Psoriasis for NEET PG: Auspitz, Koebner and Woronoff Signs, Plus the Treatment Ladder

Psoriasis is a chronic, immune-mediated skin disease. It produces well-defined red plaques with silvery scale, and its signs map neatly onto its histology. If you can explain why a scraped plaque bleeds, why a scratch grows a new lesion and why a pale ring appears as a plaque heals, you already understand most of the disease.

This guide covers the three named signs, the clinical types, the histology behind them, how severity is graded, and the treatment ladder from emollients to biologics.

Key Takeaways

• Auspitz sign: scraping the scale gives pinpoint bleeding, because dilated dermal capillaries sit just under a thinned epidermis over the papillae.

• Koebner phenomenon: new lesions appear at sites of skin injury, and the new lesions look the same clinically and histologically as the disease.

• Woronoff ring: a pale halo around a plaque that is regressing with treatment, so it points to response and not to a new problem.

• Types: plaque psoriasis is by far the commonest form; guttate, inverse, erythrodermic and pustular forms need to be told apart by pattern.

• Severity: mild disease means BSA, PASI and DLQI all at 10 or below; moderate-to-severe means BSA or PASI above 10 with DLQI above 10.

• Ladder: topicals, then phototherapy, then conventional systemics (methotrexate, ciclosporin, acitretin), then biologics and targeted agents.

What is psoriasis?

Psoriasis is a chronic inflammatory skin disease in which keratinocytes turn over too quickly and the skin thickens and scales. Plaque psoriasis is the most common pattern in every racial group, according to DermNet. A narrative review in PMC puts plaque disease at roughly 80 to 90 percent of cases.

The disease is not only cutaneous. Joint involvement (psoriatic arthritis) is estimated to affect anywhere from under 10 percent to about 40 percent of patients, and about one in five of those with joint disease present with the joints first, as summarised in the same review. The wide range is itself a fact worth remembering: no single prevalence figure is reliable.

Diagnosis is mainly clinical. A biopsy is kept for atypical presentations, which is why the bedside signs below matter.

Signs of plaque psoriasis: Auspitz, Koebner and Woronoff

Three signs are worth learning as a set, because each one reflects a different layer of the pathology. The table gives the pattern, then the sections below add the detail.

Auspitz sign

The Auspitz sign is pinpoint bleeding when the dry scale of a plaque is scraped off. DermNet and the PMC review both attribute it to dilated, twisting capillaries in the papillary dermis lying beneath a thin epidermis.

Think of it as the clinical twin of the histology: the epidermis over each dermal papilla is thin, so removing the scale tears open the capillary beneath. The sign is not unique to psoriasis; it has also been described in actinic keratosis and Darier disease, according to an Actas Dermo-Sifiliograficas article. The same article questions whether Auspitz himself described it, which is trivia, not something to build an answer on.

A related bedside observation is the "candle-grease" quality of the scale, where the silvery scale scrapes off like wax. This is a textbook description, so treat it as a qualitative pattern and pair it with the Auspitz sign when you work through a stem.

Koebner phenomenon

The Koebner phenomenon, also called the isomorphic response, is the appearance of new lesions at sites of skin injury. DermNet lists cuts, abrasions and sunburn as typical triggers. "Isomorphic" means that the new lesions are identical to the disease, both clinically and under the microscope, as the StatPearls entry describes it.

The sign is not fixed in a patient. Someone can be Koebner-negative for years and become positive later. The phenomenon is also not unique to psoriasis; vitiligo, lichen planus and warts are the other diseases usually grouped with it in textbooks, which makes it useful for comparison rather than for diagnosis.

A practical point: if a stem describes linear plaques along a scratch or surgical scar in a known psoriatic, name the phenomenon first and the disease second.

Woronoff ring

The Woronoff ring is a pale, blanched halo of fairly constant width around a psoriatic plaque that is regressing, usually after phototherapy or topical treatment. The evidence base is thinner here: descriptions come from a paper on the Woronoff ring in PMC, a reference summary of Woronoff's ring and a case report of the ring after adalimumab, which suggests it may reflect treatment response.

The PMC paper describes a hypopigmented ring around regressing lesions. Its cause was long unexplained, and older explanations involved prostaglandins. For revision, remember one idea: a Woronoff ring means the plaque is healing, not spreading.

Types of psoriasis: plaque psoriasis and its variants

Plaque psoriasis dominates, but the minor types carry the distinct clues and the different management. The percentages below come from the PMC overview; clinical features come from DermNet.

Other patterns include scalp, sebopsoriasis and palmoplantar disease. DermNet also separates small plaque disease (plaques under 3 cm) from chronic plaque disease (over 3 cm).

Nail changes are worth a separate line. Pitting is the most common finding and comes from the nail matrix, while the oil-drop (salmon) patch arises from the nail bed. Onycholysis, yellowing and ridging also occur, and nail disease is associated with inflammatory arthritis, as per DermNet.

Histology of plaque psoriasis and how it explains the signs

Each histological finding has a clinical counterpart, and learning them as pairs removes the need to memorise two separate lists. The correlations below draw on the PMC overview and histopathology reviews of psoriasiform dermatoses.

Uninvolved skin looks normal under the microscope. Spongiform pustules are not exclusive to psoriasis; they also appear in acute generalised exanthematous pustulosis, as noted in the StatPearls chapter on generalised pustular psoriasis.

Triggers and drugs that worsen psoriasis

Knowing the triggers helps you both explain a flare and avoid causing one. DermNet lists streptococcal tonsillitis and other infections (including HIV), skin injury, sunburn, dry skin, obesity, smoking, heavy alcohol use, stress and stopping oral or strong topical steroids. Sunlight usually helps; only a minority worsen with sun.

Several drug groups are listed as triggers or aggravators: lithium, antimalarials, NSAIDs, ACE inhibitors and angiotensin receptor blockers, terbinafine and immunotherapy. Beta-blockers are commonly listed too, but the evidence is not uniform, and one case-control study summarised in the PMC overview did not find a link.

DermNet's page on drug-induced psoriasis draws a useful distinction:

• Drug-induced: appears in people without a prior history and clears when the drug is stopped.
• Drug-aggravated: persists in people with a personal or family history.

The first step is to stop the offending drug when possible, though this is not always feasible (lithium is the usual example). Topical steroids have also been reported to trigger a pustular episode.

Grading severity: PASI, BSA and DLQI

Severity guides the treatment step, and the EuroGuiDerm S3 guideline sets explicit thresholds. PASI was introduced in 1978, ranges from 0 to 72, and combines body surface area with erythema, induration and scaling. DLQI measures quality of life.

A mild case is upgraded when it involves visible areas, scalp, genitals, palms or soles, when two or more fingernails show onycholysis or onychodystrophy, when itch leads to scratching, or when plaques resist treatment. So a patient with a small BSA can still be treated as moderate-to-severe.

Treatment goals in the same guideline: PASI 75 at the end of induction at minimum, with PASI 90, an absolute PASI below 2, or DLQI of 1 or less as the desired target. Response is checked at 10 to 12 weeks for fast-acting drugs and 16 to 24 weeks for slower ones.

Treatment ladder for psoriasis

The ladder runs from topicals through phototherapy and conventional systemics to biologics. Move up when the current step fails, when severity or site demands it, or when contraindications close a door. The sources used are DermNet's treatment page, the Latin America guideline and the EuroGuiDerm guideline.

Step 1: topical therapy

Emollients help every patient. Keratolytics such as urea (5 to 40 percent) and salicylic acid (0.5 to 10 percent) lift scale. Topical steroids work, but potency must match the site: weak ones for the face, flexures and genitals, potent ones for palms and soles. Tachyphylaxis limits long-term use, and potent steroids on flexures cause atrophy.

Vitamin D analogues (calcipotriol, calcitriol, tacalcitol) are used up to a limit of 100 g per week, and calcipotriol with betamethasone is often a first choice for plaque disease.

Other options are coal tar, short-contact dithranol, calcineurin inhibitors (off-label, useful on thin skin), tazarotene, roflumilast 0.3 percent and tapinarof 1 percent.

For genital and flexural disease the Latin America guideline treats topical therapy as first line, with local irritation as the limit.

Step 2: phototherapy

Narrowband UVB suits thin plaque and guttate disease, with sessions two to three times a week over roughly 20 to 30 treatments. It is considered safe in pregnancy with folic acid. PUVA is reserved for thick plaques and hand and foot disease; it carries a higher skin cancer risk, so lifetime treatments are capped, and it is avoided in pregnancy and breastfeeding.

The Latin America guideline found no meaningful PASI 75 difference between NB-UVB and PUVA, and noted useful combinations: methotrexate with NB-UVB, and acitretin with PUVA. Access is the practical limit in remote areas.

Step 3: methotrexate, ciclosporin and acitretin

These three share a theme: each has a dose range, a monitoring routine and a pregnancy rule. The table collects them. Always read doses as guideline ranges, since different guidelines start at different points.

Methotrexate is a weekly drug. Daily dosing instead of weekly is a recognised and dangerous error, and subcutaneous injection is preferred above 15 mg or to avoid overdose, as per the EuroGuiDerm guideline. Patients with respiratory symptoms should be checked for alveolitis. Prolonged use can damage the liver, so watch liver enzymes.

Ciclosporin acts fast, which makes it useful for acute flares and severe disease. Its duration is deliberately limited because of nephrotoxicity. Acitretin is especially useful in palmoplantar disease, and both acitretin and ciclosporin are avoided as first-line choices in patients with dyslipidaemia, per the second EuroGuiDerm part.

Acitretin carries a long contraception window, so attach the number three years to the drug in your notes. Its other adverse effects (liver injury, raised triglycerides, dry mucosa and skin) are standard textbook content.

Apremilast, a PDE-4 inhibitor, is another oral option, and it carries nausea, diarrhoea and reports of suicidal behaviour. Fumaric acid esters, hydroxyurea, mycophenolate and sulfasalazine are less central.

Step 4: biologics and targeted therapy

Biologics are for moderate-to-severe disease after topical or systemic failure. The classes are best learned by target.

In the EuroGuiDerm network meta-analysis, infliximab, IL-17 inhibitors and IL-23 inhibitors (except tildrakizumab) were more likely to reach PASI 90 than ustekinumab, the three older anti-TNF agents and deucravacitinib. Etanercept was inferior to adalimumab, tildrakizumab and ustekinumab.

The French systemic guideline proposes methotrexate, adalimumab or ustekinumab as first systemic choices when there are no symptomatic comorbidities.

For very extensive disease (BSA above 50 percent) or a heavy disease burden, it suggests considering an IL-17 or IL-23 inhibitor, or infliximab.

Deucravacitinib is used after contraindication, intolerance or failure of a biologic.

Screen for tuberculosis before starting any biologic. Reactivation risk is very low with IL-17 and IL-23 inhibitors, so those are suggested when latent TB cannot be treated.

Special forms of psoriasis and special situations

Some patterns change the drug choice, as set out in the French and Latin America guidelines:

• Generalised pustular flare: spesolimab, an IL-36 receptor antibody; maintenance is spesolimab, a TNF inhibitor or an IL-17 inhibitor.
• Erythrodermic psoriasis: IL-17 inhibitor, IL-23 inhibitor or infliximab first line.
• Palmoplantar pustular disease: IL-17 inhibitor, IL-23 inhibitor or ciclosporin.
• Psoriasis with inflammatory bowel disease: TNF inhibitors, IL-12/23 or IL-23 inhibitors; IL-17 inhibitors are avoided.
• Recent or active cancer: NB-UVB, acitretin or methotrexate first line.
• Nail psoriasis: adalimumab, etanercept, guselkumab, infliximab, ixekizumab, risankizumab, secukinumab or ustekinumab, with a modified NAPSI below 10 as the target.

How to study psoriasis efficiently

Build one page that links sign, histology and drug. Draw the epidermis from memory with elongated rete ridges, thin suprapapillary plates and Munro microabscesses, then write the matching sign next to each feature. If a stem gives you pinpoint bleeding, think of the thin plate over the capillary; if it gives you a pale halo, think of regression.

For drugs, learn the classes by target and the three conventional systemics by their rule: methotrexate weekly with folic acid, ciclosporin short and watched for kidney and pressure, acitretin never in pregnancy.

Memory aid (a study device written for this guide, not a published mnemonic): "Methotrexate is weekly, folic acid follows the next day; acitretin never in pregnancy." It compresses three rules from the table above into one line.

Then test yourself on the dermatology questions in the papulosquamous disorders practice set and compare the pattern with pityriasis rosea, another scaly eruption you will need to separate from psoriasis.

For wider revision of the subject, the dermatology topic overview places psoriasis among the other conditions in the specialty.

Psoriasis revision summary

Psoriasis rewards structure. The Auspitz sign, the Koebner phenomenon and the Woronoff ring each reflect a different part of the disease, from capillaries to injury response to healing. Treatment then follows severity: topicals, phototherapy, a conventional systemic with careful monitoring, and biologics chosen by target and by special site.

Learn the Woronoff ring, the candle-grease scale and the acitretin adverse effects as descriptive patterns, and spend most of your revision time on the severity thresholds, the methotrexate dose limits and the pregnancy rules.