🧑‍⚕️ Acne Vulgaris is a chronic inflammatory disorder of the pilosebaceous unit, affecting adolescents and adults. It presents with comedones, inflammatory papules/pustules, nodules, and sometimes cysts. 💡 Acne is multifactorial: genetics, hormones, immune response, microbiome, environment, and lifestyle all contribute. Early recognition and structured treatment prevents scarring and psychological morbidity.

🧬 Aetiology & Risk Factors

🧬 Genetic predisposition: First-degree relatives with acne → ↑ risk. Polymorphisms in androgen receptor, TNF-α, IL-1α, filaggrin.
💡 Androgen excess: Testosterone → DHT via 5α-reductase in sebaceous glands → sebaceous hyperplasia and ↑ sebum production 🧴.
🧪 Sebum composition: Rich in triglycerides, squalene, free fatty acids → follicular occlusion, lipid peroxidation, bacterial growth.
🧫 Follicular hyperkeratinisation: Abnormal keratinocyte differentiation → comedones. Retinoid pathways dysregulated.
🦠 Cutibacterium acnes colonisation: Triggers TLR2 → ↑ IL-1β, IL-8, TNF-α → neutrophil recruitment → pustules. Biofilm formation prolongs inflammation.
🔥 Inflammatory response: Early lesions show CD4⁺ T cells, macrophages, neutrophils → papules, pustules, nodules.
💊 Drugs: Corticosteroids, lithium, anticonvulsants, androgenic steroids.
🥗 Diet & lifestyle: High GI foods → ↑ insulin/IGF-1 → sebum synthesis; dairy may ↑ androgenic activity.
⚖️ Endocrine disorders: PCOS, Cushing’s, congenital adrenal hyperplasia → severe acne.
🌞 Environmental: UV light, occlusion, heat, humidity, pollution.

🔬 Pathophysiology (Stepwise)

Acne lesions arise from interaction of four main pathogenic processes:

Sebaceous gland hyperactivity – DHT and IGF-1 ↑ sebum. Lipid peroxidation → comedone inflammation.
Follicular hyperkeratinisation – Abnormal keratin shedding → microcomedone → clinical comedones.
Microbial colonisation – C. acnes proliferates → activates innate immunity (TLR2, inflammasome) → inflammatory cytokines.
Inflammatory cascade – Neutrophils, lymphocytes, macrophages → papules, pustules, nodules, scarring. Chronic lesions → fibrosis, hyperpigmentation, keloids.

🖼️ Illustrations

💡 Key Teaching Points

Acne is a multifactorial inflammatory disease, not just “hormones” or “hygiene.”
DHT drives sebaceous hyperplasia → androgen-blocking therapy may help.
Innate immunity (TLR2, cytokines) → target for topical retinoids and anti-inflammatory agents.
Systemic triggers (stress, diet, drugs, endocrine disorders) modulate severity and chronicity.
Pathophysiology guides stepwise treatment: retinoids normalize keratinisation, benzoyl peroxide reduces bacteria, antibiotics/isotretinoin reduce inflammation & sebaceous activity.

💊 Management – NICE-Compliant & Stepwise

Guided by severity, , and response. Educate patients on expected 8–12 week onset and safe use. Discuss psychosocial impact and adherence.

🔎 Principles

Treat all 4 pathogenic processes: sebum, hyperkeratinisation, bacterial load, inflammation.
Use combination therapy where possible to improve efficacy & reduce resistance.
Review every 8–12 weeks; adjust therapy accordingly.
Monitor for side effects (photosensitivity, irritation, antibiotic resistance, systemic toxicity).

📊 Stepwise Treatment

Severity	Recommended Therapy	Monitoring / Notes
Mild (comedonal)	Topical benzoyl peroxide 5–10% once/twice daily Topical retinoid (adapalene/tretinoin) nightly Combination therapy (adapalene + benzoyl peroxide) Topical clindamycin only with benzoyl peroxide	Reduce comedone formation and inflammation Warn about dryness/irritation; moisturise Photosensitivity 🌞 → SPF 30+ daily Review 8–12 weeks
Moderate (papules/pustules)	Topical therapy as above + oral antibiotics 3–6 months Doxycycline 100 mg/day Lymecycline 408 mg/day Erythromycin if pregnancy or tetracycline contraindicated Continue topical benzoyl peroxide + retinoid	Never oral antibiotics alone ❌ (always combine) Monitor for GI upset, photosensitivity, fungal infections Review at 12 weeks
Severe / Nodulocystic	Oral isotretinoin 0.5–1 mg/kg/day for 16–24 weeks	Specialist initiation & monitoring Baseline LFTs, fasting lipids, pregnancy test Monthly monitoring during treatment Strict pregnancy prevention programme 🚫🤰 Monitor mood, headache, dry skin, lipid levels
Hormonal Acne (Women)	COCP with anti-androgenic component (co-cyprindiol) Spironolactone (off-label, specialist guidance)	Assess clot risk, CV history before COCP Spironolactone: monitor BP/electrolytes Useful in PCOS-related acne

📌 Practical UK Notes

Benzoyl peroxide reduces resistance, use with antibiotics
Topical retinoids: start 2–3 nights/week, gradually increase
Oral antibiotics: stop at 3–6 months or if no response by 12 weeks
Isotretinoin: pregnancy prevention, monthly labs, monitor side effects
Gentle, non-comedogenic skincare; SPF ≥30 daily
Adherence: 6–12 weeks to see improvement

⚠️ Urgent / Specialist Considerations

Acne fulminans or sudden severe flare → urgent dermatology referral
Resistant acne after multiple courses → dermatology opinion
Endocrine disorders suspected (PCOS, virilisation) → endocrine/dermatology assessment

📈 Long-Term Maintenance

Topical retinoid + benzoyl peroxide to prevent relapse
Assess ongoing hormonal therapy needs
Address psychosocial impact, counselling or support groups

📚 UK Guidelines

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Acne Vulgaris ✅