Seborrhoeic Dermatitis - MD Dermatology Exam Notes

1. Definition and Overview

• Seborrhoeic dermatitis (SD): common, chronic inflammatory skin disease characterised by red/pink patches with superficial scaling.
• Affects areas with high density of sebaceous glands: scalp, face (nasolabial folds, eyebrows, glabella), central chest, and anogenital region. Also predilection for skin folds/large flexures and submammary areas.
• Distribution is usually symmetrical.
• Dandruff (pityriasis capitis) = mildest form of SD, confined to scalp, lacking visible inflammation.
• Diagnosis is clinical - no validated diagnostic criteria/scoring system exists.
• Occurs in two age peaks: infantile variant (including "cradle cap") and from puberty through adult life.

2. Epidemiology

• Adult prevalence: ~3-4% in general dermatology outpatients; higher in older age groups (14.3% in Rotterdam study, median age 67.9 years).
• Twice as common in men than women.
• Higher rates reported in fair skin; lower recognition in skin of colour (possibly under-recognition of erythema).
• Dandruff affects up to 50% of post-pubertal population worldwide.
• Infantile SD/cradle cap: peak prevalence ~72% in first 3 months of life; most clear by 1 year.
• Increased prevalence in:
  • HIV infection (35% early disease, up to 85% in AIDS - can be widespread)
  • HTLV-1 seropositivity (2-fold increase)
  • Organ transplant recipients (increases with duration of immunosuppression)
  • Parkinson disease, spinal cord injury (reduced facial movement/sebum clearance)
  • Down syndrome (31% prevalence in children)

3. Pathophysiology

• Pathogenesis not fully understood; multifactorial - involves skin mycobiome (Malassezia), sebum, and individual host susceptibility.

Causative organisms

• Malassezia yeasts - part of normal skin microbiome, not a conventional pathogen; role supported by response to antifungals and relapse coinciding with reappearance of yeast.
• M. globosa and M. restricta are commonest species on head/neck and most associated with SD/dandruff.
• Historical names: Pityrosporum (ovale, orbiculare, pachydermatis).
• Mechanism: yeast lipases/phospholipases hydrolyse sebum triglycerides → release free fatty acids (oleic acid) → irritant effect, increased keratinocyte desquamation, impaired barrier function, and triggers dandruff/SD-like changes.
• Cytokine induction: IL-1β, IL-6, IL-8, IL-10, TNF-α, TGF-β from keratinocytes; activation of Th17 immunity/IL-17.
• Increased kallikrein 5 (KLK5) in stratum corneum in dandruff.
• Raised cathepsin S and histamine in scalp - implicated in pruritus.
• Epidermis shows hyperproliferation (increased Ki-67) despite lack of overt inflammation in dandruff.

Genetics

• No clear Mendelian inheritance pattern (unlike atopic eczema/psoriasis).
• Association with HLA A32, DQB105, DRB1*01.
• GWAS: no single specific locus, but overlap with psoriasis/atopic eczema via LCE3 gene cluster.
• Rare associations: mutations in ACT1 (IL-17 signalling), complement C5 (Leiner disease), NEMO, SKT4, ZNF750 (autosomal dominant early-onset severe SD-like rash).

Environmental/lifestyle factors

• Worse in winter (impaired barrier from cold/low humidity); improves in summer (possible UV immunosuppression effect).
• Diet: high fruit intake associated with lower SD prevalence; "Western" diet pattern linked to more SD in women; possible link with vitamin D deficiency.
• Case-crossover data: flares associated with higher alcohol intake and psychological stress.
• Hair care/cosmetic practices (oils, hair extensions) can modulate Malassezia growth.

4. Clinical Features

History

• Usually begins in adolescence/early adulthood; chronic, relapsing course.
• Symptoms (itch) may be disproportionate to visible signs, especially on scalp.

Presentation by site

• Face: nasolabial folds, ear creases, eyelids, glabella, medial eyebrows - fine scaling with erythema over alar creases, nasal side walls, posterior ear folds.
• Ears: light scaling/inflammation of ear canal; can develop otitis externa with secondary bacterial/Candida infection.
• Scalp: spectrum from mild grey-white scale (dandruff, no erythema) to inflammatory eruption with thick, yellow, greasy scale/crust. Similar changes in beard.
• Eyelids: anterior blepharitis - flaky debris at lash base → conjunctival irritation, red eye; can cause meibomian gland loss and dry eye.
• Trunk (men): presternal petaloid (petal-shaped) lesions; may extend to upper back, umbilicus, axillae, groins, submammary area (glazed, pink appearance in flexures).
• Pityriasiform SD: more widespread inflammatory variant involving torso +/- limbs.
• Anogenital region: can occur in both sexes; up to 40% of women with vulvar dermatitis have extragenital SD features.
• Skin of colour: hypopigmentation may be the predominant feature with little visible inflammation; arcuate/petaloid hairline lesions.
• Post-inflammatory hyperpigmentation of nasal crease = "seborrhoeic melanosis".

Sebopsoriasis

• Psoriasis-like variant with coarser, well-defined scaling in an SD distribution; possibly represents koebnerisation of psoriasis into SD-affected skin; reported to arise in HIV-positive men on suppressive ART.

Complications

• Secondary bacterial/candidal infection of flexures.
• Widespread SD may rarely progress to exfoliative erythroderma.
• Blepharitis-related dry eye disease.

5. Differential Diagnosis

Drug-induced/exacerbated SD

• Sulphydryl-group drugs: captopril, D-penicillamine, gold salts (sodium aurothiomalate)
• Lithium, buspirone, methyldopa, chlorpromazine, cimetidine
• Interferon-α + ribavirin (hepatitis C treatment)
• Recombinant IL-2
• Targeted chemotherapy: erlotinib (EGFR inhibitor), sorafenib, sunitinib (multikinase inhibitors), dasatinib, vemurafenib (BRAF inhibitor - also causes pityriasis amiantacea)
• Topical/systemic 5-fluorouracil
• Dupilumab - new-onset SD/sebopsoriasis or head-and-neck dermatitis (4.2% in one retrospective study)

6. Classification of Severity

• No validated scoring system exists (unlike atopic eczema/psoriasis) - studies use descriptive categories.

7. Investigations

• Diagnosis is clinical; investigations rarely needed.
• Histology (not diagnostic - overlapping features of psoriasis and chronic dermatitis):
  • Spongiosis - helpful distinguishing feature (more evident in earlier lesions)
  • Older lesions show psoriasiform features: follicular plugs, orthokeratosis, parakeratosis, uneven rete ridges
  • Shoulder parakeratosis and prominent lymphocytic infiltrate favour SD
  • Perifollicular infiltrate with increased dendritic cells
  • Classic lesion: "squirting papilla" (Civatte; Pinkus and Mehregan) - capillary dilatation in dermal papillae with granulocyte migration into epidermis inciting spongiosis
  • Immunohistochemistry (Ki-67, keratin 10, caspase-5, GLUT-1) not helpful in differentiating from psoriasis

8. Quality of Life and Disease Course

• Chronic condition with flares; requires long-term/maintenance treatment.
• Impaired QoL correlates with disease severity and facial involvement (Skindex-29 mean scores: 20.5 in Spanish cohort - mild impairment; 33.97 in Chinese cohort with severe emotional impact in nearly half).
• Associated with depression and, in the elderly, with age-related loss of self-sufficiency (senescence).

9. Management

A. Topical antifungals (first-line)

• Ketoconazole 2% and ciclopirox olamine 1% - similar efficacy, both superior to placebo (2015 Cochrane review)
• Miconazole, clotrimazole - comparable to topical steroids short-term
• Sertaconazole 2% - small studies show benefit
• Bifonazole 1% - lacked efficacy in high-quality RCT
• Allylamines (terbinafine, naftifine) - effective despite lacking anti-Malassezia activity (suggests other mechanisms)
• Formulations: 2% ketoconazole foam effective long-term (up to 52 weeks); consider hair texture/grooming practices when choosing vehicle
• Resistance: ketoconazole-resistant M. restricta strains identified with long-term use

B. Keratolytics

• Salicylic acid, sulphur, coal tar, urea, lactic acid, propylene glycol, selenium sulfide (antifungal + keratolytic), zinc pyrithione, piroctone olamine
• Help remove scale, improve penetration of other agents
• Little robust efficacy evidence, especially in infantile SD/cradle cap
• Topical salicylic acid contraindicated in infancy (toxicity risk)

C. Topical anti-inflammatory/immunomodulatory agents

• Topical corticosteroids: mild potency short-term (per NICE), superior in combination with antifungal vs monotherapy; limit long-term use due to atrophy risk (especially eyelids)
• Topical calcineurin inhibitors (pimecrolimus, tacrolimus): strong RCT evidence for facial SD (unlicensed indication); improvement within 2 weeks; twice-weekly tacrolimus maintenance superior to once-weekly; longer remission than ciclopirox in 24-week study; common side effects: burning, flushing, irritation (reassure not allergic reaction)
• Topical lithium (gluconate/succinate) 8%: high-quality evidence, more effective than 2% ketoconazole in inducing remission; mechanism - inhibits GSK3β, NF-κB, STAT pathways; precipitates free fatty acids limiting yeast growth
• Other agents: 4% nicotinamide cream, metronidazole 0.75% gel (useful with coexistent acne/rosacea), crisaborole 2% (PDE4 inhibitor), roflumilast (in phase 3 trials)

D. Systemic treatment (rarely indicated)

• Oral itraconazole: most frequently reported; pulse regimen (200mg daily x1 week, then 200mg daily for first 2 days of month) superior to placebo in RCT
• Narrow-band UVB: improvement reported but short-lived (relapse ~3 weeks)
• Low-dose oral isotretinoin: unlicensed option for severe seborrhoea; RCT showed improvement
• Oral biotin: NOT effective (despite theoretical link to biotinidase deficiency)

NICE Recommendations Summary (Table 40.1)

High-yield exam points

1. SD is a clinical diagnosis; distribution follows sebaceous gland density.
2. Key organism = Malassezia (globosa/restricta) - commensal turned pathogenic via lipase-mediated free fatty acid release.
3. Classic histology = squirting papilla with spongiosis + shoulder parakeratosis.
4. Increased in HIV/AIDS, Parkinson's, transplant recipients, Down syndrome.
5. First-line treatment = topical antifungals (ketoconazole/ciclopirox); steroids for short-term flares only; calcineurin inhibitors and topical lithium for maintenance/facial disease.
6. Watch for drug-induced SD, especially with EGFR/BRAF/multikinase inhibitors and dupilumab.
7. Infantile severe/atypical SD → think Leiner disease, biotinidase deficiency, zinc deficiency.

Probiotics in Atopic Dermatitis - Short Notes

Rationale

• Based on gut microbiome-immune axis ("gut-skin axis") and the hygiene hypothesis.
• Altered gut microbiota in infancy is linked to immune dysregulation (Th2 skewing) and AD risk/severity.
• Probiotics = live microorganisms thought to restore microbial diversity, promote Treg induction, and modulate Th1/Th2 balance, reducing inflammatory cytokine drive.

Evidence - Prevention (Primary Prophylaxis)

• Best evidence is for prenatal + early postnatal supplementation in high-risk infants (family history of atopy).
• Meta-analyses (cited in Fitzpatrick's Dermatology) show probiotics reduce incidence of AD when given to mother (late pregnancy/lactation) and infant (early life) - "primary prevention" effect.
• Effect is strain-specific and most consistent with combined maternal + infant supplementation rather than infant-only.
• Not established for prevention of other atopic diseases (asthma, allergic rhinitis) - benefit appears AD-specific.

Evidence - Treatment (Established AD)

Pediatric AD

• Systematic reviews/meta-analyses (e.g., Gaikwad et al. 2025, Medicina) show moderate-to-large reduction in SCORAD with probiotic therapy (pooled Hedges' g ≈ 0.65) vs placebo.
• No significant effect on serum IgE - benefit appears independent of IgE-mediated mechanism.
• Network meta-analysis (Tan-Lim et al. 2021) found combination probiotic strains (e.g., Bifidobacterium + Lactobacillus) more effective than single strains in reducing SCORAD in children.
• Harriet Lane Handbook notes: evidence for probiotics is "limited" overall, but efficacy demonstrated specifically in prevention of atopic dermatitis.

Adult AD

• Husein-ElAhmed & Steinhoff (2023) meta-analysis (9 RCTs): significant SCORAD reduction favoring probiotics (RR -5.93).
  • Strain-specific efficacy: Lactobacillus salivarius (largest effect) > L. acidophilus > L. plantarum; no benefit with L. fermentum.
  • Greater benefit in moderate-to-severe AD than mild AD.
  • No significant change in IgE or eosinophil count.
  • Despite SCORAD improvement, no clinically meaningful improvement in Dermatology Life Quality Index (DLQI).
• Optimal dose/duration not established - major limitation across trials.

Key Strains with Reported Benefit

Textbook Consensus (Andrews', Fitzpatrick's, Dermatology 2-Vol Set)

• Probiotics are mentioned under adjunctive/complementary management of AD, not first-line therapy.
• Cochrane review (Boyle et al., cited in Fitzpatrick's): "Probiotics for treating eczema" - insufficient high-quality evidence to recommend probiotics as standard treatment.
• Stronger, more consistent data support a role in prevention (early-life supplementation) than in established disease treatment.
• Andrews' notes trials on early-life probiotic supplementation showing long-term reduction in AD incidence, and reduced AD in preterm neonates given probiotics.

Practical/Exam Takeaways

1. Not first-line or standard-of-care treatment for AD - remains adjunctive/investigational.
2. Best-supported use: primary prevention in high-risk infants via maternal (late pregnancy/lactation) + infant supplementation.
3. Treatment effect (if any) is strain-specific, more evident in moderate-to-severe disease, and IgE-independent.
4. Symptom/severity score (SCORAD) improvement does not consistently translate to quality-of-life improvement.
5. Heterogeneity in strains, doses, and durations across trials limits firm guideline recommendations - highlighted as a recurring limitation in both textbook references and recent meta-analyses (2022-2025).