Pathogenesis Of Hidradenitis Suppurativa Research Articles

Gram-negative anaerobes elicit a robust keratinocytes immune response with potential insights into HS pathogenesis.

Hidradenitis Suppurativa (HS) is a chronic autoinflammatory skin disease with activated keratinocytes, tunnel formation and a complex immune infiltrate in tissue. The HS microbiome is polymicrobial with an abundance of commensal gram-positive facultative (GPs) Staphylococcus species and gram-negative anaerobic (GNA) bacteria like Prevotella, Fusobacterium and Porphyromonas with increasing predominance of GNAs with disease severity. We sought to define the keratinocyte response to bacteria commonly isolated from HS lesions to probe pathogenic relationships between HS and the microbiome. Type strains of Prevotella nigrescens, Prevotella melaninogenica, Prevotella intermedia, Prevotella asaccharolytica, Fusobacterium nucleatum, as well as Staphylococcus aureus and the normal skin commensal Staphylococcus epidermidis were heat-killed and co-incubated with normal human keratinocytes. RNA was collected and analysed using RNAseq and RT-qPCR. The supernatant was collected from cell culture for protein quantification. Transcriptomic profiles between HS clinical samples and stimulated keratinocytes were compared. Co-staining of patient HS frozen sections was used to localize bacteria in lesions. A mouse intradermal injection model was used to investigate early immune recruitment. TLR4 and JAK inhibitors were used to investigate mechanistic avenues of bacterial response inhibition. GNAs, especially F. nucleatum, stimulated vastly higher CXCL8, IL17C, CCL20, IL6, TNF and IL36γ transcription in normal skin keratinocytes than the GPs S. epidermidis and S. aureus. Using RNAseq, we found that F. nucleatum (and Prevotella) strongly induced the IL-17 pathway in keratinocytes and overlapped with transcriptome profiles of HS patient clinical samples. Bacteria were juxtaposed to activated keratinocytes invivo, and F. nucleatum strongly recruited murine neutrophil and macrophage migration. Both the TLR4 and pan-JAK inhibitors reduced cytokine production. Detailed transcriptomic profiling of healthy skin keratinocytes exposed to GNAs prevalent in HS revealed a potent, extensive inflammatory response vastly stronger than GPs. GNAs stimulated HS-relevant genes, including many genes in the IL-17 response pathway, and were significantly associated with HS tissue transcriptomes. The close association of activated keratinocytes with bacteria in HS lesions and innate infiltration in murine skin cemented GNA pathogenic potential. These novel mechanistic insights could drive future targeted therapies.

Hidradenitis Suppurativa (part 1): definition, epidemiology, etiology, diagnosis.

Hidradenitis Suppurativa (HS) is a chronic recurrent skin disease characterized by development of autoimmune inflammation in the infundibulum of the hair follicle and apocrine sweat glands located in the axillary, inguinal, anogenital regions, submammary folds, near the areola of mammary glands and the umbilical region. HS is difficult to treat and has an extremely negative impact on the quality of life. HS is separated into a distinct clinical entity fundamentally different in etiopathogenesis from acute bacterial hidradenitis. The exact prevalence of HS is unknown, it varies greatly in different studies ranging from 0.03% to 4% in general population. The detection of IL-1, IL-23, and IL-17 in the lesions indicates the key role of autoimmune inflammation involving Th17-lymphocytes in the pathogenesis of HS. Risk factors include smoking, obesity, mechanical friction, genetic predisposition. The diagnosis of HS relies on three obligatory criteria: characteristic distribution, typical morphology of the lesions and relapsing, chronic disease course. There is no gold standard in assessing the severity of the disease, since all available scoring systems have many limitations, therefore many questions regarding this disease remain unsolved at present - from terminology and clear and most objective assessment criteria for the severity of the process to the development of native clinical guidelines.

Brodalumab for moderate-severe hidradenitis suppurativa: An open-label multicentric cohort study in real clinical practice.

The use of biological therapy is becoming increasingly common in patients with hidradenitis suppurativa (HS). Levels of serum TNF-alfa and IL17 support the role of an immune system dysregulation in the pathogenesis of HS. Brodalumab targets the receptor A of IL-17, thus having a promising role in the treatment of HS. A multicenter retrospective observational open-label study was conducted in two tertiary hospitals. Adults with moderate to severe HS under treatment with brodalumab 210 mg at week 0, 1, 2 and then every 2 weeks were included and assessed at weeks 0 and 16 which was the median follow-up time. Demographic and disease-related variables as well as response parameters (HiSCR and IHS4) and safety data were recorded and analysed. A total of 16 patients (75% males) were included in our study. 50% of patients presented an inflammatory phenotype and mean BMI was 28.37. HiSCR was achieved in 50% of patients and mean IHS4 decreased from 24.13 to 16.81 (p = 0.002). No differences were found between those who achieved HiSCR and those who did not. Grade 2 adverse events were reported in three patients with no fatal outcomes and treatment discontinuation was advised in four patients. Brodalumab seems to be effective and safe in patients with moderate to severe HS, even in those that did not respond to adalimumab, which, at the moment, is the only widely approved biologic for this indication. Thus, it stands as an interesting option for the treatment of HS.

Macrophage Polarization and Crosstalk between Macrophages and Other Cells in Hidradenitis Suppurativa

Hidradenitis suppurativa (HS), also known as acne inversa, is a chronic inflammatory disease characterized by the development of inflammatory nodules, abscesses, and pus-discharging tunnels in areas such as the axillary, inguinal, gluteal, and perianal regions. The pathogenesis of HS remains unclear, but it is being increasingly recognized to rely on the dysregulation of inflammatory responses. Central to this process are macrophages, which have emerged as key players in the inflammatory milieu of HS. These cells orchestrate inflammation via polarization and significantly influence the functions of neighboring cells. This review briefly describes macrophage polarization and crosstalk between macrophages and other cells in patients with HS with the aim of providing new therapeutic strategies for the clinical management of HS.

The NLRP3 Inflammasome Gene Is Overexpressed in Hidradenitis Suppurativa Lesions: A Preliminary Study on the Role of Pyroptosis in Disease Pathogenesis.

Hidradenitis suppurativa (HS) is a debilitating inflammatory skin disorder, and its pathogenesis remains incompletely understood. This study aimed to investigate the role of the P2X7 receptor (P2X7R) and NLRP3 inflammasome in HS pathogenesis. RNA sequencing and real-time PCR were performed to assess the gene expression levels of P2X7R and NLRP3 in the skin biopsies of HS patients and healthy controls (HC). The results of our study revealed a significantly increased expression of the NLRP3 gene in both the lesional and perilesional skin of HS patients compared to healthy controls. Moreover, the mRNA levels of NLRP3 were significantly higher in lesional skin compared to non-lesional skin in HS patients, indicating the spread of inflammation to adjacent tissues. In contrast, no significant differences in P2X7R gene expression were observed between the three groups. These findings suggest the involvement of NLRP3 inflammasomes in HS pathogenesis, while P2X7R may not play a significant role in the disease. This research sheds light on the complex inflammatory pathways in HS, highlighting the potential of NLRP3 as a therapeutic target. Understanding the molecular mechanisms underlying HS is crucial for the development of targeted treatment modalities for this debilitating condition.

Hidradenitis suppurativa, intestinal microbiome and SIBO – a comprehensive overview of the issue

Hidradenitis suppurativa, intestinal microbiome and SIBO – a comprehensive overview of the issue

Single-cell sequencing reveals Hippo signaling as a driver of fibrosis in hidradenitis suppurativa.

Hidradenitis suppurativa (HS) is a chronic inflammatory disease characterized by abscesses, nodules, dissecting/draining tunnels, and extensive fibrosis. Here, we integrate single-cell RNA sequencing, spatial transcriptomics, and immunostaining to provide an unprecedented view of the pathogenesis of chronic HS, characterizing the main cellular players and defining their interactions. We found a striking layering of the chronic HS infiltrate and identified the contribution of 2 fibroblast subtypes (SFRP4+ and CXCL13+) in orchestrating this compartmentalized immune response. We further demonstrated the central role of the Hippo pathway in promoting extensive fibrosis in HS and provided preclinical evidence that the profibrotic fibroblast response in HS can be modulated through inhibition of this pathway. These data provide insights into key aspects of HS pathogenesis with broad therapeutic implications.

An Atlas of the Hidradenitis Suppurativa Transcriptome.

Hidradenitis suppurativa (HS) is a chronic inflammatory condition of the skin. Both genetic and environmental factors contribute to the risk of developing HS, but the pathogenesis of this disease is currently not fully understood. The aim of this study was to further current understanding of the molecular background of HS with the use of global transcriptome analyses. Transcriptome profiling of perilesional and lesional skin of five patients with HS and six healthy control patients was performed by next-generation sequencing. Groups of differentially expressed genes characteristic of the skin of patients with HS were shortlisted by bioinformatic analysis. RNA sequencing followed by bioinformatic profiling revealed profound enrichment of inflammatory-related processes in both lesional and perilesional skin of patients with HS. There were, however, distinct differences in the gene expression profiles between the lesional and perilesional skin, with 1488 genes differentially expressed. Genes encoding typical proinflammatory cytokines were profoundly enriched within HS lesions. In contrast, those encoding mediators of extracellular matrix organization were highly expressed mostly in the perilesional area. Our study provides novel insights into the mechanisms underlying the pathogenesis of HS, and the results also have potential clinical implications in both diagnosis and therapeutics.

Unraveling the Epigenetic Tapestry: Decoding the Impact of Epigenetic Modifications in Hidradenitis Suppurativa Pathogenesis.

Hidradenitis suppurativa (HS) is a chronic autoinflammatory skin disorder, which typically occurs during puberty or early adulthood. The pathogenesis of HS is complex and multifactorial; a close interaction between hormonal, genetic, epigenetics factors, host-specific aspects, and environmental influences contributes to the susceptibility, onset, severity, and clinical course of this disease, although the exact molecular mechanisms are still being explored. Epigenetics is currently emerging as an interesting field of investigation that could potentially shed light on the molecular intricacies underlying HS, but there is much still to uncover on the subject. The aim of this work is to provide an overview of the epigenetic landscape involved in HS. Specifically, in this in-depth review we provide a comprehensive overview of DNA methylation/hydroxymethylation, histone modifications, and non-coding RNAs (such as microRNA-miRNA-132, miRNA-200c, miRNA-30a-3p, miRNA-100-5b, miRNA-155-5p, miRNA-338-5p) dysregulation in HS patients. An interesting element of epigenetic regulation in HS is that the persistent inflammatory milieu observed in HS lesional skin could be exacerbated by an altered methylation profile and histone acetylation pattern associated with key inflammatory genes. Deepening our knowledge on the subject could enable the development of targeted epigenetic therapies to potentially restore normal gene expression patterns, and subsequentially ameliorate, or even reverse, the progression of the disease. By deciphering the epigenetic code governing HS, we strive to usher in a new era of personalized and effective interventions for this enigmatic dermatological condition.

Tertiary lymphoid structures sustain cutaneous B cell activity in hidradenitis suppurativa.

Hidradenitis suppurativa (HS) is a chronic skin condition affecting approximately 1% of the US population. HS skin lesions are highly inflammatory and characterized by a large immune infiltrate. While B cells and plasma cells comprise a major component of this immune milieu, the biology and the contribution of these cells in HS pathogenesis are unclear. We aimed to investigate the dynamics and microenvironmental interactions of B cells within cutaneous HS lesions. Combining histological analysis, single-cell RNA sequencing, and spatial transcriptomics profiling of HS lesions, we defined the tissue microenvironment relative to B cell activity within this disease. Our findings identified tertiary lymphoid structures (TLSs) within HS lesions and described organized interactions among T cells, B cells, antigen-presenting cells, and skin stroma. We found evidence that B cells within HS TLSs actively underwent maturation, including participation in germinal center reactions and class switch recombination. Moreover, skin stroma and accumulating T cells were primed to support the formation of TLSs and facilitate B cell recruitment during HS. Our data definitively demonstrated the presence of TLSs in lesional HS skin and point to ongoing cutaneous B cell maturation through class switch recombination and affinity maturation during disease progression in this inflamed nonlymphoid tissue.

Hidradenitis suppurativa associated telomere-methylome dysregulations in blood.

Hidradenitis suppurativa (HS) is a chronic debilitating disease with a significant burden of both organic and psychological comorbidities. It has been shown that certain telomere-related genes (TRGs) affect a wide range of diseases, including HS and its associated comorbidities, but their exact role in HS pathogenesis is still unknown. To determine whether TRG methylomes can be used as biomarkers in HS. Using the Illumina HumanMethylation450 BeadChip array, we examined methylation variations associated with TRGs in HS cases and age-, sex- and ethnicity-matched healthy controls. The study utilized integrated bioinformatics statistical methods, such as a false discovery rate (FDR), the area under the receiver operating characteristic curve (AUC) and principal component analysis. There were a total of 585 different differentially methylated CpG sites identified in 585 TRGs associated with HS (474 hypomethylated and 111 hypermethylated) (FDR p-value < 0.05). A number of these CpGs have been identified as being involved in increased pain sensitivity including EPAS1, AHR, CSNK1D, DNMT1, IKBKAP, NOS3, PLCB1 and PRDM16 genes; GABRB3 as a potential alcohol addiction marker; DDB1, NSMCE2 and HNRNPA2B1 associated with cancers. Pathway analysis identified 67 statistically significant pathways, including DNA repair, telomere maintenance, mismatch repair and cell cycle control (p < 0.001). The disruption of TRGs leads to the shortening of telomeres, which is associated with HS progression, ageing, cellular senescence and an increased risk of various diseases, including cancer and associated comorbidities, such as metabolic syndrome, cardiovascular disease and inflammatory disorders. Further research is necessary to better understand the underlying mechanisms and establish causal links between TRGs and HS. The present study is the first effort to comprehend potential pathomechanisms of sporadic HS cases concentrating on PBMC methylome since ours.

Transcriptomic Analysis of Hidradenitis Suppurativa: A Unique Molecular Signature with Broad Immune Activation

Hidradenitis suppurativa is a chronic inflammatory skin disease with limited treatment options. The poorly understood pathogenesis hinders the development of effective treatments; therefore, a pressing need exists to further elucidate the molecular mechanisms in hidradenitis suppurativa. This study investigated the underlying inflammatory pathways and cell types in hidradenitis suppurativa using transcriptomic approaches with RNA sequencing of lesional and non-lesional skin biopsies from hidradenitis suppurativa, which was jointly analyzed with previously published transcriptomic data from atopic dermatitis and psoriasis patients. The differential expression and pathway enrichment analyses demonstrated the activation of multiple inflammatory processes, including the innate and adaptive immune systems, implicated in the hidradenitis suppurativa pathogenesis. In agreement, hidradenitis suppurativa exhibited a unique and heterogeneous cell type signature involving lymphoid and myeloid cells such as B cells and macrophages. Furthermore, hidradenitis suppurativa displayed increased expression of TH1/2/17 signatures with no predominant TH signatures unlike psoriasis (TH1/17) and atopic dermatitis (TH2). In summary, our study provides molecular insights into the pathomechanisms in hidradenitis suppurativa, revealing a strong and widespread immune activation, which may benefit from treatment strategies offering a broad immunomodulation of various key inflammatory pathways. Our data not only corroborate previously reported findings but also enhance our understanding of the immune dysregulation in hidradenitis suppurativa, uncovering novel and potential therapeutic targets.

Epigenetic switch reshapes epithelial progenitor cell signatures and drives inflammatory pathogenesis in hidradenitis suppurativa.

Hidradenitis suppurativa (HS) is a complex inflammatory skin disease with undefined mechanistic underpinnings. Here, we investigated HS epithelial cells and demonstrated that HS basal progenitors modulate their lineage restriction and give rise to pathogenic keratinocyte clones, resulting in epidermal hyperproliferation and dysregulated inflammation in HS. When comparing to healthy epithelial stem/progenitor cells, in HS, we identified changes in gene signatures that revolve around the mitotic cell cycle, DNA damage response and repair, as well as cell-cell adhesion and chromatin remodeling. By reconstructing cell differentiation trajectory and CellChat modeling, we identified a keratinocyte population specific to HS. This population is marked by S100A7/8/9 and KRT6 family members, triggering IL1, IL10, and complement inflammatory cascades. These signals, along with HS-specific proinflammatory cytokines and chemokines, contribute to the recruitment of certain immune cells during the disease progression. Furthermore, we revealed a previously uncharacterized role of S100A8 in regulating the local chromatin environment of target loci in HS keratinocytes. Through the integration of genomic and epigenomic datasets, we identified genome-wide chromatin rewiring alongside the switch of transcription factors (TFs), which mediated HS transcriptional profiles. Importantly, we identified numerous clinically relevant inflammatory enhancers and their coordinated TFs in HS basal CD49fhigh cells. The disruption of the S100A enhancer using the CRISPR/Cas9-mediated approach or the pharmacological inhibition of the interferon regulatory transcription factor 3 (IRF3) efficiently reduced the production of HS-associated inflammatory regulators. Our study not only uncovers the plasticity of epidermal progenitor cells in HS but also elucidates the epigenetic mechanisms underlying HS pathogenesis.

161 IL-17A and IL-17F in the pathogenesis of hidradenitis suppurativa: insights from early and chronic lesions

161 IL-17A and IL-17F in the pathogenesis of hidradenitis suppurativa: insights from early and chronic lesions

Dietary Factors and Hidradenitis Suppurativa.

Hidradenitis suppurativa (HS) is a debilitating chronic inflammatory skin condition affecting hair follicles in flexural sites. Obesity is considered to be a risk factor for HS occurrence and thought to be associated with increased severity of HS symptoms. Here, we review the literature examining the impact of dietary factors on HS. Moreover, we propose potential mechanistic links between dietary factors and HS pathogenesis, incorporating evidence from both clinical and basic science studies.

Biology of Interleukin-17 and Novel Therapies for Hidradenitis Suppurativa.

Skin disorders affect ∼40% of the human population. One of the most debilitating cutaneous disorders is Hidradenitis suppurativa (HS), a noncommunicable chronic inflammatory disease with an estimated global prevalence of 0.4% to 2.5%. In January 2011, high levels of IL-17 were discovered in skin lesions of HS patients. In the following years, translational and clinical research led to a better understanding of the pathogenesis of HS. In June 2023, more than 12 years after the initial note, secukinumab, an anti-IL-17A monoclonal antibody, was approved for the treatment of moderate to severe HS. This is the next milestone in improving the treatment of these patients after the approval of the anti-TNF-α monoclonal antibody adalimumab in 2015. In this review article, we present the IL-17 pathway in HS and discuss the use of secukinumab as a therapeutic option for this disease. Our review starts with a description of the epidemiology, clinical features, etiology, and pathogenesis of HS. An overview of the IL-17/IL-17 receptor system in general and a detailed description of the known facts about the expression and action of IL-17 in HS follow. Afterward, we consider the results of clinical trials evaluating the safety and efficacy of IL-17 inhibitors in HS. Finally, a comparison is made between secukinumab and adalimumab and the characteristics of the patients that may be particularly suitable for each of these biologics are described.

IL-17 Inhibition: A Valid Therapeutic Strategy in the Management of Hidradenitis Suppurativa.

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with a significant negative impact on the quality of life of patients. To date, the therapeutic landscape for the management of the disease has been extremely limited, resulting in a profound unmet need. Indeed, adalimumab, an anti-tumor necrosis factor (TNF)-α monoclonal antibody, is the only approved biologic agent for HS, obtaining a therapeutic response in only 50% of HS patients. Numerous clinical trials are currently ongoing to test novel therapeutic targets in HS. The IL-17-mediated cascade is the target of several biologic agents that have shown efficacy and safety in treating moderate-to-severe HS. Both bimekizumab and secukinumab, targeting IL-17 in different manners, have successfully completed phase III trials with promising results; the latter has recently been approved by EMA for the treatment of HS. The aim of this review is to summarize the current state of knowledge concerning the relevant role of IL-17 in HS pathogenesis, highlighting the key clinical evidence of anti-IL-17 agents in the treatment of this disease.

THU366 Type 1 Diabetes Complicated By Multiple Episodes Of Diabetic Ketoacidosis Secondary To Flares Of Hidradenitis Suppurativa

Abstract Disclosure: S.R. Vasavada: None. K.A. Chopra: None. L. Philipson: Grant Recipient; Self; Novo Nordisk. Background: Hidradenitis suppurativa (HS) is an inflammatory skin condition of the pilosebaceous unit characterized by subcutaneous nodules that if untreated can form purulent abscesses, fistulae, and sinus tracts. HS may result from dysregulated autoimmune response to skin flora with overexpression of inflammatory cytokines, such as IL-17A, TNF-a, IL-1B (Shah et al 2017). Although HS and type 1 diabetes both share underlying autoimmune etiologies, and autoimmune diseases have been reported in higher frequencies in HS than controls, co-incidence with type 1 diabetes is extremely rare (Straalen et al 2022). Herein, we describe a case of a patient with type 1 diabetes with recurrent admissions for diabetic ketoacidosis (DKA) secondary to HS flares. Clinical Case: 37-year-old female with medical history of type 1 diabetes, hypogammaglobulinemia, and HS presented with rectal pain and hematochezia. Previously, she had several hospitalizations due to HS flares complicated by episodes of DKA and 20+ corrective surgeries for infected HS lesions. Prior to admission, patient was treated with clindamycin lotion, spironolactone, and weekly adalimumab for HS. Patient’s initial labs showed DKA with glucose 494 mg/dL (RR 60-99 mg/dL), bicarbonate 21 mmol/L (RR 23-30 mmol/L), anion gap 16 mmol/L (RR 6-15 mmol/L), and beta hydroxybutyrate level 1.44 mmol/L (N &amp;lt;0.3 mmol/L). Hemoglobin A1c was 10.4% (RR &amp;lt;5.7%). Physical exam showed Hurley Stage 2 HS with multiple atrophic scars, boils, and double comedones on bilateral axillae. She was treated with insulin infusion and IV fluids. After anion gap closed and bicarbonate improved to 24 mmol/L (RR 23-30 mmol/L), she transitioned to regimen of insulin glargine 38 units and started mealtime insulin lispro using a ratio of 1 unit of lispro for 6 grams of carbs. Subsequent glucose values stabilized, ranging 120-200 mg/dL (RR 60-99 mg/dL) during hospitalization. She underwent colonoscopy due to concern for colonic involvement of HS, however pathology was normal. After multidisciplinary discussion with endocrinology and dermatology specialists, HS treatment with prednisone was avoided due to concern of worsening patient’s glycemic control. Patient started infliximab treatment and reported mild symptom improvement. Conclusion: This case showing a patient with multiple episodes of DKA triggered by flares of HS has demonstrated the importance of further study to improve our current understanding of the potential overlap of these two conditions to help guide future treatment decisions and improve patients’ overall quality of life. Reference: Shah A, Alhusayen R, Amini-Nik S. The critical role of macrophages in the pathogenesis of hidradenitis suppurativa. Inflamm Res. 2017;66(11):931-945. Straalen KR van, Prens EP, Gudjonsson JE (2022) Insights into hidradenitis suppurativa. J Allergy Clin Immun 149(4):1150–1161. Presentation: Thursday, June 15, 2023

Hidradenitis Suppurativa: An Interdisciplinary Problem in Dermatology, Gynecology, and Surgery-Pathogenesis, Comorbidities, and Current Treatments.

Hidradenitis suppurativa (HS), also known as acne inversa, is a chronic inflammatory disease that manifests as painful nodules, abscesses, draining dermal tunnels, and scarring in intertriginous areas such as the axillae, groin, and breasts. The nature of the disease and its chronicity have a destructive impact on mental health and quality of life. HS has an estimated global prevalence of 0.00033-4.1% and it disproportionately affects females compared to males. HS involving the female anogenital regions is reported rarely in the gynecological literature, and it can often be mistaken for other vulvar diseases. The distinct phenotypes and HS rarity cause delayed diagnosis and the implementation of effective treatment. Acne inversa is associated with several comorbidities, including metabolic disease, diabetes mellitus, inflammatory bowel diseases, and spondyloarthropathies. Although HS etiology and pathogenesis remain unclear, studies have shown that lifestyle, immunological processes, genetics, and hormonal predispositions may promote follicular hyperkeratosis, dilatation, and rupture, leading to the development of chronic tissue inflammation. This article provides updated information on HS pathogenesis, comorbidities, and treatment methods. Furthermore, we share our experience in the surgical treatment of the disease, which often proves most effective, and highlight that an interdisciplinary management approach ensures optimal outcomes.

Hidradenitis Suppurativa: A Literature Review Comparing Current Therapeutic Modalities.

Hidradenitis suppurativa (HS) is a disease with a poor prognosis, often misinterpreted as an infection, with the highest impact on the patient's quality of life among all the assessed dermatological diseases. The main aim of this study was to compare various therapeutic interventions that are currently available for the treatment of HS. The pathogenesis of HS is not well understood, but it is mostly multifactorial involving a number of factors like genetic factors, androgens, local immunity, microflora, smoking, and obesity. Despite limited evidence on their effectiveness, topical antibiotics and antiseptics are commonly employed. Due to the colonization of bacteria and the presence of biofilms in the sinus tracts formed by HS lesions, systemic antibiotics are commonly employed as the primary form of therapy. In females with HS who experience menstrual flares or display symptoms of polycystic ovary syndrome, hormonal agents are often considered to be a viable and effective therapeutic option. At present, the sole treatment approved by both the Food and Drug Administration and the European Medicines Agency for addressing moderate to severe HS is adalimumab, an antibody that targets tumor necrosis factor alpha. Many surgical procedures in the management of HS aim to address inflammation by eliminating the affected folliculo-pilosebaceous unit, sinus tracts, and associated debris to impede further progression and scarring. HS continues to pose a considerable treatment challenge, necessitating a comprehensive approach for patients. However, the available evidence for most of these treatments is limited, indicating the need for more extensive research to identify the most effective interventions for managing HS.