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This is a scalp of a 64 yr old female diagnosis is discoid lupus erythmatosus- give me a Proper caselike description for this case for my spotter in dermatology practical exam
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Case description for spotter
A 64-year-old female presents with lesions over the scalp. On examination, there are two well-defined, irregular erythematous to pink plaques over the vertex/parietal scalp, approximately 3-5 cm in size. The plaques show adherent scales with follicular plugging and focal yellowish crusting. There is associated patchy alopecia with reduction/loss of follicular openings, suggesting cicatricial (scarring) alopecia. The surrounding scalp shows no diffuse scaling.
The morphology of erythematous scaly plaques with follicular plugging and scarring alopecia is consistent with discoid lupus erythematosus (DLE) of the scalp, a form of chronic cutaneous lupus erythematosus. DLE plaques may progress to atrophy, dyspigmentation and permanent hair loss. The description is consistent with standard clinical features described by DermNet.
Provisional diagnosis:
Discoid lupus erythematosus of scalp with cicatricial alopecia.
Discoid lupus erythematosus of scalp with cicatricial alopecia.
Differential diagnoses:
- Lichen planopilaris
- Folliculitis decalvans
- Tinea capitis, particularly inflammatory tinea
- Psoriasis/seborrhoeic dermatitis with secondary hair loss
Confirmation / work-up:
- Dermoscopy: follicular keratotic plugs, perifollicular white halo, telangiectasia, dyspigmentation and absent follicular ostia.
- Skin biopsy from the active margin for histopathology and direct immunofluorescence.
- Screening for systemic involvement when clinically indicated: CBC, urinalysis, ANA and other lupus serology.
One-line viva answer:
“This is a case of discoid lupus erythematosus of the scalp, presenting as erythematous scaly plaques with follicular plugging and irreversible cicatricial alopecia.”
“This is a case of discoid lupus erythematosus of the scalp, presenting as erythematous scaly plaques with follicular plugging and irreversible cicatricial alopecia.”
What are the other questions that examiner can askme in this cae starting from medium to hard question
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Medium-level viva questions
1. What is your diagnosis?
Discoid lupus erythematosus (DLE) of the scalp causing cicatricial alopecia.
2. Why is this called cicatricial alopecia?
Because inflammation destroys the hair follicles and replaces them with fibrosis. Therefore, follicular openings are absent and hair loss in the scarred area is permanent.
3. What are the classical clinical features of DLE?
- Well-defined erythematous to violaceous plaques
- Adherent scale
- Follicular plugging
- Central atrophy and scarring
- Telangiectasia
- Hypo- or hyperpigmentation
- Scarring alopecia when the scalp is involved
A useful description is: “The triad of erythema, adherent scale/follicular plugging, and atrophic scarring.”
4. What is the carpet-tack sign?
On removing adherent scale from a DLE plaque, keratotic plugs are seen projecting from the undersurface of the scale, like the tacks of a carpet. It results from follicular plugging.
5. Common sites of DLE?
Primarily photo-exposed sites:
- Scalp
- Face, especially nose and cheeks
- Ears, particularly concha and helix
- V-area of neck
- Extensor forearms
6. What type of cutaneous lupus is DLE?
DLE is the commonest type of chronic cutaneous lupus erythematosus (CCLE).
7. How will you classify DLE?
- Localized DLE: lesions restricted to the head and neck
- Generalized DLE: lesions occur both above and below the neck
This patient has localized DLE if no lesions are present below the neck.
8. What are differentials for this scalp lesion?
- Lichen planopilaris
- Folliculitis decalvans
- Tinea capitis, especially inflammatory tinea/kerion
- Psoriasis or seborrhoeic dermatitis with hair shedding
- Central centrifugal cicatricial alopecia
- Alopecia areata, though this is non-scarring and follicular openings are preserved
9. How do you differentiate DLE from lichen planopilaris clinically?
| Feature | DLE | Lichen planopilaris |
|---|---|---|
| Plaque | Well-defined erythematous plaque | Less well-defined patches |
| Scale | Adherent scale with follicular plugging | Perifollicular scale/casts |
| Pigmentary change | Common | Less prominent |
| Atrophy/telangiectasia | Common | May occur but less characteristic |
| Trichoscopy | Follicular plugs, large yellow dots, speckled pigmentation, arborizing vessels | Perifollicular erythema and tubular perifollicular scales |
10. What is the significance of follicular plugging?
It is a characteristic sign of DLE caused by hyperkeratosis filling the follicular infundibulum. It supports the diagnosis but is not entirely specific.
Investigations examiners may ask
11. What is the confirmatory investigation?
Skin biopsy from the active edge of a lesion for histopathology. If direct immunofluorescence is required, a separate specimen is taken in the appropriate transport medium.
Do not biopsy the fully scarred central area, as it may only show fibrosis and yield nonspecific findings.
12. Describe the histopathology of DLE.
- Hyperkeratosis, often with follicular plugging
- Epidermal atrophy
- Interface dermatitis with basal-cell vacuolar degeneration
- Apoptotic keratinocytes
- Thickened basement membrane
- Dense perivascular and periappendageal lymphocytic infiltrate
- Dermal mucin deposition
- Late lesions show dermal fibrosis and follicular destruction
13. What does direct immunofluorescence show?
The lupus band test may show granular deposition of immunoglobulins, commonly IgG and IgM, with C3 at the dermoepidermal junction and around adnexal structures.
14. What tests will you order to rule out systemic lupus erythematosus?
- Complete blood count
- Urinalysis for proteinuria/hematuria
- Serum creatinine and renal function
- ANA
- If ANA positive or symptoms suggest SLE: anti-dsDNA, anti-Sm, complement C3/C4, urine protein quantification
- Clinical examination for arthritis, oral ulcers, photosensitivity, serositis, renal and neurologic features
A negative ANA does not rule out isolated DLE. Clinical assessment plus biopsy is central to diagnosis. DermNet’s diagnostic summary also notes that ANA may be absent in DLE.
15. Does every patient with DLE have SLE?
No. Most have disease limited to the skin, but every patient should be assessed at baseline and followed for symptoms/signs of systemic disease.
16. What clinical features suggest evolution to systemic disease?
- Constitutional symptoms: fever, weight loss, fatigue
- Symmetrical inflammatory polyarthritis
- Oral/nasal ulcers
- Raynaud phenomenon
- Serositis symptoms
- Cytopenias
- Proteinuria, hematuria, edema or hypertension
- Positive ANA, anti-dsDNA, anti-Sm or low complement
High-yield answer: Widespread DLE, systemic symptoms and abnormal immunological/renal tests should raise concern for SLE.
Treatment questions
17. What are the general measures?
- Explain that scarring alopecia is permanent once follicles are destroyed, so early treatment is needed to stop extension.
- Strict photoprotection: broad-spectrum sunscreen, hat, protective clothing and avoidance of intense sun.
- Stop smoking, since smoking worsens cutaneous lupus and reduces response to antimalarials.
- Avoid trauma to lesions and review drugs that can trigger lupus-like eruptions.
18. How will you treat localized scalp DLE?
For limited active disease:
- Potent or very potent topical corticosteroid in a suitable scalp vehicle, such as lotion, solution, foam or gel
- Intralesional triamcinolone for a few localized thick active plaques, administered by a trained dermatologist
- Topical calcineurin inhibitor can be considered in appropriate sites, especially where steroid adverse effects are a concern
19. How will you treat extensive, recurrent or resistant disease?
Hydroxychloroquine is the usual first-line systemic antimalarial, together with photoprotection and topical/intralesional treatment for active lesions.
If it remains resistant, a dermatologist may consider alternatives such as methotrexate, mycophenolate mofetil, retinoids, dapsone, thalidomide/lenalidomide in selected patients, or other immunomodulatory treatment depending on disease severity and contraindications.
20. What is the usual hydroxychloroquine dose?
A safe exam answer is:
“Hydroxychloroquine is generally dosed according to actual body weight, not exceeding 5 mg/kg/day.”
The exact prescribed dose must be individualized by the treating clinician.
21. What counselling and monitoring are needed for hydroxychloroquine?
- Baseline ophthalmic assessment
- Retinal screening according to local ophthalmology guidelines, generally annual screening after 5 years in low-risk patients and earlier in high-risk patients
- Calculate dose by actual body weight
- Assess renal impairment and concomitant tamoxifen use, because these increase retinal-toxicity risk
- Counsel about gastrointestinal upset, skin pigmentation and rare retinal toxicity
22. Can the alopecia be reversed after treatment?
Only non-scarred follicles may regrow hair. In established cicatricial areas, treatment prevents further destruction but does not reliably restore hair. Hair transplantation may be considered only after prolonged inactive disease, under specialist care.
Harder examiner questions
23. What is the pathogenesis of DLE?
DLE is an autoimmune, photosensitive interface dermatitis. Ultraviolet radiation causes keratinocyte injury and exposes/release nuclear antigens. In genetically susceptible individuals, dysregulated innate and adaptive immune responses, particularly type I interferon pathways and autoreactive T and B cells, cause chronic inflammation at the dermoepidermal junction and around hair follicles. Persistent inflammation ultimately destroys follicles and produces scarring.
24. Why does DLE cause permanent hair loss while alopecia areata usually does not?
- DLE: destroys the follicular epithelium and follicular stem-cell region, followed by fibrosis. It is a scarring alopecia.
- Alopecia areata: attacks the hair bulb but generally preserves the follicular stem-cell niche and follicular openings. It is a non-scarring alopecia and can regrow.
25. What trichoscopic features are seen in scalp DLE?
- Loss of follicular openings
- Follicular keratotic plugs
- Speckled pigmentation
- White structureless scarred areas
- Telangiectatic/arborizing vessels
- Perifollicular scale
- Hair shaft variability and broken hairs may be seen in active lesions
26. Why should a biopsy be taken from the active margin rather than the centre?
The active edge shows interface change, inflammation and follicular involvement, allowing diagnosis. The old centre is often only scar tissue with destroyed follicles, and it may not distinguish DLE from other end-stage cicatricial alopecias.
27. What are the important complications of long-standing DLE?
- Permanent scarring alopecia
- Cosmetic disfigurement and dyspigmentation
- Psychosocial morbidity
- Secondary infection of excoriated/crusted lesions
- Rarely, squamous cell carcinoma developing in chronic scarred DLE lesions
28. Can DLE occur with a negative ANA?
Yes. ANA is often negative in skin-limited DLE. ANA is more useful in screening for systemic involvement than in confirming isolated cutaneous DLE.
29. How is SLE classified in a patient with DLE?
DLE itself is not sufficient to diagnose SLE. Under the 2019 EULAR/ACR classification system, a positive ANA is the entry criterion, followed by weighted clinical and immunologic criteria. A score of 10 or more, with at least one clinical criterion and no more likely explanation, classifies SLE. This is a classification framework, not a substitute for clinical diagnosis.
30. What is the difference between acute, subacute and chronic cutaneous lupus?
| Type | Typical lesions | Scarring |
|---|---|---|
| Acute cutaneous lupus | Malar rash or generalized photosensitive erythema, often associated with active SLE | Usually no scarring |
| Subacute cutaneous lupus | Annular-polycyclic or papulosquamous lesions on photo-exposed trunk/arms, often anti-Ro positive | Usually no scarring |
| Chronic cutaneous lupus/DLE | Discoid plaques with adherent scale, follicular plugging, atrophy and dyspigmentation | Common, especially on scalp |
31. What is the single most important point in managing this patient?
“Recognize and treat active inflammation early to prevent progression of irreversible cicatricial alopecia, while evaluating for systemic lupus involvement.”
Rapid-fire questions
- Is DLE contagious? No.
- Is it infective? No, it is autoimmune.
- Is photosensitivity common? Yes.
- Can it cause permanent alopecia? Yes, due to follicular destruction and scarring.
- Does DLE always progress to SLE? No.
- What is the bedside sign of follicular plugging? Carpet-tack sign.
- Most useful diagnostic test? Biopsy of active lesion margin.
- First systemic drug for extensive disease? Hydroxychloroquine.
- Most important non-drug measure? Photoprotection and smoking cessation.
- What should never be promised to the patient? Hair regrowth in a completely scarred area.
Recent literature continues to examine rates and predictors of progression from DLE to SLE, so quote local teaching or your department’s standard figure rather than giving an absolute percentage in the exam. A 2025 systematic review addresses this progression question.
Clinical and dermoscopic signs of activity in a dle plaque
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Clinical signs of activity in a DLE plaque
Look especially at the advancing margin. Active disease is suggested by:
- Erythema or violaceous discoloration
- Oedema/infiltration with a raised, indurated plaque
- Adherent scale
- Follicular hyperkeratosis or plugging
- New or enlarging area of alopecia
- Crusting or erosions, if markedly inflamed or excoriated
- Symptoms of itch, burning or tenderness
Exam answer:
“An active DLE plaque has erythema, infiltration, adherent scale and follicular plugging, usually at the periphery. In contrast, inactive disease shows central atrophy, dyspigmentation, fibrosis and established scarring alopecia.”
“An active DLE plaque has erythema, infiltration, adherent scale and follicular plugging, usually at the periphery. In contrast, inactive disease shows central atrophy, dyspigmentation, fibrosis and established scarring alopecia.”
The classic teaching description is active erythema, oedema, scaling and follicular plugging, with later atrophy, telangiectasia and dyspigmentation. Goldman-Cecil Medicine, section “Discoid Lupus Erythematosus,” lines 1467-1469.
Dermoscopic/trichoscopic signs of activity
- Large yellow dots: represent prominent follicular keratotic plugging
- Follicular red dots: a helpful activity sign and associated with better potential for hair regrowth
- Thick arborizing telangiectatic vessels
- Perifollicular white halo
- Perifollicular scale
- Speckled brown pigmentation and blue-gray dots, due to pigment incontinence
- White/pink structureless areas may represent early fibrosis, so correlate with the clinical appearance and follicular openings
A practical trichoscopic answer:
“Active scalp DLE shows large follicular yellow dots due to plugging, follicular red dots, thick arborizing vessels, perifollicular white halo and perifollicular scaling, often with blue-gray dots and speckled pigmentation.”
Signs of inactive or burnt-out disease
- Smooth, atrophic, ivory-white or hypopigmented scar
- Loss of follicular ostia
- No erythema or adherent scale
- No expanding edge or symptoms
- Predominant fibrosis and fixed scarring alopecia
Important distinction: Thick arborizing vessels and large yellow dots can persist in late disease, so activity is best judged by the combination of clinical erythema/scale plus trichoscopic inflammatory signs, not a single feature alone.
These active and late-stage trichoscopic findings are summarized in DermNet’s trichoscopy reference.
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