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As time marches on, so does HS

A delayed HS diagnosis can lead to missing the window of opportunity for early treatment and make the patient nightmare even longer and more frustrating. It’s physically and mentally exhausting. By the time a diagnosis is received, patients with HS have often seen numerous providers—all while suffering the relentless torment of painful skin lesions and fighting an ongoing sense of despair.1-3

A diagnosis of HS is based on the following clinical criteria3,4:

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Image is of actual clinical trial patient.
Image is of actual clinical trial patient.

Tunnels are openings at the skin surface that can drain malodorous fluid.3


Image is of actual clinical trial patient.


Crural folds

Image is of actual clinical trial patient.

Typical locations include axillae, inframammary areas, and crural folds. HS may also occur less
frequently in other locations, including the lower abdomen, scalp, neck, and eyelids.5

How does HS vary from other differential diagnoses?

Often mistaken for infection, HS is a diagnosis of exclusion. It typically starts with the formation of single or multiple abscesses and gets progressively worse. The intertriginous areas–axillae, inframammary areas, and crural folds–are the most commonly affected sites in adults. While biopsies and cultures are not routinely recommended, a biopsy may show hyperkeratosis of a hair follicle while cultures are usually negative. Lesions may test positive, however, for Staphylococcus aureus during flares.6 Exceptions to these rules include cases where HS occurs in adolescents and children.7

Differential diagnosis examples8,9

Follicular pyoderma (including folliculitis, furuncles, carbuncles)




Similarities with HS:

nodules, abscesses, purulent discharge

Differences from HS:

primarily caused by an infection, random distribution, burning, and perilesional erythema

Acne vulgaris

Back acne


Acne scarring

Similarities with HS:

cysts with pus, inflammatory nodules, scars

Differences from HS:

varying distribution compared to HS (face, back, upper chest)

Granuloma inguinale

Similarities with HS:

localized to genital and inguinal folds

Differences from HS:

red ulcers, granulation of tissues, easily bleeds, infectious disease

Other examples

  • Pilonidal, epidermoid, dermoid, or Bartholin cysts
  • Noduloulcerative syphilis
  • Tuberculous abscess
  • Crohn’s disease (cutaneous Crohn’s)

HS disease severity is often graded using Hurley Staging2,10

Hurley Staging is considered the most commonly used severity classification. 70% of patients have mild HS (Hurley Stage I) and 30% of patients have moderate-to-severe HS (Hurley Stages II and III).12

A delayed diagnosis together with multiple misdiagnoses, mismanaged care, and inappropriate treatments contributes to disease progression and poor outcomes.3

Delays can also lead to greater disease severity at the time of diagnosis and a greater number of surgically treated sites, concomitant diseases, and work-related disruptions.2

While Hurley Staging is the first (1989) and best-known clinical scoring system used for HS, a number of other scoring systems have since been established. These include but are not limited to13:

  • 2003 Sartorius Score

  • 2010 HS Severity Index (HSSI)

  • 2012 HS-Physician Global Assessment (HS-PGA)

  • 2012 Hidradenitis Suppurativa Clinical Score (HiSCR)

  • 2017 International HS Severity Scoring System (IHS4)

  • 2019 HS Area and Severity Index (HASI)

An assessment of a patient’s disease severity or response to treatment can vary depending on which clinical scoring is used.13 Therefore, in some cases, it may be appropriate to use several measures to determine a patient’s disease severity.13

Let's listen to Cydney’s story of how and when she was diagnosed with HS.

Watch The Rest of Cydney’s Story

Nearly one-third of patients have a family history of HS5


of patients visited a physician for HS symptoms more than 5 times before an appropriate HS diagnosis was made.14

A delayed diagnosis markedly contributes to disease progression, comorbid conditions, and an increased number of surgically treated sites.2,3

The average time from symptom onset to HS diagnosis is 10 years,14 with more than 3 misdiagnoses along the way.2

Hospitalizations due to HS are trending upward, emphasizing the need
to diagnose and treat the disease earlier.

Based on a retrospective analysis of the Nationwide Inpatient Sample (NIS), the rate of hospitalizations with HS as a primary diagnosis increased from 7.9 per 100,000 all-cause hospitalizations in 2008 to 11.6 per 100,000 all-cause hospitalizations in 2017 (P<0.0001).15

Looking in the Window of Opportunity

Characterized by boils and skin scarring, HS is often misidentified as more well-known skin conditions, such as acne vulgaris or folliculitis. Because of this, it can take years for a patient with HS to receive a correct diagnosis and appropriate treatment.2

Addressing HS early, when anti-inflammatory attempts will be most effective, can decrease disease progression and may alter the natural HStory of the disease.16 This window of opportunity is the optimal time for treating HS and improving clinical outcomes, before irreversible damage and development of lesions such as fistulas, sinus tracts, and scarring.11,16

Open the Treatment Window

Natural HStory v. Disease Modification Graphic

Clinically diagnosing HS involves recognizing insidious abscesses, nodules, and tunnels as well as assessing recurrence and involvement at typical anatomic sites.3

Mild (Hurley Stage I)

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HS of the axillae with a visible, boil-like nodule.

Close-up of HS on the thigh, showing red, swollen boils/lesions.

HS lesion on the face.

HS lesion in the anogenital area.

Moderate (Hurley Stage II)

Image is of actual clinical trial patient.

HS of the axillae showing characteristic inflammatory nodules and scarring.

Image is of actual clinical trial patient.

Axillary HS with an abscess, inflammatory nodules, and scarring.

Image is of actual clinical trial patient.

HS of the abdomen with inflammatory nodules, nondraining tunnels, and scarring.

Image is of actual clinical trial patient.

Inguinal HS with inflammatory nodules, nondraining tunnels, and scarring.

Severe (Hurley Stage III)

Image is of actual clinical trial patient.

HS of the axillae with an abscess, inflammatory nodules, and scarring.

Image is of actual clinical trial patient.

Inguinal HS with multiple inflammatory nodules, draining tunnels, and scarring.

Image is of actual clinical trial patient.

HS of the breast fold with multiple abscesses, inflammatory nodules, draining tunnels, and scarring.

HS of the buttocks with tunneling and scarring.


  1. Schneider-Burrus S, Tsaousi A, Barbus S, et al. Features associated with quality of life impairment in hidradenitis suppurativa patients. Front Med (Lausanne). 2021;8:676241.
  2. Kokolakis G, Wolk K, Schneider-Burrus S, et al. Delayed diagnosis of hidradenitis suppurativa and its effect on patients and healthcare system. Dermatology. 2020;236(5):421-430.
  3. Sayed CJ, Hsiao JL, Okun MM. Clinical epidemiology and management of hidradenitis suppurativa. Obstet Gynecol. 2021;137(4):731-746.
  4. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: a publication from the United States and Canadian Hidradenitis Suppurativa Foundations: part I: diagnosis, evaluation, and the use of complementary and procedural management. J Am Acad Dermatol. 2019;81(1):76-90.
  5. Scala E, Cacciapuoti S, Garzorz-Stark N, et al. Hidradenitis suppurativa: where we are and where we are going. Cells. 2021;10(8).
  6. Jemec GBE. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012;366(2):158-164.
  7. Liy-Wong C, Kim M, Kirkorian AY, et al. Hidradenitis suppurativa in the pediatric population: an international, multicenter, retrospective, cross-sectional study of 481 pediatric patients. JAMA Dermatology. 2021;157(4):385-391.
  8. Ballard K, Shuman VL. Hidradenitis suppurativa. Stat Pearls Treasure Island, FL: StatPearls. Publishing; 2023.
  9. Saunte DML, Jemec GBE. Hidradenitis suppurativa: advances in diagnosis and treatment. JAMA. 2017;318(20):2019-2032.
  10. Lee EY, Alhusayen R, Lansang P, et al. What is hidradenitis suppurativa? Can Fam Physician. 2017;63(2):114-120.
  11. Marzano AV, Genovese G, Casazza G, et al. Evidence for a “window of opportunity” in hidradenitis suppurativa treated with adalimumab: a retrospective, real-life multicentre cohort study. Br J Dermatol. 2021;184(1):133-140.
  12. van der Zee H, Bunte M, Straalen K. Management of mild hidradenitis suppurativa: our greatest challenge yet. Br J Dermatol. 2022;186(2):355-356.
  13. Daoud M, Suppa M, Benhadou F, et al. Overview and comparison of the clinical scores in hidradenitis suppurativa: a real-life clinical data. Front Med (Lausanne). 2023;10:1145152.
  14. Garg A, Neuren E, Cha D, et al. Evaluating patients’ unmet needs in hidradenitis suppurativa: results from the Global Survey of Impact and Healthcare Needs (VOICE) Project. J Am Acad Dermatol. 2020;82(2):366-376. 
  15. Patel A, Patel A, Solanki D, et al. Hidradenitis suppurativa in the United States: insights from the National Inpatient Sample (2008-2017) on Contemporary Trends in Demographics, Hospitalization Rates, Chronic Comorbid Conditions, and Mortality. Cureus. 2022;14(5):e24755.
  16. Martorell A, Jfri A, Ochando G, et al. Present and future trends of biologic therapies and small molecules in hidradenitis suppurativa. J IMIDs. 2022;2(1):8-19.
  17. Goldburg SR, Strober BE, Payette MJ. Hidradenitis suppurativa: epidemiology, clinical presentation, and pathogenesis. J Am Acad Dermatol. 2020;82(5):1045-1058.
  18. Danese S, Fiorino G, Fernandes C, Peyrin-Biroulet L. Catching the therapeutic window of opportunity in early Crohn's disease. Curr Drug Targets. 2014;15(11):1056-1063.