Eosinophilic folliculitis

Meet the patient

A 34-year-old man who has not seen a doctor in years arrives scratching. For six weeks he has had small, intensely itchy, red bumps over his cheeks, forehead and upper chest that wake him at night; antihistamines and two courses of flucloxacillin have done nothing. On the back of his tongue is oral thrush, and his CD4, drawn the day you see him, is 80.[4]

The single question this patient is really asking is the question every EF stem turns on: is this a skin problem, or a sentinel of the immune system collapsing beneath it? Hold that question, and every variant, every biopsy and every step of the ladder slots into place.[1]

The itch that wakes the patient — what EF actually is

EF is not an infection — it is an eosinophil-driven, immune-mediated folliculitis where the itch dwarfs the rash. Eosinophils accumulate within and around the hair follicle, producing follicular spongiosis and follicular damage, with a matching peripheral blood and tissue eosinophilia.[3] It sits within the wider family of eosinophilic dermatoses — Wells syndrome, eosinophilic cellulitis, and the eosinophilic eruptions of HIV — all sharing the same Th2-eosinophil engine.[2]

The clinical problem is symptomatic, not cosmetic. The pruritus is characteristically exquisite and disproportionate to the visible lesion burden, and it drives the itch-scratch cycle: excoriation, crusting, secondary infection, and disfiguring post-inflammatory hyperpigmentation that is particularly marked in skin of colour.[4]

Etymology for viva gold: eosinophil, from the Greek eos ("dawn") and philien ("to love") — the leukocyte that stains dawn-pink with eosin dye. The eosin-lover turns out to be the itch-maker.[3]

A short history anchors the variants. Iwao Ofuji described the disease in 1970 as a chronic, annular, eosinophilic folliculitis of otherwise-healthy Japanese adults — the form that still carries his name.[5] In the 1980s and early 1990s an intensely pruritic, urticarial follicular variant emerged in patients with advanced AIDS and a CD4 under 200 to 300, and this HIV-associated form came to dominate Western practice.[4] The introduction of combination antiretroviral therapy (HAART) in the mid-1990s transformed the prognosis — immune reconstitution resolved the eruption in most patients, and population incidence fell sharply.[1]

Four variants, one histology — the classification that earns marks

One histological signature, four host contexts — and the host context decides the prognosis and the treatment. The classification below is the one the major reviews use and the distinction examiners test.[2]

[2]

The one-line discriminator: palms or soles involved, or annular polycyclic plaques with peripheral spread in a non-HIV adult, points to Ofuji; disabling itch with few lesions confined to the face and upper trunk of an immunosuppressed patient points to the HIV variant. The histology is the same — it is the host that splits them.[5]

Who gets EF, and why HIV owns the story

EF is uncommon, the epidemiology is case-series grade, and the single fact an examiner rewards is the association with advanced HIV.[1]

[1]

The dominant risk factor for the HIV variant is advanced, untreated or poorly controlled HIV, typically with a CD4 under 200 to 300; the eruption often appears at the point of profound immunodeficiency and may be the first clue to HIV in an undiagnosed patient.[4] In the pre-HAART era EF was one of the most distressing cutaneous manifestations of AIDS. Its incidence fell sharply once combination antiretroviral therapy became routine, so a new presentation now demands a careful look at ART adherence, virological failure, or a new HIV diagnosis.[4]

Beyond HIV, EF is described with haematological malignancy (CLL, non-Hodgkin lymphoma, myelodysplasia), solid-organ and stem-cell transplantation, autoimmune connective-tissue disease, and a range of drug triggers — allopurinol, carbamazepine, minocycline, leukotriene-receptor antagonists and some monoclonal antibodies.[2] Classic Ofuji has a striking over-representation in Japanese adults, a minority of cases are familial, and the pregnancy variant affects women in the third trimester and recurs.[5]

Why eosinophils attack the follicle — the Th2 story

The engine of EF is a skewed Th2 response that recruits eosinophils against the follicular unit — and every effective treatment interrupts one limb of that engine. Interleukin-4, interleukin-5, interleukin-13 and the eosinophil chemoattractant eotaxin drive the recruitment, activation and survival of eosinophils in and around the follicle.[3]

In the HIV-associated variant, progressive immunodeficiency creates a paradoxically dysregulated Th2 environment — as the CD4 count falls, the immune system loses balanced Th1/Th2 control and tips toward an IgE-rich, eosinophil-promoting cytokine milieu. Two co-factors amplify it: altered sebum lipid composition with sebaceous atrophy in advanced HIV changes what the immune system sees at the follicle, and follicular organisms (Demodex, Malassezia, skin bacteria) act as antigenic triggers in a now-hypersensitive host.[2]

The mantra: intensely itchy follicular papules — reach for the HIV test before the antihistamine.[4]

The histological cascade mirrors the cytokine story. Eosinophils first cluster in the perifollicular dermis, then invade the follicular epithelium producing eosinophilic spongiosis; degranulation generates flame figures and breaches the follicular wall. The intense pruritus — disproportionate to the visible lesion — reflects the heavy eosinophil-derived pruritogens (major basic protein, eosinophil-derived neurotoxin) dumped into the dermis.[3]

The mediators earn naming because they explain the treatment. Interleukin-5 is the dominant eosinophilopoietin — blocking it (mepolizumab-style biologics) depletes tissue eosinophils. Eotaxin (CCL11) draws primed eosinophils into the dermis; IL-4 and IL-13 skew the response to Th2 and drive IgE class-switching, which is why serum IgE is so often raised. This is the rationale for considering anti-IL-5 and anti-IL-4-receptor-alpha (dupilumab) strategies in severe, refractory disease.[3]

Why HIV-associated EF resolves with effective ART now reads as mechanism: restoring the CD4 count rebalances the Th1/Th2 axis, removes the dysregulated eosinophil-promoting milieu, and re-establishes tolerance to follicular antigens.[4]

A second strand of the pathogenesis deserves emphasis because it explains two empirical drugs. The follicle in advanced HIV is antigenically altered — sebaceous atrophy and shifted sebum lipid ratios change what the immune system sees, and Demodex and Malassezia antigens land in a hypersensitive Th2 host. An autoreactive component is suspected in classic Ofuji (circulating autoantibodies, atopic background), which is why immunomodulators — indomethacin, dapsone, cyclosporin — rather than antimicrobials own the Ofuji ladder. The leukotriene pathway is implicated too, which is why the 5-lipoxygenase-inhibiting action of itraconazole helps out of proportion to its antifungal effect.[2]

What you see at the bedside

One symptom dominates and does almost all the diagnostic work — pruritus that is severe, persistent, and disproportionate to the number of visible lesions — set over follicular papules on the seborrhoeic areas.[1]

The HIV-associated variant — the one you will meet

This is the variant most likely to be examined and the one most often seen in practice.[1]

• Distribution. The face (cheeks, forehead), upper chest, shoulders and upper back bear the brunt; the extensor arms are frequently involved, and disease can extend more widely as immunodeficiency deepens.[4]
• Morphology. Lesions begin as small (2 to 5 mm), erythematous, urticarial, follicular papules that evolve into papulopustules and may coalesce into plaques. The follicular origin is the key discriminator from acne and from non-follicular drug eruptions.
• Symptom. The pruritus is characteristically exquisite, often described as burning or stinging as well as itching, and severe enough to disrupt sleep. Excoriation is the rule; crusts, erosions and punctate scars follow.
• Secondary change. In skin of colour, the cycle of inflammation and excoriation produces striking post-inflammatory hyperpigmentation that can distress the patient long after the active papules have settled.[4]
• Temporal pattern. The course is chronic and relapsing without treatment; in advanced HIV the lesions persist until immune reconstitution is achieved.

A handful of nuances sharpen the pattern and earn marks. The papules are follicular and urticarial, so they can be transient and evanescent early on — which is why patients are sometimes dismissed as having "no rash" until you look in good tangential light. Dermoscopy is non-specific but shows follicular plugging, perifollicular erythema and a uniform peri-follicular vessel network. The distribution is strikingly symmetrical and confined to seborrhoeic, photo-exposed areas, separating EF from a drug eruption (generalised, acral) and from scabies (interdigital, flexural, genital).[1]

Classic Ofuji disease — the morphology is the discriminator

The high-yield discriminator here is annular configuration with peripheral spread in a non-HIV adult.[1]

• Annular, polycyclic or serpiginous plaques with peripheral extension: fresh papulopustules appear at the advancing edge while the centre clears, leaving hyperpigmentation.[5]
• Distribution favours the seborrhoeic areas — face, trunk and extensor surfaces; uniquely, the palms and soles may be involved in Ofuji, a feature not seen in the HIV variant.
• The typical patient is an adult without HIV, over-represented in Japanese subjects; a minority of cases are familial.
• Pruritus is variable and may be mild — a stark contrast to the HIV form.

Infantile and pregnancy-associated variants

The infantile variant presents as clusters of pruritic papulopustules on the scalp of neonates and infants, runs a self-limiting course over weeks to months, and must be separated from neonatal acne, scabies and bacterial folliculitis. The pregnancy-associated variant erupts as pruritic follicular papules in the third trimester, resolves post-partum, may recur, and is clinically and histologically distinct from polymorphic eruption of pregnancy (PUPPP).[3]

Atypical presentations — the corners examiners test

EF is on the list whenever an immunocompromised host develops new itchy follicular papules. Think of it in a transplant recipient, in newly diagnosed haematological malignancy, in an infant with scalp papulopustules refractory to antiseptics, and in a pregnant woman in the third trimester with intensely pruritic follicular lesions.[2]

The mimics that fool everyone

Pruritic follicular papules are common, several mimics overlap EF in distribution, and the discriminator for each is what gets the marks.[2]

[2]

The classic trap: the two most common errors are labelling HIV-associated EF as ordinary bacterial folliculitis (and burning through courses of antibiotics that never touch an eosinophilic disease) and missing the underlying HIV by not testing. A skin biopsy and an HIV test resolve both.[4]

A three-question structure on the itchy follicular papule in an immunocompromised host prevents error. First, are the lesions truly follicular (centred on a hair)? That narrows the list to the folliculitides and away from eczema, drug eruption and dermatitis herpetiformis. Second, is the pruritus disproportionate to the lesion count? Intense itch with few lesions favours EF, scabies or dermatitis herpetiformis over bacterial folliculitis or acne. Third, the tempo and distribution: a sudden crop of monomorphic papulopustules on the upper trunk in a hot, sweaty young adult points to Malassezia; chronic, relapsing, intensely pruritic follicular papules on the face and upper trunk in a patient with night sweats and weight loss points to EF and mandates an HIV test.[1]

The focused assessment — three objectives

A focused assessment in suspected EF has three jobs: confirm the clinical pattern, identify the host context, and screen for the mimics and the systemic triggers.[1]

History. Map the onset, distribution and tempo; characterise the pruritus (severity, diurnal pattern, sleep impact on a visual analogue scale); ask explicitly about HIV risk factors (unprotected sex, men who have sex with men, injecting drug use, prior STIs, partner risk), known HIV and current ART, pregnancy, atopy, recent new drugs, and symptoms of lymphoproliferative disease (fever, night sweats, weight loss, lymphadenopathy). A family history is relevant for Ofuji disease.[2]

Examination. Examine the seborrhoeic areas in good light — face, upper chest, shoulders, upper back and extensor arms. Confirm the follicular origin of the papules, look for the annular configuration of Ofuji, and record the secondary changes: excoriation, crusting, erosions, prurigo nodularis, lichen simplex chronicus and post-inflammatory hyperpigmentation. Dermoscopy may show follicular plugging and perifollicular erythema but is non-specific. Then a general examination — palpate for lymphadenopathy and hepatosplenomegaly (lymphoproliferative disease), and look for stigmata of HIV such as oral candidiasis, oral hairy leucoplakia and seborrhoeic dermatitis.[4]

The single most important bedside decision is whether to offer an HIV test. EF is an indication for HIV testing in any adult with new-onset, intensely pruritic, follicular papules on the face and upper trunk.[4]

Quantify the itch, because it is the main treatment target. Record severity with a 0 to 10 numerical rating scale at baseline and each visit, ask specifically about sleep (time to onset, awakenings, daytime somnolence) and about impact on daily life with the Dermatology Life Quality Index (DLQI). A baseline DLQI gives an objective endpoint against which ART, phototherapy or systemic therapy can be judged, and it documents the burden that justifies escalation. The itch of EF is characteristically worse at night and with heat, and patients often describe a burning or stinging quality distinct from ordinary itch.[1]

Investigations — biopsy, bloods, and the HIV test

EF is a clinicopathological diagnosis — the clinical pattern plus the histological signature, set in the right host context — and there is no single pathognomonic blood test.[3]

[1]

Skin biopsy is the diagnostic investigation. Histology shows eosinophilic spongiosis (eosinophils within the follicular epithelium), a perifollicular and intrafollicular eosinophilic infiltrate, occasional flame figures, and follicular damage; a neutrophilic component suggests superimposed bacterial infection.[3]

Biopsy a fresh, non-excoriated papule or papulopustule — chronic excoriated lesions show only non-specific inflammation and the diagnostic perifollicular eosinophils may be obscured. Read the histology asking "where are the eosinophils?": early disease clusters them in the perifollicular dermis and sebaceous gland, established disease invades the follicular epithelium (eosinophilic spongiosis), and late disease shows flame figures and follicular rupture. A neutrophilic infiltrate redirects the diagnosis to bacterial folliculitis; yeast within the follicle points to Malassezia; Demodex mites point to demodicidosis; subepidermal blistering with neutrophils and granular IgA points to dermatitis herpetiformis.[3]

Bloods. A full blood count demonstrates peripheral eosinophilia in roughly half and may show anaemia or lymphopenia pointing to HIV; serum IgE is frequently elevated; ESR/CRP may be mildly raised. HIV serology and a CD4 count are mandatory whenever the HIV variant is suspected — EF may be the presenting feature of HIV.[4]

Microbiology to exclude mimics. Bacterial culture of a pustule excludes staphylococcal folliculitis; KOH examination and fungal culture exclude Malassezia folliculitis (budding yeast) and dermatophyte infection; a skin scraping excludes Demodex overgrowth and scabies (mite, eggs, faeces). Direct immunofluorescence of perilesional skin excludes dermatitis herpetiformis (granular IgA at the dermal papillae).[2]

Workup for an underlying systemic trigger. When EF appears in a non-HIV, non-pregnant adult without a drug trigger, screen for lymphoproliferative disease: a peripheral blood smear, lactate dehydrogenase, serum electrophoresis, and lymph-node biopsy or imaging if there is lymphadenopathy or hepatosplenomegaly.[2]

The urgent few — when EF cannot wait

EF is rarely a dermatological emergency — but three situations demand prompt action, and the first is the one most often missed.[1]

The most important urgent action is recognising EF as the possible presenting feature of HIV. A new diagnosis of HIV must trigger immediate linkage to HIV services for confirmation, baseline CD4 and viral load, and initiation of combination antiretroviral therapy — the single most effective disease-modifying treatment for the HIV variant.[4]

The second urgent scenario is disabling, treatment-refractory pruritus with sleep deprivation. Symptom control is humanitarian as much as medical: a sedating antihistamine at night (hydroxyzine 25 mg or promethazine) buys sleep while definitive therapy is arranged, and a short course of a potent topical corticosteroid (clobetasol 0.05% or betamethasone valerate 0.1%) dampens the inflammation.[1]

The third is secondary bacterial infection of excoriated lesions — treat with a topical or oral antistaphylococcal agent (flucloxacillin 500 mg four times daily orally for 7 days, or cephalexin in penicillin-allergic patients without anaphylaxis). Severe, widespread disease or suspected erythroderma warrants same-day dermatology referral.[2]

The ladder — definitive treatment by variant

Definitive treatment is stratified by variant, and in the HIV variant the principle is fixed: optimise antiretroviral therapy, because everything else is symptomatic or adjunctive.[4]

HIV-associated eosinophilic folliculitis

[1]

The systemic agents in step 5 carry monitoring an examiner will probe. Dapsone (50 to 150 mg daily) needs G6PD screening before the first dose, a baseline full blood count, then weekly full blood counts for the first month and monthly thereafter, watching for haemolytic anaemia and methaemoglobinaemia; warn the patient about blue-grey discolouration and sulpha-drug cross-reactivity. Isotretinoin (0.5 to 1 mg/kg/day) is teratogenic and needs a pregnancy-prevention programme — reliable contraception, a negative pregnancy test before and during therapy, and avoidance of pregnancy for at least one month after stopping — with baseline and serial lipids and liver enzymes, plus mucocutaneous dryness counselling.[1]

Classic Ofuji disease

Ofuji does not respond to ART — its ladder is built on systemic anti-inflammatory and immunomodulatory agents. Oral indomethacin 25 to 75 mg daily is effective in a subset (implicating the prostaglandin pathway) and is a reasonable first choice. Dapsone 50 to 100 mg daily (after G6PD screening) and NB-UVB phototherapy are useful alternatives. Cyclosporin, colchicine and minocycline are described for refractory disease, and a short course of oral corticosteroid (prednisolone 0.5 mg/kg/day tapered over 2 to 3 weeks) can settle a severe flare.[1][5]

Pregnancy-associated and infantile variants

In pregnancy, manage with a pregnancy-safe topical corticosteroid (moderate potency, avoiding excessive potent agents) and NB-UVB, which is regarded as safe in pregnancy; avoid systemic retinoids (teratogenic) and weigh the risk-benefit of dapsone, which crosses the placenta. The condition resolves post-partum.[3]

In infants the disease is usually self-limiting: a mild topical corticosteroid (hydrocortisone 1%) and an antiseptic wash (chlorhexidine or dilute potassium permanganate) suffice; avoid systemic agents and reserve them for the rare, severe, refractory case under specialist supervision. Exclude scabies (treat the whole household with permethrin 5% if confirmed) and neonatal acne (comedones, no itch), the two principal differentials in this age group, and reassure the parents.[3]

The scenarios that bite

EF and immune reconstitution inflammatory syndrome (IRIS). When ART starts in a patient with subclinical or suppressed EF, the recovering immune system can transiently amplify the eosinophilic response, producing a flare in the first weeks of therapy. This is IRIS, not treatment failure or drug allergy — manage with topical corticosteroids and antihistamines while continuing ART; the flare settles as immune reconstitution completes.[4]

EF in haematological malignancy and post-transplant. The principle is to treat the underlying disease (the lymphoma, the transplant immunosuppression) while providing topical corticosteroids and phototherapy for symptom control. Coordinate with haematology and transplant teams — systemic agents may interact with chemotherapy or immunosuppressants.[2]

Drug-induced EF. Withdraw the suspect agent — commonly allopurinol, carbamazepine, minocycline or a leukotriene-receptor antagonist — combined with topical corticosteroids; the eruption usually resolves, and rechallenge should be avoided.[2]

EF in skin of colour. The dominant problem is post-inflammatory hyperpigmentation, which persists long after the active papules resolve and is itself a source of distress. Early, aggressive control of inflammation (phototherapy over prolonged potent topical steroids), sun protection, and reassurance about the slow resolution of pigmentation are central.[4]

When EF is missed or mistreated

The complications of untreated EF arise from the itch-scratch cycle and from the immunodeficiency beneath it — and both are under-recognised.[4]

Excoriation, crusting and erosion are followed by scarring, prurigo nodularis, lichen simplex chronicus and disfiguring post-inflammatory hyperpigmentation, particularly in skin of colour. Secondary staphylococcal infection is common and may progress to cellulitis. The sleep deprivation, anxiety and depression driven by chronic severe pruritus are under-asked — ask about them directly.[4]

The classic trap — four diagnostic pitfalls. First, missing the underlying HIV by treating EF as ordinary folliculitis without offering an HIV test. Second, misdiagnosing EF as scabies or acne and treating empirically for months without a biopsy. Third, overlooking a coexisting Malassezia or Demodex component that needs additional targeted therapy. Fourth, confusing an IRIS flare with ART failure or drug allergy and inappropriately stopping effective antiretroviral therapy.[4]

The treatment pitfalls are equally punishing. Prolonged potent topical corticosteroids on the face cause atrophy, telangiectasia and steroid rosacea. Dapsone without G6PD screening precipitates haemolytic anaemia and methaemoglobinaemia, particularly in patients of African, Mediterranean or South-East Asian descent. Isotretinoin in a woman of childbearing potential without contraception and pregnancy testing is teratogenic. Chronic phototherapy carries a cumulative skin-cancer and photoaging risk that must be weighed against the benefit, especially in immunosuppressed patients who already carry a raised skin-cancer background risk.[1]

The itch-scratch cycle deserves separate emphasis because it converts a symptomatic skin disease into a chronic, self-perpetuating one. Repeated scratching drives lichen simplex chronicus and prurigo nodularis, which themselves become intensely pruritic and lock the patient into scratching even once the EF is settling; the result is indelible post-inflammatory hyperpigmentation that can persist a year or more after disease control. The psychological burden is real — chronic, sleep-disrupting pruritus breeds anxiety, low mood and social withdrawal, which in turn lower the itch threshold and worsen the disease.[4]

Prognosis and who goes home

The prognosis is decided by the variant and, in the HIV form, by the response to ART — name the driver and you have shown understanding rather than rote recall.[1]

HIV-associated EF improves and usually resolves as the CD4 recovers above 200 to 300 cells per microlitre on effective ART; a transient IRIS flare may occur in the first weeks. Without immune reconstitution the course is chronic and relapsing, and the pruritus is debilitating.[4]

Classic Ofuji disease runs a chronic, relapsing course over years, responding variably to indomethacin, dapsone and phototherapy; sustained remission is achievable but relapse is common.[5]

Pregnancy-associated EF resolves post-partum and may recur in subsequent pregnancies; the infant is not affected. The infantile variant is self-limiting over weeks to months.[3]

Three factors drive the outcome, and naming them earns marks. First, immune reconstitution — recovery of the CD4 above 200 to 300 on effective ART is the single strongest predictor of resolution; EF that persists despite a good CD4 response should send you hunting for an additional trigger (Malassezia, Demodex, a new drug, an alternative diagnosis). Second, control of any underlying systemic disease — in EF with lymphoproliferative disease or transplant, the skin mirrors the systemic process. Third, interrupting the itch-scratch cycle early before lichenification and pigmentation become permanent.[4]

Disposition. Most patients are managed jointly by dermatology and, where relevant, the HIV, haematology or obstetric team. The safety-net is clear: return if the pruritus is uncontrolled despite first-line measures, if new lesions appear, if there are signs of secondary infection, or if ART side-effects develop. Routine follow-up is at 4 to 8 weeks to assess response, then at intervals until controlled.[2]

Special populations and regional differences

[1]

The evidence base — five sources, all case series

The evidence for EF is largely case series, case reports and expert review rather than randomised trials — a recognised limitation worth naming to an examiner.[1]

Ellis and Scheinfeld (2004, PMID 15186198) is the comprehensive treatment-options review that established the modern therapeutic ladder — topical corticosteroids, antihistamines, NB-UVB, itraconazole, indomethacin, dapsone, cyclosporin, isotretinoin.[1] Marzano and colleagues (2020, PMID 32394361) reframes EF within the wider family of eosinophilic dermatoses and updates recognition and management.[2] Long and colleagues (2016, PMID 25876839) maps the spectrum of eosinophilic skin diseases and the shared Th2 pathogenesis.[3] Parker and colleagues (2006, PMID 16734507) adds the case series of EF in HIV-infected women and reinforces that EF may be the presenting feature of HIV.[4] Katoh and colleagues (2013, PMID 23083212) synthesises the Japanese literature on Ofuji disease, including palmoplantar involvement and the immunomodulatory ladder.[5]

Regional differences are modest but real. The CD4 threshold for starting ART has fallen over time: current US (DHHS) and WHO guidance is to start ART in all patients with HIV regardless of CD4 count, which has reduced the population incidence of EF; India (NACO) has moved to the same treat-all policy.[4] The NB-UVB regimen (3 times weekly, 15 to 30 treatments) is consistent across the British Association of Dermatologists, the European Academy of Dermatology and Venereology, and the American Academy of Dermatology; what differs regionally is phototherapy access and the formality of isotretinoin pregnancy-prevention programmes (iPLEDGE in the US, the PPP in the UK, more informal counselling in India).[1]

The principal controversy is the relative place of itraconazole and indomethacin in the ladder: both have enthusiastic proponents and limited head-to-head evidence, and the choice is pragmatic — itraconazole when Malassezia is suspected, indomethacin for classic Ofuji. Where the evidence is weakest is the long-term safety of repeated phototherapy in immunosuppressed patients, in whom background skin-cancer risk is already raised.[1]

The biologics frontier is the most active area of new evidence. Because EF rides the Th2-eosinophil axis, anti-IL-5 (mepolizumab, benralizumab) and anti-IL-4-receptor-alpha (dupilumab) strategies have a sound mechanistic rationale and appear in case reports and small series for refractory EF. They remain off-label and evidence-poor, but a candidate who names the cytokine target demonstrates pathogenesis rather than recall.[3]

Exam pearls

[1] [1]

Ward-round test

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

A 34-year-old with six weeks of excruciatingly itchy follicular papules on the cheeks, forehead and upper chest, oral thrush, sleep deprivation, and no response to two courses of flucloxacillin. What are the three investigations that decide his next hour, and what is the disease-modifying step? Model: This is the HIV-associated variant of EF until proven otherwise — the itch is disproportionate, the lesions are follicular and seborrhoeic, and oral thrush in a flucloxacillin-resistant eruption is the bedside clue. The three investigations are skin biopsy of a fresh papule (eosinophilic spongiosis with perifollicular eosinophils), HIV serology, and a CD4 count (plus FBC for eosinophilia and serum IgE). The disease-modifying step is start combination ART with the HIV physician; everything else — potent topical corticosteroid, sedating antihistamine, then NB-UVB — is symptomatic or adjunctive. Do not reach for another antibiotic; you are treating an eosinophilic disease, not a staphylococcal one.[4][1]

Stem 2 — the flare two weeks into ART (answer)

A patient with HIV-associated EF starts combination ART and returns two weeks later with a worse, intensely pruritic crop of follicular papules. The registrar wants to stop the ART, suspecting a drug reaction. What has happened, and what do you do? Model: This is immune reconstitution inflammatory syndrome (IRIS), not ART failure and not drug allergy. As the CD4 recovers, the rebounding immune system transiently amplifies the eosinophilic response against follicular antigens. Continue the ART — do not stop it — and dampen the flare with a potent topical corticosteroid and a sedating antihistamine; arrange NB-UVB if severe. The eruption settles as immune reconstitution completes. Stopping effective ART here is the classic, damaging trainee error.[4]

Stem 3 — Ofuji or HIV variant? (answer)

A 40-year-old otherwise-healthy Japanese man has chronic, mildly itchy, annular polycyclic plaques on the face and trunk with peripheral extension and central hyperpigmentation; there are a few papules on the palms. HIV serology is negative. Which variant is this, and what is the first-line systemic drug? Model: This is classic Ofuji disease — the discriminator is the annular, serpiginous configuration with peripheral spread in a non-HIV adult, the Japanese background, and the palmoplantar involvement (unique to Ofuji and not seen in the HIV variant). First-line systemic therapy is oral indomethacin 25 to 75 mg daily (implicating the prostaglandin pathway); dapsone 50 to 100 mg daily (after G6PD screening) and NB-UVB phototherapy are alternatives for non-response. ART has no role here.[5][1]

Stem 4 — the woman who needs dapsone and isotretinoin (answer)

A 29-year-old woman with refractory HIV-associated EF, on effective ART, is being considered for second-line systemic therapy. What two screening steps are non-negotiable before dapsone, and what programme is mandatory before isotretinoin? Model: Before dapsone, screen for G6PD deficiency — haemolysis and methaemoglobinaemia are the preventable harms, especially in patients of African, Mediterranean or South-East Asian descent — and monitor the full blood count weekly for the first month then monthly. Before isotretinoin in any woman of childbearing potential, a pregnancy-prevention programme is mandatory: reliable contraception, a negative pregnancy test before and during therapy, and avoidance of pregnancy for at least one month after stopping. iPLEDGE in the US, the PPP in the UK, structured local counselling elsewhere. These two screens are the dose-safety pair most likely to be examined.[1]

References

1. [1]Ellis E, Scheinfeld N Eosinophilic pustular folliculitis: a comprehensive review of treatment options Am J Clin Dermatol, 2004.PMID 15186198
2. [2]Marzano AV, Genovese G, et al. Eosinophilic Dermatoses: Recognition and Management Am J Clin Dermatol, 2020.PMID 32394361
3. [3]Long H, Zhang G, Wang L, Lu Q Eosinophilic Skin Diseases: A Comprehensive Review Clin Rev Allergy Immunol, 2016.PMID 25876839
4. [4]Parker SR, Parker DC, McCall CO Eosinophilic folliculitis in HIV-infected women: case series and review Am J Clin Dermatol, 2006.PMID 16734507
5. [5]Katoh M, Nomura T, Miyachi Y, Kabashima K Eosinophilic pustular folliculitis: a review of the Japanese published works J Dermatol, 2013.PMID 23083212