Seborrhoeic Dermatitis

Meet the patient

A 34-year-old man returns to clinic with six months of intermittent scalp flaking and a salmon-pink, mildly itchy rash in his eyebrows, the creases beside his nose and behind his ears. An over-the-counter dandruff shampoo settles it for a week, then it drifts straight back.[1][2]

Two exam questions are now live and you must hold both at once. Is this seborrhoeic dermatitis or one of its mimics — scalp psoriasis, tinea capitis, atopic dermatitis? And is something driving it that changes the workup — HIV, Parkinson disease, an immunodeficient infant? Everything below exists to answer those two questions at consultant depth.[1][2]

What it is — and the three things it is not

It is a chronic, relapsing inflammatory dermatosis of skin rich in sebaceous glands. The defining morphology is erythema with greasy, yellowish scale, and it sits on one clinical spectrum: pityriasis capitis (dandruff) at the mild end, classic adult disease in the middle, and erythroderma at the severe end, with infantile cradle cap as a distinct early-life phenotype.[1][2][9]

[1] [2] [20] [21]

It is not a yeast infection. Every adult skin carries Malassezia as a commensal; disease reflects a dysregulated host response, not simple overgrowth. That single fact explains why antifungals help but never cure, and why steroids and calcineurin inhibitors work at all.[4][5][6]

It is not psoriasis, though they overlap. Where greasy yellow scale meets thick silvery plaque the examiners coin "sebopsoriasis" — overlap skin you treat as seborrhoeic dermatitis but watch for psoriatic conversion. Nail pitting and extension beyond the hairline push you toward psoriasis.[1]

It is not curable. Set that expectation on the first visit. The goals are symptom control, clearance of scale and erythema, and prevention of relapse through maintenance — not a one-off cure.[1][2]

Etymology for viva gold: seborrhoea stitches together the Greek sebos, "tallow" or "fat", and rhoia, "a flow" — literally, a flowing of grease. The word outlived its humoural origins because the greasy morphology it names is unchanged, and it still pins the disease to its sebaceous territory.[1]

The bimodal age fork — cradle cap at 3 months, adult face at 30

Two age peaks, two different patients, and a trap if you blur them. The disease is bimodal: an infantile peak in the first three months and an adult peak from puberty into the fourth decade, with a smaller second rise in the sixties.[2][20][21]

Infantile disease is the cradle cap of the first three months — thick, yellow, greasy, adherent scale on the vertex and anterior scalp, often with facial and flexural involvement, and almost always non-itchy with a comfortable, thriving baby. Most resolves spontaneously by 6 to 12 months.[20][21]

Adult disease is the chronic relapsing form you will see in clinic — scalp, face, retro-auricular skin, presternal chest and flexures, fluctuating with stress, season and comorbidity, and roughly twice as common in men because androgen-driven sebum fuels it.[1][2]

[2] [3] [8] [21]

The classic trap: cradle cap is harmless, but the infant who is failing to thrive, with diarrhoea or recurrent infection is not "just cradle cap" — that is the red flag for immunodeficiency (LAD type 1, Netherton syndrome, severe combined immunodeficiency, Omenn syndrome, hyper-IgE syndrome, Leiner disease). The comfortable, thriving baby reassures; the unwell infant escalates.[20][21]

How common, and who else gets it

A 2024 systematic review and meta-analysis pooled the global prevalence at 4.38 percent (95 percent confidence interval 3.58 to 5.17), higher in adults at 5.64 percent than children at 3.70 percent, and vanishingly rare in neonates at 0.23 percent. Most clinical series quote an adult prevalence around 1 to 3 percent, while dandruff — the mild end of the same spectrum — touches up to half of all adults at some point.[3]

The associations worth reciting on a ward round, because each one rewrites the workup:[1]

• HIV/AIDS — the headline association; disease may be severe, widespread and refractory, and can be the presenting feature of undiagnosed HIV, with prevalence rising to 30 to 40 percent in advanced immunosuppression.[8]
• Parkinson disease — prevalence 19 to 60 percent, facial-predominant, and severity may track motor decline through a substance-P and autonomic pathway.[7]
• Iatrogenic immunosuppression — transplant recipients, long-term systemic steroids, biologics, chemotherapy; often under-recognised.[1]
• Stress, fatigue and sleep loss — common flare triggers patients will name themselves.[1]
• Season — worse in winter and low humidity, better in summer with ultraviolet exposure.[1]
• Genetic susceptibility — familial clustering; lipid-metabolism and innate-immunity polymorphisms explain why carriers vary.[4]

Malassezia is necessary but not sufficient — the host-microbe axis

Stop teaching "yeast overgrowth". The modern model is a dysregulated host-microbe interaction. Most adults carry Malassezia as a commensal from infancy onward, yet only a minority develop disease — which is the whole point of the examiner's favourite line: Malassezia is necessary but not sufficient.[4][5][6]

The three species that matter are M. restricta, M. globosa and M. furfur — lipophilic, dimorphic yeasts that colonise sebaceous skin, densest where sebum is richest. They do four things that light up susceptible skin:[4][5]

• Lipases hydrolyse sebum triglycerides into free fatty acids, especially oleic acid, which penetrates the stratum corneum, disrupts barrier lipids and acts as a danger signal.
• Hyphal transformation tracks with inflammatory activity and cytokine release.
• Pigments — pityriacitrin and indoles — explain the dyspigmentation of pityriasis versicolor.
• Cell-wall beta-glucans and lipoproteins fire keratinocyte TLR2/TLR4 and downstream NF-kB signalling.[1][4]

Lesional skin then shows TLR2/TLR4 to NF-kB upregulation, NLRP3 inflammasome activation, and release of IL-1 beta, IL-6, IL-8, IL-17, IL-23, TNF-alpha and IFN-gamma — a mixed Th1/Th17 response. Healthy carriers mount tolerance; patients mount an aberrant Th1/Th17-skewed reaction with reduced Treg function. That skewed cytokine profile is exactly why PDE4 inhibition works.[4][5]

[4]

Sebaceous glands supply the triglyceride substrate, and androgen-driven sebum peaks in infancy (maternal androgens), post-puberty and again in the sixth decade — mirroring the bimodal epidemiology. Patients also show altered sebum composition (more free fatty acids, squalene and cholesterol; fewer ceramides) and barrier dysfunction with raised transepidermal water loss, which lets yeast products penetrate and sustain inflammation. Lipid and innate-immunity genes such as CARD14, IL-36RN and DEFB1 explain inter-individual variation.[4]

Neurogenic inflammation is the missing link to Parkinson disease. Substance P, a tachykinin from unmyelinated C-fibres, is upregulated in lesional skin and drives mast-cell degranulation, vasodilation, pruritus and sebaceous secretion. In Parkinson disease, dopaminergic loss disinhibits substance P release, autonomic function falls and sebum composition shifts — a triple hit that explains both the high prevalence and the tracking with motor severity.[7]

Everyone forgets: the pathway is named with Greek letters in the literature — keep NF-kB, NLRP3 and IL-17/IL-23 on your tongue in the viva, because the panel is listening for the cytokine axis, not the symbol.[4]

Where it lives — the sebaceous map

Map the distribution before you name the diagnosis. Adult disease follows the sebaceous glands onto the scalp and face, then drops onto the central chest and into the flexures:[1][2]

• Scalp — diffuse or patchy dandruff with fine greasy scale; erythema may cross the hairline onto the forehead and post-auricular skin. Pityriasis sicca is the dry, scaly, non-erythematous variant.
• Face — salmon-pink erythema with yellowish scale in the eyebrows, glabella and nasolabial folds; blepharitis with lid-margin scaling and madarosis; retro-auricular fissuring and external auditory canal involvement masquerading as otitis externa.
• Trunk — well-demarcated patches with greasy scale over the presternal area and upper back; petaloid lesions are ring- or petal-shaped plaques with a peripheral collarette of scale.
• Flexures — sharply marginated, beefy-red patches in axillae, inframammary folds, groin and umbilicus, often macerated with minimal scale.[1]

The face-and-flexure sites are the trap. Intertriginous seborrhoeic dermatitis mimics candidiasis (look for satellite pustules), inverse psoriasis (smooth, minimal scale) and erythrasma (coral-red under Wood light) — and these are exactly the sites where potent steroids do the most harm, so the diagnosis must be right before you reach for the tube.[1]

Read the morphology — and the HIV and Parkinson phenotypes

In advanced HIV, expect severe, widespread, refractory disease, sometimes erythroderma. Severity often tracks the CD4 count, and a florid presentation in a young adult with risk factors is HIV until the test comes back. The same disease in a Parkinson patient clusters on the face with prominent blepharitis and may ease when dopaminergic therapy is optimised.[7][8]

The face-off — seborrhoeic dermatitis vs psoriasis vs atopic dermatitis

The three scalp-and-face eczemas that collide in clinic, separated by morphology, distribution and a single discriminator. This is the table the fellowship panel reaches for first.[1]

[1]

The discriminator line: greasy yellow scale on sebaceous-rich sites with the nasolabial folds involved is seborrhoeic; thick silvery scale extending beyond the hairline with nail pitting is psoriasis; intense itch with flexural lichenification that spares the nasolabial folds is atopic. One sentence, three diagnoses.[1]

The rest of the differential — read it by site

The differential is site-specific, so examine first, then name the mimic. The four fellowship-favourite mimics are psoriasis, tinea capitis, atopic dermatitis and rosacea; the rest sort themselves by where the rash sits.[1]

On the scalp, distinguish from psoriasis (thick silvery plaques extending beyond the hairline, Auspitz sign, nail pitting), tinea capitis (patchy alopecia, broken hairs, black-dot or grey-patch variants, kerion, cervical lymphadenopathy — a child, not a comfortable adult), and pityriasis amiantacea (asbestos-like scale encircling shafts; a reaction pattern overlying psoriasis or severe seborrhoeic dermatitis, not a diagnosis).[1][9]

On the face, distinguish from rosacea (centrofacial flushing, papules, pustules, telangiectasia, no greasy scale, ocular involvement in half), atopic dermatitis (pruritic, xerotic, flexural, spares the nasolabial folds, personal or family atopy), periorificial dermatitis (monomorphic papules around mouth, nose and eyes with vermilion-border sparing, often steroid-induced), cutaneous lupus (photosensitive, scarring, follicular plugging; biopsy and serology), contact dermatitis (exposure history, patch testing) and pemphigus foliaceus (superficial erosions, Nikolsky sign, anti-Dsg1).[1]

On the trunk and in flexures, distinguish from inverse psoriasis (smooth, well-demarcated, minimal scale), candidiasis (beefy-red with satellite pustules, KOH positive), tinea corporis or cruris (annular, active scaly border, KOH positive), pityriasis versicolor (hypo- or hyperpigmented fine scale; KOH shows spaghetti-and-meatballs), erythrasma (brown intertriginous patches, coral-red Wood-light fluorescence from Corynebacterium minutissimum) and plain intertrigo.[1][9]

On the lid margin, distinguish seborrhoeic blepharitis from staphylococcal blepharitis (collarettes around lashes, ulceration), ocular rosacea (meibomian dysfunction, conjunctival injection) and contact blepharitis (eye-drop or cosmetic exposure).[1]

When it is generalised, think erythroderma — cutaneous T-cell lymphoma (mycosis fungoides or Sezary syndrome; poikiloderma, lymphadenopathy; biopsy essential), pemphigus foliaceus, atopic or psoriatic erythroderma, and drug-induced erythroderma. A treatment-resistant "seborrhoeic dermatitis" that keeps widening is CTCL until biopsy proves otherwise.[1]

Dermoscopy earns its keep here. Seborrhoeic dermatitis shows linear branching vessels on a yellowish background with follicular plugs and yellow scale, which separates it from psoriasis (regularly distributed dotted vessels on a light-red background) and from tinea (comma-shaped or corkscrew hairs). One look can settle a borderline scalp.[9]

Investigations — clinical first, KOH when tinea lurks

This is a clinical diagnosis; tests exist to exclude mimics, not to confirm. Reach for them when the picture is atypical, refractory, or shows alopecia and broken hairs.[1][2][9]

• Skin scraping for KOH — exclude dermatophytes (tinea capitis, corporis) or confirm Malassezia in pityriasis versicolor. Malassezia under KOH shows yeast clusters and short hyphae — "spaghetti and meatballs" (or "bananas and grapes").
• Fungal culture — when KOH is negative but tinea suspicion is high; identifies species (Trichophyton tonsurans, Microsporum canis).
• Skin biopsy — for refractory disease or suspicion of CTCL, pemphigus, lupus or Langerhans cell histiocytosis. Histology shows psoriasiform hyperplasia, follicular plugging, parakeratosis, spongiosis and a superficial perivascular lymphocytic infiltrate; PAS stain may reveal Malassezia yeasts in the stratum corneum.
• HIV test — for new, severe, widespread or refractory adult disease, especially with risk factors; first-line in many regions.
• Patch testing — when contact dermatitis is a trigger or comorbidity.
• Wood light — coral-red fluorescence flags erythrasma; pityriasis versicolor may show pale yellow-gold.
• Bloods and severity scoring — FBC, LFT, U&E and HIV serology when immunodeficiency or systemic disease is suspected; the Seborrhoeic Dermatitis Area and Severity Index (SDSI) and Dermatology Life Quality Index (DLQI) are research and quality-of-life tools.[9]

When it is an emergency — erythroderma and the unwell infant

Seborrhoeic dermatitis is rarely an emergency, but two presentations are: erythroderma, and infantile disease with systemic upset.[1][2]

The treatment ladder — antifungal first, steroid short, calcineurin to spare

Antifungals are the cornerstone — for scalp and face alike — because they hit the yeast and carry an anti-inflammatory bonus. Ketoconazole shampoo is first-line for the scalp; ketoconazole cream is first-line for the face.[11][12][13][16]

For the scalp and hair-bearing areas, the antifungal shampoo ladder:[1]

[1]

For the face, trunk and flexures, reach for a cream or gel:[10]

• Ketoconazole 2% cream — once or twice daily for 2 to 4 weeks; the workhorse first-line facial therapy, with excellent long-term safety for intermittent use.[11]
• Ciclopirox 1% cream or gel — alternative; useful for resistant or intertriginous disease.[10]
• Miconazole 2% plus hydrocortisone 1% (Daktacort) — combined antifungal and low-potency steroid; ideal when inflammation and yeast overgrowth coexist.[1]
• Selenium sulfide 2.5% lotion — alternative for truncal and petaloid disease.[13]
• Zinc pyrithione 1% cream or wash — over-the-counter maintenance option.[16]

Everyone forgets: the shampoo must sit on the scalp for 3 to 5 minutes before rinsing — anything less fails to kill Malassezia, and the patient will tell you the treatment "did not work".[1]

Anti-inflammatories — short, low-potency, then step down

Use the weakest steroid that works, for the shortest time that clears the flare — then switch to a calcineurin inhibitor for the face and flexures.[1]

• Mild face or intertrigo: hydrocortisone 1% cream or ointment once or twice daily for 1 to 2 weeks.
• Moderate scalp or trunk: betamethasone valerate 0.1% or mometasone furoate 0.1%, short 2-to-4-week courses.[1]

Never put a potent steroid on the face or in the flexures. The price is atrophy, telangiectasia, striae, perioral dermatitis and rebound flares — and potent steroids also let Malassezia flourish by stripping competing flora. This is the single most tested safety point in the topic.[1]

Calcineurin inhibitors are the steroid-sparing workhorses for facial and intertriginous disease — tacrolimus 0.1% ointment and pimecrolimus 1% cream — and crucially they do not cause skin atrophy, which is why they win the chronic-face argument. The Rigopoulos 2004 trial matched pimecrolimus 1% against betamethasone valerate 0.1% for facial disease and found them comparable; the Papp 2012 trial matched tacrolimus 0.1% against hydrocortisone 1% with comparable efficacy and the prospect of longer remission. Mind the US black-box warning (theoretical malignancy risk, causality unproven), avoid in active infection, and never under occlusion.[14][15]

Combination antifungal-plus-steroid products earn their place when both problems are live: ketoconazole 2% plus desonide 0.05% (Ketozal-D, Acuatim-D) for facial disease, miconazole 2% plus hydrocortisone 1% (Daktacort) for the napkin area and flexures, and hydrocortisone 1% plus clotrimazole 1% (Canesten HC, Lotriderm equivalents) for face and intertriginous disease.[1][10]

Refractory disease — itraconazole pulse, not oral ketoconazole

When topicals fail, the systemic of choice is itraconazole pulse — oral ketoconazole is restricted and now a historical answer.[1][2]

Oral itraconazole pulse is the modern pick for refractory or widespread disease:[1]

• Dose: 200 mg twice daily for 1 day per week for 1 to 3 months.
• Mechanism: broad-spectrum azole that accumulates in keratin and sebum.
• Evidence: open-label and small randomised trials support efficacy in refractory disease.
• Monitoring: baseline LFTs, repeat at 4 weeks and at end of treatment; avoid in heart failure (negative inotropy); mind the many CYP3A4 interactions.[1]

Oral ketoconazole — 200 mg once daily for 2 to 4 weeks — works but is restricted in most regions (FDA and EMA, 2013) because of hepatotoxicity (symptomatic hepatitis in roughly 1 in 10,000), adrenal suppression above 400 mg per day, and CYP3A4 interactions. It is now reserved for endemic mycoses; itraconazole has taken its place for seborrhoeic dermatitis. If a viva panel asks "why not oral ketoconazole?", that is the answer.[1]

Oral fluconazole — 200 to 300 mg once weekly for 4 to 8 weeks — is a third option supported by open-label series; check baseline LFTs and watch CYP2C9 and CYP3A4 substrates.[1]

The new kid — roflumilast 0.3% foam, a PDE4 inhibitor

Roflumilast is the first genuinely new topical for seborrhoeic dermatitis in years — a PDE4 inhibitor that mutes the Th1/Th17 cytokine storm by raising intracellular cAMP. The 0.3% foam is FDA-approved for adolescents and adults, backed by a 2023 phase 2a trial, the 2024 phase 3 STRATUM trial, and 52-week open-label safety data through 2026.[17][18][19]

• Phase 2a (2023): rapid, significant improvement in erythema, scaling and pruritus versus vehicle.[17]
• Phase 3 STRATUM (2024): efficacy and safety replicated across scalp, face and trunk in adolescents and adults.[18]
• 52-week open-label (2026): sustained benefit, no new safety signals — supporting long-term, steroid-sparing use.[19]

It earns its place for patients who need a steroid-sparing option, cannot tolerate topical antifungals alone, or have disease in cosmetically sensitive areas (the face, the hair-bearing scalp). Behind it, lotamilast (RVT-502) is another PDE4 inhibitor in trials, low-dose oral isotretinoin (0.1 to 0.3 mg/kg/day) has case-series support for refractory disease by shrinking sebaceous glands, and crisaborole 2% ointment is used off-label.[1]

By site — the prescription you actually write

Match the vehicle to the site. A shampoo for hair, a cream for face and trunk, a low-potency steroid or calcineurin inhibitor for the flexures and lids — and never a potent steroid where skin is thin.[1]

[1]

The associations that change the workup — HIV, Parkinson, the infant

Three associations rewrite the plan; ask for all three on the first visit.[1]

HIV/AIDS. Seborrhoeic dermatitis may be severe, widespread and refractory, can be the presenting feature of undiagnosed HIV, and prevalence climbs to 30 to 40 percent in advanced disease. Optimise ART, use potent topical antifungals and anti-inflammatories, add itraconazole pulse for refractory disease, and plan on long-term maintenance. A new, florid, refractory adult is an HIV test, not a stronger shampoo.[8]

Parkinson disease. Prevalence runs 19 to 60 percent, severity may track motor burden, and the phenotype is facial-predominant with blepharitis. Proposed drivers are autonomic dysfunction, altered sebum and the substance-P pathway; optimising dopaminergic therapy may even improve the skin. Regular antifungal shampoo, topical ketoconazole and gentle skin care carry the day.[7]

Infants (cradle cap). Conservative first-line: emollients (mineral oil, petroleum jelly, olive oil) to soften scale, then gentle brushing after 15 to 30 minutes, plus baby shampoo. Persist with short-course ketoconazole 2% cream or hydrocortisone 1% — but the Cochrane 2019 review found limited evidence for any specific intervention; emollients and gentle scale-removal remain the cornerstone. The red flags are failure to thrive, recurrent infection, diarrhoea or erythroderma — evaluate for immunodeficiency.[20][21]

Pregnancy. Topical antifungals (ciclopirox, ketoconazole 2%) are generally safe, and calcineurin inhibitors are acceptable with minimal systemic absorption; avoid oral ketoconazole and itraconazole (teratogenicity, embryotoxicity) and keep topical steroids to low-to-moderate potency, short courses.[10]

Skin of colour. Post-inflammatory hyperpigmentation is the dominant cosmetic concern — treat early and aggressively to limit dyspigmentation. The granulomatous variant (Facial Afro-Caribbean Childhood Eruption, FACE) is commoner in children with skin of colour and mimics sarcoidosis or lupus; topical antifungals and calcineurin inhibitors remain safe and effective.[1]

The preventable-harm list — what juniors get wrong

Most harm in seborrhoeic dermatitis is iatrogenic, and it is preventable. Run this list before you sign the prescription.[1]

• Potent topical steroid on the face — atrophy, telangiectasia, striae, perioral dermatitis, rebound flares, tachyphylaxis and steroid rosacea. The commonest error in the topic.
• Treating infantile cradle cap with prolonged potent steroids — systemic absorption, hypothalamic-pituitary-adrenal suppression, iatrogenic Cushing syndrome.
• Oral ketoconazole for "refractory" disease without weighing hepatotoxicity, adrenal suppression and CYP3A4 interactions — itraconazole pulse is the modern answer.
• Inadequate shampoo contact time — less than 3 to 5 minutes fails to kill Malassezia.
• Stopping the shampoo when symptoms settle — relapse is the rule; maintenance therapy is mandatory.
• Missing the diagnosis behind the diagnosis — tinea capitis in a child (where shampoo alone is inadequate), CTCL in a treatment-resistant adult, and HIV in severe refractory disease.[1][8]

The classic trap: a "severe eczema" on the face handed a potent steroid is not eczema — it is seborrhoeic dermatitis being made worse, with perioral dermatitis and steroid rosacea as the iatrogenic bonus. Reach for ketoconazole cream and a calcineurin inhibitor instead.[1]

Prognosis — no cure, good control, maintenance is the rule

Seborrhoeic dermatitis is chronic and relapsing; there is no cure, but control is excellent and relapse is preventable. Cradle cap usually self-resolves in 6 to 12 months; adult disease fluctuates with stress, season and comorbidity, and consistent therapy brings 80 to 90 percent to good control. Review at 4 to 8 weeks after starting therapy, then as needed, and keep weekly antifungal shampoo plus intermittent topical anti-inflammatory as the maintenance backbone. Safety-net the patient: never a potent steroid on the face, sunscreen to limit dyspigmentation, and treat flares early.[1][2][20][21]

The mantra

Antifungal first, steroid short, calcineurin to spare — and screen for HIV when it will not behave.[1]

Ward-round test

Stem 1. A 34-year-old man has greasy yellow scale in his eyebrows, nasolabial folds and behind his ears, with mild itch. What is the diagnosis, the first-line scalp treatment, and the one thing you must not put on his face?[1]

Answer

Diagnosis: seborrhoeic dermatitis (greasy yellow scale on sebaceous-rich sites). First-line scalp treatment: ketoconazole 2% shampoo two to three times weekly, left on for 3 to 5 minutes. Never apply: a potent topical steroid on the face — use ketoconazole 2% cream and, if inflamed, short-course hydrocortisone 1% or a calcineurin inhibitor.[1][11]

Stem 2. A 28-year-old presents with new, severe, widespread and treatment-resistant seborrhoeic dermatitis. What is the single most important next investigation, and why?[1]

Answer

HIV serology. Severe, widespread, refractory adult seborrhoeic dermatitis can be the presenting feature of undiagnosed HIV, with prevalence rising to 30 to 40 percent in advanced disease — so this is a test, not a stronger shampoo. Optimise ART alongside aggressive skin therapy if positive.[8]

Stem 3. A 2-month-old has thick yellow adherent scalp scale and is thriving and afebrile; another infant has the same scale but is failing to thrive with diarrhoea. What separates the disposition?[20]

Answer

The comfortable, thriving baby has cradle cap — emollients, gentle brushing and baby shampoo; it self-resolves by 6 to 12 months. The infant failing to thrive, with diarrhoea or recurrent infection is a red flag for immunodeficiency (LAD type 1, Netherton syndrome, SCID, Omenn syndrome, hyper-IgE syndrome, Leiner disease) — escalate, do not reassure.[20][21]

Stem 4. Give the discriminator that separates seborrhoeic dermatitis from scalp psoriasis in one sentence, and the KOH finding that separates it from tinea capitis.[1]

Answer

Greasy yellow scale confined to sebaceous-rich sites (with nasolabial-fold involvement) is seborrhoeic; thick silvery scale extending beyond the hairline with nail pitting is psoriasis. On KOH, Malassezia shows yeast clusters and short hyphae ("spaghetti and meatballs"), whereas tinea capitis shows septate hyphae with patchy alopecia and broken hairs.[1][9]

References

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12. [12]Carr MM, Pryce DM, Ive FA Treatment of seborrhoeic dermatitis with ketoconazole: I. Response of seborrhoeic dermatitis of the scalp to topical ketoconazole Br J Dermatol, 1987.PMID 2950914
13. [13]Danby FW, Maddin WS, Margesson LJ, et al. A randomized, double-blind, placebo-controlled trial of ketoconazole 2% shampoo versus selenium sulfide 2.5% shampoo in the treatment of moderate to severe dandruff J Am Acad Dermatol, 1993.PMID 8245236
14. [14]Rigopoulos D, Ioannides D, Kalogeromitros D, et al. Pimecrolimus cream 1% vs. betamethasone 17-valerate 0.1% cream in the treatment of seborrhoeic dermatitis. A randomized open-label clinical trial Br J Dermatol, 2004.PMID 15541087
15. [15]Papp KA, Papp A, Dahmer B, Clark CS. Single-blind, randomized controlled trial evaluating the treatment of facial seborrheic dermatitis with hydrocortisone 1% ointment compared with tacrolimus 0.1% ointment in adults J Am Acad Dermatol, 2012.PMID 22101215
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17. [17]Zirwas MJ, Draelos ZD, DuBois J, et al. Efficacy of Roflumilast Foam, 0.3%, in Patients With Seborrheic Dermatitis: A Double-blind, Vehicle-Controlled Phase 2a Randomized Clinical Trial JAMA Dermatol, 2023.PMID 37133856
18. [18]Blauvelt A, Stein Gold L, Bhatia N, et al. Roflumilast foam 0.3% for adolescent and adult patients with seborrheic dermatitis: A randomized, double-blinded, vehicle-controlled, phase 3 trial J Am Acad Dermatol, 2024.PMID 38253129
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20. [20]Victoire A, Magin P, Coughlan J, van der Kruis J. Interventions for infantile seborrhoeic dermatitis (including cradle cap) Cochrane Database Syst Rev, 2019.PMID 30828791
21. [21]Nobles T, Harberger S, Krishnamurthy K Cradle Cap(Archived) 2026.PMID 30285358