Papulosquamous Disorders
Papulosquamous simply means raised and scaly. That sounds like a description rather than a diagnosis, and it is, but it is a useful one because the character of the scale reflects what the epidermis is doing.
Scale is dead stratum corneum that has not been shed properly, and there are only two ways to produce it in quantity.
The epidermis can turn over too fast, so cells reach the surface before they have matured and are shed in visible clumps. That is psoriasis, and it gives thick, silvery, loosely adherent scale on a well-defined red plaque.
Or the granular layer can thicken while the basal layer is being attacked, producing a compacted surface. That is lichen planus, and it gives a violaceous flat-topped papule with a fine white lacy network on the surface.
Once you can separate those two, the rest of the group is defined largely by what it is not, and by distribution.
1. Psoriasis
Psoriasis is an immune-mediated disease in which T cells drive keratinocyte hyperproliferation. Epidermal transit time falls from around 28 days to about four, which is why the scale is so abundant.
The lesion is a well-demarcated erythematous plaque with silvery scale, typically on extensor surfaces, scalp, and the sacrum, which is the opposite distribution to eczema.
The three classical signs
Candle grease sign: scratching the scale produces a white powdery appearance, as with scraped candle wax.
Auspitz sign: removing the scale reveals pinpoint bleeding, because the dermal papillae are elongated and their capillaries lie close to a thinned suprapapillary epidermis.
Koebner phenomenon: lesions appear at sites of trauma, which is shared with lichen planus and vitiligo.
Histology matches the signs exactly: parakeratosis, absent granular layer, acanthosis with regular elongation of rete ridges, dilated papillary capillaries, and Munro microabscesses of neutrophils in the stratum corneum.
Patterns and triggers
| Pattern | Features |
|---|---|
| Chronic plaque | Commonest; extensors, scalp, sacrum |
| Guttate | Small drop-like lesions, often after streptococcal throat infection, in young people |
| Pustular | Sterile pustules; generalised form is a medical emergency |
| Erythrodermic | Over 90 per cent body surface; thermoregulatory and fluid failure |
| Inverse | Flexural, moist, often lacking scale |
Nail changes include pitting, onycholysis, subungual hyperkeratosis and the oil-drop sign, and nail involvement correlates strongly with psoriatic arthritis, which makes examining the nails a way of estimating joint risk rather than a cosmetic observation.
Drugs that provoke or worsen psoriasis are worth knowing as a group: lithium, beta blockers, antimalarials, and, importantly, systemic corticosteroid withdrawal, which can precipitate generalised pustular psoriasis. This is the reason systemic steroids are avoided in psoriasis.
Psoriasis is more than skin
Psoriasis is now understood as a systemic inflammatory disease, and the associations are examinable and clinically consequential: psoriatic arthritis, metabolic syndrome, obesity, non-alcoholic fatty liver disease, cardiovascular disease and depression.
Guidelines now direct active assessment for these comorbidities rather than treating the skin alone.
Treatment
Topical treatment for limited disease uses vitamin D analogues such as calcipotriol, topical corticosteroids, and coal tar or dithranol.
Phototherapy with narrowband ultraviolet B is used for extensive disease, and it remains widely used in India because it is inexpensive and effective, though it requires repeated hospital attendance.
Calcipotriol and topical steroid are often combined, since the vitamin D analogue normalises keratinocyte differentiation while the steroid suppresses inflammation, and the combination reduces the irritation that calcipotriol alone can cause.
Systemic therapy uses methotrexate, ciclosporin and acitretin, and acitretin is absolutely contraindicated in women of childbearing potential because of teratogenicity that persists for years after stopping.
Biologics have transformed severe disease. Agents targeting tumour necrosis factor alpha, interleukin-17 and interleukin-23 achieve much higher rates of near-complete clearance than conventional systemic agents. Data also suggest interleukin-23 inhibitors may be associated with lower rates of subsequent dyslipidaemia, hypertension, diabetes and major adverse cardiovascular events than other biologic classes, which fits the systemic inflammation model.
2. Lichen Planus
Lichen planus is a T cell-mediated attack on basal keratinocytes, and everything about it follows from damage at that specific level.
The six Ps describe it: purple, polygonal, planar, pruritic, papules and plaques.
Wickham striae are the fine white lacy lines on the surface, produced by focal thickening of the granular layer.
Distribution favours flexor wrists, forearms, ankles and the lower back, which is again the opposite of psoriasis. Koebner phenomenon occurs.
Histology shows hyperkeratosis without parakeratosis, wedge-shaped hypergranulosis, irregular acanthosis giving a saw-tooth rete pattern, and a dense band-like lymphocytic infiltrate at the dermo-epidermal junction with basal cell degeneration.
Because the basal layer contains melanocytes, its destruction releases pigment into the dermis, which is why lichen planus heals with prominent post-inflammatory hyperpigmentation, particularly in Indian skin.
Sites and associations
Oral lichen planus produces a lacy white network on the buccal mucosa and, in its erosive form, painful ulcers with a small but real risk of squamous carcinoma requiring long-term follow-up.
Nail disease can cause longitudinal ridging and, in severe cases, pterygium formation with permanent nail loss. Scalp disease is lichen planopilaris and causes scarring alopecia, which is irreversible.
The association with hepatitis C is well described, and testing is reasonable in patients with extensive, oral or atypical disease.
Lichenoid drug eruption mimics lichen planus and should be considered where the eruption is widespread and photodistributed, with antihypertensives, antimalarials and antituberculous drugs among the culprits.
3. Pityriasis Rosea
A self-limiting eruption, probably related to human herpesvirus 6 and 7 reactivation.
It begins with a single herald patch, an oval scaly plaque, followed one to two weeks later by a shower of smaller oval lesions on the trunk.
The lesions align along skin cleavage lines, producing the Christmas tree pattern on the back, and each has a collarette of scale attached at the periphery pointing inward.
It resolves spontaneously over six to eight weeks and needs only reassurance and emollients, and telling the patient the expected duration at the first visit prevents a series of anxious return visits.
The essential exclusion is secondary syphilis, which can look almost identical but characteristically involves the palms and soles, lacks a herald patch, and is accompanied by generalised lymphadenopathy. Serology settles it, and missing it has consequences.
4. Seborrhoeic Dermatitis and Pityriasis Rubra Pilaris
Seborrhoeic dermatitis produces greasy yellowish scale on the scalp, eyebrows, nasolabial folds and presternal area, related to Malassezia and treated with antifungal shampoos and mild topical steroid.
Two clinical signals matter. Severe, extensive or abruptly worsening seborrhoeic dermatitis in an adult should prompt consideration of HIV infection. And it is common and often severe in Parkinson disease.
Pityriasis rubra pilaris is worth recognising because of one sign. It produces orange-red scaly plaques with follicular keratotic papules and, characteristically, islands of completely normal skin within otherwise confluent erythema. Those spared islands are the diagnostic clue, and psoriasis does not produce them.
5. Pityriasis Lichenoides and the Parapsoriasis Group
Two further groups appear in differential lists and are separated by tempo and by risk.
Pityriasis lichenoides exists on a spectrum. The acute form produces crops of papules that necrose and crust, resolving with varioliform scars, while the chronic form gives scaly papules that resolve with post-inflammatory change. Both wax and wane over months, and lesions of different ages coexist, which is the useful clue.
Large plaque parapsoriasis matters because it is the condition that can evolve into mycosis fungoides, the commonest cutaneous T cell lymphoma. It produces broad, poorly defined, slightly scaly patches, characteristically on sun-protected sites such as the buttocks and inner thighs, sometimes with fine wrinkling and atrophy.
Small plaque parapsoriasis, by contrast, produces narrow finger-like patches on the trunk and behaves benignly.
The practical rule is that a persistent scaly patch on covered skin in an adult that fails repeated treatment deserves a biopsy, and often more than one over time, since early mycosis fungoides is histologically subtle and can masquerade as eczema or psoriasis for years.
6. Eczema, the Other Scaly Disease
Eczema is the main differential for everything in this chapter, and one histological word separates it: spongiosis, meaning intercellular oedema within the epidermis.
That oedema explains the clinical picture. Fluid between keratinocytes produces vesicles when acute, weeping and crusting when they rupture, and lichenification with thickened skin markings when the process becomes chronic from scratching.
The border is the practical discriminator. Psoriasis is sharply demarcated; eczema fades into surrounding skin. Psoriatic scale is silvery and loose; eczematous scale is finer and often accompanied by excoriation.
Atopic dermatitis
Atopic dermatitis is a barrier disease as much as an immune one. Filaggrin loss-of-function impairs the stratum corneum, allowing water loss and allergen entry, which drives type 2 inflammation, which further degrades the barrier.
Distribution changes predictably with age, which is a reliable examination point.
| Age | Distribution |
|---|---|
| Infant | Face, scalp, extensor surfaces; napkin area spared |
| Child | Flexures: antecubital and popliteal fossae, wrists, ankles |
| Adult | Flexures, hands, eyelids, with lichenification |
The sparing of the napkin area in infants is explained by the moisture and occlusion of a nappy, which protects rather than irritates in this condition.
Eczema herpeticum is the emergency: monomorphic punched-out erosions in a patient with atopic dermatitis who deteriorates rapidly, caused by disseminated herpes simplex across a defective barrier. It requires urgent systemic aciclovir.
Contact dermatitis
Irritant contact dermatitis is direct chemical damage, requires no prior sensitisation, occurs in anyone given enough exposure, and is commonest on the hands of people who wash frequently.
Allergic contact dermatitis is a type IV delayed hypersensitivity, requires prior sensitisation, affects only sensitised individuals, and can appear at sites distant from the contact. Patch testing identifies the allergen; prick testing does not, since the mechanism is cell-mediated rather than IgE-mediated.
Common Indian allergens include nickel in jewellery, parthenium weed causing an airborne pattern on exposed skin, hair dye containing paraphenylenediamine, and footwear rubber chemicals.
Using topical corticosteroids properly
Two principles prevent most of the harm and most of the failure.
Potency is matched to site, not to severity alone. The face, flexures and genitalia absorb far more drug than the palms and soles, so mild preparations are used there while very potent ones may be needed on thick skin. Long-term potent steroid on the face produces atrophy, telangiectasia and perioral dermatitis.
Quantity is prescribed, not left to guesswork. The fingertip unit, the amount from the distal crease to the tip of an adult index finger, covers roughly two adult palm areas. Under-prescribing is the commonest reason topical treatment appears to fail, because patients apply far less than the amount studied in trials.
7. When Papulosquamous Disease Becomes Dangerous
Erythroderma is inflammation involving more than about 90 per cent of the body surface, and it is a dermatological emergency regardless of cause.
The skin's failure is physiological rather than cosmetic. Massive cutaneous vasodilatation causes high-output cardiac failure and hypothermia from heat loss. Scaling causes protein and fluid loss. The barrier is lost, so infection follows.
Causes are worth grouping: psoriasis, eczema, drug reaction, cutaneous T cell lymphoma and pityriasis rubra pilaris.
In an older patient with erythroderma of unclear cause, cutaneous T cell lymphoma must be excluded, and repeated biopsies over time are often required because early histology is non-specific.
Management is supportive first: warmth, fluid and protein replacement, emollients, and treating infection, with cause-specific treatment following.
8. Worked Examples
Example 1. A 24-year-old develops a shower of small scaly papules over the trunk two weeks after a sore throat. Both parents have psoriasis. What is the diagnosis and what should be done?
Guttate psoriasis, precipitated by streptococcal pharyngitis. The drop-like lesions appearing over days in a young person after a throat infection, on a background of family history, is the classic presentation.
Confirm the streptococcal trigger with a throat swab and antistreptolysin O titre, and treat any active infection. The eruption often resolves over weeks to months, and phototherapy with narrowband ultraviolet B is useful for extensive disease. A substantial proportion of patients later develop chronic plaque psoriasis, which is worth mentioning honestly. Systemic corticosteroid should be avoided, since withdrawal can precipitate generalised pustular psoriasis.
Example 2. A 45-year-old has itchy violaceous flat-topped papules on the flexor wrists with fine white lines on their surface, and a lacy white pattern on the buccal mucosa. What is the diagnosis, and what two things would you check?
Lichen planus, with the six Ps and Wickham striae, and characteristic oral involvement.
First, check hepatitis C serology. The association with hepatitis C is well described and is reasonable to test for in patients with oral or extensive disease.
Second, check the drug history. A lichenoid drug eruption can be clinically indistinguishable, and antihypertensives, antimalarials and antituberculous drugs are among the recognised culprits, so identifying one avoids treating a drug reaction with immunosuppression. Erosive oral disease additionally requires long-term follow-up because of a small risk of squamous carcinoma.
Example 3. A patient with extensive plaque psoriasis is given oral prednisolone by a general practitioner, with rapid improvement. Two weeks after finishing the course he develops widespread sterile pustules, fever and malaise. Explain.
Generalised pustular psoriasis precipitated by systemic corticosteroid withdrawal. Systemic steroid suppresses psoriasis dramatically, which is exactly why it is tempting, but withdrawal produces a rebound that can convert stable plaque disease into a life-threatening pustular form.
Generalised pustular psoriasis is a medical emergency with fever, systemic upset, hypoalbuminaemia and a risk of sepsis and cardiovascular collapse, and it requires admission. This is the reason systemic corticosteroids are avoided in psoriasis, and it is one of the most reliably examined pieces of prescribing knowledge in dermatology.
Example 4. A 68-year-old man has had generalised red scaly skin for four months with itch, having failed treatment for presumed eczema. What is the diagnosis category, what is the immediate concern, and what must be excluded?
Erythroderma, defined as inflammation of more than about 90 per cent of the body surface, and it is a dermatological emergency in its own right.
The immediate concerns are physiological. Massive cutaneous vasodilatation produces high-output cardiac failure and heat loss with hypothermia, scaling causes protein and fluid loss, and barrier failure invites infection. Management therefore begins with warmth, fluid and protein replacement, emollients and treatment of infection before any cause-specific therapy.
What must be excluded is cutaneous T cell lymphoma, particularly in an older patient with erythroderma of unclear cause that has not responded to treatment for a presumed benign cause. Early histology is frequently non-specific, so repeated biopsies over time, with immunophenotyping and T cell receptor gene rearrangement studies, are often required.
Example 5. Explain why psoriasis produces pinpoint bleeding when the scale is removed, while lichen planus does not.
Because the two diseases damage different parts of the epidermis and remodel the dermal papillae differently.
In psoriasis, keratinocyte turnover accelerates so that transit time falls from around 28 days to about four. The rete ridges elongate regularly, the dermal papillae become tall and their capillaries dilated and tortuous, and the epidermis directly above those papillae becomes thinned. Removing the adherent scale therefore strips a very thin layer over dilated superficial capillaries, which bleed at discrete points corresponding to each papilla. That is the Auspitz sign.
In lichen planus the attack is on basal keratinocytes, and the surface response is hyperkeratosis with wedge-shaped hypergranulosis rather than parakeratosis. There is no suprapapillary thinning and no papillary capillary dilatation, so the scale is compact and adherent and its removal does not expose vessels. The visible surface change instead is Wickham striae, which are the thickened granular layer seen through the surface.
Summary
Scale reflects epidermal behaviour: fast turnover gives silvery psoriatic scale, basal attack gives lichen planus with Wickham striae.
Psoriasis affects extensors, scalp and sacrum; lichen planus affects flexor wrists and ankles.
Auspitz sign occurs because suprapapillary epidermis is thin over dilated papillary capillaries.
Psoriasis histology: parakeratosis, absent granular layer, regular acanthosis, Munro microabscesses.
Lichen planus histology: hypergranulosis, saw-tooth rete, band-like junctional infiltrate.
Basal layer destruction releases melanin, so lichen planus leaves marked hyperpigmentation.
Guttate psoriasis follows streptococcal throat infection in young people.
Lithium, beta blockers and antimalarials worsen psoriasis.
Systemic corticosteroid withdrawal can precipitate generalised pustular psoriasis.
Psoriasis is a systemic inflammatory disease with metabolic and cardiovascular associations.
Acitretin is absolutely contraindicated in women of childbearing potential.
Biologics targeting TNF-alpha, IL-17 and IL-23 achieve far higher clearance rates.
Oral erosive lichen planus carries a small risk of squamous carcinoma.
Lichen planopilaris causes irreversible scarring alopecia; nail disease can cause pterygium.
Lichen planus is associated with hepatitis C, and lichenoid drug eruption mimics it.
Pityriasis rosea has a herald patch and a Christmas tree pattern with an inward-facing collarette.
Secondary syphilis mimics pityriasis rosea but involves palms and soles and lacks a herald patch.
Severe adult seborrhoeic dermatitis should prompt consideration of HIV.
Islands of sparing within erythema indicate pityriasis rubra pilaris.
Erythroderma causes high-output failure, hypothermia, protein loss and infection, and in the elderly requires exclusion of cutaneous T cell lymphoma.
