Psoriasis

Meet the patient

A 34-year-old man has had itchy, scaly plaques on his elbows, knees and scalp for ten years, worse each winter. His nails are now pitted with oil-drop discolouration, and for six weeks his mornings have begun with stiff, swollen fingers that only loosen after an hour.^[1][7]

Two questions decide his clinic letter: what is this plaque? (morphology and the IL-23 axis) and is the inflammation spilling into his joints and his metabolism? (PsA screening and comorbidity). Hold those two and the rest of the topic slots into place.^[1]

One disease, five faces — own the morph

The plaque is the anchor; every other variant is the same IL-23-driven process wearing a different mask. The cutaneous hallmark is a well-demarcated erythematous plaque with silvery-white micaceous scale. Sort the variants by morphology and distribution — the examiner's favourite discriminator game:^[1]

Three named signs every candidate must produce at the bedside:^[1]

• Auspitz sign — pinpoint bleeding when you lift the scale, from the dilated capillary loops in the dermal papillae.
• Koebner phenomenon — new plaques appear in lines of trauma (a scratch, a tattoo, a sunburn).
• Woronoff ring — a pale halo around a resolving plaque, marking the edge of the cytokine field.^[1]

Etymology for viva gold: psoriasis is from the Greek psora, "itch" — the disease was named for the symptom patients actually complain of. Auspitz, Koebner and von Zumbusch are 19th-century physicians whose names outlived them because the signs they described are unchanged.^[1]

Who gets it, and what lights the fuse

About 2 to 3 percent of the world carries psoriasis — more in Northern Europeans, less in some African and East Asian populations — with a bimodal onset in the late teens and again in the fifties.^[1]

^{[1] [2]}

Genetics sets the stage. About 30 percent have an affected first-degree relative; HLA-Cw6 in the PSORS1 locus on chromosome 6p21 is the strongest susceptibility allele and tracks with early-onset and guttate disease; further loci include IL-12B, IL-23R, TRAF3IP2 and TNFAIP3.^[1]

Environmental triggers light the fuse — know the list, because removing the trigger can switch the disease off:^[1]

• Infection — group A beta-haemolytic streptococcal pharyngitis fires guttate psoriasis; HIV worsens it.
• Drugs — lithium, beta-blockers, antimalarials (chloroquine and hydroxychloroquine), interferon, and rapid withdrawal of systemic corticosteroids.
• Trauma — the Koebner phenomenon.
• Lifestyle — psychological stress, obesity, smoking and alcohol all raise onset and severity.
• Pregnancy — often improves, then flares postpartum; pustular psoriasis of pregnancy is impetigo herpetiformis.^[1]

The IL-23 to Th17 to IL-17 axis — the cytokines you must name

Name the axis and you have named the disease and every modern drug. Psoriasis is dysregulated innate and adaptive immunity in genetically susceptible skin, and the central pathway is a self-amplifying cytokine loop.^[1]

The four-step cytokine loop, in consultant shorthandShowHide

1. Initiation — trauma or infection activates keratinocytes and innate cells; the antimicrobial peptide LL-37 binds nucleic acid and fires plasmacytoid dendritic cells through TLR7 and TLR9.
2. Dendritic-cell activation — myeloid dendritic cells release IL-23 and IL-12, which drive Th17 and Th1 cells.
3. Effector phase — Th17 cells release IL-17A, IL-17F and IL-22; Th1 cells release IFN-gamma and TNF-alpha.
4. Keratinocyte response — cytokines shorten keratinocyte transit from about 28 days to 3 to 5 days, forcing parakeratosis and pumping out LL-37, beta-defensins and S100 chemokines that re-feed the loop.^[1]

The cytokine table is the bridge from mechanism to therapy — each row maps to a drug class:^[1]

Generalised pustular psoriasis has its own genetics. Loss-of-function mutations in IL36RN (the IL-36 receptor antagonist) unleash IL-36 signalling, neutrophil chemotaxis and pustule formation; CARD14 mutations mark other pustular phenotypes.^[28]

Read the plaque, the nail and the joint

The plaque is symmetric and extensor; the nail is pitted; the joint is inflammatory — and the joint is the one you must not miss. Chronic plaque psoriasis gives well-demarcated, dull-red plaques with silvery scale on elbows, knees, the lumbosacral area and scalp; pruritus varies, and fissuring on palms or soles can be the symptom that brings the patient in.^[1]

^[1]

The variants you must describe in one line each:^[1]

• Guttate — abrupt 1 to 10 mm drop-like salmon-pink papules on trunk and proximal limbs, classically 2 to 3 weeks after streptococcal pharyngitis; often resolves, may become plaque.
• Inverse — smooth, shiny, well-demarcated erythema in axillae, groin and inframammary folds; scale is minimal because of moisture.
• Pustular — palmoplantar pustulosis (sterile pustules on palms and soles, linked to smoking); generalised pustular psoriasis of von Zumbusch (an emergency); acropustulosis of infancy (not true psoriasis).
• Erythrodermic — generalised erythema and scale over more than 90 percent of BSA; a medical emergency.^[1][26]

Atypical presentations examiners test: late-onset disease in the elderly (drug triggers common), severe refractory psoriasis in HIV, impetigo herpetiformis in the third trimester, and guttate or scalp presentations in children.^[1]

The mimics — discriminate, don't list

The diagnosis is usually clinical; biopsy is for the uncertain, the atypical, and the rule-out before systemic therapy. A 4 mm punch biopsy from an active plaque settles doubt.^[1]

Extensor plaques — nummular eczema (coin-shaped, exudative, less demarcated), lichen planus (purple polygonal papules, Wickham striae, flexor wrists), tinea corporis (annular, central clearing, KOH positive), secondary syphilis (coppery papules on palms and soles, lymphadenopathy), subacute cutaneous lupus (photosensitive annular plaques, anti-Ro).^[1][5]

Scalp — seborrhoeic dermatitis (greasy yellow scale, eyebrows and nasolabial folds), tinea capitis (alopecia, cervical lymphadenopathy, KOH positive), lichen planopilaris (perifollicular erythema, scarring alopecia).^[5]

Inverse sites — candidiasis (satellite pustules, KOH positive), erythrasma (coral-red under Wood lamp), Hailey-Hailey disease (painful erosions, family history).^[5]

Nails — onychomycosis (yellow-brown subungual scale, KOH or PCR positive), lichen planus (ridging, pterygium), alopecia areata (fine geographic pitting, no oil-drop).^[5]

Histology is viva gold: regular acanthosis with elongated rete ridges, parakeratosis with a diminished granular layer, Munro microabscesses (neutrophils in the stratum corneum), spongiform pustules of Kogoj (neutrophils in the upper epidermis), and dilated tortuous dermal papillary capillaries — the last is the anatomical basis of Auspitz sign.^[4]

Dermoscopy adds a bedside discriminator: regularly distributed dotted vessels on a red background with uniform white scale — distinct from lichen planus (Wickham striae, peripheral vessels) and eczema (yellow scale, irregular vessels).^[6]

The four severity numbers — score skin, life and joint

PASI scores the skin, DLQI scores the life, NAPSI scores the nail, and CASPAR decides the joint. Know each tool and when it applies — these are the numbers that gate every escalation decision.^[1][8]

Practical severity bands drive the ladder: mild is BSA under 3 percent with DLQI under 6 (topical alone); moderate is BSA 3 to 10 percent or quality-of-life impairment; severe is BSA over 10 percent, PASI 10 or higher, or DLQI 10 or higher.^[1]

Screen for psoriatic arthritis at every visit — up to 30 percent develop it. The PEST tool is five yes/no questions; any positive answer earns a rheumatology referral.^[8]

The CASPAR criteria classify psoriatic arthritis with 91 percent sensitivity and 98 percent specificity, applied to a patient with inflammatory articular disease (joint, spine or entheseal):^[1][7]

• Current psoriasis (2 points) — or a personal or family history (1 point).
• Typical psoriatic nail dystrophy (1 point).
• Negative rheumatoid factor (1 point).
• Current dactylitis or a history of dactylitis (1 point).
• Juxta-articular new-bone formation on radiograph (1 point).^[1][7]

The number rule: CASPAR 3 or more equals psoriatic arthritis. Do not let a tender joint leave clinic without scoring it.^[7]

The investigations you actually order

Most psoriasis is diagnosed clinically; bloods exist to map comorbidity and clear the runway for systemic therapy — not to confirm the rash.^[1]

Baseline for every patient: FBC, LFT, urea and electrolytes, creatinine, fasting lipids and HbA1c (comorbidity), CRP or ESR (inflammatory activity), blood pressure and BMI (metabolic and cardiovascular risk), and a NAPSI if nails are involved.^[1]

Before any systemic or biologic agent, clear the runway: hepatitis B surface antigen and core antibody, hepatitis C antibody and HIV; tuberculosis screening with IGRA or Mantoux (treat latent TB before a biologic); a pregnancy test for women of childbearing potential before methotrexate, acitretin or a biologic; and a liver fibrosis assessment (fibroscan or biopsy) before methotrexate.^[1]

The topical ladder — match potency to site

Topicals are first-line for mild disease and an adjunct for everything else. The cardinal rule is to match potency and vehicle to the site — never a potent steroid on the face.^[1]

Site-specific pearls the viva rewards:^[1]

• Scalp — calcipotriol plus betamethasone scalp solution or foam; salicylic acid or coal-tar shampoo for scale; part the hair and apply to skin, not hair.
• Face, flexures, genitals — a low-potency steroid or a calcineurin inhibitor; avoid potent steroids.
• Palms and soles — a very potent steroid under occlusion; salicylic acid for hyperkeratosis; often acitretin or phototherapy.
• Nails — intralesional triamcinolone, topical vitamin D or corticosteroid, or systemic therapy for functional impairment.^[1]

Phototherapy — narrowband first, PUVA last

Narrowband UVB (NB-UVB, 311 nm) is the first-line phototherapy for widespread plaque or guttate psoriasis: two to three sessions a week for 15 to 20 sessions, with the dose titrated to the minimal erythema dose or skin type; remission typically lasts 3 to 6 months.^[10]

PUVA (psoralen plus UVA) is more effective but carries a higher long-term risk of squamous cell carcinoma and melanoma, so it is reserved for refractory disease or after NB-UVB has failed, and is contraindicated in pregnancy and significant photosensitivity.^[1]

Excimer laser (308 nm) targets localised plaques and scalp disease without exposing uninvolved skin.^[1]

The systemic ladder — four conventional agents, four personalities

When topicals and phototherapy are insufficient, four conventional systemic agents cover most moderate-to-severe disease — each with a distinct personality, monitoring burden and danger. Indications are moderate-to-severe disease, significant nail or palmoplantar involvement, psoriatic arthritis, or failure of topical and phototherapy.^[1][11]

Methotrexate — the workhorse, given weekly, never daily.^[11][13]

• Dose: 5 to 10 mg once weekly by mouth for the first week, then escalated quickly to a target of 15 to 25 mg weekly. The maximum is 25 mg weekly. Subcutaneous dosing at the same dose is an option when the response is inadequate or gastrointestinal tolerance is poor.
• Folic acid: a supplement is necessary; it improves tolerability but may slightly reduce efficacy.
• Liver toxicity: published data do not allow the risk of hepatic fibrosis to be quantified; type 2 diabetes and obesity significantly increase it. Serum procollagen III is the most validated monitoring test, complemented by FibroTest and elastography.^[13]

Methotrexate is weekly. Daily dosing has no place in psoriasis treatment; initiation by the oral route is preferred, with subcutaneous dosing reserved for poor response or intolerance.^[13]

Ciclosporin — the rapid responder.^[11][14]

• Dose: 2 to 5 mg/kg/day.
• Onset: one of the most effective and rapidly acting systemic treatments; virtually all manifestations of the disease can respond.
• Course: single or intermittent short courses for all except the most severe cases, because this is safer than continuous treatment.
• Combination: combines with any topical treatment for a dose-sparing effect, and with other systemic drugs in severe disease to spare the dose of each agent.^[14]
• Toxicities: nephrotoxicity and hypertension are the main side effects. Susceptibility varies between individuals, so careful monitoring is required. Concurrent ultraviolet therapy is discouraged because it raises non-melanoma skin cancer risk.^[11][14]

Acitretin — the retinoid.^[11][15]

• Acitretin, the active metabolite of etretinate, is the most widely used systemic retinoid in psoriasis.
• It is highly efficacious as monotherapy in some specific clinical subtypes of psoriasis, and it spares the dose of conventional systemic drugs and biologics when used in combination.
• It suits long-term maintenance therapy. Side effects are common but usually mild, and good results depend on patient selection, gradual dose escalation and counselling.^[15]

Apremilast — the oral PDE4 inhibitor.^[11][16]

• Dose: 30 mg twice daily.
• Mechanism: works intracellularly to regulate inflammatory mediators.
• Efficacy: in ESTEEM 1, 33.1 percent of patients reached PASI 75 at week 16 versus 5.3 percent on placebo; most patients re-randomised to apremilast maintained PASI 75 through week 52.
• Safety: most adverse events were mild or moderate, and no new significant adverse events emerged with continued exposure.^[16]

Biologics — three targets, one decision tree

Biologics are for moderate-to-severe plaque psoriasis refractory to or unsuitable for topical, phototherapy and conventional systemic therapy — and for active psoriatic arthritis. Before the first dose, screen for infection (IGRA or Mantoux for TB, hepatitis B and C serology, HIV), update vaccination (pneumococcal, influenza, COVID-19; live vaccines are contraindicated on therapy), counsel on pregnancy, and check baseline FBC, LFT and creatinine.^[1]

TNF-alpha inhibitors — proven in skin, joint and inflammatory bowel disease:^[1]

IL-17 inhibitors — the fastest, deepest skin clearance, with one absolute contraindication:^[18]

IL-23 inhibitors — the highest sustained clearance, with convenient dosing:^[20]

Ustekinumab — the IL-12 and IL-23 p40 blocker. In PHOENIX 1, ustekinumab 45 mg or 90 mg was given at weeks 0 and 4 and then every 12 weeks. PASI 75 at week 12 was reached by 67.1 percent of the 45 mg group and 66.4 percent of the 90 mg group, versus 3.1 percent on placebo, and every-12-week maintenance held the response for at least a year in most patients.^[17]

Choosing a biologic turns on the comorbidity, not just the skin:^[1]

• Skin-dominant disease, no PsA: an IL-23 or IL-17 inhibitor for the highest clearance.
• Psoriatic arthritis: a TNF or IL-17 inhibitor; IL-23 inhibitors also work.
• Comorbid inflammatory bowel disease: avoid IL-17 inhibitors (they may flare IBD) — prefer a TNF inhibitor or ustekinumab.
• Cardiovascular disease: TNF inhibitors may carry cardiovascular benefit; IL-17 and IL-23 data are evolving.
• Pregnancy: data are limited; TNF inhibitors (especially later in pregnancy) have the most experience, and avoid live vaccines in the infant for 6 months after in-utero exposure.^[1][30]

^[1]

Biologic failure has two flavours. Primary failure is inadequate response after an adequate trial (typically 12 to 16 weeks); secondary failure is loss of response after initial improvement (think immunogenicity, dosing, adherence, weight gain, smoking). Options are dose escalation, shortening the interval, or switching to a different mechanism class.^[12]

Small molecules — deucravacitinib, the TYK2 that is not a JAK

Deucravacitinib is an oral, selective TYK2 inhibitor for moderate-to-severe plaque psoriasis, blocking signalling downstream of IL-23, IL-12 and type I interferon without directly binding JAK1, JAK2 or JAK3.^[1]

• Dose: 6 mg once daily.
• Efficacy: in POETYK PSO-1, PASI 75 at week 16 was 58.4 percent versus 12.7 percent on placebo and 35.1 percent on apremilast, and efficacy was maintained through week 52.
• Safety: adverse event rates were similar to placebo and apremilast.^[25]

The high-yield line: deucravacitinib is TYK2-selective, not a pan-JAK inhibitor — a different safety profile from tofacitinib and baricitinib.^[25]

The preventable-harm list — psoriasis is a systemic disease

Psoriasis is not just skin, and the harm that shortens these patients' lives is cardiovascular and metabolic, not cutaneous. Screen and manage every patient holistically.^[1][2]

Everyone forgets: the cardiovascular risk is independent of the traditional risk factors — a patient with severe psoriasis carries excess MI and stroke risk even with a clean lipid profile, so treat the whole vessel, not just the plaque.^[31]

The immune emergencies — erythroderma, von Zumbusch, impetigo herpetiformis

Humour is off for the rest of this section.^[1]

Erythrodermic psoriasis is a medical emergency. Erythema and scale cover more than 90 percent of BSA, and the skin fails as a barrier: hypothermia, dehydration, electrolyte disturbance, high-output cardiac failure, infection and protein loss. Admit, resuscitate fluids and electrolytes, regulate temperature, enforce bed rest, and use ciclosporin or infliximab for rapid control — avoid systemic corticosteroids, because their withdrawal precipitates rebound pustular or erythrodermic flares.^[1]

Generalised pustular psoriasis (von Zumbusch) is a dermatology emergency. Widespread sterile pustules on erythematous skin come with fever, malaise, leucocytosis and hypocalcaemia; the dangers are sepsis, dehydration and organ dysfunction, and it can be life-threatening. Triggers include infection, pregnancy, corticosteroid withdrawal, hypocalcaemia and IL36RN mutations. Admit, give supportive care, and treat with ciclosporin (rapid onset), acitretin, methotrexate or a biologic (infliximab, secukinumab or guselkumab), and treat the trigger.^{[1][26][27][28]}

Impetigo herpetiformis is generalised pustular psoriasis of pregnancy, usually in the third trimester: grouped pustules on an erythematous base with fever, leucocytosis and hypocalcaemia, endangering both mother and fetus. It needs urgent dermatology and obstetrics co-management. Methotrexate, acitretin and PUVA are contraindicated; options include systemic corticosteroids, ciclosporin and biologics case by case.^[1][29][30]

The classic trap: a course of systemic corticosteroids can convert stable plaque psoriasis into pustular or erythrodermic crisis on withdrawal. Resist the steroid reflex.^[1]

On any biologic, severe infection, fever or unexplained systemic symptoms means hold the biologic and run a sepsis work-up.^[1]

Pregnancy, children and the elderly

In pregnancy, the rule is the safest effective therapy. Topicals are generally safe (avoid high-potency steroids over large areas); narrowband UVB is safe and PUVA is contraindicated; methotrexate, acitretin and PUVA are contraindicated; ciclosporin, some TNF inhibitors later in pregnancy, and ustekinumab may be used with caution. In breastfeeding, prefer topicals and avoid methotrexate and acitretin.^[1][30]

In children, guttate and scalp presentations dominate; first-line is topical therapy and phototherapy, with methotrexate, ciclosporin, etanercept and ustekinumab on specialist protocols, and biologics increasingly used for severe paediatric plaque disease.^[1]

In the elderly, weigh the higher burden of comorbidity and polypharmacy: methotrexate and ciclosporin need careful monitoring against renal and hepatic function, cardiovascular risk and frailty, and biologics are often well tolerated but carry a higher infection risk.^[1]

Prognosis and the treat-to-target mantra

Psoriasis is chronic and relapsing; there is no cure, but modern biologics can clear the skin in most well-selected patients. The treat-to-target goals are clear or almost clear skin, minimal symptoms, preserved function, and prevention of comorbidity.^[1]

The mantra: score the skin (PASI), the life (DLQI) and the joint (CASPAR) — every visit — and escalate until clear.^[1]

Follow-up intervals track the therapy: review topicals at 4 to 8 weeks; reassess phototherapy after 10 to 15 sessions and escalate if there is no response; monitor systemic agents by agent and review clinically every 3 months once stable; and assess biologic primary response at 12 to 16 weeks, then every 3 to 6 months.^[1]

Guidelines and landmark trials — name them in the viva

Major guidelines: the AAD-NPF (2020 to 2021) separate topical, systemic non-biologic and biologic guidance and emphasise treat-to-target; the EuroGuiDerm (2020) gives European consensus on systemic treatment, strong on biologic sequencing and monitoring; NICE NG507 (UK) recommends topical vitamin D plus corticosteroid first-line, narrowband UVB or systemic therapy for moderate-to-severe disease, and biologics only after conventional systemic therapy has failed or is contraindicated; the BAD biologic eligibility criteria often require PASI 10 and DLQI 10 despite two conventional systemic therapies.^{[1][9][11][12]}

Landmark trials to name: PHOENIX (ustekinumab, 2008), ERASURE and FIXTURE (secukinumab, 2014), UNCOVER (ixekizumab, 2016), VOYAGE (guselkumab, 2017), ECLIPSE (guselkumab versus secukinumab, 2019), UltIMMa (risankizumab, 2018), reSURFACE (tildrakizumab, 2017), AMAGINE (brodalumab, 2015), ESTEEM (apremilast, 2015), and POETYK PSO-1 and PSO-2 (deucravacitinib, 2023).^[1]

Ward-round test

1. A 19-year-old, two weeks after a sore throat, with raindrop papules on the trunk — diagnose, explain and treatShowHide

Guttate psoriasis, the classic post-streptococcal variant: group A beta-haemolytic streptococcal pharyngitis fires an IL-17-driven eruption 2 to 3 weeks later in an HLA-Cw6-susceptible host. Confirm with a throat swab and antistreptolysin titre, treat any active infection, and reach for narrowband UVB — guttate disease often resolves spontaneously and may never become chronic plaque.^[1]

2. A patient on adalimumab develops new bloody diarrhoea — what happened, and which biologic class is nextShowHide

A flare of inflammatory bowel disease — and the trap is that IL-17 inhibitors can worsen IBD, so they are the wrong switch. Continue TNF-alpha blockade (adalimumab or infliximab are proven in Crohn disease and ulcerative colitis) or move to ustekinumab (IL-12 and IL-23 p40), which also treats IBD. Avoid secukinumab, ixekizumab, brodalumab and bimekizumab here.^[1][32]

3. Stable plaque psoriasis flares into erythroderma two weeks after a steroid taper — your first 12 hoursShowHide

Erythrodermic psoriasis is a medical emergency — the barrier has failed. Admit, secure IV access, resuscitate fluids and correct electrolytes, regulate temperature, enforce bed rest, and start ciclosporin or infliximab for rapid control. Do not restart systemic corticosteroids — their withdrawal is precisely what precipitated this, and re-withdrawal will deepen the crisis. Screen for infection and watch for high-output cardiac failure.^[1]

4. A woman planning pregnancy is on methotrexate for severe psoriasis — what do you stop, for how long, and what is allowedShowHide

Stop methotrexate now — it is teratogenic; wait at least three months before conception. Acitretin is stricter still: contraindicated for 3 years after stopping in women of childbearing potential. Safe in pregnancy: topical therapy (avoid high-potency steroids over large areas) and narrowband UVB. Ciclosporin and some TNF inhibitors later in pregnancy may be used with specialist input; PUVA is contraindicated.^[1][30]

References32ShowHide

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