Acne Vulgaris is the most common chronic skin condition of adolescence, affecting up to 80–90% of teenagers worldwide 🌍. It is a disease of the pilosebaceous unit, characterised by comedones, inflammatory papules/pustules, and in severe cases, nodules and cysts. Although often dismissed as “cosmetic,” acne can cause significant scarring and psychological morbidity. 💡 Remember: acne is not caused by poor hygiene.

📊 Epidemiology

• Peak onset: 12–18 years; often persists into the mid-20s, occasionally beyond.
• More severe in males (androgen-driven), but more persistent in females.
• Common across all ethnic groups; post-inflammatory pigmentation more problematic in darker skin tones.
• Strong genetic influence – family history is a risk factor.

🧬 Pathophysiology

Acne arises from a combination of 4 interlinked processes within the pilosebaceous unit:

1. Sebum overproduction due to androgen stimulation of sebaceous glands.
2. Follicular hyperkeratinisation → formation of keratin plugs (comedones).
3. Colonisation with Cutibacterium acnes (formerly Propionibacterium acnes) → promotes inflammation.
4. Inflammatory cascade → papules, pustules, nodules, scarring.

Additional factors: diet (high glycaemic index foods, dairy 🥛), drugs (steroids, lithium, antiepileptics), and endocrine disorders (e.g. PCOS).

🔎 Clinical Features

• Lesions: open comedones (blackheads), closed comedones (whiteheads), papules, pustules, nodules, cysts.
• Distribution: face, chest, shoulders, and back.
• Symptoms: may be itchy or painful; often psychological distress is prominent.
• Variants:
  • Acne conglobata – severe, nodulocystic, sinus tracts, scarring.
  • Acne fulminans – sudden, ulcerative acne with systemic upset (fever, arthralgia, ↑ESR/CRP).

⚖️ Differential Diagnoses

• Rosacea 🌹 (no comedones, later age, flushing, telangiectasia).
• Perioral dermatitis (papules around mouth, spares vermillion border).
• Folliculitis (monomorphic pustules, bacterial/fungal causes).
• Drug-induced acneiform eruptions (steroids, lithium, anti-TB drugs).
• Keratosis pilaris (rough follicular papules on arms/thighs).

⚠️ Complications

• Physical: Atrophic scarring (ice-pick, boxcar), hypertrophic scars, keloids.
• Pigmentation: Post-inflammatory hyperpigmentation (esp. darker skin).
• Psychological: Depression, anxiety, social withdrawal, suicidal ideation.
• Systemic: Acne fulminans (rare, emergency).

🧪 Investigations

• Diagnosis is clinical ✅ – based on morphology and distribution.
• Consider investigations if:
  • Sudden severe onset → exclude drug-induced acneiform rash.
  • Signs of hyperandrogenism (oligomenorrhoea, hirsutism, obesity) → screen for PCOS (testosterone, LH, FSH, prolactin, pelvic US).
  • Refractory acne → consider culture/swabs (to exclude Gram-negative folliculitis).

💊 Management (Stepwise)

Treatment depends on severity, duration, and impact. Always consider psychological burden.

🌍 Lifestyle & Self-care Advice

• 🧴 Use gentle cleansers; avoid excessive washing or scrubbing (can worsen irritation).
• 🚫 Avoid oily/cosmetic products that are “comedogenic.”
• 🍫 Diet: evidence is mixed, but high-GI foods & dairy may exacerbate acne in some patients.
• ⏳ Emphasise adherence: treatments take 6–8 weeks before improvement is seen.

🧠 Exam Pearls

– Comedones = diagnostic of acne vulgaris. Rosacea never has comedones. – Always combine oral/topical antibiotics with benzoyl peroxide to prevent resistance. – Isotretinoin is highly effective but carries risks: teratogenicity, mood disturbance, hepatotoxicity, ↑ triglycerides. – Psychological morbidity is common: always ask about mood & self-esteem. – Acne fulminans = sudden severe acne + systemic upset → dermatology emergency.

🖼️ Illustrations