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Acne Vulgaris

Table of Contents

  • Key Points ⚡
  • Introduction
  • Aetiology
  • Risk Factors
  • Clinical Features
  • Associated Conditions
  • Differential Diagnosis
  • Investigations
  • Management
  • Complications
  • References
  • Related Notes
  • Test Yourself

Key Points ⚡

  • Acne vulgaris: disorder of the pilosebaceous unit, characterized by pustules, papules, comedones; common in adolescents.
  • Aetiology: increased sebum production, bacterial colonization (P. acnes), multifactorial but highly heritable (up to 80%).
  • Risk factors: hormonal shifts (puberty, PCOS), medications (steroids, antiepileptics), high glycemic index foods, chemical exposure (e.g., halogenated aromatic compounds).
  • Clinical features: onset ~12-17 years, cyclical worsening in females, common on face, chest, upper back; mild to severe presentations.
  • Scarring: ice pick, boxcar, anetoderma, hypertrophic, keloid; pigmented macules may persist post-inflammation.
  • Investigations: primarily clinical; skin swabs for persistent/unusual cases; hormonal tests for severe female acne.
  • Management: topical therapies (salicylic acid, benzoyl peroxide, retinoids—teratogenic), systemic therapies (OCPs, spironolactone—contraindicated in pregnancy), oral antibiotics (tetracyclines, erythromycin), isotretinoin for moderate to severe cases (monitor LFTs, cholesterol).
  • Complications: post-inflammatory hyperpigmentation and scarring.

Introduction

Acne vulgaris is the most common dermatological condition. It is a disorder of the pilosebaceous unit characterized by pustules, papules, and comedones. Acne severity and presentation can vary widely among different populations and ethnic groups.

Aetiology

  • Acne involves increased sebum production due to androgenic hormones, bacterial colonization by Propionibacterium acnes, and immune system activation likely triggered by bacteria.
  • Highly heritable with up to 80% familial prevalence in severe phenotypes.

Risk Factors

Precipitating Factors

  • Hormonal shifts during puberty or disorders causing excess androgens (PCOS, congenital adrenal hyperplasia).
  • Exogenous androgen use: steroids, testosterone.

Exacerbating Factors

  • Medications: steroids, antiepileptics, EGFR inhibitors.
  • Occlusion: cosmetics, shaving products, topical skin products.
  • Diet: high glycemic index foods (strong association), dairy (weaker association).
  • Occupational exposure to chemicals (halogenated aromatic compounds).

Relieving Factors

  • Low glycemic load diet and avoidance of comedogenic products may help.

Clinical Features

History

  • Onset commonly around 12-17 years (early puberty).
  • Females may note cyclical changes with menstrual cycle.
  • History should include lifestyle, diet, skincare, medications, family history, prior treatments.

Examination

  • Comedones:
  • Closed (whiteheads): blocked follicle covered by skin.
  • Open (blackheads): blocked follicle exposed to air.
  • Inflammatory lesions: papules (<1 cm), pustules, nodules (>1 cm), cysts.
  • Scarring: ice pick, boxcar, anetoderma, hypertrophic, keloid.
  • Pigmented macules: non-raised, usually fade over time.

Associated Conditions

  • PCOS: common endocrine disorder in women causing increased androgen levels, exacerbating acne.

Differential Diagnosis

  • Acne rosacea
  • Perioral dermatitis
  • Folliculitis
  • Drug eruptions
  • Seborrheic dermatitis

Investigations

  • Diagnosis mainly clinical.
  • Skin swab for persistent/unusual cases.
  • Hormonal panel (androgens) for severe female acne.

Management

Topical Therapies

  • Salicylic acid (keratolytic).
  • Benzoyl peroxide (antibacterial).
  • Topical retinoids (teratogenic; start low dose, alternate days).

Systemic Therapies

  • Oral contraceptive pills (OCP), e.g. cyproterone acetate for antiandrogen effect.
  • Spironolactone (antiandrogen; contraindicated in pregnancy).

Antibiotics

  • Oral tetracyclines (doxycycline, minocycline) and erythromycin for moderate acne.
  • Anti-inflammatory effect more important than antibacterial.

Isotretinoin

  • For moderate to severe or cystic acne.
  • Markedly reduces sebum production and inflammation.
  • Teratogenic; requires regular monitoring (LFTs, lipids, pregnancy tests).

Other Therapies and General Care

  • Use non-comedogenic skincare products and gentle non-soap cleansers.
  • Advise low glycemic index diet.
  • Avoid picking or scratching lesions.

Complications

  • Post-inflammatory hyperpigmentation and scarring (keloid, hypertrophic).
  • Psychological impact including low self-esteem and depression.

References

  • British Association of Dermatologists. Handbook for Medical Students and Junior Doctors. 2020.
  • Bhate & Williams. Epidemiology of acne vulgaris. 2012.
  • Spencer et al. Diet and acne: A review of the evidence. 2009.
  • DermNet NZ. Acne. 2014.
  • eTG Complete. Acne. 2015.
  • Australasian College of Dermatologists. Acne Scarring. 2020.
  • Basal Cell Carcinoma (BCC)
  • Cellulitis
  • Cutaneous Squamous Cell Carcinoma (SCC)
  • Erythema Multiforme
  • Erythema Nodosum

Test Yourself

  • [Link to practice questions or quizzes if available]