Acne vulgaris

Meet the patient

A 16-year-old boy is referred because his acne is "not responding to everything". Cheeks, jaw and upper back carry a mix of open comedones, angry papules and three deep nodules on the chest that have already left a dent. He has quietly stopped swimming. His mother asks whether "the strong tablet" is safe.[1][4]

Two exam questions are now live, and everything below exists to answer them: is this scarring nodular disease that needs isotretinoin now? and if he starts it, how do you keep him off the teratogenicity list?[1]

The four pathogenic factors — plug, sebum, bug, fire

Every acne lesion is the same four-step machine, and every drug you will ever name attacks one step. Learn the four and you can derive the whole pharmacopoeia from memory.[1]

1. Plug — follicular hyperkeratinisation. Infundibular keratinocytes desquamate abnormally and block the pore, forming the microcomedone — the precursor lesion you cannot yet see.
2. Sebum — androgen-driven sebaceous glands overproduce, and the sebum itself turns pro-inflammatory (low linoleate, an altered squalene-to-oleic acid ratio).
3. Bug — Cutibacterium acnes, anaerobic and lipophilic, colonises the plugged, oily follicle.
4. Fire — C. acnes binds Toll-like receptor 2 on keratinocytes and sebocytes, firing IL-1 alpha, IL-8 and TNF-alpha; neutrophils and a Th17 response then amplify the inflammation.[6][7]

[1]

The therapeutic map drops straight out of the four factors — each pathogenic step has a drug class that targets it, and the table below is the spine of every prescription you will write:[1]

Why sebum composition matters, not just volume

Androgens drive the amount of sebum, but acne-prone sebum is also abnormal in composition — depleted linoleate and a shifted squalene-to-oleic acid ratio that lowers the follicular barrier and is itself pro-inflammatory. This is why a drug that simply suppresses sebum (isotretinoin, causing up to 90 percent reduction within weeks) is so disproportionately effective, and why sebum biology — not lesion count alone — is the rational target in severe disease.[6]

Viva nugget on the names: acne is almost certainly a corruption of the Greek akme, "the peak" — the peak of life, when androgens surge and the pilosebaceous unit first misbehaves. Comedo comes from the Latin comedere, "to eat up", the matter once imagined to be devoured within the pore. Both words outlived their metaphors because the lesions they name are unchanged.[4]

Classify by the dominant lesion — the four faces of acne

Classification is not bookkeeping — it dictates the drug. Name the dominant lesion first, then the severity, and the treatment ladder writes itself. The face-off every candidate must reproduce:[1]

[1]

Severity is then graded mild, moderate or severe from lesion type, count, extent and scarring, sharpened by three named scales. You do not need all three at the bedside, but examiners expect you to name them and their bands:[1][3]

The special forms and life stages that earn extra marks

Most acne is adolescent, but a string of named variants turn up in vivas — cluster them by age and trigger:[1]

• Neonatal acne — tiny papulopustules in the first weeks of life, blamed on maternal androgens; self-limiting.
• Infantile acne — onset between 3 and 12 months; may persist and merits follow-up to exclude androgen excess.
• Adolescent acne — the common form, driven by pubertal androgens.
• Adult or persistent acne — increasingly recognised, especially in women; often hormonal, jawline and lower-face predominant.
• Acne conglobata — severe, chronic, nodulocystic disease with grouped comedones, abscesses and sinus tracts.
• Acne fulminans — acute, ulcerative, febrile, systemic; the dermatology emergency covered below.
• Acne mechanica — occlusion and friction from helmets, masks and instruments.
• Drug-induced acneiform eruptions — corticosteroids, androgens, lithium, EGFR inhibitors, mTOR inhibitors, isoniazid.
• SAPHO syndrome — synovitis, acne, pustulosis, hyperostosis, osteitis; acne can be the presenting clue.[1][4][26]

How common, who, and what lights the fuse

Acne is among the commonest skin diseases on earth. Peak prevalence is in adolescence — roughly 85 percent of people aged 12 to 24 years — but a substantial minority carry disease into their third and fourth decades, and adult female acne is now a distinct and growing phenotype you will see weekly.[5]

The risk and exacerbating factors, grouped so they stick:[1]

• Genetics — a family history predicts earlier onset and more severe disease.
• Androgens — pubertal, menstrual-cycle, PCOS or exogenous androgens all raise sebum output.
• Diet — high-glycaemic-load diets and skimmed milk are the most consistent associates; the evidence for chocolate and whey is weaker.
• Stress — psychological stress flares acne through neuroendocrine pathways.
• Occlusion and friction — occlusive clothing, masks, helmets, topical oils and cosmetics.
• Medications — corticosteroids, androgens, lithium, phenytoin, isoniazid, EGFR and mTOR inhibitors.
• Smoking — the link is inconsistent, but some studies tie it to non-inflammatory and adult acne.[1][4][25]

[1]

Read the lesions — morphology and distribution

The lesion tells you the stage; the distribution tells you the phenotype. Run morphology and site together and you have already half-classified the patient.[1]

• Comedones — the non-inflammatory lesions. Open comedones (blackheads) are dilated follicular openings with oxidised keratin and sebum; closed comedones (whiteheads) are small, skin-coloured papules with no visible pore.
• Inflammatory lesions — erythematous papules, pustules, nodules and cysts.
• Secondary changes — excoriations, crusting, post-inflammatory erythema, post-inflammatory hyperpigmentation and scarring.[1]

On distribution: the face (forehead, cheeks, nose, chin, jawline) is classic, with adult female acne clustering on the lower face and jaw. Do not forget the trunk — back and chest, especially in males — because truncal acne carries the highest scarring risk and is overlooked the moment treatment focuses only on the face.[1]

The classic trap: examining only the face. A patient with a clean forehead and a scarred back has severe disease, and a back-focused question is an examiner favourite. Always ask the patient to expose the back and chest.[1]

Spot the mimics — the acneiform face-off

Not every papulopustular face is acne. The discriminator is almost always comedones — true acne has them, the mimics usually do not — plus the distribution and the trigger.[1][20]

[1] [20]

When to investigate — and when not to

Acne is a clinical diagnosis. Reach for tests only when the picture is atypical, resistant, or pointing at an endocrine cause — never to confirm ordinary acne.[1]

Investigate when you see any of:[1]

• Sudden severe acne, or acne resistant to standard therapy.
• Signs of hyperandrogenism — hirsutism, androgenic alopecia, voice change, clitoromegaly.
• Menstrual irregularity, infertility or galactorrhoea.
• Prepubertal acne (before androgens ought to be driving it).[1]

The endocrine first-line panel is testosterone, DHEAS, LH and FSH, prolactin, 17-hydroxyprogesterone, with a pelvic ultrasound if PCOS is suspected. Before isotretinoin or hormonal therapy, take baseline full blood count, liver function tests, fasting lipids and a pregnancy test; further monitoring follows local protocol and the pregnancy-prevention programme.[1][10]

Topical therapy — the multimodal foundation

Topicals are first-line for mild acne and a part of almost every regimen. Both the AAD and EuroGuiDerm guidelines push multimodal therapy — combine agents that hit different pathogenic factors, because monotherapy breeds resistance and underperforms.[1]

Fixed-dose combinations improve adherence and efficacy — adapalene 0.1 to 0.3 percent plus benzoyl peroxide 2.5 percent, tretinoin plus clindamycin, and benzoyl peroxide plus clindamycin or erythromycin. They suit mixed comedonal and inflammatory acne and cut the risk of antibiotic resistance.[1]

The classic trap: prescribing a topical antibiotic alone. Topical antibiotic monotherapy is the single surest way to breed resistant C. acnes, it is prohibited by every guideline, and pairing it with benzoyl peroxide suppresses the very resistance you would otherwise create.[8][9]

Systemic antibiotics — stewardship is the exam

Oral tetracyclines are first-line for moderate-to-severe inflammatory acne, chosen as much for their anti-inflammatory as their antibacterial effect. The doses and the cautions every candidate owns:[1]

Antibiotic stewardship — the sentence that earns the marks. Limit oral antibiotic courses to 3 to 6 months, always combine with benzoyl peroxide or a topical retinoid, never use antibiotic monotherapy, and have a maintenance plan for the day the course ends. A Cochrane review found minocycline offers no clinically important advantage over other tetracyclines and carries more adverse events — so do not reach for it first.[1][10][12]

Hormonal therapy — the adult-female lever

Hormonal therapy is the lever in adult female acne, especially with perimenstrual flares, jawline predominance, or biochemical or clinical hyperandrogenism. Two agents do most of the work.[1]

• Combined oral contraceptives (COCs) reduce ovarian androgen output and raise sex-hormone-binding globulin. Those with anti-androgenic progestogens — drospirenone, cyproterone acetate, chlormadinone acetate — are the most effective, with benefit apparent after 3 to 6 months.
• Spironolactone, an aldosterone antagonist with anti-androgen effects, at 50 to 200 mg daily — start low and titrate. Monitor potassium and blood pressure at higher doses, and avoid it in pregnancy.[1][13][14]

For mild-to-moderate adult female acne — jawline and lower-face papules, often perimenstrual, fewer comedones than in adolescence — first-line is a topical retinoid plus BPO, adding a COC or spironolactone (or an oral tetracycline) for refractory disease. Clascoterone, a topical androgen-receptor inhibitor, offers a non-antibiotic, anti-androgen option for those who want to avoid systemics.[10][13][15]

Isotretinoin — the one drug that changes everything

Isotretinoin is the most effective acne therapy that exists, producing long-term remission in 60 to 80 percent of patients after a single 5 to 7 month course, because it is the only drug that hits all four pathogenic factors at once. Reach for it when:[1]

• There is severe nodulocystic or scarring acne at presentation.
• Moderate acne is scarring or refractory to at least 3 months of combination therapy (topical retinoid plus BPO plus an oral tetracycline).
• Acne is producing scarring despite treatment.
• There is relapse after one or more courses of oral tetracyclines or hormonal therapy.
• Acne is severe and psychosocially disabling even with low lesion counts.[1]

The isotretinoin mantra

Start at 0.5, aim for 120 to 150, stop a month before conception, never with a tetracycline. Say it as one breath and you have the dosing, the relapse target, the teratogenicity rule and the one dangerous interaction.[1][2][3]

The conventional regimen is 0.5 to 1 mg/kg/day for 16 to 24 weeks, to a cumulative target of 120 to 150 mg/kg for maximal sustained remission. Begin at 0.5 mg/kg/day (about 40 mg/day in a 70 kg adolescent), hold for 4 weeks to judge tolerability and any flare, then escalate to 1 mg/kg/day in divided doses with the largest meal. Most courses finish within 5 to 7 months; shorter courses relapse earlier, longer ones rarely add benefit.[1][2][3]

Isotretinoin pharmacology — why food, teratogenicity and interactions follow

Isotretinoin is the naturally occurring geometric isomer of all-trans retinoic acid, given as a soft-gelatin capsule whose bioavailability doubles with a fatty meal (hence "with the largest meal"). It binds nuclear retinoic acid receptors (RAR-alpha, beta, gamma) and rewires the genes controlling epidermal proliferation, differentiation and sebaceous activity. It hits all four factors: sebaceous gland atrophy with up to 90 percent sebum reduction within 6 weeks; normalised follicular keratinisation; reduced C. acnes through an altered follicular milieu; and an anti-inflammatory effect from TLR inhibition and reduced neutrophil chemotaxis and Th17 signalling. Its lipophilicity dictates the dosing, its placental transfer dictates the teratogenicity, and its cytochrome P450 3A4 metabolism dictates the interactions — never combine with tetracyclines (benign intracranial hypertension), vitamin A supplements (additive toxicity) or methotrexate. The elimination half-life is about 21 hours, but tissue effects persist long after plasma clearance.[1]

The dosing protocol table is the one to reproduce verbatim in a viva:[1]

Teratogenicity — humour off

Isotretinoin is an absolute teratogen. This is the single most important safety fact on the page, and no leeway is acceptable. Patients of childbearing potential require two complementary contraceptive methods (or abstinence plus one), monthly negative pregnancy tests, and enrolment in a risk-management programme — iPLEDGE in the United States, or the local pregnancy-prevention programme in the EU, UK and Australia. Stop isotretinoin at least one month before attempting conception, and avoid blood, marrow and organ donation until one month after the last dose.[1][2][3]

Pregnancy on isotretinoin is a hard stop. If a patient conceives on the drug, stop it immediately and refer to a teratology service — the risk of severe fetal malformation is high and unavoidable once exposure has occurred.[1]

The common adverse effects and how you manage them

Side effects are dose-dependent and usually manageable: cheilitis in over 90 percent, xerosis, dry eyes, epistaxis, myalgia, mild-to-moderate hypertriglyceridaemia and transaminitis. Manage them conservatively — emollients, lip balm, preservative-free ocular lubricants, and lipid and liver monitoring at baseline and at 4 to 8 week intervals. The controversies around mood change and inflammatory bowel disease are real but unresolved; ask about mood at every visit and document it.[1]

Acne fulminans — the systemic emergency

Acne fulminans is a dermatology emergency: sudden, ulcerative, necrotic nodulocystic acne with systemic toxicity. It classically strikes adolescent males aged 12 to 20 years with a personal or family history of severe acne, evolving over days to weeks from truncal papulopustules into haemorrhagic, ulcerative, necrotic nodules that ooze and crust. The eruption is accompanied by fever, malaise, weight loss, lymphadenopathy, hepatosplenomegaly, arthralgia, myalgia and bone pain.[23][24]

Triggers to name in the viva: recent commencement of isotretinoin (the commonest iatrogenic precipitant), high-dose vitamin B12, androgens, systemic corticosteroids paradoxically during withdrawal, and Epstein-Barr virus infection. Osteolytic lesions of the clavicles, sternum, ribs, pelvis and long bones reflect a sterile neutrophilic osteomyelitis.[23]

Laboratory findings are neutrophilic leucocytosis, raised erythrocyte sedimentation rate and C-reactive protein, anaemia of chronic disease and elevated transaminases; radiographs or MRI may show the osteolytic bone lesions. Skin biopsy shows a dense dermal neutrophilic infiltrate with follicular rupture and ulceration — and distinguishing it from pyoderma gangrenosum and Sweet syndrome may need clinicopathological correlation.[1]

The management ladder — humour off, this is preventable harm. Admit or arrange urgent same-day dermatology review. Initial therapy is prednisolone 0.5 to 1 mg/kg/day for 2 to 4 weeks to dampen the inflammatory storm, then introduce low-dose isotretinoin at 0.1 to 0.25 mg/kg/day once fever and ESR have settled. The corticosteroid is tapered over 4 to 8 weeks as isotretinoin is titrated upward. Adjuncts include dapsone 50 to 100 mg daily (after G6PD screening), salicylic acid soaks and intralesional triamcinolone for active nodules, and biologic agents — adalimumab or anakinra — for refractory, corticosteroid-dependent disease. NSAIDs ease the osteoarticular pain. Early aggressive therapy limits the permanent pitted and cribriform atrophic scarring across the trunk that otherwise marks these patients for life.[23][24]

Acne conglobata — suppurative, scarring, chronic

Acne conglobata is the chronic, suppurative counterpart without systemic features. It affects adult men aged 18 to 30 on the trunk, buttocks, proximal limbs and chest, with grouped inflammatory nodules, deep bridging cysts, double-headed comedones and sinus tracts that heal with bridging, hypertrophic and keloidal scarring. General health is preserved and there are no constitutional or haematological abnormalities — that absence is the discriminator from fulminans.[1]

It runs a continuous rather than relapsing-remitting course, is disfiguring and resists conventional therapy. Isotretinoin at 0.5 to 1 mg/kg/day to a cumulative target of at least 120 mg/kg is the cornerstone, often combined with intralesional corticosteroids for individual cysts, dapsone for neutrophil-rich disease, and wide excision with grafting or secondary-intention healing for retracted sinus tracts. Because the truncal scars are severe, refer early — before fibrosis is established.[1][2]

Procedural and adjunctive therapy

Procedural treatments are adjuncts, not substitutes for medical therapy. Reach for them once active acne is controlled, or for the lesions drugs cannot reach:[1]

• Intralesional corticosteroids — triamcinolone acetonide 2.5 to 5 mg/mL into inflammatory nodules and cysts; keep the concentration low to avoid atrophy.
• Chemical peels — salicylic acid, glycolic acid, Jessner solution; modest benefit for comedones and post-inflammatory hyperpigmentation.
• Light and laser — photodynamic therapy, blue and red light, pulsed-dye laser; generally less effective than pharmacotherapy but useful adjuncts.
• Comedone extraction — for individual resistant comedones; never a substitute for medical therapy.
• Scar revision — subcision, microneedling, fractional laser, TCA CROSS, fillers; best delayed until active acne is quiet.[1][18][22]

Special scenarios — pregnancy, children, skin of colour

Pregnancy rewrites the formulary. Avoid topical and oral retinoids (including isotretinoin), oral tetracyclines and spironolactone. Prefer topical azelaic acid, topical erythromycin, benzoyl peroxide to limited areas, and gentle skin care. For isotretinoin specifically, iPLEDGE or its equivalent is mandatory — two forms of contraception and negative pregnancy tests throughout.[1]

In children, neonatal and infantile acne are usually self-limiting, but investigate for androgen excess if severe or persistent. Tetracyclines are contraindicated under 8 years because of tooth discolouration and bone effects; topical retinoids and BPO are generally well tolerated in pre-adolescents.[1][26]

In skin of colour, post-inflammatory hyperpigmentation and keloid scarring are the dominant risks. Emphasise gentle skin care, avoid overly irritating regimens, treat inflammation promptly, and lean on azelaic acid or retinoids for pigmentary sequelae. Photoprotection is non-negotiable.[1][22]

Scarring and the post-inflammatory aftermath

Scarring is the permanent complication, and early treatment is the only prevention. Atrophic scars — ice-pick, boxcar and rolling — dominate on the face; hypertrophic scars and keloids dominate on the trunk. Established scars need procedural intervention; early inflammatory disease needs prompt, adequate treatment, and topical retinoids may reduce early scarring.[20][21][22]

Risk factors for scarring: severe inflammatory or nodular disease, truncal involvement, a family history of scarring, delayed or inadequate treatment, and picking. Validated tools such as the atrophic acne scar risk assessment tool help pick the patients who benefit from early isotretinoin or close follow-up.[21]

Post-inflammatory hyperpigmentation and erythema are common in darker skin types and after inflammatory lesions — treat the underlying acne, use photoprotection, and consider azelaic acid or retinoids.[1]

The psychosocial weight — ask about mood

Acne can disable a life as surely as a chronic disease. Quality-of-life scores may match those of asthma, epilepsy or diabetes, and the condition carries real depression, anxiety, social withdrawal and, rarely, suicidal ideation. The lesion count and the distress often do not correlate — a "mild" face can carry a severe burden.[11]

So screen routinely. Ask directly about mood, sleep, school or work, and relationships, and refer for mental-health support the moment distress, depression or any suicidal ideation appears. This is never an afterthought.[1][11]

Guidelines, landmark agents and the debate

Three guideline families shape practice, and a handful of new agents have reshaped the options. Know the guideline, the year, and what each added.[1]

• AAD 2024 — the current evidence-based guideline; strongly recommends topical retinoids, BPO and fixed-dose combinations, and emphasises antibiotic stewardship and hormonal options for adult females.
• AAD 2016 — the foundational guideline covering topical, systemic, procedural and special-population management.
• EuroGuiDerm 2016 and the 2026 update — the European S3 evidence-based guideline, covering mild-to-severe acne, maintenance, pregnancy and paediatric considerations.[1][2][3][27]

The AAD 2024 guideline was significant enough to draw a published response from Del Rosso and colleagues the following year — a reminder that even consensus guidance in acne is actively debated, and that reading the guideline plus its critique is the fellowship-level standard.[28]

The landmark agents to name with a one-line evidence hook:[15]

• Clascoterone — the first topical androgen-receptor inhibitor; effective for facial acne in patients 12 years or older.
• Sarecycline — a narrow-spectrum tetracycline with reduced gut-flora impact and low resistance rates.
• Tazarotene 0.045 percent lotion — a once-daily retinoid effective for moderate-to-severe acne.
• The 2022 network meta-analysis — supported topical retinoid plus BPO combinations and oral isotretinoin among the most effective options, and underpinned the cost-effectiveness case for early effective therapy.[15][16][17][18][19]

Ward-round test

Stem 1. A 15-year-old boy has papules, pustules and two nodules on his chest, already scarring. He has used a topical retinoid plus benzoyl peroxide and 3 months of doxycycline with little change. What is the next step, and what do you check before prescribing?[1]

Answer

This is scarring nodular acne refractory to adequate combination therapy — an isotretinoin indication. Counsel on teratogenicity and the pregnancy-prevention programme, take baseline full blood count, liver function, fasting lipids and a pregnancy test, and start at 0.5 mg/kg/day, titrating toward a cumulative 120 to 150 mg/kg. Ask about mood and document it.[1]

Stem 2. A 17-year-old boy, day 10 of isotretinoin, develops flaring nodules, fever, arthralgia and ulcerative lesions on his back. Name the diagnosis and the first drug.[23]

Answer

Isotretinoin-flared acne fulminans. Do not escalate the isotretinoin dose — start prednisolone 0.5 to 1 mg/kg/day, then reintroduce low-dose isotretinoin at 0.1 to 0.25 mg/kg/day once the systemic inflammation has settled. Same-day dermatology review or admission.[23][24]

Stem 3. A 28-year-old woman has jawline papules flaring premenstrually, regular cycles, no hirsutism. What is the first-line systemic option, and what do you monitor?[13]

Answer

Spironolactone 50 to 200 mg daily (or a combined oral contraceptive) for classic adult female hormonal acne. Monitor potassium and blood pressure at higher doses, and confirm she is not pregnant before starting.[13]

Stem 4. A patient asks for "just the antibiotic cream" for her comedonal acne. What do you say, and why?[8]

Answer

No — topical antibiotic monotherapy is prohibited by stewardship; it breeds resistant C. acnes and offers nothing a retinoid or benzoyl peroxide does not. Comedonal acne wants a topical retinoid, with or without BPO.[8][9][10]

References

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2. [2]Zaenglein AL, Pathy AL, Schlosser BJ, et al. Guidelines of care for the management of acne vulgaris J Am Acad Dermatol, 2016.PMID 26897386
3. [3]Nast A, Dréno B, Bettoli V, et al. European evidence-based (S3) guideline for the treatment of acne - update 2016 - short version J Eur Acad Dermatol Venereol, 2016.PMID 27514932
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14. [14]van Vloten WA, van Haselen CW, van Zuuren EJ, et al. The effect of 2 combined oral Contraceptives containing either drospirenone or cyproterone acetate on acne and seborrhea Cutis, 2002.PMID 12096825
15. [15]Hebert A, Thiboutot D, Stein Gold L, et al. Efficacy and Safety of Topical Clascoterone Cream, 1%, for Treatment in Patients With Facial Acne: Two Phase 3 Randomized Clinical Trials JAMA Dermatol, 2020.PMID 32320027
16. [16]Moore A, Green L, Bruce S, et al. Once-Daily Oral Sarecycline 1.5 mg/kg/day Is Effective for Moderate to Severe Acne Vulgaris: Results from Two Identically Designed, Phase 3, Randomized, Double-Blind Clinical Trials J Drugs Dermatol, 2018.PMID 30235387
17. [17]Tanghetti EA, Werschler WP, Lain T, et al. Tazarotene 0.045% Lotion for Once-Daily Treatment of Moderate-to-Severe Acne Vulgaris: Results from Two Phase 3 Trials J Drugs Dermatol, 2020.PMID 31985914
18. [18]Mavranezouli I, Daly CH, Welton NJ, et al. A systematic review and network meta-analysis of topical pharmacological, oral pharmacological, physical and combined treatments for acne vulgaris Br J Dermatol, 2022.PMID 35789996
19. [19]Mavranezouli I, Welton NJ, Daly CH, et al. Cost-effectiveness of topical pharmacological, oral pharmacological, physical and combined treatments for acne vulgaris Clin Exp Dermatol, 2022.PMID 36258288
20. [20]Dessinioti C, Antoniou C, Katsambas A. A cross-sectional study of clinical factors associated with acne facial scarring in patients with active acne J Eur Acad Dermatol Venereol, 2018.PMID 29194788
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22. [22]Tan J, Tanghetti E, Baldwin H, et al. The Role of Topical Retinoids in Prevention and Treatment of Atrophic Acne Scarring: Understanding the Importance of Early Effective Treatment J Drugs Dermatol, 2019.PMID 30909329
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28. [28]Del Rosso JQ, Zaenglein A, Callender V, et al. Response to Reynolds et al's Guidelines of care for the management of acne vulgaris J Am Acad Dermatol, 2025.PMID 39251025