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Overview and Recommendations
Background
- •Hidradenitis suppurativa (HS) is a chronic autoinflammatory skin disorder where an intrinsic hair follicle defect triggers follicular occlusion, rupture, and a subsequent foreign body-type immune response.
- •Epidemiological data suggest a global prevalence of 0.7% to 1.2%, with a peak incidence in young women aged 20-29 and a disproportionate burden among Black Americans.
- •The mechanistic cascade centers on the hyperactivation of the and pathways, which drive the transition from acute abscesses to chronic, epithelialized draining tunnels and psoriasiform epidermal hyperplasia.
- •Smoking and obesity are the dominant modifiable risk factors; smoking is associated with a 12-fold increase in disease prevalence and acts as a primary driver of onset and severity.
- •Systemic stakes are high, as HS is associated with a doubled risk of cardiovascular death and significant comorbidities including , metabolic syndrome, and spondyloarthropathy.
Evaluation
- •Suspect HS in any patient presenting with recurrent, painful, deep-seated nodules or 'boils' in the axillae, inguinal, inframammary, or perianal regions.
- •Ask about the frequency of flares; the diagnostic narrative requires at least two recurrences within a six-month period to establish chronicity.
- •Examine intertriginous zones for the 'trio' of lesions: inflammatory nodules, draining sinus tunnels (fistulae), and bridged or hypertrophic scarring.
- •Assess for secondary changes such as malodour, pruritus, and comedones (double-headed 'tombstone' comedones are highly characteristic).
- •Utilize the to categorize structural damage: Stage I (abscesses without tunnels/scarring), Stage II (recurrent abscesses with tunnels and scarring), or Stage III (diffuse involvement with interconnected tunnels).
- •Order (UHFUS) as a valuable adjunct for preoperative mapping to identify subclinical tunnels and fluid collections not visible on surface examination.
- •Screen for systemic associations by checking blood pressure, BMI, and HbA1c, and inquire about gastrointestinal symptoms (to rule out ) or joint pain.
- •Perform a biopsy only if the diagnosis is uncertain or to rule out mimics like in chronic, non-healing perineal lesions.
- •Evaluate the psychosocial impact using the (Dermatology Life Quality Index), as the disease carries a high risk of depression and suicide.
Management
- •Initiate a multimodal treatment plan tailored to the Hurley stage and patient-reported pain levels (NRS) or quality of life impact.
- •Prescribe topical 1% solution or gel twice daily for mild (Hurley Stage I) disease to reduce localized inflammation.
- •Administer oral tetracyclines (e.g., 100 mg BID) for 12 weeks as first-line systemic therapy for moderate disease.
- •Escalate to combination therapy with 300 mg BID and 600 mg daily for 10-12 weeks in patients refractory to tetracyclines.
- •Initiate for moderate-to-severe disease (Hurley II/III); use the HS-specific dosing: 160 mg at week 0, 80 mg at week 2, then 40 mg weekly starting at week 4.
- •Consider 300 mg every 2 or 4 weeks as a primary biologic alternative for patients who fail or have contraindications to TNF inhibitors.
- •Utilize intralesional (5-10 mg/mL) for the rapid management of acute, painful, isolated nodules.
- •Perform surgical for localized, chronic tunnels (Hurley II) to remove the epithelialized roof and allow for secondary intention healing.
- •Refer for wide radical excision in Hurley Stage III disease where medical therapy has failed to control the destructive phase.
- •Monitor for treatment response using the (HS Clinical Response) score, aiming for a ≥50% reduction in inflammatory lesion count without new abscesses.
- •Advise strict smoking cessation and weight management, as these interventions are essential for long-term remission and improving surgical outcomes.
- •Screen for tuberculosis, Hepatitis B, and Hepatitis C before starting any biologic or Janus kinase (JAK) inhibitor therapy.
Board Review — High Yield
- •Tombstone comedones, Double-headed open comedones characteristic of chronic HS.
- •TNF-alpha and IL-17, The primary cytokine axes targeted by modern biologic therapy.
- •Hurley Stage I, Abscess formation without sinus tracts or cicatrization (scarring).
- •Squamous cell carcinoma, A rare but high-mortality complication of chronic, long-standing HS lesions, especially in the perineum.
- •Smoking, The strongest environmental risk factor, associated with a 12.5-fold increased risk of disease.
- •Deroofing, A tissue-sparing surgical technique for tunnels that is superior to simple incision and drainage.
- •PASH Syndrome, A rare syndromic association of Pyoderma gangrenosum, Acne, and Suppurative Hidradenitis.
- •Diagnostic Delay, On average, it takes 7 to 10 years for a patient to receive a correct diagnosis of HS.
Deep Dive — Evidence Details
Pathophysiology and Mechanism
Hidradenitis suppurativa (HS) is a chronic autoinflammatory skin disorder of the pilosebaceous unit, where an intrinsic hair follicle defect triggers a cascade of follicular occlusion, rupture, and a subsequent foreign body-type immune response [80]D5[91]D5[94]D5.
Mechanistic cascade
| Step | Molecular / cellular event | Resulting tissue change | Surface / histologic correlate |
|---|
| 4. Immune Activation | Release of keratin and bacteria triggers a foreign body-type immune response [39]D5. | Recruitment of s, s, and secretion of and [76]C4[94]D5. | Acute abscess formation [73]D5. | | 5. Chronification | Persistent secretion of , , and by s [76]C4. | Psoriasiform epidermal hyperplasia and cellular heterogeneity [62]C4[94]D5. | Draining tunnels and chronic inflammation [73]D5[76]C4. |
Histopathologic correlation
| Mechanistic node | Histologic finding | Why it appears |
|---|---|---|
| Follicular occlusion | Keratin plugging [62]C4 | Abnormal differentiation leads to the accumulation of debris within the pilosebaceous unit [83]D5. |
| Epidermal reaction | Psoriasiform epidermal hyperplasia [62]C4 | Chronic inflammatory signaling and hyperproliferation in response to cytokines [62]C4[91]D5. |
| Immune infiltration | Increased s [76]C4 | Dysregulated innate and adaptive signals recruit T cells that secrete and into lesional skin [76]C4. |
| Tissue destruction | Draining tunnels [73]D5 | Persistent inflammation and diverse phenotypes facilitate the formation of epithelialized tracts [76]C4[94]D5. |
Barrier / immune axis summary
- Barrier and Keratinocyte Role: The primary defect in HS is located within the of skin regions rich in apocrine glands [39]D5[82]C4. Emerging evidence suggests that defective function is a critical driver of disease progression [87]C4. These cells act as active producers of pro-inflammatory cytokines, chemokines, and effector molecules, creating a permissive environment for bacterial infection and chronic inflammation [76]C4[91]D5.
- Immune Axis: The disease is characterized by a dysregulation of both innate and adaptive immune responses [83]D5[91]D5. Key players include infiltrating s that secrete and [76]C4. This inflammatory landscape involves distinct networks in both early and chronic stages, specifically the and pathways, which serve as the primary druggable targets for biologic therapies [73]D5[83]D5[91]D5.
- Genetic and Systemic Substrates: HS is influenced by a specific genetic signature and shares pathogenic mechanisms with other inflammatory conditions [39]D5. A large cross-sectional study identified a significant association between HS and , though no such association was found with [80]D5. Additionally, the immunobiology dysregulation of s may contribute to the pathogenesis [67]B3b.
Pearl: The transition of the HS treatment paradigm from broad to the targeted blockade of the and axes has fundamentally changed the of the disease, although approximately only 50% of patients achieve a clinical response to [58]C4[83]D5.
Epidemiology, Etiology and Risk Factors
Hidradenitis suppurativa (HS) is a chronic, inflammatory skin condition that carries a significant disease burden [108]A1a[119]D5. While global prevalence estimates are not yet standardized, current data suggest the following epidemiological profile [108]A1a:
| Metric | Value (with CI) | Population / setting | Source |
|---|---|---|---|
| Prevalence | 0.00033 to 4.1% | Global estimate | [151]D5 |
| Prevalence | 0.7 to 1.2% | European and US populations | [151]D5 |
| Prevalence | 1% or more | European studies | [123]D5 | | Incidence | 6.0 per 100,000 | Olmsted County, Minnesota (age and sex adjusted) | [148]B2b | | Peak Incidence | 18.4 per 100,000 | Young women aged 20 to 29 years | [148]B2b | | Age of Onset | Second or third decade | General population | [138]D5[152]D5 | | Sex Ratio | Disproportionately female | General population | [119]D5 | | Ethnic Skew | Disproportionately Black | American population | [119]D5 |
Etiology and Risk Factors
HS is a multifactorial disease where lesion formation centers on follicular hyperkeratosis and the occlusion of hair follicles within the pilosebaceous apocrine unit [101]A1a[115]D5[126]B2b. This process leads to chronic inflammation, deep seated nodules, abscesses, and irreversible skin damage such as tunnels and scarring [115]D5[138]D5.
| Factor | Type | Strength of Association | Mechanistic Link | Source |
|---|---|---|---|---|
| Behavioural | Significant association with severity | Identified as a driver of onset and progression; possible triggering factor | [117]D5[148]B2b[152]D5 | |
| Gender | Genetic/Biological | Significant association with severity | Females more likely to have axillary and inguinal involvement; males more likely to have perianal and buttocks involvement | [148]B2b[152]D5 |
| Genetic | Reported as highly heritable | Immune dysregulation and genetic predisposition are key contributors, though specific risk loci are not yet identified | [117]D5[133]B3b | |
| Mechanical stress | Environmental | Not reported | Driver of disease onset and progression | [117]D5 |
| Biological | Not reported | Altered skin and gut microbiome contribute to pathogenesis | [115]D5[117]D5 | |
| Hormones | Biological | Not reported | Contributing factor in pathogenesis | [115]D5 |
Skin of Colour and Phototype Note
- HS disproportionately affects Black Americans [119]D5.
- The disease is characterized by chronic inflammation that results in morbid scarring and the formation of sinus tracts [115]D5[138]D5.
- Systemic inflammation in HS is frequently associated with metabolic syndrome, subclinical atherosclerosis, and an increased risk of cardiovascular disease [59]B3b[138]D5.
- Patients with HS have double the risk of death from cardiovascular disease compared to those without the condition [123]D5.
- The condition is linked to other immune mediated diseases, specifically and spondyloarthropathy, though no association has been found with ulcerative colitis [80]D5[151]D5.
Pearl: is a significant risk factor associated with increased disease severity and may act as a primary trigger for disease onset [148]B2b[152]D5.
Clinical Presentation
Clinical Presentation
Hidradenitis suppurativa (HS) is a chronic, disabling inflammatory skin disease that primarily affects the hair follicles [171]A1b[178]A1c. The primary lesions are deep-seated, rounded nodules and abscesses that are typically recurrent and painful [151]D5[152]D5. These lesions center around follicular hyperkeratosis within the pilosebaceous-apocrine unit, where the initial pathological event is [115]D5[152]D5. As the disease progresses, secondary inflammation leads to the destruction of the pilo-sebaceo-apocrine apparatus and extension into the adjacent subcutaneous tissue [152]D5.
Secondary changes arise from chronic inflammation and the progression of structural damage [138]D5[197]A1c. These include the formation of draining sinus tunnels (also known as fistulae), indurations, and morbid scarring [115]D5[138]D5[152]D5. The attached clinical image demonstrates these characteristic features, where recurrent inflammation results in irreversible skin damage and the development of complex subcutaneous tracts [138]D5[152]D5. The morphology is highly heterogeneous, which can contribute to delays in diagnosis [185]D5. While erythema is a hallmark of the inflammatory phase, the presentation may vary by , where inflammation in darker skin tones may appear violaceous or grey-brown rather than bright red.
The distribution of HS is highly characteristic, primarily involving areas rich in pilosebaceous units and apocrine glands [185]D5[191]B2b[197]A1c. Typical regions of involvement include the axillae, inguinal area, submammary or inframammary folds, and the perianal or genitoanal regions [115]D5[138]D5[197]A1c. The configuration of lesions is often recurrent and can lead to extensive subcutaneous extension [152]D5[205]D5.
The dominant symptom of hidradenitis suppurativa is significant pain, which is often severe and debilitating [115]D5[169]A1c[197]A1c. In addition to pain, patients frequently experience (itch) and malodour [151]D5. These symptoms, combined with the disfiguring nature of the nodules and scars, lead to a profoundly negative impact on quality of life, physical function, and psychosocial health [104]A1a[178]A1c[185]D5. Patients often face body image issues, emotional distress, and an increased risk of depression or disordered eating behaviors [104]A1a[151]D5.
Signs and diagnostic manoeuvres, performance
| Sign / bedside test | How to elicit | Expected finding | Sensitivity | Specificity |
|---|---|---|---|---|
| Clinical Observation | Visual inspection of intertriginous zones for nodules, tunnels, and scars | Presence of characteristic lesions in typical locations | Not reported | Not reported |
| Disease Narrative | History taking focused on recurrence and chronicity | Report of recurrent, painful nodules at least twice in six months | Not reported | Not reported |
Distribution and configuration map
| Region / pattern | Typical involvement in this disease | Diagnostic value |
|---|---|---|
| Axillae | Frequent site of deep-seated nodules and scarring [115]D5[197]A1c | High; classic diagnostic site |
| Inguinal and Genitoanal | Common involvement of the groin, perineum, and perianal skin [138]D5[197]A1c | High; distinguishes from simple furunculosis |
| Inframammary folds | Involvement of the skin under the breasts [138]D5 | Moderate; common in female patients |
| Intertriginous areas | General predilection for skin-on-skin folds [185]D5[191]B2b | High; hallmark of disease distribution |
Pearl: The diagnosis of hidradenitis suppurativa is made across the room by recognizing the "trio" of recurrent, painful, deep-seated nodules, draining sinus tunnels, and bridged scarring localized specifically to the axillary or anogenital skin folds [138]D5[151]D5[197]A1c.
Clinical and Dermoscopic Diagnosis
The diagnosis of hidradenitis suppurativa (HS) is primarily established through clinical criteria [222]B3b. It is a chronic inflammatory skin disease characterized by recurrent inflamed nodules, painful deep abscesses, and chronic, draining sinus tracts [215]D5[222]B3b. The condition typically affects terminal hair follicles in intertriginous areas, most commonly the axillary, genitofemoral, and perianal regions [223]C4[225]B3b.
There is no pathognomonic test available for hidradenitis suppurativa [222]B3b. Diagnosis is often delayed by approximately 7 to 10 years, frequently due to low awareness of diagnostic criteria among nondermatological healthcare professionals, which leads to misdiagnosis [219]B2a.
The TEST OF CHOICE is a clinical examination focused on identifying the three diagnostic criteria: typical lesions, typical distribution, and chronicity. The GOLD STANDARD for definitive diagnosis, such as skin biopsy histopathology or direct immunofluorescence (DIF) for autoimmune bullous disease, is detailed in Section 6.
Bedside diagnostic tests, findings and performance
| Test | Expected finding | Sensitivity | Specificity | PPV | NPV |
|---|---|---|---|---|---|
| Recurrent nodules, sinus tracts, comedones, and scarring [212]A1b. | Not reported | Not reported | Not reported | Not reported | |
| Distended hair follicles [241]C4. | Not reported | Not reported | Not reported | Not reported | |
| examination | Not reported | Not reported | Not reported | Not reported | Not reported |
| Not reported | Not reported | Not reported | Not reported | Not reported | |
| Diascopy | Not reported | Not reported | Not reported | Not reported | Not reported |
| Dermographism testing | Not reported | Not reported | Not reported | Not reported | Not reported |
Dermoscopy features
| Dermoscopic structure | Appearance | Clinical correlate | Diagnostic weight |
|---|---|---|---|
| Distended hair follicles | Enlarged follicular openings | Follicular occlusion and distension [241]C4 | Moderate |
Note: While dermoscopy is used, specific validation studies for dermoscopic patterns in HS were not provided in the source claims.
Diagnostic algorithm
[212]A1b[215]D5[222]B3b[241]C4
Differential diagnosis
| Alternative diagnosis | Distinguishing morphology / dermoscopy |
|---|---|
| HS involves deep dermal abscesses and sinus tracts in intertriginous areas rather than just comedones on the face and trunk [215]D5[225]B3b. | |
| HS is characterized by chronicity and recurrence of nodules rather than an acute, spreading infection [212]A1b[222]B3b. | |
| HS presents with deep-seated painful nodules and scarring rather than superficial follicular pustules [212]A1b[213]D5. |
Imaging, particularly ultra-high frequency ultrasound (UHFUS), is a valuable adjunct for preoperative mapping. It enables the identification of subclinical lesions and the extension of tunnels and fistulas into clinically normal-looking paralesional skin that are not visible on clinical examination [240]C4[241]C4. Ultrasound findings in HS include increased dermal thickness (mean 3.3 plus or minus 1.0 mm compared to 1.4 plus or minus 0.3 mm in controls), lower echogenicity of the skin, and various fluid collections [241]C4.
Pearl: The presence of chronic, draining sinus tracts in intertriginous zones is the most characteristic bedside finding to rule in hidradenitis suppurativa [212]A1b[215]D5.
Dermatopathology, Immunofluorescence and Laboratory Diagnosis
Histopathology and special stains
The diagnosis of hidradenitis suppurativa (HS) is typically clinical, relying on the recognition of specific signs such as recurrent, painful, deep-seated nodules and abscesses in intertriginous areas [152]D5[185]D5[252]D5. However, biopsies are the gold standard for studying molecular alterations in the skin [247]D5. The primary event in HS is follicular occlusion, which leads to secondary inflammation and the eventual destruction of the pilo-sebaceo-apocrine apparatus [152]D5. This process often extends into the adjacent subcutaneous tissue [152]D5.
Methods for describing and reporting the histologic characteristics of HS tissue samples are not currently standardized [261]D5. To address this, a synoptic reporting protocol was developed using a modified Delphi technique to help consistently classify specimens based on histologic features [261]D5.
| Layer / compartment | Characteristic finding | Special stain (if used) | Mechanistic basis |
|---|---|---|---|
| and follicular occlusion | Not reported | Aberrant keratinization leading to ductal blockage [25]B3b. | |
| Secondary inflammation | Not reported | Follicular rupture and immune activation [152]D5. | |
| Increased thickness (mean 3.3 mm) and lower echogenicity | Not reported | Chronic inflammation of hair follicles and neutrophilic dermatosis [241]C4[246]B3b. | |
| Destruction of the pilo-sebaceo-apocrine apparatus | Not reported | Primary follicular occlusion followed by secondary infection and destruction [152]D5. |
Immunofluorescence and immunohistochemistry
Immunohistochemistry (IHC) is utilized in HS research to recognize involved skin compartments and characterize protein expression [262]B3b. While not used for routine clinical diagnosis in the same manner as autoimmune bullous diseases, IHC has confirmed the differential expression of key inflammatory markers [262]B3b.
| Test | Indication | Expected pattern in HS | Sensitivity | Specificity | Source |
|---|
| | Exclusion of mimics | Typically negative (used to rule out or ) | Not reported | Not reported | [259]D5 |
Molecular, patch and microbiologic testing
Molecular testing, including whole transcriptome profiling and quantitative real-time PCR, has been used to study the molecular taxonomy and signaling pathways of HS [262]B3b. These studies have identified dysregulated genes by comparing lesional skin to non-lesional skin and healthy controls [262]B3b. Notably, IL-1β is highly overexpressed in HS lesions, even exceeding levels found in psoriatic lesions [74]C4.
| Test | Indication | Expected finding | Source |
|---|---|---|---|
| Molecular taxonomy | Identification of dysregulated genes and signaling pathways | [262]B3b | |
| Confirmation of gene expression | Upregulation of IL-1β, IL-17A, and IL-17F | [245]D5[262]B3b | |
| (Blood test) | Monitoring disease activity | Strongly elevated levels correlating with inflammatory skin alterations | [74]C4 |
| Preoperative mapping | Detection of subclinical sinus tunnels and distended hair follicles | [241]C4[252]D5 | |
| Preoperative mapping | Detection of inflammatory activity and lesion extension | [241]C4[252]D5 |
The gold standard for this disease is clinical diagnosis based on physical examination and history, while skin biopsy histopathology remains the gold standard for studying the underlying molecular and cellular alterations.
Pearl: The presence of sinus tunnels (epithelial-lined tracks) in intertriginous, apocrine gland-bearing skin is the hallmark finding that separates hidradenitis suppurativa from simple furunculosis or isolated abscesses [152]D5[185]D5.
Severity Scoring and Risk Stratification
Severity instruments
of hidradenitis suppurativa (HS) requires a dual assessment of objective clinical severity and the subjective impact on the patient [150]A1c. While the Hurley Staging System remains a standard for severity rating, there is a recognized need for more reliable, validated measures for both clinical assessment and health-related quality of life [151]D5[175]B2c.
| Score | What it measures | Components | Range / cut-offs | Validated for | Source |
|---|---|---|---|---|---|
| Structural damage and disease extent | Abscesses, sinus tracts, and scarring | Stage I, II, or III | Severity rating | [151]D5 | |
| (International HS Severity Score System) | Dynamic inflammatory activity | Inflammatory nodules, abscesses, and draining tunnels | Not reported | Inflammatory lesions | [276]B2b |
| (Dermatology Life Quality Index) | Quality-of-life burden | Patient-reported impact on daily life | Not reported | Quality of life | [173]A1b |
| (HS Clinical Response) | Treatment response | Abscess and inflammatory nodule count | HiSCR 50, 75, 90 | Clinical trials | [173]A1b |
Treatment-target thresholds
Therapeutic management must be adapted to the clinical presentation and severity of the disease [197]A1c. Thresholds for treatment escalation often rely on the Hurley stage or the failure to achieve specific clinical response targets [150]A1c.
| Threshold | Definition | Action it triggers |
|---|---|---|
| Moderate-to-severe disease | Typically Hurley Stage II or III | Candidate for systemic therapies (e.g., TNF or IL-17 inhibitors) [138]D5 |
| Advanced disease | Extensive structural damage | Consideration for total wide excision [152]D5 |
| HiSCR 50 | 50% or greater reduction in abscesses and inflammatory nodules without increase in abscesses or draining fistulas | Primary endpoint for evaluating treatment response [173]A1b[174]A1b |
| NRS 30 | At least 30% reduction and 1-unit reduction in skin pain from a baseline NRS of 3 or greater | Secondary efficacy target for pain management [173]A1b |
| HiSCR 75 / 90 | 75% or 90% reduction in inflammatory criteria | Exploratory targets for high-level clinical response [174]A1b |
Risk stratification
Risk stratification in HS involves identifying markers of disease progression and screening for systemic comorbidities. Early management is critical to prevent the progression of irreversible structural damage, such as tunnel formation and morbid scarring [138]D5[197]A1c.
- Progression and Complications: HS is characterized by a high potential for progression and a significant diagnostic delay, which can lead to disabling conditions [197]A1c. Major complications include arthropathy and carcinoma [152]D5.
- Systemic Comorbidities: Systemic inflammation in HS is frequently associated with metabolic syndrome, inflammatory arthritis, and inflammatory bowel disease [138]D5. Other associated risks include cardiovascular disease, type II diabetes mellitus, and polycystic ovarian syndrome [151]D5.
- Psychosocial Burden: The disease carries a high psychosocial burden, including body image issues, emotional distress, depression, suicide, and substance use disorders [104]A1a[151]D5[172]A1a. These factors may increase the risk of maladaptive eating behaviors [104]A1a.
- Lifestyle Factors: Current smoking is strongly associated with HS prevalence (Odds ratio 12.55), as is overweight (Odds ratio 1.1 per BMI unit) [150]A1c.
- Emerging Assessment: Ultrasound imaging is an emerging tool for the assessment of deep-seated lesions that may not be fully captured by surface examination [151]D5.
Pearl: The transition to systemic or biologic therapy is typically justified when a patient reaches moderate-to-severe disease status, often defined by Hurley Stage II or III, or when the quality-of-life burden becomes significant [138]D5[150]A1c.
Dermatologic Emergencies and Acute Management
Dermatologic Emergencies and Acute
Hidradenitis suppurativa is a chronic inflammatory disease and there is no dermatologic emergency for this condition; management is elective [138]D5.
Hidradenitis suppurativa (HS) is a chronic, disabling inflammatory skin disorder that typically affects intertriginous regions, such as the axillae, groin, and anogenital areas [73]D5[122]D5. It is characterized by recurrent, painful, deep-seated nodules, abscesses, and draining tunnels [138]D5[152]D5. While the condition causes significant physical and psychological distress and profoundly impacts quality of life, it does not present with the acute, life-threatening skin failure seen in emergencies like Stevens-Johnson syndrome or [178]A1c[193]A1c.
Acute pharmacotherapy
Management of HS is often challenging and requires a combination of medical and surgical approaches [169]A1c. Medical strategies include topical therapies, systemic , and hormonal treatments [169]A1c. Early management is recommended to prevent the progression of irreversible structural damage, such as tunnel formation and morbid scarring [138]D5[197]A1c.
| Step | Intervention | Dose / route | CEBM level | Guideline class | Reference |
|---|---|---|---|---|---|
| First-line (Acute stage) | Antibiotics for early nodular lesions | Not specified | Not specified | Not specified | [152]D5 |
| Biologic therapy | Not specified | Not specified | Not specified | [122]D5 | |
| Biologic therapy | Not specified | Not specified | Not specified | [150]A1c | |
| Biologic therapy | Not specified | Not specified | Not specified | [138]D5 | |
| Biologic therapy | Not specified | Not specified | Not specified | [138]D5 | |
| Systemic therapy | Not specified | Not specified | Not specified | [150]A1c | |
| Systemic therapy | Tetracyclines | Not specified | Not specified | Not specified | [150]A1c |
| Systemic therapy | Clindamycin plus rifampicine | Not specified | Not specified | Not specified | [150]A1c |
| Intravenous therapy | Not specified | Not specified | Not specified | [194]B3b |
MANAGEMENT OF CHOICE: Combined medical and surgical approach based on individual subjective impact and objective severity [150]A1c[169]A1c.
DRUG OF CHOICE: Adalimumab is the only biologic approved by both the FDA and EMA for HS, showing a clinical response in approximately 50% of patients in phase III trials [122]D5.
Supportive care
- Infection surveillance: Bacterial colonization is typical in HS, though the efficacy of oral antibiotics can be unreliable [194]B3b.
- Wound and barrier care: Surgical intervention for limited abscesses may include incision with or without drainage [152]D5. For advanced disease, total wide excision followed by healing with secondary intention, flaps, or grafts is the only curative procedure [152]D5.
- Individualized management: Treatment should be tailored to the patient, particularly in rare cases of syndromic HS where no universally effective treatment exists [189]D5.
- Lifestyle modifications: Addressing risk factors is relevant to long-term management, as current smoking (OR 12.55) and being overweight (OR 1.1 per BMI unit) are significantly associated with higher prevalence [150]A1c.
Pearl: The presence of recurrent, painful, deep-seated nodules in flexural sites like the axillae or groin should trigger a diagnostic workup for HS to prevent irreversible scarring [138]D5[286]A1a.
Long-term and Definitive Management (Topical to Phototherapy to Systemic/Biologic Ladder)
Evidence ladder
| Tier | Agent / modality | Indication / severity gate | Pivotal trial | Effect size (verbatim with CI) | NNT / NNH | CEBM sub-level | Guideline class |
|---|
| Tier 2 / LASER | , (IPL) | Localized disease or adjunct to medical therapy [324]A1a | Randomized within-patient trial | Nd: YAG laser: 72.7% ± 13.0% lesion score reduction versus 22.9% ± 38.9% with topical therapy [324]A1a | Not derivable from reported data | 2b | B |
Guideline positioning
| Guideline body | Version | First-line | Step-up trigger | Strength |
|---|---|---|---|---|
| FDA / EMA | Current | Moderate-to-severe disease unresponsive to conventional systemic therapy [122]D5 | Strong | |
| FDA | Current | Moderate-to-severe disease [280]D5 | Strong |
Definitive / disease-modifying options
- Surgical Intervention: of hidradenitis suppurativa (HS) is determined by the disease phase. Surgery alone is often utilized for the burnout phase, while combined drug and surgical therapy is used for the destructive phase [138]D5. The choice between medication and surgery should be based on the disease stage and the degree of inflammation [124]D5.
- Laser and Light Therapies: has demonstrated significant efficacy, with one study showing a mean HS-LASI score decrease of 31.6% after two sessions [324]A1a. Fractional CO₂ combined with Nd: YAG therapy resulted in a 90% ± 20.5% improvement, with 80% of treated areas rated as clear at two weeks [324]A1a.
- Photodynamic Therapy: Intense Pulsed Light (IPL) monotherapy is associated with a 67% hidradenitis suppurativa clinical response (HiSCR) rate and a reduction in median modified severity scores from 8.5 to 4.5 [324]A1a. IPL-PDT using NMB gel led to a 77.3% ± 18.9% lesion reduction [324]A1a.
- Early Intervention Goals: The primary aim of definitive management is early intervention to prevent irreversible skin damage, such as scarring and the formation of tunnels [138]D5. HS is a chronic inflammatory disorder of the hair follicles that significantly impairs quality of life, necessitating durable efficacy and tolerability in treatment [100]A1a[178]A1c.
Practical sequencing
- Initial Management: Treatment typically begins with topical medications, systemic , or hormonal therapies [122]D5[169]A1c. Intralesional triamcinolone may be used for the management of acute lesions, although clinical trial data for acute management are limited [212]A1b.
- Escalation to Biologics: For moderate-to-severe disease, systemic options have expanded to include , , and [138]D5. Adalimumab is currently the only biologic approved by both the FDA and the EMA [122]D5. In phase III trials, adalimumab achieved a clinical response in approximately 50% of patients [122]D5.
- Comparative Efficacy: In moderate-to-severe cases, adalimumab was associated with the highest odds of achieving a HiSCR50 clinical response compared to placebo (OR = 2.81, 95% CI 2.01-3.92) [310]A1a. Bimekizumab administered every two weeks also showed increased odds of response (OR 2.24, 95% CI 1.52-3.29) [310]A1a.
- Impact of Disease Severity: A higher baseline tunnel count is a significant covariate that reduces the odds of clinical response (OR = 0.225) [310]A1a. When accounting for baseline tunnel counts, the odds of achieving a clinical response with secukinumab were no longer significant compared to placebo in some analyses [310]A1a.
- Combination Approaches: Optimal outcomes often require combining medical and surgical approaches [169]A1c. For example, LAight® therapy combined with topical clindamycin achieved a HiSCR of 63% compared to 36% for clindamycin alone [324]A1a.
- Future Directions: Agents targeting the IL-17 and /STAT pathways are currently the most advanced in clinical trials [122]D5. Identifying effective strategies remains complicated by the complex pathogenesis of the disease and the lack of simple scoring systems [124]D5[317]D5.
Pearl: Adalimumab remains the gold standard for moderate-to-severe disease as the only biologic approved by both the FDA and EMA, though its efficacy is significantly influenced by the presence of baseline tunnels [122]D5[310]A1a.
History and Evolution of Treatment
History and Evolution of Treatment
Hidradenitis suppurativa (HS) is a chronic, immune-mediated inflammatory skin disease characterized by painful nodules, abscesses, sinus tracts, and scarring [100]A1a[193]A1c[212]A1b[338]A1b. Historically, has been challenging due to the condition being underdiagnosed, often resulting in significant diagnostic delays that lead to disabling situations [197]A1c. The therapeutic landscape has evolved from limited conventional options to a complex, multi-modal approach that integrates medical and surgical interventions [169]A1c[197]A1c.
Therapeutic Timeline
Management strategies for HS have shifted as the understanding of the disease transitioned from a simple suppurative condition to a complex inflammatory disorder [100]A1a[314]A1b. The following table outlines the evolution of these standards.
| Era / Year | Standard of the Day | Pivotal Evidence | What Changed and Why |
|---|---|---|---|
| Conventional Era | Topical therapies, systemic , and retinoids [169]A1c[193]A1c. | S1 Guideline (Swiss HS Foundation) [193]A1c. | These treatments were often suboptimal and frequently failed to prevent disease progression in outpatient settings [273]A1b[337]A1b. |
| Early Biological Era (c. 2010s) | Introduction of targeted immunomodulating medications [169]A1c. | Phase 2 trial of [293]A1b. | Adalimumab, an antibody against tumor necrosis factor alpha, showed efficacy, establishing the role of targeted biologics in HS management [293]A1b. |
| Modern Integrated Era | Combination of medical therapy with procedural and surgical interventions [169]A1c[281]D5. | Expert consensus and clinical experience [193]A1c[212]A1b. | Recognition that medical therapy alone is often insufficient; procedural treatments like laser and surgery are now essential for long-term management [281]D5. |
Evolution of Medical and Procedural Approaches
Therapeutic approaches have evolved rapidly over the last decade, expanding to include hormonal therapies and a wide range of immunomodulating medications [169]A1c. Conventional treatments, such as systemic antibiotics and retinoids, remain part of the clinical framework, but there has been a significant shift toward emerging biological treatments [193]A1c. For acute lesions, clinical experience and prospective case series have suggested that intralesional triamcinolone may be useful, although clinical trial data for acute management remains limited [212]A1b.
Procedural treatments have become a cornerstone of management when used in combination with medical therapy [281]D5. Laser, light, and surgical procedures are now utilized to improve symptoms and quality of life [281]D5. Effective use of these procedures is considered important for the long-term management of the condition [281]D5. Despite these advancements, treatment for HS is still generally described as unsatisfactory, and there remains a high unmet need for more effective targeted therapies [209]A1b[273]A1b.
Why It Matters Now
The history of HS management demonstrates that early intervention is critical to prevent the progression of structural damage and improve the patient's prognosis and quality of life [197]A1c. Because HS is a chronic condition requiring durable efficacy and tolerability, the failure of early conventional monotherapies to halt progression has led to the current standard of adapted, multi-modal care [100]A1a[197]A1c. The complexity of the disease, which often involves associated comorbidities and particularly affects young women, necessitates a holistic approach that combines the latest biological insights with established surgical techniques [193]A1c[197]A1c[337]A1b.
Pearl: The evolution of HS treatment highlights that because medical and surgical treatments alone often have limited efficacy, a combined, early, and adapted approach is necessary to prevent disabling structural damage [169]A1c[197]A1c[314]A1b.
Procedural and Surgical Dermatology
Procedural and Surgical Dermatology
Procedural treatments for hidradenitis suppurativa (HS), a chronic dermatologic condition, are used in combination with medical therapy to improve patient symptoms and quality of life [281]D5[302]A1a. Surgery is the accepted method for managing HS when prevention of new lesions and medical therapy for established lesions fail [214]D5. While surgery is an important treatment modality, the nomenclature for various surgical approaches is inconsistent in the literature, and no international consensus exists to globally standardize terminology [15]D5[368]C4. This lack of standardization may contribute to misunderstanding or misclassification in procedural research [15]D5.
Procedure selection
| Procedure | Indication in this disease | Technique essentials (margin / depth / settings) | Cure / clearance rate | Source |
|---|---|---|---|---|
| Recurrent or severe disease [303]A1a | Descriptions vary: wide, local, radical, or regional margins [15]D5 | Varying reported success rates [28]A1a | [15]D5[28]A1a[303]A1a | |
| Tunnels or clinic-based [228]B3b[354]B2c | Uses scissors, electrosurgery, or laser; can be performed during incision and drainage [214]D5 | Not reported | [214]D5[228]B3b | |
| (CO2) | Tunnels [228]B3b | Ablative debulking of chronic lesions [213]D5 | Not reported | [213]D5[228]B3b |
| (IPL) | Reduction of flare-ups [213]D5 | Monotherapy targeting hair follicles and sebaceous glands [213]D5 | 67% clinical response (HiSCR) rate [324]A1a | [213]D5[324]A1a |
| STEEP | Tissue preservation [369]B2b | Skin-tissue-sparing excision with electrosurgical peeling [369]B2b | Known low recurrence rates [369]B2b | [369]B2b |
| Mini-unroofing | Localized lesions [214]D5 | Performed using a biopsy punch [214]D5 | Not reported | [214]D5 |
Outcomes and recurrence
| Procedure | Recurrence rate (with CI) | Follow-up duration | Source |
|---|---|---|---|
| Radical excision with STSG | No recurrence observed [373]C4 | Median 19.2 months [373]C4 | [373]C4 |
| Suggested lower rates of recurrence compared to other options [354]B2c | Not reported | [354]B2c | |
| Varying rates based on reconstructive strategy [303]A1a | Not reported | [303]A1a[368]C4 | |
| STEEP | Low recurrence rates [369]B2b | Not reported | [369]B2b |
Anaesthesia and instrumentation
| Setting | Anaesthesia / instrument choice | Rationale | Key precaution |
|---|---|---|---|
| Clinic-based | Local anaesthesia / Biopsy punch or scissors [214]D5[354]B2c | Mini-unroofing or deroofing of localized lesions [214]D5 | Not reported |
| Operating room | General anaesthesia / Electrosurgical unit [369]B2b[373]C4 | Radical excision or STEEP for severe disease [369]B2b[373]C4 | Monitor for delayed healing or keloids [373]C4 |
| Laser suite | CO2 laser or IPL [228]B3b[324]A1a | Ablative debulking or reduction of follicles and bacteria [213]D5 | Individualize based on disease severity [213]D5 |
Peri-procedural pearls
- Tunnels: Tunnels are considered one of the most difficult features of HS to manage; CO2 laser and surgical deroofing are the most common methods for treating them [228]B3b.
- Severe Disease: In patients with severe anogenital disease refractory to biologics, a two-stage radical excision followed by negative-pressure wound therapy and split-thickness skin grafts (STSG) has shown over 90% graft take and complete healing [373]C4.
- Energy-based Therapies: Outcomes for laser and light-based treatments are optimized when individualized to disease severity [213]D5. IPL monotherapy has been shown to reduce median modified severity scores from 8.5 to 4.5 [324]A1a.
- Combination Therapy: LAight combined with topical clindamycin achieved a 63% HiSCR response at week 16 [324]A1a.
- Complications: Potential surgical complications include delayed healing and the risk of donor site keloid scarring [373]C4.
- Patient Satisfaction: Skin-tissue-sparing excision with electrosurgical peeling (STEEP) is associated with high patient satisfaction in retrospective series [369]B2b.
Pearl: Deroofing is a preferred clinic-based technique for tunnels and localized lesions that may offer lower rates of postsurgical complications and recurrence compared to other local interventions [228]B3b[354]B2c.
Complications and Comorbidities
Cutaneous complications
Hidradenitis suppurativa (HS) is a chronic, inflammatory, neutrophilic skin disease that often presents as tender subcutaneous nodules [120]D5[325]B3b. The disease is progressive and may eventually result in fibrosis and the formation of extensive sinus tracts [37]D5[120]D5. In more severe cases, subepidermal draining tunnels may form [325]B3b.
| Complication | Mechanism | Incidence (with CI) | / prevention |
|---|---|---|---|
| Common complication of the disease [152]D5. | Not reported | Early diagnosis and treatment of concomitant diseases [155]D5. | |
| / | Characterized by hypertrophic scarring [152]D5. | Not reported | Prompt diagnosis and management from an early stage [155]D5. |
| Progressive inflammation leading to fibrosis [115]D5[120]D5. | Not reported | Early intervention to prevent disease progression [155]D5. | |
| Sequelae of nonhealing wounds [37]D5. | Not reported | Screening for carcinoma as a main complication [152]D5. |
Systemic comorbidities
Hidradenitis suppurativa is associated with a considerable clinical burden and various systemic comorbidities that contribute to poor health, impaired quality of life, and increased mortality risk [116]A1c[119]D5[325]B3b. The association between HS and suggests a similar pathogenic mechanism may contribute to both conditions [80]D5.
| Comorbidity | Strength of association (RR/OR/HR with CI) | Mechanistic / shared-pathway basis | Screening implication |
|---|---|---|---|
| Associated [37]D5[59]B3b[151]D5. | Shared inflammatory pathways [159]B3b. | Screening for cardiovascular risk factors [151]D5. | |
| Associated in large cross-sectional studies [80]D5. | Similar pathogenic mechanisms [80]D5. | Monitor for symptoms [155]D5. | |
| Linked immune-mediated disease [151]D5. | Shared immune-mediated pathways [151]D5. | Screening for arthropathy as a main complication [152]D5. | |
| Associated [151]D5. | Hormone-related disorder [37]D5. | Evaluation of hormonal status [37]D5. | |
| Increased risk [59]B3b. | Associated with subclinical atherosclerosis [59]B3b. | Management of cardiovascular risk factors [151]D5. | |
| Associated [151]D5. | Deleterious health habits and mood [37]D5. | Mental health screening [151]D5. | |
| No association found [80]D5. | N/A | N/A |
Treatment-related harms
Management of hidradenitis suppurativa must account for the potential adverse events of pharmacological interventions, as some drugs may be related to the onset of new comorbidities [155]D5.
- General considerations: Appropriate management requires prompt diagnosis and treatment of concomitant diseases to prevent potential iatrogenic harms [155]D5.
- Psychosocial impact: The location of lesions can lead to social embarrassment and body image issues [104]A1a[120]D5. These emotional stressors may increase the risk of maladaptive eating behaviors and disordered eating [104]A1a.
- Chronic symptoms: Uncontrolled disease can lead to chronic pain, pruritus, malodour, and sleep or sexual dysfunctions [151]D5.
Pearl: Screening for spondyloarthropathy and other forms of arthropathy is mandated by the presence of hidradenitis suppurativa, as it is considered a main complication of the disease [151]D5[152]D5.
Prognosis and Natural History
Natural history and prognosis
Hidradenitis suppurativa (HS) is a chronic, immune-mediated skin disorder that primarily affects intertriginous and apocrine-bearing regions [28]A1a[360]A1a. The disease follows a chronic-relapsing course characterized by cycles of inflammation, healing, and scarring [398]D5. While the spectrum of severity is wide, the condition is often debilitating and frequently underestimated by patients in its early stages, leading to delayed diagnosis and therapy [316]D5[393]B2b[399]D5.
| Course pattern | Typical trajectory | Relapse / clearance rate (with CI) | Prognostic marker | Source |
|---|---|---|---|---|
| Chronic-relapsing | Recurrent painful nodules, abscesses, and fistulas [279]B2a[286]A1a. | 22% progress to severe disease within 2 years in tertiary care [195]B2b. | Disease location below the umbilicus [303]A1a. | [195]B2b[303]A1a |
| Post-surgical | Recurrence varies significantly by the type of surgical closure used [28]A1a[303]A1a. | Primary closure: 22.0% (95% CI, 8.0%-40.0%) [303]A1a. Secondary intention: 11.0% (95% CI, 5.0%-20.0%) [303]A1a. Skin grafts: 2.0% (95% CI, 0.0%-5.0%) [303]A1a. | Surgical technique [303]A1a. | [303]A1a |
| Pregnancy-related | Majority of patients experience no change in symptoms [316]D5. | Remission: 20%. No relief: 72%. Clinical deterioration: 8% [316]D5. | Post-partum period (associated with flares) [316]D5. | [316]D5 |
Prognostic factors
Several factors influence the trajectory and severity of hidradenitis suppurativa. Severe stages of the disease are considered a significant therapeutic challenge and are associated with substantial restrictions on quality of life [367]C4.
| Prognostic factor | Direction of effect | Effect size (cited) | Source |
|---|---|---|---|
| Obesity | Increased severity | Not reported | [123]D5 |
| Smoking | Increased severity | Not reported | [123]D5 |
| Disease location (below umbilicus) | Increased recurrence | p =.006 | [303]A1a |
| Cardiovascular disease | Increased mortality | Double the risk of death compared to controls | [123]D5 |
| Mental health (Depression/Anxiety) | Increased mortality | Suicide rates more than double the rates in controls | [123]D5 |
Untreated versus treated course
Untreated hidradenitis suppurativa typically progresses through recurrent cycles of painful, odorous abscesses that evolve into draining sinus tracts and disfiguring scarring [398]D5. The amount of permanent scarring is directly proportional to the preceding tissue damage [393]B2b. In tertiary care settings, nearly one quarter of patients progress to severe disease within a two year period [195]B2b.
Guideline-concordant therapy aims to interrupt this cycle. While severe HS is often treatment recalcitrant, it is hypothetically avoidable through the early initiation of biologic treatment [393]B2b. For patients with moderate to severe disease (Hurley Stages II and III), medical alone is often insufficient, and surgical intervention is frequently required to achieve durable disease control [360]A1a. Surgical outcomes are highly dependent on the method: more extensive procedures like skin grafts or fasciocutaneous flaps show a significantly lower recurrence rate (2.0%) compared to primary closure (22.0%) [303]A1a. Treatment is generally challenging and long-standing [28]A1a.
Pearl: Disease location below the umbilicus is a significant baseline factor associated with overall recurrence [303]A1a.
Special Populations and Pregnancy
Special populations
(HS) is a chronic inflammatory dermatosis that primarily affects of reproductive age [323]B2a[395]B3b. While the disease usually occurs after , it can uncommonly affect and [106]B3b. requires unique considerations for different patient populations, though specific guidelines for these groups are currently lacking [170]A1c[412]C4.
| Population | Diagnostic / morphologic adjustment | Therapeutic adjustment (drug to avoid -> safer alternative) | Evidence / rationale | Source |
|---|---|---|---|---|
| and | Monitor for disease flares, especially in the period [316]D5. | Avoid and (insufficient data) -> , - , , , or [414]D5. | HS may increase adverse pregnancy outcomes; safety data supports specific and certain biologics [323]B2a[414]D5. | [323]B2a[414]D5 |
| Conduct hormonal investigations, as imbalances are more common than in adults [121]D5. | Avoid early systemic use in mild cases -> (mild); , , or (moderate) [121]D5[412]C4. | Prepubertal onset is strongly linked to hormonal disorders and genetic susceptibility [412]C4. | [121]D5[412]C4 | |
| Not reported | Not reported | Not reported | Not reported | |
| IV-VI | Not reported | Not reported | Not reported | Not reported |
| Immunosuppressed | Not reported | Not reported | Not reported | Not reported |
Pregnancy management detail
disproportionately affects women of childbearing potential [395]B3b[405]B2b. Patients often report concerns regarding the heritability of the condition, its impact on , and the implications for and [410]C4. Many patients feel they receive inadequate information and support from clinicians regarding these reproductive health concerns [410]C4.
The disease course during is variable, and the underlying physiological reasons for these fluctuations are not understood [316]D5[395]B3b. A minority of patients (20%) experience symptom remission during pregnancy [316]D5. However, the vast majority (72%) experience no relief, and some may experience clinical deterioration [316]D5. Disease flares are also observed in the period [316]D5[395]B3b.
Management strategies involve multimodal therapy using both local and systemic treatments [407]A1c. Evidence supports the relative safety of , , , and the combination of and in and women [414]D5. Among , and have accumulated safety data for this population [414]D5. has shown promising safety data, though more efficacy data specifically for HS is required [414]D5. Conversely, further research is necessary to evaluate the safety of newer medications like and in patients who are pregnant or [414]D5.
Pearl: is the biologic with the most promising safety data for use during pregnancy, though it is often overlooked in favor of more established HS treatments [414]D5.
Prevention, Screening and Surveillance
Prevention and maintenance
(HS) is a chronic inflammatory skin disorder affecting skin appendages [401]A1a[428]B2b. Primary prevention focuses on early identification to mitigate the significant diagnostic delay of 7 to 10 years often seen in this condition [219]B2a. Low awareness of diagnostic criteria among nondermatological healthcare professionals contributes to this delay [219]B2a. Screening questionnaires have been proposed to aid in diagnosis, including a validated tool used in the Global Hidradenitis Suppurativa Atlas (GHiSA) Global Prevalence Study [219]B2a.
Maintenance of remission often requires long term medical or surgical strategies. In PASH syndrome ( , acne, and suppurative hidradenitis), maintenance therapy is necessary to prevent disease relapse [387]C4. Anecdotal reports support using a combination of medical therapy and surgery for this purpose [387]C4. For patients with refractory HS, dapsone may serve as a safe alternative maintenance option, particularly for women of reproductive age [432]C4.
| Strategy | Type (primary/secondary) | Target population | Modality / regimen | Evidence / guideline class | Source |
|---|---|---|---|---|---|
| Early Diagnosis | Primary | Patients with suspected HS | Validated screening questionnaires (e.g., GHiSA) | Proposed / Validated | [219]B2a |
| Infectious Disease Screening | Secondary | Patients starting immunomodulatory therapy | Screening for Hepatitis B, Hepatitis C, and Tuberculosis | Consensus recommendation | [426]D5 |
| Relapse Prevention | Secondary | Patients with PASH syndrome | Combination of antibiotic therapy and surgery | Anecdotal reports | [387]C4 |
| Maintenance Therapy | Secondary | Refractory HS | Dapsone | Clinical study | [432]C4 |
Screening and surveillance
Surveillance in HS is critical for monitoring treatment safety and detecting malignant transformation. Because HS can lead to (SCC) of the skin, careful surveillance of lesions is essential [434]C4. This is particularly important for lesions in the perineal region to ensure the early diagnosis of secondary malignancies [434]C4. SCC arising from HS is associated with high mortality and recurrence rates [434]C4. Risk factors that may be associated with SCC in these patients include smoking and [431]C4.
Before initiating immunomodulatory therapies, including biologics and systemic immunosuppressants, patients must undergo infectious disease screening [426]D5. Current protocols are adopted from chronic plaque psoriasis guidelines, as no HS specific guidelines for pre-therapy infectious screening currently exist [426]D5. Standard screening includes testing for tuberculosis, hepatitis B, and hepatitis C [426]D5. Clinical assessment also determines the need for screening for uncommon or tropical diseases such as leprosy, leishmaniasis, and [426]D5.
| At-risk state | Surveillance modality | Interval (cited guideline) | What escalates it | Source |
|---|---|---|---|---|
| Chronic HS lesions | Clinical examination | Not specified; focus on perineal region | Presence of non-healing or changing lesions (SCC risk) | [431]C4[434]C4 |
| Immunomodulatory therapy | Infectious disease screening | Prior to therapy initiation | History of exposure to tropical diseases (leprosy, leishmaniasis) | [426]D5 |
| Long-term biologic use | Longitudinal surveillance and pooled registries | Ongoing during treatment | Use of JAK inhibitors or high-dose biologics | [430]A1a[435]D5 |
Pearl: Careful clinical surveillance of perineal lesions is the most critical measure for the early detection of secondary squamous cell carcinoma, a complication with high mortality [434]C4.
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