Psoriasis Management
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Direct answer
Well-demarcated, silvery-scaled plaques on extensor surfaces, scalp and the natal cleft, with nail pitting and Koebner phenomena, are managed by a ladder running from topical calcipotriol plus corticosteroid combinations, through narrowband UVB phototherapy, to methotrexate, ciclosporin or acitretin, and on to biologics targeting TNF, IL-17 or IL-23. Severity is graded with the PASI score, and treatment choice follows body surface area, site, functional impact and comorbidity rather than histology, since the diagnosis is clinical. Abrupt withdrawal of potent topical or systemic steroids is a recognised trigger for erythrodermic or pustular flares, which is why steroids are never maintenance in plaque psoriasis.
What you must remember
- Auspitz sign (pinpoint bleeding on scale removal), candle grease scaling, the Koebner isomorphic phenomenon and nail oil-drop change with pitting are the four clinical signs examiners quote.
- First-line topical: a combined calcipotriol plus potent corticosteroid (such as betamethasone) application once daily outperforms either alone; monotherapy with a potent steroid is time-limited to about four weeks, especially on the face and flexures.
- Scalp: keratolytic tar or salicylic acid shampoos to lift scale before steroids; face and flexures: tacrolimus or pimecrolimus, not potent steroids.
- Phototherapy: narrowband UVB three times weekly is the standard outpatient course; psoralen plus UVA suits palmoplantar disease.
- Systemics: methotrexate 7.5 to 15 mg once weekly with folic acid the next day, monitoring full blood count and liver profile; ciclosporin 2.5 to 5 mg per kg for rapid control, limited by hypertension and renal impairment; acitretin for pustular and erythrodermic disease, highly teratogenic for years after stopping.
- Biologics: anti-TNF agents such as etanercept and adalimumab, anti-IL-17 agents such as secukinumab, and anti-IL-23 or IL-12/23 agents such as guselkumab and ustekinumab; all demand latent tuberculosis and hepatitis B screening first.
- Triggers: streptococcal pharyngitis for guttate flares in the young (ASO titre, treat the focus), beta-blockers, lithium, antimalarials, rapid steroid withdrawal, alcohol, smoking, obesity and stress; excess metabolic and cardiovascular comorbidity must be managed alongside the skin.
A treatment pathway from plaque to biologic
A 38-year-old man has plaque psoriasis affecting 12 per cent body surface area, both elbows and knees, the scalp and the natal cleft, with nail pitting that interferes with his work as a mechanic. He has gained weight and drinks alcohol most evenings.
Step one: grade and stage. PASI is calculated from erythema, induration and desquamation across four body regions; his PASI of about 18 with a poor Dermatology Life Quality Index places him in the moderate-to-severe bracket where topicals alone will not succeed.
Step two: control the triggers. Alcohol counselling, weight reduction and smoking cessation are prescribed as deliberately as any ointment; a throat swab and ASO titre are checked since sore throats preceded flares.
Step three: use topicals as adjuncts, not the plan. Calcipotriol-betamethasone once daily to body plaques, a weekend maintenance rhythm once cleared; tar-salicylic acid shampoo then a steroid lotion for the scalp; tacrolimus ointment for the natal cleft and any facial extension.
Step four: step up to phototherapy or systemic. Narrowband UVB three times weekly for twelve to sixteen weeks suits his extensive plaques; if he relapses quickly, methotrexate 15 mg weekly with folic acid 5 mg the following day begins after baseline blood count, liver profile, serology for hepatitis B and C, and documentation of alcohol abstinence.
Step five: reserve biologics for failure, intolerance or major functional impact. Screening for latent tuberculosis with Mantoux or IGRA and chest radiograph precedes anti-TNF therapy; anti-IL-17 is avoided where inflammatory bowel disease coexists; response is tracked with PASI 75 or PASI 90.
Where the exam tries to catch you
The steroid withdrawal trap is the perennial answer: a patient with psoriasis given oral prednisolone or over-using potent topical steroids returns with pustular or erythrodermic psoriasis, and the correct next step is supportive care with acitretin or ciclosporin under dermatology, never more steroid. The second trap is site-directed prescribing, with stems offering potent steroids for the face or flexures where the answer is a calcineurin inhibitor. Indian vivas probe the methotrexate schedule, expecting the once-weekly dose with folic acid the next day, because the historic daily-dose error causes fatal pancytopenia; and they probe the streptococcal link, expecting ASO testing and tonsillar focus treatment in guttate disease of the young.
Frequently asked questions
Which topical combination is first-line for plaque psoriasis?
Calcipotriol with a potent corticosteroid such as betamethasone, applied once daily, which clears faster than either component alone.
What is the standard phototherapy regimen?
Narrowband UVB three times weekly for a course of several months, with PUVA reserved for palmoplantar and selected cases.
How is methotrexate prescribed in psoriasis?
7.5 to 15 mg once weekly with folic acid the following day, with blood count and liver monitoring and alcohol moderation.
Why is abrupt steroid withdrawal dangerous in psoriasis?
It can precipitate erythrodermic or generalised pustular psoriasis, the two medical emergencies of the disease.
Which screening precedes biologic therapy?
Latent tuberculosis testing and chest radiograph, hepatitis B and C serology, and assessment for demyelinating disease or heart failure depending on the agent.