5.1 Psoriasis: Variants, Psoriatic Arthritis, Comorbidity & European Management
Key Takeaways
- Psoriasis affected about 3.9% of adults in the 27-country EADV Burden of Skin Diseases survey, and roughly 20% to 30% of patients develop psoriatic arthritis.
- European consensus defines moderate-to-severe psoriasis by the "rule of tens": PASI above 10, body surface area above 10%, or DLQI above 10, with special sites able to upgrade severity.
- The CASPAR criteria diagnose psoriatic arthritis with inflammatory joint, spine, or entheseal disease plus at least 3 points from psoriasis, nail dystrophy, negative rheumatoid factor, dactylitis, and juxta-articular new bone.
- IL-17 inhibitors should be avoided in patients with inflammatory bowel disease; TNF-alpha monoclonal antibodies, ustekinumab, or IL-23 inhibitors are preferred when Crohn disease coexists.
- Generalised pustular psoriasis is linked to IL36RN mutations, and the anti-IL-36 receptor antibody spesolimab is approved in the EU for treating GPP flares.
5.1 Psoriasis: Variants, Psoriatic Arthritis, Comorbidity & European Management
Psoriasis is one of the most common chronic diseases seen by dermatologists and a core General Dermatology topic. Questions usually test four things: recognising the clinical variant, scoring severity, spotting psoriatic arthritis, and choosing a systemic drug that suits the patient's comorbidities.
Pathogenesis and Triggers
- Genetics: the strongest susceptibility locus is PSORS1, containing HLA-C*06:02, which is linked to early-onset (type I) and guttate disease.
- Immunology: dendritic cells release IL-23, which maintains Th17 cells. These produce IL-17A, IL-17F, and IL-22, which drive keratinocyte proliferation and neutrophil recruitment. TNF-alpha amplifies the loop. This is why IL-17 and IL-23 blockers work so well.
- Triggers: streptococcal throat infection (guttate psoriasis), physical trauma (Koebner phenomenon), stress, smoking, alcohol, obesity, HIV, and drugs. Classic drug triggers are lithium, beta-blockers, antimalarials, interferon, and rapid withdrawal of systemic corticosteroids (which can provoke pustular flares). Anti-TNF drugs can cause paradoxical psoriasis, often palmoplantar pustular.
Clinical Variants
| Variant | Key Features | Points to Remember |
|---|---|---|
| Chronic plaque | Well-demarcated, salmon-red plaques with silvery scale on extensors, scalp, sacrum; Auspitz sign | About 80–90% of cases |
| Guttate | Showers of small drop-like papules on the trunk in children and young adults | Often 2–3 weeks after streptococcal pharyngitis; may clear or become chronic |
| Inverse (flexural) | Glazed, red, scale-poor plaques in axillae, groins, submammary and intergluteal folds | Differentials: candidiasis, erythrasma, tinea, intertrigo |
| Scalp | Thick adherent scale extending just beyond the hairline | Common first site; may cause temporary hair shedding |
| Nail | Pitting and leukonychia (matrix); onycholysis, oil-drop spots, subungual hyperkeratosis, splinter haemorrhages (bed) | Nail disease is a marker of psoriatic arthritis risk |
| Palmoplantar pustulosis | Sterile yellow-brown pustules on palms and soles | Strongly linked to smoking; can be part of SAPHO syndrome |
| Generalised pustular (GPP, von Zumbusch) | Sudden sheets of sterile pustules on red skin, fever, leucocytosis | Emergency; IL36RN mutations; triggers include steroid withdrawal and pregnancy (impetigo herpetiformis) |
| Erythrodermic | More than 90% of body surface red and scaling | Risk of fluid loss, hypothermia, infection, high-output heart failure |
| Acrodermatitis continua of Hallopeau | Pustules on the distal fingers or toes, nail destruction | Often resistant to treatment |
Histology: confluent parakeratosis, Munro microabscesses in the stratum corneum, spongiform pustules of Kogoj, loss of the granular layer, regular acanthosis with thin suprapapillary plates, and dilated tortuous papillary capillaries.
Psoriatic Arthritis (PsA)
PsA affects roughly 20–30% of patients and usually follows the skin disease by about 10 years. Risk factors include nail disease, scalp and intergluteal or perianal involvement, and severe skin disease. Patterns include distal interphalangeal disease, asymmetric oligoarthritis, symmetric polyarthritis, spondylitis, and arthritis mutilans. Dactylitis ("sausage digit") and enthesitis (for example at the Achilles tendon) are typical.
CASPAR criteria: inflammatory articular disease (joint, spine, or entheseal) plus at least 3 points from:
| Criterion | Points |
|---|---|
| Current psoriasis | 2 |
| Personal history of psoriasis (if no current psoriasis) | 1 |
| Family history of psoriasis (if no personal history or current psoriasis) | 1 |
| Typical psoriatic nail dystrophy (pitting, onycholysis, hyperkeratosis) | 1 |
| Negative rheumatoid factor | 1 |
| Current dactylitis, or history recorded by a rheumatologist | 1 |
| Juxta-articular new bone formation on hand or foot radiographs | 1 |
Dermatologists should ask about joint symptoms at every visit. Screening questionnaires such as the PEST (Psoriasis Epidemiology Screening Tool) help, and suspected PsA should be referred early to rheumatology.
Comorbidity
Moderate-to-severe psoriasis is associated with obesity, metabolic syndrome, type 2 diabetes, dyslipidaemia, hypertension, cardiovascular disease, non-alcoholic fatty liver disease, depression, and inflammatory bowel disease (especially Crohn disease). Management includes screening for cardiovascular risk factors and mood, and advice on weight, smoking, and alcohol.
Measuring Severity
- PASI (Psoriasis Area and Severity Index): 0 to 72, combining erythema, induration, and scale with area in four body regions.
- BSA: the patient's palm with fingers is about 1% of body surface.
- DLQI (Dermatology Life Quality Index): 10 questions, 0 to 30.
- Rule of tens (European consensus, Mrowietz 2011): PASI > 10, BSA > 10%, or DLQI > 10 means moderate-to-severe disease. Mild disease by area can be upgraded when visible areas, scalp, genitals, palms and soles, or nails are significantly involved, or when itch is severe.
- Treatment goals: the European consensus judged success by at least PASI 75, or PASI 50–75 with DLQI ≤ 5. Newer guidance increasingly uses absolute PASI targets (for example PASI ≤ 3) and DLQI 0–1.
European Treatment Ladder
| Level | Options | Notes |
|---|---|---|
| Topical | Vitamin D analogue plus corticosteroid (calcipotriol + betamethasone dipropionate fixed combination); corticosteroids; calcipotriol alone; dithranol; tar; calcineurin inhibitors for face and flexures (off-label) | Fixed combination is standard first-line topical therapy |
| Phototherapy | Narrowband UVB (311 nm); PUVA | Limited by cumulative dose and skin cancer risk with PUVA |
| Conventional systemic | Methotrexate, ciclosporin, acitretin, fumarates (dimethyl fumarate), apremilast (PDE4), deucravacitinib (TYK2) | Acitretin is not immunosuppressive but is teratogenic for 3 years |
| Biologics | TNF-alpha (adalimumab, etanercept, infliximab, certolizumab pegol); IL-12/23 (ustekinumab); IL-17 (secukinumab, ixekizumab, brodalumab, bimekizumab); IL-23 p19 (guselkumab, risankizumab, tildrakizumab) | In the EU most biologics are licensed for patients who are candidates for systemic therapy |
Matching the Drug to the Patient (EuroGuiDerm approach)
- Psoriatic arthritis: methotrexate, TNF-alpha inhibitors, IL-17 inhibitors, IL-23 inhibitors, or ustekinumab. For axial disease, TNF or IL-17 blockers have the best evidence.
- Inflammatory bowel disease: avoid IL-17 inhibitors, which can worsen or trigger Crohn disease. TNF monoclonal antibodies (adalimumab, infliximab), ustekinumab, or IL-23 inhibitors are preferred. Etanercept does not treat IBD.
- Pregnancy wish: certolizumab pegol has minimal placental transfer. Avoid methotrexate, acitretin, and fumarates.
- Heart failure (NYHA III–IV) or demyelinating disease: avoid TNF-alpha inhibitors.
- Latent tuberculosis: IL-17 and IL-23 inhibitors carry a lower reactivation risk than TNF inhibitors; treat latent infection first either way.
Generalised Pustular Psoriasis
GPP is a medical emergency. It is linked to loss-of-function mutations in IL36RN (deficiency of the IL-36 receptor antagonist, DITRA). Spesolimab, an anti-IL-36 receptor antibody, is approved in the EU for GPP flares in adults. Other options include acitretin, ciclosporin, and infliximab, plus supportive care for fluid, temperature, and infection.
A 45-year-old man has joint pain and swelling of the right index finger along its whole length. He has current plaque psoriasis and nail pitting, and his rheumatoid factor is negative. How many CASPAR points does he have from these features, and does he meet the criteria?
A 32-year-old woman with severe plaque psoriasis also has active Crohn disease. Which biologic class should be avoided?
A patient has psoriasis covering 6% of body surface, with a PASI of 7, but has thick plaques on both palms that stop him working, and a DLQI of 14. How should his disease be classified under the European consensus?
A 38-year-old woman develops fever and widespread sheets of sterile pustules on red skin. Genetic testing shows a loss-of-function mutation in IL36RN. Which targeted treatment is approved in the EU for flares of this condition?