SUMMARY

Acne vulgaris is a chronic inflammatory condition with a substantial psychosocial burden. Early effective therapy reduces the risk of permanent scarring and mental health impacts.

Combination topical therapy is recommended as initial and maintenance treatment for most patients (e.g. benzoyl peroxide and a topical retinoid). Topical antibiotics should not be used long-term, or as monotherapy, because of the risk of antibiotic resistance.

Management has shifted away from prolonged oral antibiotic courses. If oral antibiotics are used, they should be time-limited (generally no more than 3 months) and paired with a non-antibiotic topical therapy.

Oral isotretinoin is the most effective option for severe, scarring or treatment-resistant acne. Recent safety updates emphasise baseline and ongoing assessment of mental health, counselling about possible sexual adverse effects and stringent pregnancy prevention.

The combined oral contraceptive and spironolactone are effective systemic options for women with persistent acne that can reduce reliance on repeated or prolonged antibiotic courses.

Light-based therapies and physical therapies (e.g. comedone extraction) can be useful adjuncts, ideally accessed through dermatologists.

 

Introduction

Acne vulgaris is the common form of acne. It is an inflammatory skin condition that affects up to 85% of adolescents, may persist into adulthood (particularly in women), and is increasingly approached as a chronic relapsing disease.1,2 Early effective therapy reduces the risk of permanent scarring and mental health impacts.1

 

Pathogenesis

The pathogenesis of acne is multifactorial and includes androgen-driven sebaceous gland activity leading to increased sebum production, abnormal follicular keratinisation, Cutibacterium acnes–associated inflammation, and dysregulated innate and adaptive immune responses.1,3

Genetic susceptibility has the strongest supporting evidence as a determinant of disease expression and severity. There is low to moderate evidence for the impact of potentially modifiable factors, including dairy intake, high glycaemic-load diet, stress, and obesity and other metabolic factors.4-9

 

Sequelae and psychological impact

Acne sequelae can include a range of atrophic and hypertrophic or keloid scarring morphologies. Scarring risk correlates with severity, delayed control, and behaviours such as picking and excoriation.1

Post-inflammatory dyspigmentation may occur; this may be more prominent and persistent in darker skin phototypes.

Acne can markedly impair quality of life and social functioning. Meta-analyses demonstrate consistent associations between acne and depression, anxiety and suicidality, with psychosocial impact not always proportional to lesion counts alone. Greater impact is seen in females and adults.10-12 These data support early effective treatment and routine enquiry about mood, emotional distress, body image concerns and social withdrawal.1,10-12

 

Clinical presentation and severity

Acne typically affects seborrhoeic areas (face, chest, back). Lesion types include:

  • Non-inflammatory – open and closed comedones.
  • Inflammatory – papules, pustules, nodules, cysts.

Severity may be broadly described as:

  • Mild – limited open and closed comedones with few inflammatory lesions.
  • Moderate – extensive comedones, more numerous papules/pustules, limited nodules.
  • Severe – conglobate acne (severe nodulocystic acne), extensive truncal involvement, scarring, or marked psychosocial morbidity.
 

Diagnosis and assessment

Assessment should incorporate lesion type and severity, as described above, along with duration, prior treatments, scarring and psychological impact.1

The key clinical separator for acne vulgaris versus other conditions is the presence of comedones: both open comedones (blackheads) and closed comedones (whiteheads), the latter often becoming more apparent with gentle stretching of the skin.

Differential diagnoses

Important differentials include:1

  • rosacea
  • periorificial dermatitis
  • hidradenitis suppurativa
  • folliculitis due to infection with Staphylococcus aureus, Malassezia (yeast) or gram-negative bacteria associated with prolonged antibiotics
  • acneiform drug eruptions (Box 1).13

Drug-induced acne or acne-like (acneiform) eruptions should be considered when onset is abrupt, morphology is monomorphic, comedones are absent or distribution is atypical (e.g. trunk or extremities).

Box 1 Examples of drugs that may cause acne or acneiform (acne-like) eruptions

  • systemic corticosteroids (e.g. prednisolone)
  • testosterone and anabolic steroids (e.g. danazol, nandrolone)
  • lithium
  • some antiepileptics (e.g. phenytoin, phenobarbital, carbamazepine, lamotrigine)
  • vitamin B12
  • Janus kinase (JAK) inhibitors (e.g. upadacitinib)
  • some targeted cancer therapies (including BRAF and EGFR inhibitors)
BRAF = proto-oncogene B-Raf; EGFR = epidermal growth factor receptor

Comorbid conditions

Polycystic ovary syndrome (polyendocrine metabolic ovarian syndrome) is a highly prevalent endocrine disorder (8 to 13% of reproductive‑age women), and acne is one of its core hyperandrogenic manifestations. A thorough history and endocrine assessment are warranted in women with menstrual irregularities, late-onset or rapidly worsening acne, hirsutism, infertility or other hyperandrogenic features.1

Follicular occlusion disorders are a group of conditions in which hair follicles become blocked with keratin and then rupture, resulting in intense, chronic inflammation. They include acne conglobata, hidradenitis suppurativa (acne inversa), dissecting cellulitis of the scalp and pilonidal sinus. These conditions often coexist, forming the ‘follicular occlusion tetrad’. While often confused with standard acne vulgaris, these disorders are frequently more resistant to standard treatments, leading to extensive scarring and sinus tract formation.14,15

 

Principles of acne management

Key goals are to reduce active lesions, prevent scarring and dyspigmentation, and improve quality of life. Treatment should address multiple pathogenic pathways, be matched to severity and skin type and include education and adherence support.1,16

General advice and education

General advice includes:

  • discouraging picking and squeezing
  • minimising the use of irritants such as comedogenic cosmetics, including occlusive hair waxes if the forehead is involved, which can cause and exacerbate acne
  • avoidance of abrasive scrubs and over-washing
  • gentle cleansing once or twice daily
  • daily non-comedogenic moisturiser with sunscreen to reduce the risk of light-induced post-inflammatory dyspigmentation.

When selecting a moisturiser for acne-prone skin, patients should be advised to look for products labelled ‘non-comedogenic’, which means they are formulated to avoid clogging pores. These tend to be water-based, lightweight gels or fluid lotions that rely on humectants like hyaluronic acid and glycerin to draw moisture into the skin, rather than heavy occlusives or oils that sit on the surface and trap debris. It's worth noting, however, that ‘non-comedogenic’ is not a regulated claim, so checking the ingredient list directly is the more reliable approach. Key ingredients to avoid include coconut oil, cocoa butter, isopropyl myristate, oleic acid and lanolin, while skin-friendly options like niacinamide, squalane, and dimethicone are generally well-tolerated.

Discussion about diet (e.g. avoiding high glycaemic load and dairy products) should be offered as an adjunct, while emphasising that evidence is modest and individual responses can vary. Dietary discussions should acknowledge that any changes should be balanced and sustainable.1,3,17,18

Patient education and supportive counselling can help address common myths about acne (Box 2).

Box 2 Acne myths to address with patients

Myth: ‘Acne is caused by poor hygiene.’
Truth: Acne reflects follicular and inflammatory pathways; over-washing can worsen irritation.

Myth: ‘You should let acne run its course.’
Truth: Delayed control increases scarring risk and psychosocial harm; early treatment helps.

Myth: ‘Sun exposure clears acne.’
Truth: Any short-term improvement is outweighed by photoageing and skin cancer risk; recommend non-comedogenic sunscreen.

Myth: ‘Make-up makes acne worse.’
Truth: While some products may exacerbate acne, non-comedogenic products are generally acceptable; advise gentle removal.

Myth: ‘Oral antibiotics and supplements are harmless long-term.’
Truth: Prolonged antibiotics promote resistance and have diminishing benefit; supplements vary in evidence and safety.


 

Topical acne therapies

Topical therapy is the first-line treatment for most mild acne and remains central for moderate acne and maintenance therapy. Contemporary guidance favours combination regimens (especially therapies with complementary mechanisms) rather than sequential monotherapy.1,16

Topical retinoids

Topical retinoids (adapalene, tretinoin, tazarotene and trifarotene) are core therapy for most patients (including for maintenance). They reduce microcomedone formation and are comedolytic and anti-inflammatory. They can also improve scarring, dyspigmentation and early textural change over time.1,16,19-21

The topical retinoids vary in potency and irritancy, but their efficacy is similar. Adapalene has the best tolerability for long‑term acne control, while tretinoin and trifarotene have the most data for acne‑related hyperpigmentation and early scarring.22,23

Practical prescribing to improve retinoid tolerability

To minimise irritant dermatitis, introduce topical retinoids gradually (e.g. 2 to 3 evenings per week initially) and increase frequency only as tolerated, recognising that some patients may only be able to tolerate intermittent use. Advise patients to apply a thin film of retinoid over the entire acne-prone area rather than spot treating (after using a cream-based cleanser or a mild soap free liquid cleanser to gently remove makeup and dirt without stripping the skin of its natural oils). Counsel that irritation, dryness and erythema are common in the first few weeks and often improve with persistence. Using a moisturiser regularly – either before the retinoid, after it, or both – can substantially improve tolerability.1,16 Daily sunscreen use is mandatory.

Benzoyl peroxide and fixed-dose combinations

Benzoyl peroxide has antibacterial and anti-inflammatory effects. Fixed combinations with other topical therapies (retinoid or antibiotic) can improve efficacy and simplify regimens and are recommended as first-line therapy. Patients should be warned about bleaching of fabrics and hair with benzoyl peroxide and potential for irritant dermatitis.1,16,24

Topical antibiotics

Topical antibiotics (clindamycin or erythromycin) are used for their anti-inflammatory action rather than their antibacterial effect. They should not be used long-term or as monotherapy because of the risk of antibiotic resistance. Where used, they should be in fixed combination with benzoyl peroxide or a retinoid and should be time-limited (generally up to 12 weeks).1,2

Other topical agents and newer options

Azelaic acid and salicylic acid may be useful adjuncts or alternatives in selected patients (e.g. intolerance to retinoids, pregnancy planning) and can assist with dyspigmentation.1,16

Topical clascoterone, an androgen receptor inhibitor, provides modest improvements in inflammatory and non-inflammatory lesions in clinical trials and may be an option, particularly for patients seeking non-systemic anti-androgen therapy.25,26

Maintenance therapy

For most patients, maintenance should rely on a topical retinoid, with or without benzoyl peroxide and without continued topical antibiotics.1,16

 

Oral acne therapies

Oral therapies may be indicated for moderate acne that persists despite appropriate use of topical therapies and for severe acne.

Before commencing oral therapy for persistent moderate acne, explore the patient’s adherence to general measures and topical therapies and assess their expectations, emphasising that improvement is gradual, over weeks to months.

The changing role of oral antibiotics

Oral antibiotics can be helpful for short-term control of moderate to severe inflammatory acne.1,16 Benefit is greatest early (up to approximately 12 weeks) and extended or repeated courses increase the risk of antibiotic resistance.1,16

Oral antibiotics should be used as a time-limited ‘bridge’ alongside non-antibiotic topical therapies (e.g. retinoid, benzoyl peroxide), avoiding concurrent topical antibiotics. Once inflammation is controlled, the antibiotic should be stopped.

Rather than cycling antibiotics when there is no response, or relapse occurs, clinicians should revisit the diagnosis, treatment adherence and triggers, and consider alternatives such as hormonal therapy (in women) or isotretinoin.

When oral antibiotics are indicated, tetracyclines (e.g. doxycycline, minocycline) are first line. The most common adverse events are gastrointestinal symptoms such as upper abdominal discomfort and nausea. The use of tetracyclines in pregnant people during fetal dental development may lead to yellowing of the teeth and enamel hypoplasia in the child. Photosensitivity and intracranial hypertension are also noted in some tetracycline users. Uncommon but serious reactions with minocycline include drug-induced lupus erythematosus, autoimmune hepatitis, systemic hypersensitivity reactions and hyperpigmentation with long-term use.27-29 Macrolides or trimethoprim-sulfamethoxazole are generally reserved for patients who cannot take tetracyclines.1,16

Hormonal therapies and spironolactone

The combined oral contraceptive and spironolactone (an oral aldosterone antagonist with anti-androgenic effects) reduce androgen-mediated sebum production and can be effective for females, particularly those with late-onset or persistent acne, or acne with features of jawline predominance and perimenstrual flares.1,16 Progesterone-only contraceptives are not effective and may worsen acne.30

Randomised trials demonstrate that spironolactone improves acne outcomes in women and is a reasonable antibiotic-sparing alternative for persistent moderate acne.31-33 In practice, it is commonly used alongside topical therapy and can be combined with an oral contraceptive.1,31-33

Typical spironolactone starting doses are 25 to 50 mg daily, titrated based on response and tolerability (often to 100 mg daily; sometimes up to 150 mg in selected patients). Adverse effects include menstrual irregularity, breast tenderness, fatigue and polyuria.31-33

Spironolactone-induced hyperkalaemia is rare in otherwise healthy young patients without renal or cardiovascular disease or interacting drugs; measuring baseline renal function and electrolytes can be considered, with follow-up guided by comorbidities and dose.1,31

Spironolactone is contraindicated in pregnancy because of the risk of feminisation of a male fetus; effective contraception should be employed in patients with childbearing potential and the drug should be stopped immediately if pregnancy occurs or is suspected.1

Isotretinoin

Oral isotretinoin is the most effective disease-modifying therapy for acne and is indicated for severe nodular or conglobate disease, scarring acne, widespread comedonal acne, substantial psychosocial morbidity or acne that persists despite adequate topical combinations and an appropriate trial of other systemic therapies (e.g. tetracycline and/or hormonal therapy).1,34 At the time of writing, isotretinoin can only be initiated in Australia by a dermatologist or physician.34

Isotretinoin is teratogenic, so pregnancy must be excluded before initiation, and avoided during treatment and for at least 1 month after cessation.34

Dose-dependent adverse effects

Common dose-dependent adverse effects of isotretinoin include cheilitis (inflammation of the lips), xerosis (dry skin), photosensitivity and transient increases in lipids.1,34

Mental health and sexual adverse effects

In 2025, Australia’s Therapeutic Goods Administration (TGA) published safety warnings and advice based on reports of psychiatric and sexual adverse events associated with isotretinoin.35

Psychiatric adverse effects

Although large observational studies and meta-analyses have not shown a consistent causal association between oral isotretinoin and suicide or psychiatric disorders, and mental health may improve as acne clears, individual vulnerability and rare idiosyncratic psychiatric reactions are possible.36 The TGA recommends proactive screening and counselling regarding potential for mental health changes (including depression, psychotic behaviours and suicidal thoughts).35

Sexual adverse effects

Although rare, there are reports of erectile dysfunction, decreased libido, vulvovaginal dryness, anhedonia, and gynaecomastia in males. There is more consistent evidence for vaginal dryness than for true global sexual dysfunction.36,37

Box 3 provides guidance for managing patients prescribed isotretinoin.

Box 3 A practical approach for managing patients prescribed isotretinoin35-39

  • Exclude pregnancy before initiating isotretinoin in females with childbearing potential.
  • Counsel female patients about the risk of teratogenicity and the need for effective contraception during isotretinoin treatment and for at least 1 month after stopping (often dual-method contraception depending on individual circumstances and local practice). Remind the patient about the teratogenicity risk and review their adherence to contraception regularly during treatment.
  • Check the patient’s lipid profile and liver function tests at baseline, then 8 weeks after commencing isotretinoin. Ongoing testing is only required in higher risk patients.
  • Document baseline mental health history and screen for current psychiatric symptoms; ask about mood and suicidality at follow-up visits. For patients with pre-existing mental illness, involve both their GP and mental health clinicians.
  • In appropriate circumstances, provide anticipatory counselling about possible sexual adverse effects and invite patients to report any change in libido, arousal or genital comfort and sensation during therapy.
  • If pregnancy, severe mood change, suicidality, or distressing sexual dysfunction occurs, pause therapy and arrange urgent clinical review and appropriate non-GP specialist input.
GP = general practitioner

 

Light and physical therapies for acne

Light and physical therapies are used primarily as adjuncts to conventional pharmaceutical acne treatment and ideally accessed through dermatologists. They target pathogenic mechanisms, including Cutibacterium acnes, sebaceous gland activity, follicular hyperkeratinisation and inflammation. These modalities are generally well tolerated, associated with few systemic adverse effects and considered safe for use in pregnancy.40-42

Light and laser-based therapies

There is a range of light- and laser-based therapies for acne vulgaris, including narrowband visible light devices (red or blue light), intense pulsed light and infrared lasers.43,44 Major guidelines position these as adjuncts rather than replacements for evidence-based medical therapy.16 Systematic reviews suggest modest-to-moderate improvements primarily in inflammatory lesions but with low-to-moderate certainty.43,44

Recent systematic reviews and consensus statements indicate that light and laser-based therapies can be performed safely during or shortly after isotretinoin treatment, without an increased risk of adverse scarring or delayed healing.45

Photodynamic therapy

Photodynamic therapy involves topical application of photosensitisers (e.g. 5-aminolevulinic acid or methyl aminolevulinate) followed by visible light activation (red or blue light), resulting in selective sebaceous gland damage and reduction of C. acnes. It is effective for moderate-to-severe or treatment-resistant acne, but it can be limited by post-treatment erythema.46,47

Mechanical and procedural modalities

Comedone extraction (the manual removal of open and closed comedones) provides immediate clinical improvement and patient satisfaction.46 This is an important adjunctive treatment for patients with comedonal acne that has not become inflamed. It should only be performed by clinicians trained in these procedures.

Chemical peels (e.g. salicylic acid, glycolic acid) promote exfoliation, reduce follicular occlusion, and improve post-inflammatory hyperpigmentation.46,48

 

When to refer to a dermatologist

Box 4 outlines when referral to, or advice from, a dermatologist may be considered. Shared-care models can improve treatment access and continuity, with dermatologists initiating systemic therapy and GPs supporting monitoring and adherence.34,35

Box 4 When to involve a dermatologist1,16

Refer or seek advice when:

  • conglobate acne (severe nodulocystic acne) or acne fulminans (severe inflammatory nodulocystic acne sometimes with systemic symptoms) are suspected
  • rapid scarring is present
  • there is extensive comedonal acne, particularly extensive closed comedones
  • there is inadequate response to two appropriate regimens (e.g. topical combination therapy and a time-limited oral antibiotic course with or without hormonal therapy)
  • isotretinoin is being considered
  • diagnosis is uncertain or an alternative diagnosis is suspected (e.g. hidradenitis suppurativa, drug-induced acneiform eruption)
  • the patient is a very young child
  • there is virilisation or suspected endocrine disorder (may be co-managed with an endocrinologist)
  • there is significant psychological morbidity, body dysmorphic concerns or suicidality; consider psychiatry input.

 

Conclusion

Contemporary acne management prioritises early combination topical therapy, antimicrobial stewardship (ensuring time-limited antibiotic use where indicated), broader uptake of hormonal options (including spironolactone) in women and appropriate access to isotretinoin with strengthened counselling and monitoring regarding pregnancy prevention and mental health. Light or physical therapies may be useful adjuncts for acne management in some people. Adopting these principles, individualising care and collaborating with dermatologists when needed can reduce the long-term physical and psychological sequelae of this common disease.

This article was finalised on 15 June 2026.

Conflicts of interest: Belinda Welsh has received support from Candela, Galderma and Novartis for educational activities. Laxmi Iyengar declared no conflicts of interest.

This article is peer reviewed.

 

Australian Prescriber welcomes Feedback.

 

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CPD for GPs - reflective questions

  • Identify and summarise 3 key points relevant to your scope of practice.
  • Identify the key clinical learnings that may be incorporated into the clinical assessment, work-up and/or management plan for appropriate patients.
  • If relevant, would you change any of your management strategies for those patients identified by appropriate screening, examination and investigation.

Submit answers

 

Laxmi Iyengar

Dermatology Research Fellow, Skin Health Institute, Melbourne

General Practitioner, Endeavour Hills Medical Centre, Melbourne

Adjunct Lecturer, Department of General Practice, Monash University, Melbourne

Belinda Welsh

Dermatologist & Director, Complete Skin Specialists, Melbourne

Consultant Dermatologist, Royal Children’s Hospital, Melbourne