Hidradenitis Suppurativa MCQ — NEET PG Practice Question | NEETPGAI
Hidradenitis Suppurativa
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hand Dermatology
A 28-year-old woman with a 6-year history of hidradenitis suppurativa presents with recurrent, painful inflammatory nodules and purulent drainage from sinus tracts in the bilateral axillae and inguinal folds. She has tried topical clindamycin, oral doxycycline, and hormonal therapy without sustained improvement. Examination reveals multiple interconnected sinus tracts with rope-like scarring consistent with Hurley stage III disease. Her BMI is 32 kg/m², and she continues to smoke 15 cigarettes daily. The treatment approach marked **A** in the diagram—combining adalimumab (anti-TNF biologic) with wide surgical excision—is indicated. Which of the following best explains why TNF-α inhibition is effective in this patient's condition?
A. TNF-α is produced exclusively by apocrine glands and inhibiting it reduces sebum production
B. TNF-α directly causes follicular hyperkeratosis and occlusion of the pilosebaceous unit
C. TNF-α is a key driver of the aberrant IL-17/IL-23 axis and dysregulated innate immunity underlying HS pathogenesis
D. TNF-α is the primary bacterial pathogen driving secondary infection in HS sinus tracts
Explanation
Why option B is right
TNF-α is a central cytokine in the aberrant IL-17/IL-23/TNF-α axis that drives the pathogenesis of hidradenitis suppurativa. The NEJM 2019 adalimumab trials (PIONEER I and II) and AAD HS Guidelines 2019 establish that TNF-α inhibition is effective because HS is fundamentally an inflammatory disorder of dysregulated innate immunity, not a primary bacterial infection. By blocking TNF-α, adalimumab suppresses the inflammatory cascade that perpetuates follicular rupture, deep dermal inflammation, and sinus tract formation. This is why adalimumab is FDA-approved and level 1 evidence for moderate-to-severe HS refractory to conventional therapy.
Why each distractor is wrong
Option A: TNF-α is not a bacterial pathogen. Bacterial infection is a secondary phenomenon in HS, not the primary driver. The pathogenesis centers on follicular occlusion and aberrant innate immunity, not bacterial colonization. TNF-α inhibition works because it targets the underlying inflammatory dysregulation, not because it is antimicrobial.
Option C: Follicular hyperkeratosis and occlusion of the pilosebaceous unit are the initiating events in HS pathogenesis, but TNF-α does not directly cause these structural changes. Rather, TNF-α is part of the downstream inflammatory response that amplifies tissue destruction after follicular rupture. TNF-α inhibition does not reverse hyperkeratosis but prevents the inflammatory cascade that follows.
Option D: TNF-α is produced by multiple cell types (macrophages, dendritic cells, T cells, keratinocytes) throughout inflamed skin, not exclusively by apocrine glands. Apocrine glands are the anatomic location of disease, but TNF-α's role is systemic and immunologic, not related to sebum production. Sebum reduction is not the mechanism of TNF-α inhibition in HS.
High-YieldNEET PG
HS is a chronic inflammatory disorder of dysregulated innate immunity (IL-17/IL-23/TNF-α axis), NOT a primary bacterial infection—this is why antibiotics alone fail and biologics succeed.
NEJM 2019 Adalimumab in HS; AAD HS Guidelines 2019
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