Skip to content

Module 3: Acne and Rosacea

  1. Describe the pathophysiology and aetiological factors of acne vulgaris and rosacea, including hormonal influences, microbial involvement (e.g., Cutibacterium acnes), and inflammatory pathways.

  2. Differentiate the clinical subtypes and severity grading of acne and rosacea, and correlate these with appropriate diagnostic criteria and patient history.

  3. Formulate evidence-based management plans for acne and rosacea, incorporating pharmacological (topical and systemic), non-pharmacological, and lifestyle interventions, while considering patient-specific factors such as age, comorbidities, and psychosocial impact.

1. Pathophysiology and Clinical Presentation

Section titled “1. Pathophysiology and Clinical Presentation”
  • Understand the four pathogenic factors:

    • Sebum overproduction (androgen-driven).

    • Follicular hyperkeratinization leading to comedone formation.

    • Cutibacterium acnes proliferation in the pilosebaceous unit.

    • Inflammatory response involving cytokines and neutrophils.

  • Differentiate lesion types:

    • Non-inflammatory: open (blackheads) and closed (whiteheads) comedones.

    • Inflammatory: papules, pustules, nodules, cysts.

  • Recognize distribution patterns:

    • Face (T-zone), chest, upper back, shoulders.
  • Classify severity:

    • Mild: comedonal.

    • Moderate: papulopustular.

    • Severe: nodulocystic or conglobata.

Table 3.1: Types of Lesions

Lesion TypeDescription
Superficial lesionsOpen and closed comedones (blackheads and whiteheads) — comedones
Papules (small, tender red bumps)
Pustules (white or yellow “squeezable” spots)
Deeper lesionsNodules (large painful red lumps)
Pseudocysts (cyst-like fluctuant swellings)
Secondary lesionsExcoriations (picked or scratched spots)
Erythematous macules (red marks from recently healed spots, best seen in fair skin)
Pigmented macules (dark marks from old spots, mostly affecting those with dark skin)
Scars of various types — scars

Comedones, papules, and pustules in acne

Fig. 3.1: Acne — comedones, papules, and pustules

Image sourced from DermNet.

  • Identify key features:

    • Persistent centrofacial erythema, telangiectasia, papules/pustules.
  • Understand subtypes:

    • Erythematotelangiectatic: flushing, visible vessels.

    • Papulopustular: acne-like lesions without comedones.

    • Phymatous: thickened skin, rhinophyma.

    • Ocular: blepharitis, conjunctivitis, dry eyes.

Papular rosacea on the cheeks

Papulopustular rosacea on the cheeks

Fig. 3.2: Rosacea of the cheeks

  1. Papular rosacea of the cheeks
  2. Papulopustular rosacea of the cheeks

Image sourced from DermNet.

  • Recognize triggers:

    • Heat, alcohol, spicy food, UV exposure, stress.

2. Diagnostic Reasoning and Clinical Skills

Section titled “2. Diagnostic Reasoning and Clinical Skills”
  • History taking:

    • Onset, duration, progression, aggravating/relieving factors.

    • Menstrual history (for hormonal acne).

    • Medication history (e.g., steroids, lithium).

    • Psychosocial impact (school, work, relationships).

  • Physical examination:

    • Lesion morphology, distribution, and presence of scarring.

    • Rule out differential diagnoses: perioral dermatitis, seborrhoeic dermatitis, lupus, steroid-induced acne.

  • Investigations (if indicated):

    • Hormonal profile (e.g., PCOS suspicion).

    • Skin swabs (if secondary infection suspected).

    • Dermoscopy (for rosacea telangiectasia).

  • Topical therapy (first line for mild to moderate):

    • Retinoids: adapalene, tretinoin — normalize keratinization.

    • Benzoyl peroxide: antibacterial and keratolytic.

    • Topical antibiotics: clindamycin, erythromycin (always combine with benzoyl peroxide to prevent resistance).

  • Systemic therapy:

    • Oral antibiotics: doxycycline, minocycline (moderate–severe).

    • Hormonal therapy: combined oral contraceptives, anti-androgens (e.g., spironolactone).

    • Isotretinoin: for severe nodulocystic acne — requires monitoring for teratogenicity, liver function, and lipids.

  • Adjunctive care:

    • Non-comedogenic skincare.

    • Avoid over-washing or abrasive scrubs.

    • Sun protection.

  • Topical agents:

    • Metronidazole, azelaic acid, ivermectin.

    • Brimonidine gel for transient vasoconstriction (erythema).

  • Systemic therapy:

    • Doxycycline (low dose for anti-inflammatory effect).

    • Isotretinoin (low dose for refractory cases).

  • Procedural options:

    • Laser or IPL for telangiectasia.
  • Lifestyle modification:

    • Identify and avoid triggers.

    • Use gentle cleansers and sunscreen.

4. Psychosocial Impact and Communication Skills

Section titled “4. Psychosocial Impact and Communication Skills”
  • Acknowledge emotional burden:

    • Acne and rosacea can lead to low self-esteem, social withdrawal, and depression, especially in adolescents and young adults.
  • Empathetic communication:

    • Validate patient concerns.

    • Set realistic expectations for treatment timelines (e.g., 6–8 weeks for visible improvement).

  • Patient education:

    • Importance of adherence.

    • Avoiding self-medication or overuse of cosmetics.

  • Referral:

    • Consider mental health support for patients with significant psychological distress.

Case 1: Acne Vulgaris in an Adolescent Female

Section titled “Case 1: Acne Vulgaris in an Adolescent Female”

Clinical Scenario: A 17-year-old female presents with a 6-month history of worsening acne on her face and upper back. She reports oily skin and irregular menstrual cycles. She has tried over-the-counter facial cleansers with minimal improvement. Examination reveals multiple closed comedones, inflammatory papules, and a few pustules on the cheeks and forehead. No nodules or cysts are noted.

Discussion Points:

  • Pathophysiology: Discuss the role of androgens, sebum production, follicular hyperkeratinization, and Cutibacterium acnes.

  • Differential diagnosis: Consider PCOS, steroid-induced acne, or acneiform eruptions.

  • Severity grading: Mild to moderate inflammatory acne.

  • Investigations: Consider a hormonal profile (LH, FSH, testosterone) if PCOS is suspected.

  • Management:

    • Topical retinoid + benzoyl peroxide.

    • Consider oral contraceptives if PCOS is confirmed.

    • Emphasize adherence and realistic expectations.

Clinical Scenario: A 45-year-old man presents with persistent facial redness and occasional pustules on his nose and cheeks. He reports frequent flushing after drinking alcohol or eating spicy food. He denies comedones or oily skin. Examination reveals centrofacial erythema, telangiectasia, and a few papulopustular lesions. No nodules or cysts are seen.

Discussion Points:

  • Diagnosis: Papulopustular rosacea.

  • Differentiation from acne: Absence of comedones, older age group, presence of flushing and telangiectasia.

  • Triggers: Alcohol, spicy food, temperature changes.

  • Management:

    • Topical metronidazole or ivermectin.

    • Oral doxycycline (low dose) for inflammation.

    • Lifestyle modification and sun protection.

    • Consider laser therapy for telangiectasia.

Tap an answer to check yourself — the correct option and an explanation appear once you choose.

Q1 A 17-year-old girl with moderate inflammatory acne (closed comedones, papules, and a few pustules) has not improved with over-the-counter cleansers. Which is the most appropriate first-line treatment?

Q2 A 45-year-old man has centrofacial erythema, telangiectasia, and papulopustules with flushing after alcohol and spicy food. Which feature is most characteristic of rosacea and not typically seen in acne vulgaris?

SAQ

List four pathogenic mechanisms involved in acne vulgaris and explain how each contributes to lesion formation.

Reveal model answer
Model answer
  1. Sebum overproduction — driven by androgens (particularly during puberty), producing a lipid-rich, anaerobic environment in the pilosebaceous unit that promotes bacterial proliferation and comedone formation.

  2. Follicular hyperkeratinization — increased keratinocyte proliferation combined with reduced desquamation obstructs the pilosebaceous duct; this results in non-inflammatory lesions — open comedones (blackheads) and closed comedones (whiteheads).

  3. Colonization by Cutibacterium acnes — anaerobic bacteria proliferate within the blocked follicle, producing lipases and proteases that degrade sebum and release pro-inflammatory fatty acids, further stimulating the immune response.

  4. Inflammatory response — activation of innate immunity triggers cytokine and neutrophil recruitment, converting comedones into inflammatory lesions: papules and pustules (superficial) and nodules and cysts (deeper). Severe or persistent inflammation can lead to scarring and post-inflammatory pigmented macules.

Additional contextual points:

  • Acne most commonly affects the face (T-zone), chest, upper back, and shoulders — areas with the highest density of sebaceous glands.
  • Severity is graded as mild (predominantly comedonal), moderate (papulopustular), or severe (nodulocystic or conglobata).
  • Aggravating factors include hormonal changes (e.g., menstrual cycle, PCOS), medications (e.g., steroids, lithium), and occlusion.

SAQ 2: Comparison of Acne Vulgaris and Rosacea

Section titled “SAQ 2: Comparison of Acne Vulgaris and Rosacea”

SAQ

Compare and contrast acne vulgaris and rosacea in terms of age of onset, lesion types, distribution, presence of comedones, and common triggers.

Reveal model answer
Model answer
FeatureAcne VulgarisRosacea
PathophysiologyAndrogen-driven sebum overproduction; follicular hyperkeratinization; Cutibacterium acnes colonization; inflammatory cytokine/neutrophil responseChronic vascular and inflammatory disorder; neurovascular dysregulation causing trigger-induced vasodilation; dysregulation of innate immunity
Age of onsetAdolescents and young adults (12–25 years)Adults >30 years (peak 40–60 years)
Lesion typesOpen/closed comedones (blackheads/whiteheads); papules, pustules; nodules and cysts (severe); scarring and pigmented maculesPersistent erythema and flushing; telangiectasia; papules and pustules (without comedones); phymatous skin thickening (e.g., rhinophyma); ocular involvement (blepharitis, dry eyes)
DistributionFace (T-zone), chest, upper back, shouldersCentral face: cheeks, nose, chin, forehead
ComedonesPresent — hallmark of acneAbsent — key distinguishing feature
TriggersHormonal changes, oily skin, occlusion, medications (steroids, lithium), stressAlcohol, spicy food, heat, UV sun exposure, emotional stress, hot beverages
InvestigationsUsually clinical; hormonal profile (LH, FSH, testosterone) if PCOS suspected; skin swabs if secondary infection suspectedUsually clinical; rule out lupus and seborrhoeic dermatitis; dermoscopy for telangiectasia; ophthalmology referral if ocular symptoms
Psychosocial impactLow self-esteem, social withdrawal, depression — especially in adolescents and young adultsFacial redness may cause embarrassment and anxiety; often under-recognized
OSCE

Station: A 17-year-old girl is distressed about acne that has not responded to over-the-counter medication. Counsel her on the aetiology and treatment.

Self-assess against checklist

Tick each point you covered, then check your score.

  • Introduces self and confirms the patient’s identity; establishes a non-judgmental, empathetic tone.
  • Explains that acne is a multifactorial condition involving four key mechanisms: androgen-driven sebum overproduction, follicular blockage (hyperkeratinization), Cutibacterium acnes bacterial colonization, and the resulting inflammatory response.
  • Explains the lesion spectrum: non-inflammatory lesions (blackheads and whiteheads) progress to inflammatory lesions (papules, pustules, nodules, cysts) in more severe disease.
  • Describes typical distribution: face (T-zone), chest, and upper back.
  • Asks about menstrual history and any suspicion of PCOS as a contributory hormonal factor.
  • Asks about current or recent medications that may worsen acne (e.g., steroids, lithium).
  • Outlines the treatment plan for mild-to-moderate acne: topical retinoid (adapalene or tretinoin) to normalize keratinization, combined with benzoyl peroxide for its antibacterial and keratolytic effects.
  • Explains that if topical antibiotics (clindamycin, erythromycin) are prescribed, they must always be combined with benzoyl peroxide to prevent antibiotic resistance.
  • States that oral antibiotics (doxycycline, minocycline) are considered for moderate-to-severe disease, and that isotretinoin is reserved for severe nodulocystic acne with appropriate monitoring (teratogenicity, liver function, lipids).
  • Sets realistic expectations: visible improvement typically takes 6–8 weeks; initial dryness or irritation from retinoids is expected.
  • Advises on gentle, non-comedogenic skincare: mild cleansers, avoiding abrasive scrubs or over-washing, and daily sun protection.
  • Advises against picking or squeezing lesions, which worsens inflammation and increases the risk of scarring.
  • Acknowledges psychosocial impact: validates concerns about self-esteem, social withdrawal, and the emotional burden of acne, particularly in adolescents.
  • Mentions that mental health support or referral should be considered if significant psychological distress is present.
  • Emphasises adherence to treatment and confirms a follow-up plan.

OSCE 2: Rosacea — Trigger Identification and Lifestyle Advice

Section titled “OSCE 2: Rosacea — Trigger Identification and Lifestyle Advice”
OSCE

Station: A 40-year-old plantation manager is concerned about a chronic “red face” over the last three months. Counsel him on the management of the skin condition.

Self-assess against checklist

Tick each point you covered, then check your score.

  • Introduces self and confirms patient identity; adopts an empathetic and non-dismissive tone.
  • Takes a focused history: onset and duration of facial redness, presence of flushing episodes, history of pustules or papules, any eye symptoms (dryness, grittiness, blepharitis).
  • Explains the diagnosis of rosacea: a chronic vascular and inflammatory condition affecting the central face, characterized by persistent erythema, telangiectasia, and papulopustular lesions without comedones.
  • Distinguishes rosacea from acne: older age group, no comedones, prominent flushing and telangiectasia — key differences the patient should understand.
  • Explains the four recognized subtypes: erythematotelangiectatic (flushing, visible vessels), papulopustular (acne-like lesions without comedones), phymatous (thickened skin, rhinophyma), and ocular (blepharitis, conjunctivitis, dry eyes).
  • Identifies and counsels on common triggers: alcohol, spicy food, hot beverages, heat and temperature changes, UV sun exposure, and emotional stress.
  • Recommends keeping a personal trigger diary to identify and systematically avoid individual aggravating factors.
  • Advises on sun protection: broad-spectrum sunscreen daily, wide-brimmed hats, and avoiding prolonged exposure during peak sun hours.
  • Recommends gentle skincare: mild non-irritating cleansers, avoiding exfoliants, astringents, and abrasive scrubs.
  • Explains topical treatment options available for rosacea: metronidazole, azelaic acid, and ivermectin for papulopustular disease; brimonidine gel for transient control of erythema.
  • Explains that oral doxycycline at a low dose is used for its anti-inflammatory effect in moderate papulopustular rosacea, and that isotretinoin (low dose) may be considered for refractory cases.
  • Discusses procedural options: laser or IPL therapy for telangiectasia; surgical correction for rhinophyma in phymatous disease.
  • Addresses psychosocial impact: acknowledges that persistent facial redness can cause embarrassment and anxiety, and that this burden is often under-recognized.
  • Emphasises that rosacea is a chronic, relapsing condition; encourages realistic expectations and regular follow-up.

Essential Learning Notes: Acne vs. Rosacea

Section titled “Essential Learning Notes: Acne vs. Rosacea”

Table 3.2: Essential Learning Notes — Acne vs. Rosacea

AspectAcne VulgarisRosacea
PathophysiologyIncreased sebum production (androgen-driven)
Follicular hyperkeratinization
Cutibacterium acnes colonization
Inflammatory response
Chronic vascular and inflammatory disorder
Dysregulation of innate immunity
Neurovascular dysregulation
Trigger-induced vasodilation
Age of onsetAdolescents and young adults (12–25 years)Adults >30 years (peak 40–60 years)
Lesion typesComedones (open/closed)
Papules, pustules
Nodules, cysts (severe)
Erythema, telangiectasia
Papules, pustules
Phymatous changes (e.g., rhinophyma)
Ocular involvement
DistributionFace (T-zone), chest, backCentral face (cheeks, nose, chin, forehead)
TriggersHormonal changes, oily skin, occlusion, stressAlcohol, spicy food, heat, sunlight, emotional stress
ComedonesPresentAbsent
InvestigationsUsually clinical diagnosis
Hormonal profile if PCOS suspected
Consider swabs if secondary infection
Clinical diagnosis
Rule out lupus, seborrhoeic dermatitis
Ophthalmology referral if ocular symptoms
Topical treatmentRetinoids (adapalene, tretinoin)
Benzoyl peroxide
Topical antibiotics (clindamycin)
Metronidazole
Azelaic acid
Ivermectin
Brimonidine (for erythema)
Systemic treatmentOral antibiotics (doxycycline, minocycline)
Hormonal therapy (OCPs, spironolactone)
Isotretinoin (severe cases)
Oral doxycycline (low-dose)
Isotretinoin (refractory cases)
Procedural optionsComedone extraction
Chemical peels
Laser for scarring
Laser or IPL for telangiectasia
Surgery for rhinophyma
Psychosocial impactHigh in adolescents; may affect self-esteem and social interactionOften under-recognized; facial redness may cause embarrassment or anxiety
Patient educationAdherence to treatment
Avoid picking/squeezing
Gentle skincare, sun protection
Trigger avoidance
Gentle skincare
Sun protection
Chronic nature and relapse risk