Erythema annulare centrifugum (EAC)

Meet the patient

A 42-year-old man arrives with three weeks of slowly enlarging, mildly itchy rings over his flanks and thighs. He has been treating himself with a friend's clotrimazole for ten days, and the rings kept marching outward. Between his toes you find peeling scale; a KOH of the toe web is positive, but a KOH of the ring's leading edge is negative.^[1]

Two exam questions are now live, and they are the two that define EAC: why is the KOH negative when the eruption is so clearly ring-shaped? and what is the ring reacting to? The first answer is the id reaction; the second is the trigger hunt. Hold those two questions and the rest of the page slots into place.^[1][3]

The one feature that earns the mark — the trailing inner scale

EAC is the prototype figurate erythema, and the diagnosis lives in the scale. First drawn by Darier in 1916, it presents as slowly expanding annular or polycyclic erythematous plaques whose single distinguishing feature is the trailing inner scale: a fine, white scale lying just INSIDE the advancing edge, like a wake behind a boat. In tinea the scale LEADS on the outer border; in EAC it TRAILS on the inner border. That one observation, made before any test, is half the diagnosis.^[3]

EAC is not a disease — it is a cutaneous echo of a distant immunological event. It is a type IV (delayed, cell-mediated) hypersensitivity reaction to a remote antigen, most often a dermatophyte antigen shed from a focus of tinea, the classic id reaction. In roughly half of cases no trigger is found; the rest trace to drugs, other infections, foods, autoimmune thyroid disease, pregnancy, and rarely malignancy.^[1]

Why EAC earns its own ward round — three reasons, in the order they bite. First, it is routinely mistaken for tinea and mistreated with topical antifungals; the trailing scale and a negative KOH stop that error. Second, in a minority it is paraneoplastic (PEACE — paraneoplastic erythema annulare centrifugum eruption), so persistent or atypical rings demand a malignancy search. Third, individual lesions resolve but the course is chronic and relapsing, so the real cure is trigger eradication, not ring suppression.^[2][4]

The classic trap: reach for a topical antifungal the moment you see a ring, and you have just mistreated an immunological eruption for weeks. Tinea leads with its scale; EAC trails. Confirm with KOH before you prescribe.^[1]

Etymology for viva gold: annulare, Latin for ring; centrifugum, fleeing the centre. Darier's 1916 name was already the diagnosis — the ring runs outward and leaves its scale in the wake.^[3]

Why the ring expands — a type IV chase across the skin

The expanding ring is the visible footprint of activated T-cells migrating outward through the skin. A distant antigen is processed and presented to naive T-cells; they home to skin and release cytokines (interferon-gamma, interleukin-2, tumour necrosis factor-alpha) that recruit the advancing erythematous edge. The trailing scale is the desquamating epidermis the front has already passed.^[1][3]

The mechanism runs as a four-step chain a final-year candidate should reproduce:^[1]

1. Sensitisation — a distant antigen (dermatophyte from tinea, a drug hapten, a food or mould antigen, or a tumour antigen) is taken up by Langerhans cells and dermal dendrocytes and presented in the draining node, seeding antigen-specific memory T-cells.^[1]
2. Cutaneous homing and the id reaction — when antigen re-enters the circulation, sensitised T-cells home to skin via cutaneous lymphocyte-associated antigen binding E-selectin on dermal endothelium. The eruption breaks out at a site DISTANT from the antigen source. Tinea pedis drives EAC on the trunk: the trunk is reacting to fungal antigens that reached it haematogenously though the trunk itself is not infected — which is exactly why the KOH of the ring is negative.^[1]
3. The coat-sleeve and the expanding edge — antigen-specific T-cells cluster around superficial dermal venules and release the cytokines that build the perivascular infiltrate: the tight, coat-sleeve "cuffing" pattern, with eosinophils when a drug or parasite is driving it. The front then marches outward at the characteristic 2 to 5 mm per day.^[3][19]
4. The trailing scale — as the edge advances, the epidermis behind it desquamates into the fine inner scale. The scale trails because it is the residue of inflammation that has already passed — the inverse of tinea, where the growing fungus scales the LEADING border. It is often so subtle you miss it unless you stretch the skin or sight it in tangential light.^[1]

Why the centre clears — behind the advancing edge the T-cell clone exhausts or the local antigen is cleared, so the centre returns towards normal, often leaving transient post-inflammatory hyperpigmentation. New rings appear at the periphery as fresh clones activate, producing the migratory, polycyclic pattern that evolves over weeks.^[3]

The coat-sleeve — histology that fits the name

Biopsy is not needed in the typical case, but the histology is examinable and the pattern is unmistakable. The hallmark is the coat-sleeve (tight perivascular, "cuffing") lymphocytic infiltrate of the superficial and mid-dermis — lymphocytes packed around venules like a sleeve around an arm. It is not entirely specific, but in the right clinical context it is strongly supportive. Always request PAS or GMS stains to exclude an occult dermatophyte in the biopsied skin.^[3]

^[3]

How common, who, and the trigger profile

EAC is uncommon but not rare, and risk factor is almost a synonym for trigger. Most data come from case series and reviews rather than population studies, so memorise the shape of the trigger list, not an incidence.^[3][5]

^{[3] [5]}

EAC can occur at any age, from infancy to old age, but most cases present in adults between the third and sixth decades, with no sex predominance. A seasonal pattern is described in a minority, with spring and autumn peaks, and an annually recurring variant comes back at the same time each year in affected individuals.^[4]

Because EAC is reactive, run the trigger hunt in this order — commonest and most treatable first:^[1]

• Dermatophyte (tinea) infection — the most common identifiable trigger worldwide, and the dominant driver where dermatophytosis is endemic. EAC is a distal id reaction to tinea pedis, cruris, corporis, or unguium; the ring is immunologically mediated, so it is KOH-negative at the annular border even though the distant tinea is KOH-positive.^[1]
• Drugs — take a careful drug history, including recently started or changed medications. Culprit classes include beta-lactam antibiotics, NSAIDs, allopurinol, antimalarials (hydroxychloroquine), finasteride, and hormonal agents.^[5]
• Underlying malignancy (PEACE) — rare but the one you cannot miss. Lymphoma (Hodgkin and non-Hodgkin), mycosis fungoides and Sézary syndrome, leukaemia, and solid tumours (lung, breast, prostate, gastrointestinal) are all reported. The EAC may precede the cancer diagnosis, making it a genuine cutaneous sentinel.^[2]
• Autoimmune thyroid disease — under-recognised; check thyroid status in idiopathic EAC.^[1]
• Pregnancy — a benign gestational form is described and typically resolves postpartum.^[5]
• Foods and additives — blue cheese (Aspergillus mould antigens), tomatoes, and preservatives or dyes are reported, particularly in recurrent disease.^[1]

EAC in the figurate family — scale tells them apart

EAC is one of several reactive erythemas that expand in rings; the scale, the distribution, and the tempo tell them apart. All share expanding ring or arc morphology; none shares EAC's trailing inner scale.^[3]

^[3]

The discriminator line: only EAC trails its scale on the inside. The others either carry no scale (marginatum, migrans), concentric wood-grain leading scale (gyratum repens), or target morphology (multiforme).^[3]

Classification by trigger

Because EAC is a reactive pattern, the clinically useful axis is the cause:^[1]

1. Idiopathic — no trigger found in up to half of cases.
2. Infective — dermatophyte (tinea) id reaction is the commonest identifiable cause; also Candida, bacterial (streptococcal), viral (EBV, hepatitis, HIV), and in the tropics parasitic (Ascaris, Entamoeba, filaria).
3. Drug-induced — finasteride, aceclofenac, cimetidine, chloroquine, hydroxychloroquine; also NSAIDs and allopurinol.
4. Food and additives — blue cheese (hypersensitivity to blue cheese Penicillium); food allergy is listed among the associated causes.
5. Autoimmune — autoimmune thyroid disease (Hashimoto's, Graves').
6. Paraneoplastic (PEACE) — Hodgkin and non-Hodgkin lymphoma, mycosis fungoides and Sézary syndrome, leukaemia, and solid tumours.
7. Physiological — pregnancy (benign gestational variant).
8. Seasonal — annually recurring EAC, a benign relapsing variant.^[1][2][4]

Tinea or EAC? The bedside fork — KOH settles it

The single most examined distinction is EAC versus tinea corporis, and the bedside KOH settles it. Both make annular, erythematous, expanding lesions; the scale location and the KOH tell them apart. This is the fork every examiner reaches for.^[1]

^[1]

Everyone forgets: a negative KOH in an annular lesion is EAC, not resistant tinea. Escalating the antifungal is the wrong move — the ring is not infected, it is reacting. Go find the distant focus.^[1]

The KOH test — the decisive bedside manoeuvre

KOH microscopy of the active border is the single most useful confirmatory test. Scrape scale at the advancing edge onto a slide, apply 10 to 20 per cent potassium hydroxide, gently heat, and read it under the microscope. Tinea shows branching septate hyphae (positive); EAC shows none (negative). A negative KOH plus the trailing-scale morphology confirms EAC clinically.^[1]

Then KOH the distant sites — feet, groin, nails, and scalp in children. These are often positive and pinpoint the antigen source driving the id reaction. The lesion is negative; the trigger is positive — that asymmetry is the diagnosis.^[1]

The rest of the differential — discriminators, not lists

Beyond tinea, a handful of annular erythemas enter the differential; each is dismissed by one feature. Run them by scale, distribution, tempo, and a confirmatory test.^[3]

• Granuloma annulare — annular plaques of small, firm, skin-coloured or erythematous dermal papules with a non-scaly, palpable border. No surface scale at all. Dorsal hands and feet, fingers, extensor extremities. Histology shows palisading granulomatous inflammation and mucin.^[3]
• Urticaria — transient wheals that appear and resolve within 24 hours at any given site; no scale; individual lesions migrate rapidly. EAC is fixed for days to weeks and carries a trailing scale. The tempo (under 24 hours versus days) is the discriminator.^[3]
• Psoriasis — well-demarcated, thick, erythematous plaques with thick silvery adherent scale on extensors (elbows, knees), scalp, and sacrum, often with nail changes. The scale is thick and leading, not fine and trailing.^[3]
• Erythema migrans (Lyme) — usually a single lesion at a tick bite site, expands rapidly over days, uniform red border without scale, plus a tick-exposure history. EAC is multiple, has trailing scale, and has no tick link.^[3]
• Erythema multiforme — typical target lesions (dusky or bullous centre, pale oedematous middle ring, erythematous outer ring) on extensor limbs, palms, soles, and mucosa, with acute onset over 24 to 48 hours after HSV or mycoplasma infection or a drug.^[3]
• Subacute cutaneous lupus erythematosus (SCLE) — annular or polycyclic lesions on photosensitive (sun-exposed) skin — upper back, shoulders, chest, arms — often with a peripheral scale and anti-Ro or SSA positivity (around 70 per cent). Photosensitive distribution plus a positive antinuclear or anti-Ro antibody separates it.^[3]
• Pityriasis rosea — oval, salmon-pink patches with a collarette (peripheral) scale following Langer's lines in a Christmas-tree distribution on the trunk, typically after a herald patch.^[3]

The dangerous mimic — mycosis fungoides. Early cutaneous T-cell lymphoma can present as persistent annular or figurate erythematous patches that mimic EAC and refuse to respond to topical therapy. The distinguishing features are persistence beyond months, atypical morphology, and biopsy evidence of atypical lymphocytes with epidermotropism. Any EAC that does not resolve or that progresses atypically must be biopsied — a classic fellowship pitfall.^[2]

The ward-round assessment — confirm, then hunt

EAC is a clinical diagnosis supported by KOH. The bedside round has two jobs: confirm the trailing-scale morphology with a negative KOH, and hunt the trigger — which is the key to definitive management.^[1]

History

Probe the recognised triggers in order:^[1]

1. Onset and tempo — when did it start, and how fast do rings expand? (EAC: days to weeks; urticaria: hours.)^[1]
2. Symptoms — is it itchy? (EAC: variable, often mild.) Any fever, weight loss, night sweats, or lymphadenopathy? (Red flags for lymphoma.)^[2]
3. Infection history — tinea pedis, cruris, unguium, corporis, or capitis? Recent sore throat (streptococcal), viral illness (EBV, hepatitis), or candidal infection?^[1]
4. Drug history — list every medication started or changed in the preceding weeks: penicillins, NSAIDs, allopurinol, hydroxychloroquine, finasteride, hormones.^[5]
5. Dietary history — blue cheese, tomatoes, processed foods with additives, preservatives, or dyes.^[1]
6. Thyroid and autoimmune history.^[1]
7. Pregnancy — in women of reproductive age, consider gestational EAC.^[5]
8. Malignancy history and B-symptoms — known malignancy, fever, drenching night sweats, weight loss.^[2]

Examination

Combine lesion assessment with a deliberate search for the trigger and for malignancy red flags:^[1]

^[1]

Distribution — what EAC involves and what it spares

The distribution is one of the most useful clues, with characteristic involved and spared sites:^[3]

^[3]

Symptoms

EAC is frequently asymptomatic. When symptomatic, the dominant symptom is mild and variable pruritus, which may be absent entirely. Significant pruritus raises an alternative (tinea, eczema, urticaria) or a coexisting dermatosis. Pain and systemic symptoms are not features of uncomplicated EAC — their presence should prompt investigation for malignancy or another diagnosis.^[3]

Timeline

The timeline is chronic and migratory, distinct from the acute tempo of urticaria or erythema multiforme:^[4]

• Onset — insidious over days to weeks; the patient often cannot date the first lesion.^[1]
• An individual lesion — expands over days to weeks, reaches several centimetres, then resolves centrally over further weeks, leaving hyperpigmentation that fades.^[3]
• The eruption — chronic and relapsing; new rings appear as old ones resolve, so the eruption migrates across the skin. An untreated episode may last weeks to months, occasionally years.^[4]
• Post-inflammatory hyperpigmentation — common but temporary; fades without scarring.^[1]

Refractory or atypical EAC — biopsy for mycosis fungoides, scan for PEACE

Most EAC is benign and self-limiting, but two scenarios change everything: an eruption that will not settle, and an eruption with systemic symptoms. Both demand the same reflex — stop treating the ring and start investigating the patient.^[2]

The features that should raise paraneoplastic EAC (PEACE) and trigger a malignancy workup:^[2]

• EAC refractory to treatment of an identified trigger (tinea cleared, eruption persists).^[2]
• EAC with systemic symptoms — fever, weight loss, night sweats (B symptoms).^[2]
• Lymphadenopathy or hepatosplenomegaly on examination.^[2]
• New EAC in an older patient with no obvious trigger.^[2]
• EAC with an atypical or rapidly progressive morphology.^[2]

^[2]

Investigations — confirm in atypical cases, hunt the trigger in all

EAC is a clinical diagnosis. Investigations exist to exclude tinea with KOH, confirm the diagnosis in atypical cases with biopsy, and identify the trigger. Routine bloods are otherwise unremarkable in uncomplicated EAC.^[3]

Skin biopsy

Biopsy is not required in the typical case but is indicated when the diagnosis is uncertain, the eruption is atypical or refractory, or mycosis fungoides must be excluded. The characteristic finding is the coat-sleeve tight perivascular lymphocytic infiltrate described above, with or without eosinophils and focal overlying parakeratosis (the trailing scale); PAS or GMS stains exclude an occult dermatophyte.^[3]

Fungal studies

Fungal studies both exclude tinea at the eruption site and identify the distant focus driving the id reaction:^[1]

• KOH of the EAC border — negative (confirms EAC, excludes tinea at the eruption site).^[1]
• KOH or fungal culture of distant sites — feet, groin, nails, scalp. A positive distant site identifies the antigen source and directs definitive treatment.^[1]
• Fungal culture of distant tinea sites identifies the organism (Trichophyton rubrum, T. mentagrophytes, and others) and confirms the trigger.^[1]

Trigger workup

When no obvious trigger is found on history and examination, a focused laboratory workup is warranted:^[2]

• Full blood count with differential — screen for leukaemia, lymphoma (abnormal lymphocytes), and eosinophilia (parasite, drug reaction).^[2]
• ESR or C-reactive protein — non-specific, but elevation supports an inflammatory or neoplastic process.^[2]
• Thyroid function tests (TSH, free T4) and thyroid antibodies — detect autoimmune thyroid disease.^[1]
• Liver function tests and LDH — LDH elevation raises concern for lymphoma.^[2]
• Streptococcal serology (ASO or anti-DNase B) — if post-streptococcal.^[1]
• Viral serology (EBV, hepatitis B and C, HIV) — if a viral trigger is suspected.^[1]
• Chest X-ray — baseline screen for occult malignancy, lymphadenopathy, or tuberculosis.^[2]

When is malignancy screening indicated?

A full age-appropriate malignancy screen (CT chest, abdomen, and pelvis or PET-CT; lymph node biopsy if lymphadenopathy) is reserved for refractory, atypical, or systemically symptomatic EAC, or where the FBC, LDH, or examination raise concern. It is not warranted in every case of idiopathic EAC — the paraneoplastic association is real but uncommon.^[2]

Treat the trigger, not the ring — the management spine

The eruption is a reaction; treat the cause, not the skin. Symptomatic treatment of the eruption is secondary and often unnecessary, because uncomplicated EAC is self-limiting. Over-treatment — particularly prolonged topical corticosteroids — does not alter the course and risks skin atrophy.^[1][5]

Is specific treatment usually necessary?

No. Uncomplicated EAC is self-limiting; in most cases no specific treatment is required beyond trigger identification and eradication. Symptomatic topical therapy is added only if the eruption is pruritic or cosmetically distressing, and systemic therapy is reserved for the rare refractory case.^[5]

Step 1 — eradicate the trigger (definitive)

Trigger eradication is the only definitive treatment. Without it, the eruption recurs.^[1]

Step 2 — symptomatic topical therapy

If the eruption is pruritic or cosmetically distressing, topical therapy helps. It does not prevent new lesions and does not alter the underlying course.^[5]

• Topical corticosteroids — betamethasone valerate 0.1 per cent or mometasone furoate 0.1 per cent cream or ointment, once or twice daily to active lesions for 1 to 2 weeks. Reduces inflammation and pruritus. Avoid prolonged use on the face and intertriginous areas.^[5]
• Topical calcineurin inhibitors — tacrolimus 0.1 per cent ointment (or pimecrolimus 1 per cent cream) twice daily. A steroid-sparing alternative, particularly on the face, flexures, and for longer courses.^[5]
• Emollients — reduce the prominence of the trailing scale and soothe mild irritation.^[5]

Step 3 — oral antihistamines

Antihistamines are symptomatic cover for pruritus only; they do not change the course of the eruption. For night-time itch, a sedating antihistamine such as hydroxyzine or chlorphenamine helps sleep and settles the itch; these older agents are effective in itchy eruptions but cause marked sedation and anticholinergic effects. For daytime use, second-generation agents such as cetirizine or loratadine cause significantly less sedation. EAC is often only mildly symptomatic, so many patients need none of this.^[5][7][17]

Step 4 — systemic therapy for refractory disease

A minority of cases are chronic, extensive, or refractory to trigger treatment and topical therapy. The evidence base is limited to case reports and small uncontrolled series; there are no randomised trials.^[5][7]

• Short-course oral corticosteroid — for extremely symptomatic disease, a brief systemic course can induce remission; recurrences are common when it is stopped, so reserve this for severe, extensive, or disabling eruptions.^[7]
• Azithromycin 250 mg once daily until clearance — in an open study of 10 patients with idiopathic EAC, 8 cleared with no relapse on follow-up.^[8]
• Erythromycin — in a small series of chronic relapsing EAC, all 8 patients responded within two weeks of starting treatment; three relapsed and responded again on re-treatment.^[9]
• Dapsone — reported to clear EAC in a case report.^[10]
• Topical vitamin D analogues plus narrowband UVB — a calcipotriol-resistant case cleared with topical calcitriol combined with 311 nm narrowband UVB over four weeks, and a separate chronic case cleared with topical calcipotriol alone after three months.^[11][12]
• Metronidazole — reported in a single case report.^[13]
• Ustekinumab — recurrent EAC during ustekinumab treatment for psoriasis has been reported; the drug is not an established therapy and any biologic use belongs under specialist supervision.^[14]

Specific subtypes — the ones that change the plan

Paraneoplastic EAC (PEACE)

PEACE is the rare association of EAC with underlying malignancy, and Chodkiewicz and Cohen consolidated the literature in 2012. The commonest reported malignancies are lymphoma (Hodgkin and non-Hodgkin), leukaemia, mycosis fungoides and Sézary syndrome, and solid tumours (lung, breast, prostate, gastrointestinal, ovarian). EAC may precede the cancer diagnosis by months, making it a genuine cutaneous sentinel. The eruption is often extensive, atypical, and refractory to conventional therapy; it typically resolves with successful treatment of the tumour and recurs with tumour relapse. Any refractory or atypical EAC warrants a malignancy workup (FBC, LDH, lymph node exam, imaging).^[2]

Drug-induced EAC

Drug-induced EAC resolves with withdrawal of the culprit. Case reports implicate finasteride, aceclofenac, cimetidine, chloroquine, hydroxychloroquine, and interferon-alpha, among many others. A careful drug history — including over-the-counter and herbal preparations — is essential. Stop the suspected drug and treat symptomatically while the eruption settles.^[5][17]

Tinea-triggered EAC (the id reaction)

Tinea-triggered EAC is the single most common identifiable cause and the prototypical id reaction. The patient has a focus of dermatophyte infection (tinea pedis, cruris, onychomycosis, or corporis) shedding fungal antigens; these reach the skin and trigger a distant, KOH-negative reaction on the trunk. The distant tinea is KOH-positive; the EAC lesions are KOH-negative. Treatment is antifungal therapy directed at the distant focus; in one paediatric series, five children treated empirically with oral fluconazole all improved and three cleared entirely. The EAC settles as the fungal load falls.^[1][18]

Food-additive and pregnancy-associated EAC

• Food-additive EAC — the classic case is Shelley's patient whose eruption flared with each blue-cheese challenge (a hypersensitivity to blue cheese Penicillium). An elimination diet with rechallenge identifies a food culprit; worth exploring in idiopathic or recurrent disease.^[15]
• Pregnancy-associated EAC — reported in case reports; one patient's eruption remitted during two pregnancies and recurred in between. Distinguish from the specific dermatoses of pregnancy (polymorphic eruption of pregnancy or PUPPP, pemphigoid gestationis, intrahepatic cholestasis of pregnancy) by morphology and bile acid testing. Moderate-potency topical corticosteroids for symptom cover; avoid systemic therapy where possible.^[16][7]

Annually recurring EAC

A distinctive seasonal variant recurs each year at the same time (classically spring or autumn), as Maurelli and colleagues described. It is benign, runs a self-limiting course in each episode, and needs no additional workup once the trigger pattern is recognised. Reassurance is the mainstay.^[4]

Special populations and regional triggers

^{[1] [2]}

The adjustments above all follow one principle: identify and treat the trigger, and lower the threshold for malignancy workup in the immunocompromised and the elderly.^[1][2]

Pitfalls — the RINGS mnemonic

The classic pitfalls in EAC centre on misreading the scale, missing the trigger, and overlooking malignancy:^[2][3]

Three more pitfalls that cost marks:^[2][3]

• Mycosis fungoides masquerading as EAC — any persistent, atypical, or progressive figurate eruption must be biopsied. Cutaneous T-cell lymphoma can mimic EAC for years.^[2]
• Over-treating with prolonged topical corticosteroids — these do not alter the course and risk skin atrophy, telangiectasia, and striae.^[5]
• Missing a drug cause or thyroid disease — take a thorough drug history and check TFTs in idiopathic EAC.^[1]

Prognosis and disposition

The prognosis is benign — self-limiting and non-scarring, though chronic and prone to recurrence. EAC eventually resolves spontaneously, but the course is chronic (weeks to months, occasionally years). Recurrence is common, particularly when the trigger persists or recurs (recurrent tinea pedis, re-exposure to a culprit drug or food, inadequately treated malignancy); recurrence does not imply failure of the original treatment if the trigger was genuinely eradicated. Lesions resolve with post-inflammatory hyperpigmentation that fades, and the skin returns to normal. In PEACE, the prognosis is that of the underlying malignancy — the EAC may resolve with successful cancer treatment and recur with tumour relapse, serving as a tumour marker.^[2][4]

Factors that predict a longer or more refractory course — address them proactively:^[2]

• Persistence or recurrence of the trigger — the dominant determinant of relapse.^[1]
• Failure to identify a trigger (idiopathic EAC) — longer duration, higher chance of chronicity.^[4]
• Underlying malignancy (PEACE) — a refractory course that mirrors tumour activity.^[2]
• Immunocompromise — more extensive, more refractory disease.^[2]

Disposition follows the trigger and the red flags:^[3]

• Primary care — most straightforward cases (tinea-triggered, drug-induced) are managed here with trigger identification and symptomatic topical therapy.^[1]
• Dermatology referral — for refractory, atypical, or extensive disease; when biopsy is needed to exclude mycosis fungoides; when systemic therapy is contemplated; and for phototherapy or biologic considerations.^[2]
• Haematology or oncology referral — when PEACE is suspected (B-symptoms, lymphadenopathy, abnormal FBC or LDH).^[2]

Guidelines, evidence, and regional differences

There is no single international guideline for EAC. Practice rests on narrative reviews, the 2024 systematic review of treatment outcomes, and the principles of figurate erythema diagnosis. Key consensus points: clinical diagnosis with KOH to exclude tinea; treat the underlying trigger; topical corticosteroids for symptomatic relief; biopsy atypical or refractory lesions.^[3][5]

The evidence base is limited and largely observational — case reports, case series, narrative reviews, and one systematic review of treatment outcomes. There are no randomised controlled trials.^[5]

• Geng et al. (2024) — a systematic review of treatment outcomes in EAC, published as a letter with no abstracted outcome data; it anchors the principle that trigger eradication is the cornerstone and systemic agents are reserved for refractory disease.^[5]
• Chodkiewicz and Cohen (2012) — consolidated the PEACE literature; established EAC as a recognised, if rare, cutaneous marker of malignancy, chiefly lymphoma.^[2]
• Boehner et al. (2021) — an update and diagnostic approach to the figurate erythemas; set out a structured diagnostic algorithm that discriminates the differentials by temporal evolution and clinical or histological phenotype.^[3]
• Ilkit et al. (2012) — the definitive review of cutaneous id reactions; established dermatophyte-triggered EAC as the prototypical id reaction.^[1]
• Maurelli et al. (2021) — a new case series of annually recurring EAC, characterising this benign seasonal variant.^[4]

Regional differences

The trigger spectrum and the threshold for malignancy workup vary substantially by region:^[1]

^[1]

Controversies

Several areas remain genuinely contested:^[5]

• Role of systemic therapy — the antibiotic, anti-inflammatory, and biologic options all rest on case reports or small uncontrolled series; none is established as standard.^[5][7]
• Malignancy workup threshold — no consensus on how aggressively to investigate idiopathic EAC for occult malignancy; most reserve imaging for refractory, atypical, or systemically symptomatic disease.^[2]
• Whether idiopathic EAC is truly idiopathic — many cases likely carry an unrecognised trigger (occult tinea, food additive, thyroid disease); a thorough recurrent search often uncovers a cause.^[1]

The mantra, and the high-yield pearls

The mantra: trailing inner scale, negative KOH — treat the trigger, not the ring.^[1][3]

Ward-round test

Stem 1 — the ring that did not respond to clotrimazole (answer)ShowHide

A 42-year-old man has three weeks of expanding rings on the flanks and thighs, partially treated with topical clotrimazole. The rings keep growing. You find toe-web scale; the ring's KOH is negative and the toe-web KOH is positive. What is the diagnosis, and what is the definitive treatment? Model: This is erythema annulare centrifugum as a dermatophyte id reaction — a hypersensitivity reaction to fungal antigens from the distant tinea pedis. The trailing inner scale and the KOH-negative ring with a KOH-positive distant focus make the diagnosis. Definitive treatment is antifungal therapy directed at the distant tinea; in the reported paediatric series, empiric oral fluconazole improved every child treated and cleared three of five. The ring is immunological, so escalating topical antifungals on the ring itself is the wrong move.^[1][18]

Stem 2 — refractory rings with night sweats (answer)ShowHide

A 68-year-old presents with six months of extensive, atypical figurate rings that have not responded to repeated topical corticosteroids. He reports drenching night sweats and has lost weight. What must you do next? Model: This is paraneoplastic EAC (PEACE) until proven otherwise. The refractory course, the atypical morphology, and the B-symptoms (night sweats, weight loss) are red flags for lymphoma. Do a full malignancy workup — FBC with differential, LDH, thorough lymph node exam, chest X-ray, and CT chest, abdomen, and pelvis or PET-CT, with lymph node biopsy if lymphadenopathy is found. Biopsy the skin to exclude mycosis fungoides. Refer urgently to haematology or oncology.^[2]

Stem 3 — the mimic that will not settle (answer)ShowHide

A 55-year-old has figurate erythematous patches on the trunk that have been labelled EAC for two years. They have not resolved with topical corticosteroids or antifungals. What is the classic fellowship trap, and what is the single most important next step? Model: The trap is mycosis fungoides (cutaneous T-cell lymphoma) masquerading as refractory EAC. Early mycosis fungoides presents as persistent annular or figurate patches that resist topical therapy. The single most important next step is skin biopsy for histology with assessment for atypical lymphocytes and epidermotropism. Any EAC that persists, progresses, or behaves atypically must be biopsied — cutaneous T-cell lymphoma can mimic EAC for years before diagnosis.^[2]

Stem 4 — the rapidly migrating wood-grain eruption (answer)ShowHide

A 60-year-old smoker develops concentric, wood-grain rings with leading scale that migrate daily across the trunk. What is the diagnosis, and what does it demand? Model: This is erythema gyratum repens, not EAC — the concentric wood-grain scaling, the leading (not trailing) scale, and the rapid daily migration distinguish it. It is strongly paraneoplastic (around 80 per cent have an underlying cancer, classically lung, breast, or gastrointestinal). It demands an urgent malignancy search — imaging and targeted workup — rather than antifungals or topical steroids.^[3]

References19ShowHide

1. [1]Ilkit M, Durdu M, Karakaş M Cutaneous id reactions: a comprehensive review of clinical manifestations, epidemiology, etiology, and management Crit Rev Microbiol, 2012.PMID 22300403
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