Acne fulminans

Meet the patient

A 16-year-old boy is sent to the dermatology on-call clinic. Three days ago his mild forehead acne "went mad": his chest and back are now covered in large, ragged, bleeding nodules under black haemorrhagic crusts, he cannot bear a shirt touching his skin, he has a fever of 39 °C, and his knees and shoulders ache so much he has stopped going to the gym. His mother, almost as an aside, mentions he started "something for bulk" from the supplement shop last month.[1]

Three exam questions are now live, and this page exists to answer them: what is this? (the FUS triad), what set it off? (the supplement and drug history), and — the one that hurts patients when it is missed — which drug comes first, the steroid or the retinoid?[6]

What acne fulminans is — and what it is not

Acne fulminans (AF) — historically acute febrile ulcerative acne conglobata and acne maligna — is the apex of the acne severity spectrum: an explosive eruption of large, tender, ulcerative nodules covered in necrotic haemorrhagic crust on the chest, back and shoulders, with fever, arthralgia, myalgia and raised inflammatory markers.[1][2]

The feature that separates AF from every other acne is systemic inflammation. Uncomplicated acne vulgaris, severe nodulocystic acne and even acne conglobata do not cause fever or raise the ESR. The moment your patient with "bad acne" has a temperature and a leukocytosis, you have left ordinary acne behind — this is an immune-complex emergency, and the clock on permanent scarring has already started.[3][6]

Learn the severity spectrum once and reproduce it verbatim — examiners ask for the tiers by name:[1]

[1] [2]

The classic trap: acne conglobata and acne fulminans are conflated at the bedside every year. Conglobata is chronic, indolent and systemic-symptom-free; fulminans is acute, ulcerative and febrile. One earns a retinoid; the other earns a steroid first.[2][6]

Etymology for viva gold: fulminans is from the Latin fulmen, "lightning" — the eruption strikes like a bolt, over hours to days, not the slow burn of conglobata. The name is the natural history.[2]

The follicular occlusion tetrad — the four Hs

Acne fulminans overlaps with the follicular occlusion tetrad, four conditions driven by the same machinery — occlusion and rupture of the pilosebaceous unit, then a neutrophilic, scarring inflammatory response:[1]

[1]

All four share one pathway — follicular occlusion, rupture, neutrophilic abscess, sinus tract, fibrosis — and they coexist often enough that finding one should make you look for the other three.[1]

When acne fulminans co-occurs with pyogenic arthritis, pyoderma gangrenosum and hidradenitis, name the syndrome out loud: PAPASH (Pyogenic arthritis, Acne, Pyoderma gangrenosum, Suppurative Hidradenitis), an autoinflammatory disorder linked to PSTPIP1 mutations. Naming it changes the pathway — it points you to IL-1 blockade rather than another round of antibiotics.[1][7]

The broader autoinflammatory family to hold in your head: SAPHO (Synovitis, Acne, Pustulosis, Hyperostosis, Osteitis), and the PAPA / PAPASH / PASH / PsAPASH cluster, all driven by PSTPIP1/CD2BP1 mutations and IL-1β over-production. This is the rationale for anakinra and canakinumab in refractory disease, and for TNF-α inhibitors when bone lesions dominate.[7][8]

Who gets it — and what lights the fuse

Acne fulminans is rare, heavily male, and almost always adolescent. It accounts for well under one percent of all acne and probably affects only a few hundred new patients a year in large Western populations — yet it is over-represented in exams precisely because its management is a high-yield exception to every other acne rule.[2][3]

[1]

Why adolescent males? Three mechanisms stack. Pubertal testosterone and dihydrotestosterone enlarge the sebaceous gland and drive sebum output — the substrate for C. acnes — and males produce more sebum than females at this age. The androgen-driven CD4+ T-cell response to C. acnes is more intense in males. And the trunk follicle in adolescent boys is large, deep and sebum-rich, primed to rupture when antigen load surges.[1]

The recognised triggers, memorised as a table because the supplement history is the one candidates forget:[1]

[1] [5]

The bodybuilding and sports-supplement history is mandatory in any adolescent male with severe acne. Whey protein, creatine and over-the-counter "testosterone boosters" are increasingly recognised precipitants, and the history is frequently concealed — ask directly, ask without judgement, and ask the parent out of the room.[5]

It is not the bug — it is the immune storm

[1] [2]

Acne fulminans is a hypersensitivity reaction to Cutibacterium acnes antigen, not a bacterial infection. That single sentence explains the sterile cultures, the systemic symptoms, the bone lesions and — most importantly — why the first drug is a steroid, not an antibiotic. Three mechanisms compose the storm.[1]

First, a Type III (immune-complex) hypersensitivity. Circulating immune complexes of C. acnes antigen, IgG/IgM and complement deposit in tissue; complement activation generates C5a, a potent neutrophil chemoattractant. The same deposition drives the systemic features — fever, arthralgia, myalgia, occasional erythema nodosum — and the osteolytic lesions, sacroiliitis and cutaneous ulceration when complexes land in bone, synovium and skin.[1][2]

Second, neutrophilic infiltration and tissue destruction. C5a, IL-8 (CXCL8) and leukotriene B4 recruit a dense neutrophilic infiltrate around the ruptured follicle. In a susceptible host these neutrophils fail to clear the organism and instead degranulate, releasing elastase, collagenase and proteases that destroy the follicular wall, dermal collagen and overlying epidermis — producing the ragged ulcer under its haemorrhagic crust. This is why cultures are sterile: the inflammation is the host's, not the bacterium's.[1][2]

Third, the autoinflammatory (IL-1) axis. A subset of AF — especially the PAPA/PAPASH overlap — is driven by PSTPIP1/CD2BP1 mutations that over-produce IL-1β via inflammasome activation. IL-1β amplifies neutrophil recruitment, drives osteitis and fever, and is the mechanistic reason anakinra and canakinumab work when steroids and retinoids have failed.[7][8]

Why isotretinoin can itself precipitate AF — read this twice. Isotretinoin rapidly remodels the pilosebaceous unit: it shrinks the gland, normalises keratinisation and slashes sebum output. In a susceptible host that sudden remodelling releases a large bolus of C. acnes antigen into the dermis, lighting the immune-complex cascade described above. High starting doses and pre-existing severe inflammation raise the risk, and cases are documented even at low dose. This is the mechanistic basis of the cardinal rule — never start isotretinoin alone in acne fulminans.[4][6]

Read the patient, not just the skin

The picture is dramatic and unfolds over days to weeks — classically in an adolescent boy with mild pre-existing acne who deteriorates explosively. Examine the skin, but also take the temperature, feel the joints, and ask about mood.[1]

The cutaneous features, in the order they appear:[1][2]

• Onset — sudden, often over hours to days; a dramatic fall-off from mild acne.
• Morphology — large, tender, inflammatory nodules and plaques that rapidly ulcerate under necrotic, haemorrhagic crust; the crust is extensive and adherent, and removing it reveals a ragged, bleeding base.
• Distribution — chest, back and shoulders, less prominently the face; comedones are inconspicuous compared with ordinary acne.
• Pain — exquisite; the patient often cannot lie on his back or wear a shirt.
• Scarring — severe atrophic, keloidal and hypertrophic scarring is inevitable and develops within weeks.[1][2]

[1]

The musculoskeletal features are the ones candidates forget and examiners love:[9]

• Osteolytic bone lesions, most characteristically in the medial clavicle and sternum, also long bones and spine — producing localised bone pain, swelling and warmth, and occasionally the presenting complaint.
• Sacroiliitis that may mimic ankylosing spondylitis but is usually HLA-B27 negative.
• Enthesopathy and myopathy contributing to the myalgia and stiffness.
• Pathological fracture as a rare complication of extensive osteolysis.

[9]

Three atypical presentations to name in the viva. In a female, AF should trigger a hunt for hyperandrogenism (PCOS, congenital adrenal hyperplasia, adrenal or ovarian tumour). In an adult, suspect exogenous androgen or testosterone therapy. And the high-yield trap — a patient started on isotretinoin for severe nodulocystic acne who flares with systemic symptoms within the first weeks has isotretinoin-induced acne fulminans: stop or reduce the isotretinoin and introduce corticosteroids.[4]

The differential — and the one discriminator

A complete differential separates mimics with overlapping cutaneous morphology from those with overlapping systemic features. AF sits at the intersection of severe acne and the neutrophilic dermatoses, so both lists matter.[1]

[1]

The wider list, each with the one discriminator that earns the mark:[2][6]

• Dissecting cellulitis of the scalp — boggy, sinus-tract-forming scalp lesion in a young man; part of the tetrad; no systemic features.
• Sweet syndrome (acute febrile neutrophilic dermatosis) — tender erythematous plaques on the upper body with fever and leukocytosis; classically linked to AML, IBD and drugs; dense dermal neutrophilic infiltrate on biopsy; steroid-responsive. Distinguished from AF by the absence of folliculocentric ulcerative acne.
• Staphylococcal furunculosis or carbuncle — tender abscesses with positive culture; lacks the conglobate acneiform background and the polyarticular arthralgia.
• Atypical infection (atypical mycobacteria, disseminated fungi such as sporotrichosis or blastomycosis) — consider in the immunocompromised or endemic-area patient; biopsy and tissue culture are essential.
• Behçet disease or bowel-associated dermatitis-arthritis syndrome — oral and genital aphthae, pathergy, erythema-nodosum-like lesions, bowel symptoms; sterile pustules but not ulcerative acne.
• Severe nodulocystic acne without AF — no systemic symptoms, normal WBC, ESR and CRP; the single most important exclusion.

[2] [6]

The bedside discriminator is one sentence: systemic symptoms (fever, arthralgia, myalgia) plus raised inflammatory markers (leukocytosis, ESR, CRP) point to acne fulminans; their absence points to conglobata or severe nodulocystic acne.[1]

The FUS triad and the bedside round

Diagnose AF on the triad — fever, ulcerative trunk nodules, systemic inflammation on bloods — and on little else. It is a clinical diagnosis; investigations confirm and stage, they do not make the call.[1]

[1]

All three must be present to call it acne fulminans rather than severe nodulocystic acne or acne conglobata — two of three is not AF.[1]

Run the focused examination in this order:[1]

• Skin — count and map the ulcerative nodules; photograph for monitoring; look for secondary infection (surrounding cellulitis, pus, lymphangitis).
• Musculoskeletal — palpate the sternoclavicular joints, clavicles, sternum and sacroiliac joints for tenderness, swelling and warmth; examine every peripheral joint for synovitis; check range of movement.
• Abdomen — hepatosplenomegaly.
• Shins — erythema nodosum.
• General — temperature, weight and recent weight loss, lymphadenopathy, blood pressure.

[1]

The risk-factor and comorbidity screen is where the diagnosis is actually made — the skin only confirms what the history suggests:[5]

• Substance and supplement history — anabolic-androgenic steroids, "testosterone boosters", whey protein, creatine, BCAAs. Frequently concealed; ask directly and non-judgementally, and apart from the parent.
• Drug history — recent isotretinoin initiation; testosterone therapy.
• Mental health — screen for depression, anxiety, school refusal and suicidal ideation with a validated tool (PHQ-A or HADS). The sudden disfigurement is psychologically devastating in an adolescent; this is a mandatory, not optional, part of the assessment.
• Sexual and reproductive — in females, menstrual history, hirsutism, PCOS screen; in any female who may receive isotretinoin, contraception and a pregnancy test are mandatory.

[5] [6]

For severity and response monitoring, lesion counts and serial photographs are the practical bedrock; the fever chart and the CRP/ESR/WBC trend are the objective measures that fall fastest with corticosteroids. GAGS (Global Acne Grading System) and CADI (Cardiff Acne Disability Index) may frame quality of life but are not diagnostic.[3]

Investigations that earn their keep

Acne fulminans is a clinical diagnosis; investigations support it, exclude mimics and stage systemic involvement. Do not over-investigate the classic case — do look hard at the atypical one.[1]

[1]

Skin swabs and tissue cultures are typically sterile — the inflammation is immune-complex-mediated, not infective. Send them to exclude secondary staphylococcal or streptococcal infection (which can supervene on ulcerated skin) and to guide adjunctive antibiotics; send bacterial, mycobacterial and fungal cultures only if an infective mimic is plausible.[1]

Biopsy is not required in classic cases but is indicated when the diagnosis is uncertain, when pyoderma gangrenosum, Sweet syndrome or infection must be excluded, or when an overlap syndrome is suspected. Histology shows follicular rupture with a dense perifollicular and mid-dermal neutrophilic infiltrate, necrosis of the follicular wall, haemorrhage and a mixed infiltrate extending into the subcutis — non-specific but supportive. The neutrophilic dermatoses are excluded by folliculocentricity: pilosebaceous units sit at the centre of the inflammation.[2]

Any patient with bone or joint pain must be imaged. X-ray of the clavicle, sternum and symptomatic long bones may show osteolytic lesions, periosteal reaction, sclerosis or osteitis — the medial clavicle is the classical site. MRI is more sensitive, showing bone-marrow oedema and soft-tissue inflammation earlier, and is preferred for sacroiliitis and early disease. Whole-body Tc-99m scintigraphy maps multifocal osteitis when SAPHO overlap is suspected; CT occasionally defines cortical destruction in refractory lesions.[9]

Corticosteroids FIRST — the cardinal rule

[1]

The rationale is the pathophysiology. Corticosteroids broadly suppress the immune-complex cascade, complement activation, neutrophil recruitment and cytokine release that define AF. They bring fever and arthralgia under control within 24 to 72 hours and halt the appearance of new ulcerative lesions, buying the time needed to introduce isotretinoin safely later. This is the one paragraph where there is no room for creativity — the steroid comes first, every time.[1]

The goals of immediate management are four: suppress the life-disrupting immune-complex inflammation, prevent the rapid and permanent scarring that appears within days to weeks, relieve pain and systemic upset, and address the psychological crisis.[1]

Supportive and resuscitative measures run alongside the steroid:[6]

• Admission is warranted for severe systemic upset, inability to eat or sleep, suspected secondary infection or sepsis, extensive ulceration requiring nursing care, or suicidal ideation. Most patients can be managed as outpatients with close follow-up.
• Analgesia and antipyresis — paracetamol 1 g four times daily; avoid NSAIDs where possible (they may worsen acne and, combined with steroids, raise gastrointestinal risk), though a short course is acceptable for severe bone pain.
• Wound care for ulcerated lesions — gentle saline or dilute-antiseptic cleansing, non-adherent dressings, hydrocolloid or foam for exudative ulcers, debridement of loose crust only. Avoid aggressive debridement — pathergy is not a feature of AF, but trauma delays healing.
• Psychological first aid — explain the diagnosis and prognosis honestly, involve the family, and arrange prompt adolescent mental-health input for any sign of depression or suicidal ideation.
• Exclude infection — send blood and skin cultures; start empirical anti-staphylococcal antibiotic (for example flucloxacillin) only if secondary infection is clinically evident.[6]

The four-step regimen — steroid first, retinoid second

The definitive regimen is a sequential combination of systemic corticosteroid then low-dose isotretinoin, with careful tapering and monitoring. It is endorsed by the evidence-based recommendations of Greywal and colleagues (JAAD 2017), which remain the most widely cited guidance in the absence of any randomised trial.[6]

The four steps, with the doses and timings examiners expect verbatim:[1]

Everyone forgets the overlap. Step 2 is not "stop the steroid, start the retinoid" — the two run together for weeks. The steroid cover is precisely what makes the retinoid safe to introduce; dropping the steroid too early is the classic rebound-flare error.[4][6]

Adjunctive and supportive therapies, with the doses and the one rule that catches candidates — no tetracyclines alongside isotretinoin (benign intracranial hypertension risk):[1]

Monitoring during therapy has two masters — the isotretinoin and the steroid:[1]

• Lipids (fasting triglycerides, cholesterol) and LFTs monthly during isotretinoin; it raises triglycerides and transaminases.
• Glucose, blood pressure, weight, bone density if steroids are prolonged.
• Mood and suicidality at every visit — both the disease and isotretinoin carry mood risks; active surveillance is the safe position.
• Infection — dual steroid-plus-isotretinoin immunosuppression demands a low threshold for cultures.
• Pregnancy in females on isotretinoin — strict contraception, monthly beta-hCG, an iPLEDGE-equivalent programme where applicable.

[1]

Refractory disease and the biologics

A minority of patients are refractory to, or intolerant of, the corticosteroid-plus-isotretinoin regimen, or relapse on tapering. The recent literature (Taudorf 2024; Woźna 2024) supports off-label biologic therapy — but only on the basis of case reports and small series. There are no randomised trials in acne fulminans; the disease is too rare.[7][8]

[7] [8]

Special situations — name the subtype, change the plan

Isotretinoin-induced acne fulminans — a patient started on isotretinoin for severe nodulocystic acne who, within the first weeks, develops ulcerative nodules with fever, arthralgia and leukocytosis. Documented even at low starting dose. Management: reduce or stop the isotretinoin, start oral prednisolone 0.5–1 mg/kg/day until inflammation is controlled, then reintroduce isotretinoin at 0.25–0.5 mg/kg/day with continued steroid cover and gradual uptitration.[4][6]

Testosterone or anabolic-steroid-induced acne fulminans — bodybuilders and athletes using testosterone or anabolic-androgenic steroids may develop an eruption indistinguishable from idiopathic AF. Cessation of the offending agent is central — without it, standard therapy is less effective and relapse is likely. Then run the usual prednisolone-then-low-dose-isotretinoin regimen, with doping-control or sports-medicine liaison where relevant.[5]

Acne fulminans with prominent osteoarticular disease (SAPHO overlap) — when bone pain, sacroiliitis or clavicular osteitis dominate, consider SAPHO. Add NSAIDs first-line for pain and osteitis (caution with concurrent steroids), bisphosphonates (pamidronate, zoledronic acid) for refractory hyperostosis and bone pain, and TNF-α inhibitors for refractory osteoarticular disease.[7][9]

Autoinflammatory syndromes (PAPA, PAPASH, PASH, PsAPASH) — when AF coexists with pyoderma gangrenosum, pyogenic arthritis or hidradenitis, suspect a PSTPIP1-associated syndrome. Management is multidisciplinary (dermatology, rheumatology, genetics) and centres on IL-1 blockade (anakinra, canakinumab), often with TNF-α inhibitors, alongside isotretinoin for the acne component.[7]

Female patients — rule out hyperandrogenism: PCOS (free testosterone, LH/FSH, DHEAS, 17-OH progesterone), congenital adrenal hyperplasia, and adrenal or ovarian tumour if suspicion is high. Spironolactone 50–200 mg/day helps androgen-driven background acne but does not treat the acute fulminant flare — steroids and isotretinoin do. Pregnancy prevention with isotretinoin is absolute: two reliable contraceptive methods, monthly beta-hCG; isotretinoin is profoundly teratogenic.[3]

Resource-limited settings — where biologics are unavailable or unaffordable, the steroid-plus-low-dose-isotretinoin regimen remains the workhorse and is highly effective for the great majority. Pulsed oral azithromycin (500 mg daily for 3 days every 2–4 weeks) is a reasonable adjunct when tetracyclines are contraindicated by co-prescribed isotretinoin or simply unavailable.[8]

Scarring is inevitable

Severe atrophic, keloidal and hypertrophic scarring is the principal long-term morbidity and cannot be prevented — only limited. Early treatment reduces its extent; it does not remove it. Set that expectation honestly with the patient and family at the first visit.[6]

Scar revision is deferred until the disease is quiescent — usually 6 to 12 months after completion of isotretinoin, because active inflammation and recent isotretinoin both raise the risk of poor healing from procedural interventions:[1]

• Atrophic scars — fractional CO2 laser, microneedling, subcision, the CROSS technique with trichloroacetic acid for ice-pick scars, hyaluronic acid fillers.
• Hypertrophic or keloidal scars — intralesional triamcinolone (10–40 mg/mL every 4–6 weeks), silicone gel sheeting, pulsed-dye laser, 5-fluorouracil injections.
• Post-inflammatory hyperpigmentation — sun protection, hydroquinone in adult skin, azelaic acid, retinoids after the isotretinoin course is complete.[6]

How patients with acne fulminans come to harm (the preventable list)

• Isotretinoin started alone — the cardinal error; precipitates or worsens the immune-complex flare.[4]
• Too-rapid steroid taper — rebound flare that can be worse than the original presentation.[6]
• Anabolic-steroid or supplement trigger missed — relapse is guaranteed while the driver persists.[5]
• Suicidal ideation overlooked — the sudden disfigurement in an adolescent is devastating; a mandatory screen is skipped at the patient's peril.[6]
• Secondary infection or sepsis missed on ulcerated skin — sterile cultures are the rule, but staphylococcal cellulitis can supervene.[1]
• Osteolytic bone lesions overlooked — clavicular osteolysis can precede the skin eruption; any bone pain warrants imaging.[9]
• iPLEDGE or contraception failure — isotretinoin is absolutely teratogenic; the programme must be followed rigorously in the adolescent population.[3]
• Pyoderma gangrenosum misdiagnosed as AF — AF is folliculocentric; PG is an ulcer with an undermined border. The treatments diverge.[7]

Prognosis and disposition

Fever and systemic symptoms typically resolve within 24 to 72 hours of starting corticosteroids. Cutaneous inflammation — new lesions, pain, crusting — settles over 1 to 3 weeks. Complete clearance of active disease usually requires the full 4 to 6 month isotretinoin course.[2][8]

Relapse occurs if isotretinoin is stopped prematurely, the steroid taper is too rapid, or an ongoing trigger (anabolic steroids, supplements) persists. A full cumulative dose of isotretinoin (120–150 mg/kg) is the best protection against relapse.[8]

Bone lesions usually resolve over months once inflammation is controlled; chronic osteitis and pathological fracture are uncommon, and sacroiliitis persists in a minority with SAPHO overlap.[9]

Long-term outlook. Systemic disease has an excellent prognosis with appropriate therapy and leaves no permanent systemic sequelae in most patients. Cutaneous scarring is the dominant long-term morbidity and is lifelong. Mortality is rare and reported only with uncontrolled sepsis from secondary infection, or with suicide — which is why the mental-health screen is not optional.[2]

Disposition. Most patients are managed as outpatients with close (initially weekly) dermatology follow-up. Admit for severe systemic upset, extensive ulceration requiring nursing care, suspected sepsis or secondary infection, or suicidal ideation. Every patient should be under a dermatologist; rheumatology and adolescent mental-health input follow the clinical picture.[1]

Evidence, guidelines and regional deltas

There are no randomised controlled trials in acne fulminans — the disease is too rare. Every recommendation rests on expert consensus, narrative and systematic reviews, case series and case reports. Name that limitation in the viva; it is itself a mark-scorer.[6][8]

The names that earn marks:[1]

• Greywal and colleagues (JAAD 2017) — the most widely cited evidence-based recommendations for AF and its variants; endorses corticosteroid first, low-dose isotretinoin second.[6]
• Trave and colleagues (2023) — a systematic review of AF and its multiple associated factors: epidemiology, triggers (anabolic steroids, isotretinoin, supplements) and management.[1]
• Gutiérrez-Meré and colleagues (2023) — a narrative review of the clinical features, pathophysiology and treatment ladder.[2]
• Taudorf and colleagues (JDDG 2024) — a clinical and literature review of TNF-α inhibitor treatment, establishing the biologic evidence base for refractory disease.[7]
• Woźna and colleagues (Frontiers in Medicine 2024) — a recent case report and literature review of AF treatment.[8]
• Jemec and Rasmussen (JAAD 1989) — the classic case report and review of the bone lesions, establishing clavicular and sternal osteolysis as characteristic.[9]
• Fakih and colleagues (2020) — a key case report of AF induced by a low dose of isotretinoin, reinforcing the rule against isotretinoin monotherapy.[4]

[1] [1]

Controversies to handle calmly. The optimal steroid duration and taper has no trial-defined schedule; consensus favours 4 weeks of induction followed by a 2–3 month taper. The role and timing of biologics is case-report level — some reserve them for true refractory disease, others use them earlier in severe osteoarticular or autoinflammatory overlap. Causality of dietary supplements (whey, BCAAs, creatine) is hard to prove but the systematic reviews note the strength of the association. And the debate over whether isotretinoin independently causes depression or suicidality persists; in AF the disease itself is a major mood risk, so active surveillance is the safe position regardless of the underlying debate.[1][5][6]

The mantra, and the mnemonic

[1] [6]

The mantra: steroids to cool the fire, retinoid to finish the job.[4][6]

Ward-round test — three stems, thirty seconds each

Stem 1 — the boy from the top of the topic (answer)

The 16-year-old with a three-day explosion of ulcerative, haemorrhagic-crusted trunk nodules, fever of 39 °C, arthralgia and a supplement history. The registrar wants to start isotretinoin now. What is the diagnosis and what do you do in the next hour? Model: This is acne fulminans — the FUS triad (fever and systemic upset, ulcerative trunk nodules, systemic inflammation on bloods) in an adolescent male, with a bodybuilding supplement the likely trigger. Do not start isotretinoin alone — it can precipitate or worsen the immune-complex flare. Confirm with FBC, ESR, CRP (expect leukocytosis and marked elevation), send blood and skin cultures (expect sterile), check beta-hCG if female, and start oral prednisolone 0.5–1 mg/kg/day as the first drug. Counsel the family honestly about inevitable scarring, screen mood, and plan to add low-dose isotretinoin at 0.5 mg/kg/day only after two to four weeks of steroid cover.[1][6]

Stem 2 — the flare after starting isotretinoin (answer)

A 19-year-old started isotretinoin two weeks ago for severe nodulocystic acne. He now has new ulcerative nodules, fever, knee pain and a WCC of 16. What happened, and what is the first change to his prescription? Model: This is isotretinoin-induced acne fulminans — documented even at low dose, from abrupt antigen release as the pilosebaceous unit remodels. Reduce or stop the isotretinoin and start oral prednisolone 0.5–1 mg/kg/day to control the immune-complex flare; reintroduce isotretinoin at 0.25–0.5 mg/kg/day only once inflammation is quiescent, under continued steroid cover, with gradual uptitration. Continuing isotretinoin monotherapy, or simply pushing the dose higher, is the cardinal error.[4]

Stem 3 — the clavicle pain that came first (answer)

A 15-year-old boy presents with medial clavicular pain, swelling and warmth, low-grade fever, and — on closer questioning — a fortnight of worsening ulcerative trunk acne. Bloods show leukocytosis and a CRP of 80. X-ray of the clavicle shows an osteolytic lesion. What links the bone and the skin, and what is the mechanism? Model: The osteolytic bone lesion is part of the acne fulminans, not a separate infection — clavicular and sternal osteolysis is characteristic and can precede the skin eruption. The shared mechanism is Type III immune-complex deposition: circulating complexes of C. acnes antigen, antibody and complement deposit in bone, synovium and skin, generating C5a, recruiting neutrophils and driving both the cutaneous ulceration and the osteolysis. Cultures are sterile. Treat the underlying AF with corticosteroids first; the bone lesions usually heal over months as inflammation is controlled. Consider SAPHO overlap if sacroiliitis or palmar-plantar pustulosis is present.[9]

References

1. [1]Trave I, Donadoni R, Cozzani E, et al. Acne fulminans and its multiple associated factors: a systematic review Eur J Dermatol, 2023.PMID 38465543
2. [2]Gutiérrez-Meré R, Tajes I, Diéguez P, et al. [Translated article] Acne Fulminans: A Narrative Review Actas Dermosifiliogr, 2023.PMID 37506824
3. [3]Dall'oglio F, Puglisi DF, Nasca MR, et al. Acne fulminans G Ital Dermatol Venereol, 2020.PMID 33084268
4. [4]Fakih A, Goens J, Grozdev I, et al. Acne fulminans induced by a low dose isotretinoin: case report and review of the literature Dermatol Online J, 2020.PMID 33423422
5. [5]Zamil DH, Perez-Sanchez A, Katta R Acne related to dietary supplements Dermatol Online J, 2020.PMID 32941710
6. [6]Greywal T, Zaenglein AL, Baldwin HE, et al. Evidence-based recommendations for the management of acne fulminans and its variants J Am Acad Dermatol, 2017.PMID 28619551
7. [7]Taudorf EH, Jensen MB, Bouazzi D, et al. Tumor necrosis factor-α inhibitor treatment of acne fulminans - a clinical and literature review J Dtsch Dermatol Ges, 2024.PMID 38128111
8. [8]Woźna J, Korecka K, Stępka J, et al. Acne fulminans treatment: case report and literature review Front Med (Lausanne), 2024.PMID 39139785
9. [9]Jemec GB, Rasmussen I. Bone lesions of acne fulminans. Case report and review of the literature J Am Acad Dermatol, 1989.PMID 2521643