several new biological preparations, including anti-IL-1A monoclonal antibody (MABp1), anti-IL-17A monoclonal antibody (CJM112), and humanized anti-IL-17A and IL-17F monoclonal antibody (bimekizumab), are under investigation.[7]

  Guselkumab Top

Guselkumab, a human monoclonal antibody specific to the p19 subunit of IL23, has been shown to be effective in the treatment of severe Hurley Stage III HS.[33] Currently approved for the treatment of moderate-to-severe psoriasis, guselkumab has also proven effective in several recent studies in treatment of HS Hurley Stages II/III and may be considered a treatment option if patients respond poorly to established therapies or have contraindications to ADA.[33],[24] Several positive case report and retrospective case study results have been published with GUS 100 mg at weeks 0, 4, and then recurrent 8-week intervals.[33],[24] While still awaiting publication from a recently complete phase II randomized, placebo-controlled, double-blind study (NCT03628924), IL-23 has been demonstrated to play an important role in the pathogenesis of HS.[33],[24] As such, inhibition of this factor can lead to significant improvement in severe HS refractory to other standard therapies.[31] Guselkumab is undergoing clinical trials to evaluate safety and efficacy in larger patient cohorts.[35],[36]

  Surgery Top

While medication treatment options for HS continue to be explored, surgery has long been an available modality of achieving remission in patients with severe or recalcitrant disease. The primary goal of surgery is removal of the diseased tissue to prevent reoccurrence, with the surgical techniques of deroofing versus wide local excision having the greatest body of literature supporting outcomes.[8] Patients with Hurley Stage II or III disease with sinus tract formation may require surgery, as monotherapy with medications alone is insufficient to induce remission.[8] Of note, the role of medications in such cases is to eliminate the acute inflammatory process prior to surgery.[37] An interesting surgical technique discussed by Daveluy is that of carbon dioxide laser excision of sinus tracts. Prior to excision, cryoinsufflation, a technique that involves injecting liquid nitrogen into HS tracts, is used to delineate the surgical field.[38],[39] This technique may also be used prior to other surgical procedures (deroofing, wife local) as well, allowing for more precise excision of tracts.[8]

  Conclusions and Perspectives Top

This review offers a synthesized a comparison of the currently available and investigational immunotherapies for treatment of HS. As many different therapies are available for treatment of HS ranging from topical and oral to subcutaneous and surgical, the authors of this review have devised a theoretical treatment algorithm that may be used for reference when managing patients [Figure 1].
Figure 1: Hidradenitis treatment algorithm. Management of hidradenitis suppurativa takes on a tiered approach that depends largely on severity of disease and response to first-line medications. For any stage of the disease, efforts must be taken to alleviate pain, manage infection, and counsel the patient for smoking cessation if applicable. For mild, Hurley Stage I disease, topical clindamycin combined with oral tetracyclines or dual therapy with oral clindamycin and rifampin can be used. Laser therapy and local excision of lesions can be used in addition to medical therapy. As the severity of the disease progresses to Hurley Stage II and III, triple antibiotic therapy can be attempted with clindamycin, rifampin, and metronidazole. If the disease remains refractory to antibiotic treatment, wide surgical excision can be attempted. In patients who are not surgical candidates or in whom disease remains refractory, ertapenem or biologics such as adalimumab and infliximab can be used

Click here to view

As the pathophysiology of HS is further studied and better understood, biologics continue to be developed that more specifically and accurately target the underlying pathology of HS. ADA is the only currently FDA-approved biologic for the treatment of HS, but this fact is subject to change pending further research in and studies conducted on the other biologics in similar classes.

Early diagnosis and treatment of HS is essential for successful treatment and improvement of quality of life, and the field of biologics is ever expanding to provide more varied options to tailor treatment to the patient. Surgery is an effective option for late-stage HS or disease that is resistant to medical therapy. Further studies are needed to more comprehensively evaluate the new biologics on the market, but the available research shows promising results for the management of HS in the future.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Kelly G, Sweeney CM, Tobin AM, Kirby B. Hidradenitis suppurativa: The role of immune dysregulation. Int J Dermatol 2014;53:1186-96.  Back to cited text no. 1
Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: A comprehensive review. J Am Acad Dermatol 2009;60:539-61.  Back to cited text no. 2
Habif, T. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. Vol. 7. Amsterdam: Elsevier; 2016. p. 215-63.  Back to cited text no. 3
Jørgensen AR, Thomsen SF, Karmisholt KE, Ring HC. Clinical, microbiological, immunological and imaging characteristics of tunnels and fistulas in hidradenitis suppurativa and Crohn's disease. Exp Dermatol 2020;29:118-23.  Back to cited text no. 4
Sartorius K, Lapins J, Emtestam L, Jemec GB. Suggestions for uniform outcome variables when reporting treatment effects in hidradenitis suppurativa. Br J Dermatol 2003;149:211-3.  Back to cited text no. 5
Zouboulis CC, Desai N, Emtestam L, Hunger RE, Ioannides D, Juhász I, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatol Venereol 2015;29:619-44.  Back to cited text no. 6
Włodarek K, Ponikowska M, Matusiak Ł, Szepietowski JC. Biologics for hidradenitis suppurativa: An update. Immunotherapy 2019;11:45-59.  Back to cited text no. 7
Narla S, Lyons AB, Hamzavi IH. The most recent advances in understanding and managing hidradenitis suppurativa. F1000Res 2020;9:v1000-49.  Back to cited text no. 8
Hendricks AJ, Hsiao JL, Lowes MA, Shi VY. A comparison of international management guidelines for hidradenitis suppurativa. Dermatology 2021;237:81-96.  Back to cited text no. 9
Zouboulis CC, Bechara FG, Dickinson-Blok JL, Gulliver W, Horváth B, Hughes R, et al. Hidradenitis suppurativa/acne inversa: A practical framework for treatment optimization – systematic review and recommendations from the HS ALLIANCE working group. J Eur Acad Dermatol Venereol 2019;33:19-31.  Back to cited text no. 10
Dessinioti C, Zisimou C, Tzanetakou V, Stratigos A, Antoniou C. Oral clindamycin and rifampicin combination therapy for hidradenitis suppurativa: A prospective study and 1-year follow-up. Clin Exp Dermatol 2016;41:852-7.  Back to cited text no. 11
Gener G, Canoui-Poitrine F, Revuz JE, Faye O, Poli F, Gabison G, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: A series of 116 consecutive patients. Dermatology 2009;219:148-54.  Back to cited text no. 12
Mendonça CO, Griffiths CE. Clindamycin and rifampicin combination therapy for hidradenitis suppurativa. Br J Dermatol 2006;154:977-8.  Back to cited text no. 13
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  [Figure 1]

  [Table 1], [Table 2], [Table 3]


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