Psoriasis

Psoriasis is a long-term inflammatory disease in which the immune system speeds up the growth of skin cells. Instead of renewing over weeks, the outer skin builds up within days and forms thick, red, scaly patches called plaques. It is not an infection and it is not contagious: you cannot catch it from another person. There is no permanent cure yet, but modern treatment can clear the skin completely or almost completely for many people.

Psoriasis affects about 1 to 2 people in every 100 in Europe, men and women equally. It can start at any age, including childhood, but most often begins in young adulthood.

The most typical form is plaque psoriasis: well-defined, red, thickened patches with silvery-white scale, often on the elbows, knees, scalp and lower back. On brown or black skin the patches may look purple, grey or dark brown. Itching is common.

Psoriasis can also appear as many small drop-like spots (guttate), as smooth red areas in body folds (inverse), or as pits and thickening of the nails. Rarer forms cause pus-filled blisters that are not an infection (pustular) or redness over nearly the whole body (erythrodermic).

Psoriasis results from an inherited tendency combined with triggers that set off the immune system. Common triggers include:

• throat infections, especially "strep throat"
• injury to the skin, such as cuts, burns or tattoos, where new lesions can appear
• stress, smoking, heavy alcohol use and excess weight
• certain medicines, such as lithium, beta blockers (for the heart and blood pressure) and antimalarial medicines (used for malaria or for autoimmune diseases such as lupus)
• stopping systemic corticosteroids can set off a severe flare; this is why they are rarely used for psoriasis

Never stop a prescribed medicine on your own because you suspect it; talk to the doctor who prescribed it.

A dermatologist can usually recognise psoriasis by examining the skin, scalp and nails. If the picture is unclear, a small skin sample (biopsy) is examined under a microscope. No blood test confirms psoriasis, but blood tests are needed before some treatments.

• Creams, ointments and foams: corticosteroids (anti-inflammatory steroid creams), vitamin D-type medicines (slow skin-cell growth), calcineurin inhibitors (non-steroid anti-inflammatory creams, useful on the face and in skin folds) and scale-softening products.
• Light therapy (phototherapy): controlled sessions of narrowband UVB light, usually a few times a week over several weeks.
• Tablets or injections acting on the whole body: methotrexate, ciclosporin, acitretin and newer tablets such as apremilast. Methotrexate is taken once a week, never daily.
• Biologics: targeted injected or infused medicines that block specific immune signals (TNF, IL-17, IL-23 or IL-12/23).

Some of these medicines can harm an unborn baby and must not be used in pregnancy, when planning a pregnancy or while breastfeeding. With acitretin, women who could become pregnant must continue reliable contraception for 3 years after the last dose, and nobody who has taken it may donate blood during that time. Men should also tell their doctor if they plan to father a child.

What can you do yourself?

• Moisturise daily to soften scale and reduce itching.
• Use your treatment as prescribed. Stopping can lead to a flare, so talk to your doctor first.
• Stop smoking, limit alcohol and aim for a healthy weight.
• Avoid injuring your skin or picking at the scale.
• Protect yourself from sunburn, and do not use sunbeds as a treatment.

Psoriasis is usually lifelong, with improvements and flares that are hard to predict. Many people achieve good control, though treatment may need to change over time. Mild psoriasis is not known to shorten life, but severe psoriasis is linked to a higher risk of heart disease.

What are the complications?

About 1 in 5 people with psoriasis develop psoriatic arthritis, an inflammation of the joints and of the places where tendons attach to bone. Swollen fingers or toes, heel pain, or back stiffness that is worse in the morning should be reported, because early treatment can prevent lasting joint damage.

People with psoriasis, especially severe psoriasis, are also more likely to have heart disease, diabetes, fatty liver and depression, so your doctor may check your weight, blood pressure and mood.

Living with the condition

Psoriasis can affect confidence, relationships, work and sleep. Tell your doctor if it affects your mood or daily life; this counts when choosing treatment.

• Psoriasis is a chronic immune-related disease. It is not contagious.
• Clear or almost clear skin is a realistic goal for many people.
• Tell your doctor if you are planning a pregnancy.

When to see a doctor

See a doctor if you have a persistent scaly rash, if treatment is not working, or if you have joint pain, swelling or morning stiffness, which may be signs of psoriatic arthritis.

Seek urgent medical care if:

• redness spreads over most of your body (this may be erythrodermic psoriasis, a serious form of the disease)
• you develop widespread pus-filled spots with fever or feel unwell, including in pregnancy (this may be generalised pustular psoriasis)
• you take methotrexate and develop a sudden dry cough with breathlessness, or fever, mouth sores, a sore throat or unusual bleeding (a possible serious reaction affecting the lungs or bone marrow)
• you have thoughts of harming yourself (these may be a sign of depression and need immediate help)

Contact your doctor at once if you may be pregnant while taking methotrexate, acitretin or another medicine you were warned about, or within the time after stopping that your doctor gave you (3 years for acitretin), or if you took extra methotrexate by mistake. If you take a biologic or another immune-suppressing medicine, seek care promptly for fever, a persistent cough or signs of infection, and ask your doctor before any vaccination.

Psoriasis affects an estimated 125 million people worldwide [1]. A systematic analysis of 168 studies found prevalence ranging from 0.14% in east Asia to 1.99% in Australasia, with 1.92% in western Europe and 1.83% in central Europe [2]. The Romanian textbook gives a national prevalence of about 1.3% [3]. Men and women are affected equally, and about 15% of cases begin before the age of 16 [3]. Early-onset (type I) disease has a stronger familial pattern, whereas late-onset (type II, after 40 years) is sporadic [3]. Pooled prevalence of psoriatic arthritis (PsA) among patients with psoriasis is 19.7% overall, 22.7% in European patients and 3.3% in those under 18 years [4].

Psoriasis arises from genetic susceptibility acting together with environmental triggers [5]. HLA-C*06:02, within the PSORS1 locus on chromosome 6p21.3, is the principal risk allele for chronic plaque disease [3,5]. Familial aggregation is reported in 20–40% of cases [3]. Recognised triggers include streptococcal infection, stress, smoking, obesity and alcohol [5]. The Romanian textbook lists lithium, beta blockers, synthetic antimalarials, NSAIDs and tetracyclines as causal, and interferon, ACE inhibitors and terbinafine as less clearly established; this is a 2014 textbook list rather than a graded evidence review [3]. Withdrawal of systemic corticosteroids can provoke erythrodermic or pustular relapse [6]. TNF inhibitors can paradoxically trigger psoriasis in 1.5–5% of treated patients, most often as palmoplantar pustulosis [7]. In children, about 30% of cases follow rhinopharyngeal (streptococcal) infection [3]. The Köbner phenomenon occurs in about 20% of patients, typically 7–14 days after trauma [3].

The IL-23/IL-17 axis is the key pathogenic driver of plaque psoriasis, and TNF-α also contributes, as shown by the efficacy of agents targeting each of these pathways [1,5]. In the traditional model, the initiation phase begins when complexes of DNA and the antimicrobial peptide LL-37, released by injured keratinocytes, stimulate plasmacytoid dendritic cells to secrete IFN-α, which activates myeloid dendritic cells [8]. Myeloid dendritic cells produce large amounts of IL-23, which sustains T cells producing IL-17 [9]. IL-17A/F and IL-22 drive keratinocyte proliferation and impaired differentiation [8]. Keratinocytes in turn release antimicrobial peptides, CCL20 and CXCL chemokines that recruit neutrophils, macrophages, dendritic cells and CCR6+ cells, and IL-17C, creating a self-amplifying feed-forward loop [9]. Tissue-resident memory T cells persist after clearance and contribute to recurrence at the same sites [8]. IL-36 signalling is the central pathway in generalised pustular psoriasis (GPP) [10].

Chronic plaque psoriasis (psoriasis vulgaris) accounts for more than two-thirds of cases [3]. It presents with well-demarcated erythematous plaques bearing lamellar, silvery-white scale [3]. Three classical bedside signs are the candle-grease sign, the Auspitz sign (pinpoint bleeding on removal of scale) and the Köbner phenomenon [3]. Disease may be limited to characteristic sites:

• Scalp: lesions extend beyond the hairline; hair is not matted, and pruritus is frequent [3].
• Flexures (inverse psoriasis): bright red, smooth, sparsely scaly plaques in the inguinocrural, axillary and retroauricular folds [3].
• Palmoplantar: diffuse or insular keratoderma, disabling and difficult to treat [3].
• Nails (about 50% of patients): pitting, leukonychia, trachyonychia, oil-drop discoloration, onycholysis, splinter haemorrhages and subungual hyperkeratosis [3].
• Mucosae (5–19%): geographic tongue, fissured tongue, circinate erythema of the oral mucosa and cheilitis [3].

Guttate psoriasis is frequent in young people and often follows infection [3].

Erythrodermic psoriasis presents with generalised erythema, scaling and infiltration, fever, dermatopathic lymphadenopathy and intense pruritus, with a risk of dehydration and infection; it may arise de novo or complicate chronic disease [3].

Pustular psoriasis comprises generalised and localised forms. GPP is defined by the international consensus criteria given under Diagnosis [11]. Localised forms include palmoplantar pustular disease (Barber type) and acrodermatitis continua of Hallopeau, which may progress to nail loss and osteolysis [3]. Pustular psoriasis of pregnancy (impetigo herpetiformis in older terminology) occurs in the last trimester and carries maternal and fetal risk [3].

Skin of colour: erythema appears purple, lilac or grey rather than red, plaques may be thicker with greyish scale, and lasting dyspigmentation can be the main complaint [12]. Erythema may be underestimated in Fitzpatrick types 5 and 6 when scoring severity [13]. Prevalence of plaque psoriasis is lower but disease tends to be more severe, with a worse impact on quality of life and lower uptake of biologics [12]. Definitions of ethnicity and skin of colour are inconsistent across this literature, which limits generalisation [12].

Psoriatic arthritis presents in several patterns: asymmetric oligoarthritis with dactylitis, distal interphalangeal disease, arthritis mutilans, symmetric seronegative polyarthritis and axial disease [3]. Skin lesions precede joint disease in about 75% of cases [3]. Classification uses the CASPAR criteria [14].

Psoriatic plaques show punctate, globular or coiled vessels at conventional 10× dermoscopy, with white scale; the distinctive feature is their uniform distribution, because red dots also occur in lichen planus, porokeratosis and pityriasis rosea [15]. A persistent pattern of dilated, branched capillaries despite clinical remission suggests ongoing disease activity [15]. In one study, trichoscopy of scalp psoriasis showed red dots, silvery-white scale and the "hidden hair" sign [15]. These data come from a narrative review, and dermoscopy is not required for routine management [15].

Diagnosis is clinical in most cases [3]. Biopsy is reserved for atypical presentations, and for GPP the essential criterion is macroscopically visible sterile pustules on an erythematous base, not restricted to the acral region or within psoriatic plaques [11].

Severity assessment. The PASI, a physician global assessment, the affected BSA and the DLQI are the standard instruments [16]. PASI and BSA are not validated in children, and the Nail Psoriasis Severity Index is used for nail disease in specialist settings [13]. The 2011 European consensus, retained in the EuroGuiDerm guideline, defines moderate-to-severe disease as (PASI >10 or BSA >10%) and DLQI >10, and mild disease as PASI ≤10, BSA ≤10% and DLQI ≤10 [7]. Mild disease is "upgraded" to moderate-to-severe by major involvement of visible areas, major scalp involvement, genital involvement, onycholysis or onychodystrophy of at least two fingernails, itch leading to scratching, or recalcitrant plaques [7]. The International Psoriasis Council proposes instead a dichotomy: candidates for topical therapy versus candidates for systemic therapy, the latter meeting at least one of BSA >10%, disease in special areas, or failure of topical therapy [17].

Baseline work-up. Assess for PsA at least annually, especially in the first 10 years after onset; a validated tool such as PEST helps, although it does not detect axial disease [13]. In severe psoriasis, NICE advises cardiovascular risk assessment at presentation and every 5 years [13]. Ask about mood and assess for depression at severity reviews and when escalating treatment [13]. Severe or atypical psoriasis is an HIV indicator condition [13]. Before systemic therapy, obtain a history of infections, malignancy, liver and renal disease and concomitant medication, along with the tests listed under Management [7].

The established plaque shows parakeratosis, regular elongation of rete ridges, a reduced or absent granular layer, thinning of the suprapapillary plates and tall dermal papillae with dilated capillaries [3]. Munro microabscesses in the stratum corneum and spongiform pustules of Kogoj in the epidermis are characteristic [3].

The alternatives follow the Petrescu textbook list [6]. Discriminating features reflect clinical convention, not diagnostic-accuracy studies.

Condition	Discriminating features
Nummular eczema	Coin-shaped plaques with vesicles, oozing and crusting, intense itch; no silvery lamellar scale or Auspitz sign
Chronic eczema	Ill-defined edge, lichenification
Seborrhoeic dermatitis	Greasy yellowish scale, central face and scalp without a sharp edge beyond the hairline; overlap exists as sebopsoriasis
Pityriasis rosea	Herald patch, collarette scale, Christmas-tree distribution, self-limiting
Tinea corporis	Annular, active scaly border with central clearing; positive KOH preparation
Lichen planus	Violaceous polygonal papules, Wickham striae, oral lesions
Parapsoriasis	Persistent patches with fine scale; biopsy if atypical
Hailey-Hailey disease (flexures)	Family history, painful macerated erosions with fissures
Mycosis fungoides	Patches of varying shape and fixed distribution in sun-protected sites; atypical lymphocytes with epidermotropism
Secondary syphilis	Copper-coloured papules including palms and soles, mucosal lesions, positive serology
Pityriasis rubra pilaris	Salmon-orange plaques with islands of sparing, follicular papules, orange palmoplantar keratoderma
Intertrigo or candidiasis (flexures)	Satellite pustules, positive mycology; no plaques elsewhere
Onychomycosis (nails)	Positive mycology; pitting and oil-drop change favour psoriasis; the two may coexist
Bowen disease or superficial BCC	Solitary persistent plaque; confirm by biopsy
Cutaneous lupus (subacute or discoid)	Photodistribution, scarring in discoid disease; serology and biopsy
Pityriasis lichenoides chronica	Guttate mimic with mica-like scale; biopsy
Hand eczema or tinea (palmoplantar disease)	Vesicles or fissuring; positive mycology in tinea
Tinea capitis (scalp)	Broken hairs, alopecia, positive mycology
Psoriasiform drug eruption	Recent drug exposure; improvement on withdrawal
Extramammary Paget disease (genital or flexural)	Persistent, unresponsive plaque; biopsy
Erythroderma of another cause	Sézary syndrome, drug eruption, atopic dermatitis, PRP; history, blood film and biopsy
AGEP (versus GPP)	Recent drug exposure, rapid resolution on withdrawal

Principles. Psoriasis cannot currently be cured; management aims to minimise physical and psychological harm by treating early, identifying and preventing associated multimorbidity, encouraging lifestyle change and personalising treatment [5]. PASI 75 is the minimum target, and PASI 90 or an absolute PASI <2 is the desirable goal [16]. Assess response at 10–12 weeks for fast-acting treatments and at 16–24 weeks for slower ones, then every 8–12 weeks during maintenance [16]. If the target is not reached, adjust the dose, combine treatments or change the drug [16]. Systemic corticosteroids should not be used in routine management, because relapse on withdrawal can take an erythrodermic or pustular form; use is reserved for exceptional situations [6].

Step 1: limited disease (topical therapy). Topical corticosteroids, vitamin D analogues, calcineurin inhibitors and keratolytics remain the mainstay of mild disease [1,18]. NICE (2012 recommendations, revised 2017, minor updates to December 2025) gives the most explicit regimens [13]:

• Trunk and limbs (adults): potent corticosteroid once daily plus a vitamin D analogue once daily, applied separately, for up to 4 weeks. If control is not achieved by 8 weeks, use the vitamin D analogue alone twice daily; if that fails after 8–12 weeks, use a potent corticosteroid twice daily for up to 4 weeks or coal tar. Calcipotriol/betamethasone once daily for up to 4 weeks is an option where a once-daily product aids adherence [13]. In children, consider once-daily calcipotriol (over 6 years) or a potent corticosteroid (over 1 year); adult durations may not apply [13].
• Scalp: potent corticosteroid once daily for up to 4 weeks, changing formulation or removing scale first if needed, then calcipotriol/betamethasone once daily for up to 4 weeks [13].
• Face, flexures and genitals: mild or moderate corticosteroid for a maximum of 2 weeks (1–2 weeks per month) and never potent agents; if unsatisfactory in adults, a calcineurin inhibitor twice daily for up to 4 weeks, started by a clinician experienced in psoriasis and off-label [13].
• Safety limits: no more than 8 weeks of continuous potent or 4 weeks of very potent corticosteroid at any site, a 4-week break between courses, and no very potent agents in children [13]. Continuous use can cause irreversible atrophy, unstable disease and, over more than 10% of body surface, systemic effects; review adults on intermittent potent courses, and children on any corticosteroid, at least annually [13].
• Review: 4 weeks after a new topical in adults and 2 weeks in children [13].

Calcipotriol is limited to 100 g per week [6]. Salicylic acid 3–10% or urea 15–25% prepare thick plaques, but salicylic acid over large areas at high concentration risks salicylism [3,6]. Short-contact dithranol, 0.1–3% for 10–30 minutes, remains an option in resistant disease [3,13].

Step 2: phototherapy. Narrowband UVB (about 311 nm) is the most commonly prescribed light therapy [1,3,6]. It is offered for plaque or guttate disease not controlled topically, 2–3 times weekly, with a faster response at 3 sessions a week, and is not used routinely as maintenance [13]. Do not use PUVA with a genetic predisposition to skin cancer, such as xeroderma pigmentosum or familial melanoma, and note that later ciclosporin adds to the risk, particularly after more than 150 PUVA treatments [13]. PUVA risk rises with the number of treatments: avoid it where alternatives exist in patients with a history of skin cancer, after 150 treatments and in children, and offer lifelong surveillance after 150 treatments or skin cancer [13]. Keep a permanent record of cumulative UV treatments, and protect the eyes and genitals [13,19].

Step 3: systemic therapy. Systemic treatment is strongly recommended for moderate-to-severe disease, selected by efficacy, safety, comorbidities and individual patient factors [16]. Guidelines differ on sequence. EuroGuiDerm recommends a conventional systemic agent for most patients who need systemic treatment, and suggests following its options overview for severe disease [7]. The German S3 guideline (2026), adapted from EuroGuiDerm, suggests a biologic with a first-line label or deucravacitinib when systemic therapy is started for the first time, especially in particularly severe disease [16]. The French guideline (2025) proposes methotrexate, adalimumab or ustekinumab as first-line options without symptomatic comorbidity, and IL-17 inhibitors, IL-23 inhibitors or infliximab for very severe disease (BSA >50%) [19]. Reimbursement in several European countries still requires failure of, or a contraindication to, a non-targeted treatment [19]. EU labels for etanercept, infliximab and adult apremilast are themselves restricted to patients who failed, cannot take or do not tolerate other systemic therapy [20,21,22].

Comparative efficacy. The 2025 Cochrane network meta-analysis (204 trials, 67 889 participants, induction phase of 8–24 weeks) found all interventions superior to placebo for PASI 90 [23]. Anti-IL-17 agents performed best as a class, and infliximab, xeligekimab, bimekizumab, ixekizumab and risankizumab ranked highest, with high-certainty evidence for bimekizumab and moderate certainty for the others [23]. Clinical effectiveness among these drugs was similar, and these are SUCRA rankings from induction-phase data [23]. No difference from placebo was found for serious adverse events, but this analysis had few events and mostly low-certainty evidence [23].

Conventional systemic agents

• Methotrexate: usual starting and maintenance dose 15 mg once weekly, increased to 20 mg if response is insufficient; 25 mg benefits only a small subgroup, and higher doses are not recommended [16]. NICE instead starts at 5–10 mg weekly and escalates, assessing response after 3 months at target dose [13]. Subcutaneous administration is preferred for doses above 15 mg or where there is a risk of overdose [16]. Give folic acid 5 mg once weekly, 24 hours after methotrexate [7]. At baseline check blood count with differential, ALT, AST, γGT, ALP, creatinine, urinalysis, a pregnancy test, and hepatitis B, hepatitis C and HIV serology [16]. Repeat the blood count within 2 weeks, then every 3 months with liver enzymes and creatinine; the 2026 S3 adds risk-adapted testing in the first 3 months, for example in diabetes, obesity or steatosis, whereas EuroGuiDerm adds checks every 4 weeks during the first two months [7,16]. Reduce the dose or stop if leukocytes are <3.0, neutrophils <1.0 or platelets <100 (×10⁹/L) [16]. If liver enzymes exceed 2–3 times baseline, repeat, seek specialist advice and consider reducing or stopping; FIB-4 and elastography are further options [16]. Absolute contraindications include severe infection, severe liver disease, severe renal dysfunction, pregnancy, breastfeeding or a wish for pregnancy, alcohol abuse, bone marrow failure, immunodeficiency, acute peptic ulcer, significantly reduced pulmonary function and inability to understand weekly dosing [7,16]. EuroGuiDerm recommends against methotrexate at eGFR <30 mL/min/1.73 m² [7]. The UK Metoject PEN label halves the dose at creatinine clearance 30–59 mL/min and prohibits use below 30 [24]. Co-trimoxazole should be avoided because it increases the risk of bone marrow toxicity, with rare acute megaloblastic pancytopenia reported [16,24]. Some NSAIDs raise methotrexate levels and should be given at a different time of day [7,16]. Reliable contraception is needed in women and men; the label specifies at least 6 months after stopping in women and 3 months in men [7,24]. Warn patients about pneumonitis (dry cough with dyspnoea) and early signs of pancytopenia [16].
• Ciclosporin: 2.5–3 mg/kg/day in 2 divided doses for rapid or short-term control [13,19,25]. Most physicians reserve it for short-term induction [7,26], although NICE and the label allow the lowest effective dose as maintenance [13,25]. Increase gradually after 1 month if there is no response, up to a maximum of 5 mg/kg/day, which may be used from the start when rapid improvement is needed; stop if response is inadequate after 6 weeks at 5 mg/kg/day [25]. NICE assesses response after 3 months at the optimum dose [13]. NICE limits continuous use to 1 year except in severe or unstable disease without alternatives, whereas EuroGuiDerm cautions about irreversible renal change with use of up to two years [7,13]. Measure blood pressure on two occasions [7] and establish baseline eGFR from at least two measurements [25]. Check blood count, liver enzymes, sodium, potassium, creatinine and uric acid at baseline and weeks 4, 8, 12 and 16, then every 4–8 weeks, with urinalysis at baseline, week 4 and from week 16, and lipids at baseline, week 8 and from week 16 [7]. If eGFR falls more than 25% below baseline on more than one measurement, reduce the dose by 25–50%, and stop if it does not improve within a month [25]. Absolute contraindications are impaired renal function, uncontrolled hypertension, severe infection, current or previous malignancy (possible exceptions: treated basal cell carcinoma, squamous carcinoma in situ), simultaneous PUVA or extensive previous UV exposure with high skin cancer risk, severe hepatic disease and breastfeeding [7]. Do not combine with UVB or PUVA, and stop if hypertension cannot be controlled [25]. St John's wort is contraindicated [25]. Other interactions include rifampicin, which lowers ciclosporin levels, and NSAIDs, which add nephrotoxicity [7,25]. Consider stopping one week before elective surgery [7].
• Acitretin: start with 25–30 mg daily for 2–4 weeks and adjust; 25–50 mg daily for a further 6–8 weeks usually gives the best result, up to a maximum of 75 mg/day, taken with a fatty meal or whole milk [7,27]. NICE targets 25 mg daily, escalates to 50 mg only when no other option exists, and assesses response after 4 months [13]. It is teratogenic: strict contraception runs from at least 4 weeks before treatment until 3 years after it, with monthly pregnancy tests according to national regulations, and blood donation is prohibited for the same period [7,27]. It is contraindicated in pregnancy, breastfeeding, severe hepatic or renal impairment, chronically raised blood lipids, and with tetracyclines, methotrexate, vitamin A or other retinoids [27]. EuroGuiDerm monitors blood count at baseline, week 8 and every 12 weeks; liver enzymes at baseline and weeks 4 and 8; fasting lipids at baseline, week 4 and every 12 weeks; and creatinine and fasting glucose at baseline [7]. The UK label is stricter for liver function: every 1–2 weeks for 2 months, then every 3 months [27]. Ask about spinal and joint symptoms, and advise alcohol abstinence [7]. Diabetes, hypertriglyceridaemia and previous pancreatitis are relative contraindications [7].
• Dimethyl fumarate: titrated from 30 mg once daily to a maximum of 720 mg/day over 9 weeks [28]. Do not start if leukocytes are <3.0 or lymphocytes <1.0 (×10⁹/L); check blood count with differential every 3 months, stop at leukocytes <3.0, test monthly if lymphocytes fall to 0.7–1.0, and stop if <0.7 is confirmed on repeat [28]. The label warns of progressive multifocal leukoencephalopathy and Fanconi syndrome [28]. It is contraindicated in severe gastrointestinal disease, severe hepatic or renal impairment, pregnancy and breastfeeding [28].

Targeted oral agents

• Apremilast (PDE4 inhibitor): 30 mg twice daily after a 5-day titration; reduce to 30 mg once daily if creatinine clearance is <30 mL/min [22]. It is contraindicated in pregnancy, and the label warns of depression and suicidal ideation and behaviour [22]. Reconsider if there is no benefit by 24 weeks; rifampicin reduces exposure and risks loss of efficacy [22].
• Deucravacitinib (TYK2 inhibitor): 6 mg once daily with no renal dose adjustment; consider stopping if there is no benefit after 24 weeks [29]. Contraindicated in clinically important active infection [29]. Screen for tuberculosis before starting [29]. It is not recommended in severe hepatic impairment, and the label warns of malignancy, MACE and venous thromboembolism by extrapolation from a JAK inhibitor trial [29]. The S3 adds baseline creatine kinase and other tests as expert opinion beyond the label, and advises warning patients about herpes zoster [16].
• Icotrokinra (oral IL-23 receptor antagonist peptide): 200 mg once daily on an empty stomach; consider stopping if there is no benefit after 24 weeks [30]. Contraindicated in clinically important active infection, and live vaccines are not recommended during treatment or within 3 days of stopping [30].

Biologics (adult EMA product information, subcutaneous unless stated)

Target	Drug	Induction	Maintenance	Label notes
TNF-α	Adalimumab	80 mg, then 40 mg one week later	40 mg every 2 weeks	Reassess at 16 weeks; label allows intensification if response is inadequate [31]
TNF-α	Etanercept	25 mg twice weekly or 50 mg once weekly; alternatively 50 mg twice weekly for up to 12 weeks	25 mg twice weekly or 50 mg once weekly, until remission, up to 24 weeks	Stop if no response after 12 weeks; continuous use beyond 24 weeks may suit some adults [20]
TNF-α	Infliximab (IV)	5 mg/kg at weeks 0, 2, 6	5 mg/kg every 8 weeks	Stop if no response after 14 weeks (4 doses) [21]
TNF-α	Certolizumab pegol	400 mg at weeks 0, 2, 4	200 mg every 2 weeks; 400 mg every 2 weeks if response insufficient	Reconsider if no benefit by 16 weeks [32]
IL-12/23 p40	Ustekinumab	45 mg at weeks 0, 4	45 mg every 12 weeks	90 mg if >100 kg; consider stopping if no response by 28 weeks [33]
IL-17A	Secukinumab	300 mg at weeks 0, 1, 2, 3, 4	300 mg monthly	Consider stopping if no response by 16 weeks; 300 mg every 2 weeks may help if ≥90 kg [34]
IL-17A	Ixekizumab	160 mg at week 0, 80 mg at weeks 2, 4, 6, 8, 10, 12	80 mg every 4 weeks	Consider stopping if no response after 16–20 weeks [35]
IL-17RA	Brodalumab	210 mg at weeks 0, 1, 2	210 mg every 2 weeks	Consider stopping if no response after 12–16 weeks; contraindicated in active Crohn's disease [36]
IL-17A/F	Bimekizumab	320 mg at weeks 0, 4, 8, 12, 16	320 mg every 8 weeks	Consider stopping if no improvement by 16 weeks; every 4 weeks after week 16 may help if ≥120 kg without clearance [37]
IL-23 p19	Guselkumab	100 mg at weeks 0, 4	100 mg every 8 weeks	Consider stopping if no response after 16 weeks [38]
IL-23 p19	Risankizumab	150 mg at weeks 0, 4	150 mg every 12 weeks	Consider stopping if no response after 16 weeks [39]
IL-23 p19	Tildrakizumab	100 mg at weeks 0, 4	100 mg every 12 weeks	200 mg may help if high burden or >90 kg; consider stopping if no response by 28 weeks [40]

Before any biologic or deucravacitinib check for active infection, skin cancer and lymphadenopathy, review vaccination needs, and arrange contraception; laboratory tests include blood count, liver enzymes, hepatitis B and C serology, HIV serology and a pregnancy test where relevant [7,16]. Tuberculosis screening under EuroGuiDerm uses medical history, chest X-ray and TST and/or IGRA according to local regulations; the 2026 S3 revised the IGRA and chest X-ray indications [7,41]. After a positive IGRA, exclude active disease by history, examination and chest X-ray [41]. In BCG-vaccinated patients, IGRA is preferred over TST [7]. In latent infection, preventive therapy is rifampicin for 4 months, isoniazid plus rifampicin for 3 months, or isoniazid for 9 months [41]. Rifampicin lowers ciclosporin and apremilast exposure [22,25]. Preventive therapy is suggested against when starting acitretin, apremilast, ciclosporin, dimethyl fumarate or methotrexate, unless there is another indication [41]. Preventive therapy is recommended before TNF inhibitors (reactivation risk increased) and suggested before ustekinumab and deucravacitinib, and the S3 suggests against deucravacitinib in latent infection unless no other option exists; for IL-17 and IL-23 inhibitors, where evidence is insufficient, it may be considered and the label leaves it optional [41]. A 4-week interval before starting immunosuppression is customary, with shorter intervals considered feasible in urgent psoriasis [41]. Stay alert to tuberculosis during therapy [7]. The German guidance comes from a low-incidence setting (about 4 000–5 000 cases a year) [41], whereas Romania notified 46.3 cases per 100 000 in 2024 [42], so national protocols and pulmonology advice should take precedence.

Viral hepatitis. Decide treatment with a hepatitis specialist if HBsAg or HBV DNA is positive [41]. Patients who are anti-HBc positive and HBsAg negative need ALT, AST, HBsAg and HBV DNA at least every three months [41]. A positive anti-HCV with negative HCV RNA, without prior antiviral therapy, indicates cured infection and does not require referral [41].

Long-term strategy. Off-label dose intensification has limited safety data [19]. Dose reduction may be considered after at least one year of treatment if disease has been in remission or at low activity (PASI <2) for several months, with the patient informed of the relapse risk [19]. A 2026 international consensus agreed a two-step algorithm for adalimumab, etanercept and ustekinumab; evidence for IL-17 and IL-23 inhibitors remains limited [43]. Guideline recommendations apply equally to biosimilars [16]. Repeat blood count and liver enzymes every 3–6 months during biologic treatment [16], and re-examine for infection, skin cancer and lymphadenopathy [7].

Site-specific and guttate disease. In guttate psoriasis, a systematic review of low-quality evidence found phototherapy best supported, with narrowband UVB most effective, and topical corticosteroids and calcipotriol as the first-line topicals; antibiotic treatment showed minimal connection with remission, and 17.5–38.9% of cases progress to chronic plaque disease [44]. Nail disease responds poorly to topical treatment and justifies systemic therapy when severe [13]. Intralesional triamcinolone improved nail psoriasis in a meta-analysis of six randomised and observational studies (odds ratio 2.35, 95% CI 1.20–4.60) [45]. For scalp disease with severe symptoms or impaired quality of life, the Spanish consensus prefers IL-17 and IL-23 inhibitors [46].

Generalised pustular psoriasis is a dermatological emergency requiring same-day specialist assessment, as does erythroderma [13]; full management is covered in the pustular psoriasis article. For a flare, spesolimab 900 mg is given as a single intravenous dose, with a further 900 mg after one week if symptoms persist, in patients aged 12 years or older weighing at least 40 kg [47]. In the phase 2 Effisayil 1 trial, 19 of 35 patients (54%) on spesolimab versus 1 of 18 (6%) on placebo had no visible pustules at week 1 [10].

Erythrodermic psoriasis: exclude other causes of erythroderma and manage fluids, temperature and infection risk [3]. French guidance recommends IL-17 inhibitors, IL-23 inhibitors or infliximab first line [19].

Palmoplantar pustular disease: French guidance suggests IL-17 inhibitors, IL-23 inhibitors or ciclosporin first line [19].

Psoriatic arthritis: refer as soon as PsA is suspected [13]. EuroGuiDerm suggests a synthetic DMARD such as methotrexate first line for most patients with moderate-to-severe skin disease and active joint involvement, and recommends a biologic after inadequate response to at least one synthetic DMARD, or first line in severe active joint disease [7].

Pregnancy and planning pregnancy. Weigh the uncertain risks of untreated maternal disease (associated with preterm birth, caesarean delivery and pre-eclampsia) against fetal drug exposure [7]. Methotrexate and acitretin are contraindicated in women planning conception; acitretin should generally be avoided in women of child-bearing potential, given the 3-year contraception requirement [7,27]. Fumarates, apremilast and deucravacitinib are also contraindicated in women planning conception, with a suggestion against use [7]. Moisturisers, low- to moderate-potency topical corticosteroids or UVB phototherapy are usually first line in pregnancy [48]. Ciclosporin is suggested as the first-line conventional agent in women planning conception and when systemic therapy must be started in the second or third trimester [7]. Certolizumab pegol is the recommended first-line biologic in the same situations, because all other licensed biologics are actively transferred to the fetus in the second and third trimesters [7]. EuroGuiDerm suggests stopping biologics other than certolizumab in the second and third trimesters [7]. Around 65% of patients worsen post partum [7].

Infant vaccination. EuroGuiDerm recommends against live or live attenuated vaccines in infants whose mothers received biologics beyond 16 weeks' gestation, up to 6 months of age (12 months after maternal infliximab), unless benefit clearly outweighs the theoretical risk [7]. This applies directly to BCG scheduling [7,21].

Breastfeeding. Methotrexate, acitretin, ciclosporin, fumarates and apremilast should not be used [7,27]. Transfer of certolizumab into breast milk is none or minimal, and no or minimal levels of infliximab, adalimumab and ustekinumab were found in a study of women with IBD [7].

Men. EMA recommends stopping methotrexate three months before attempting conception [7]. French guidance differs, stating that it may be continued on the basis of reassuring data [19]. EuroGuiDerm suggests barrier contraception for men taking acitretin [7].

Children. Paediatric EMA labels include adalimumab from 4 years for severe disease, etanercept from 6 years for chronic severe disease after other therapies, and secukinumab, ixekizumab (from 25 kg), risankizumab, ustekinumab, guselkumab and apremilast (from 20 kg) from 6 years, with weight-based dosing [20,22,31,33,34,35,38,39]. Icotrokinra is licensed from 12 years and 40 kg [30]. The AAD-NPF paediatric guideline addresses this population specifically [49].

Older adults. Use lower methotrexate doses and monitor renal function regularly, with caution if creatinine clearance is <60 mL/min [16].

Heart disease. EuroGuiDerm recommends against TNF inhibitors in advanced congestive heart failure; adalimumab, infliximab and certolizumab pegol are contraindicated in NYHA class III/IV, and etanercept requires caution [7,21,31,32]. French guidance suggests methotrexate, IL-12/23, IL-17 or IL-23 inhibitors, or apremilast in advanced heart failure [19]. In ischaemic heart disease, EuroGuiDerm suggests methotrexate as preferred first-line therapy and TNF inhibitors, ustekinumab and IL-17 inhibitors as preferred targeted agents, and suggests against ciclosporin or acitretin [7].

Neurological and autoimmune disease. TNF inhibitors should be avoided in demyelinating disease, and EuroGuiDerm suggests against them where a first-degree relative has multiple sclerosis if alternatives exist [7]. Concomitant lupus erythematosus or multiple sclerosis is a relative contraindication [7].

Inflammatory bowel disease. Secukinumab, ixekizumab and bimekizumab are not recommended in IBD, and brodalumab is contraindicated in active Crohn's disease [34,35,36,37]. With both conditions, French guidance recommends a TNF inhibitor, IL-12/23 inhibitor or IL-23 inhibitor approved for both [19]; the 2026 S3 update added risankizumab and guselkumab as recommended options [41].

Cancer. After recent malignancy, EuroGuiDerm recommends topical therapy, narrowband UVB (unless the malignancy was cutaneous or high risk) and/or acitretin, with methotrexate suggested after inadequate response [7]. French guidance lists methotrexate first line [19], and the 2026 S3 modified this chapter [41]. Biologics and apremilast are decided case by case with the oncologist [7,19].

Liver disease. In cirrhosis or advanced fibrosis, biologics or apremilast are suggested [19].

Chronic kidney disease. Biologics are suggested at all stages [7,19]. At eGFR ≥30 mL/min/1.73 m², acitretin, apremilast, fumarates and methotrexate may be used, with careful dosing [7]. Below this level, EuroGuiDerm recommends against ciclosporin, fumarates and methotrexate, and impaired renal function is in any case an absolute contraindication to ciclosporin [7]; acitretin is contraindicated in severe renal impairment [27], and apremilast is reduced to 30 mg once daily [22]. Work with a nephrologist from CKD stage 3 [7].

HIV. In well-controlled HIV, French guidance suggests the standard algorithm with HIV specialists, except for deucravacitinib [19].

Depression. Brodalumab requires caution given reported suicidal ideation and behaviour, although a causal link has not been established [7].

Vaccination. Complete vaccinations before starting systemic treatment where possible [7]. Live attenuated vaccines should be avoided during systemic immune-modifying therapy, in line with each product's label; non-live vaccines can generally be given, though response may be reduced [7]. Withholding methotrexate for 2 weeks after vaccination may be considered [41].

Pooled cohort data show increased relative risks of myocardial infarction (1.17), stroke (1.19) and cardiovascular death (1.46), and a greater risk in severe (1.41) than in mild disease (1.18) [50]. Psoriasis is also a risk factor for venous thromboembolism, relevant during admission, surgery or immobility [13]. These are observational associations. For patients at high or very high cardiovascular risk, French guidance recommends methotrexate or a TNF inhibitor [19]. This is not proven cardioprotection: in CIRT, low-dose methotrexate did not reduce cardiovascular events in patients with atherosclerosis, in a population not selected for psoriasis (hazard ratio 0.96, 95% CI 0.79–1.16) [51]. Associated conditions also include PsA, metabolic syndrome, IBD and depression [5,52]. Complications of GPP include hypoalbuminaemia, hypocalcaemia and hepatic involvement [3].

Sustained clearance is achievable with current agents, but the comparative data are mostly short term [23]. Whether early systemic treatment can modify the disease course is under study and is not established [16].

No intervention is proven to prevent psoriasis. Reducing modifiable triggers such as smoking, obesity and alcohol is part of management [5]. In GPP, subcutaneous spesolimab prevents flares (phase 2b Effisayil 2 trial) [53]. The labelled regimen is a 600 mg loading dose, then 300 mg every 4 weeks [47].

• Icotrokinra (2025–2026): this oral IL-23 receptor antagonist peptide gave an IGA 0/1 response in 65% versus 8% and PASI 90 in 50% versus 4% at week 16 in ICONIC-LEAD (684 participants aged 12 and over) [54]. It was superior to placebo and to deucravacitinib in ICONIC-ADVANCE 1 and 2 [55]. The FDA approved it in March 2026 [56]. EU marketing authorisation was issued on 18 September 2026 for adults and adolescents aged 12 years and over weighing at least 40 kg who are candidates for systemic therapy [57].
• Spesolimab (2021–2023) was the first IL-36 receptor-targeted therapy shown to treat and prevent GPP flares [10,53].

• Myelosuppression on methotrexate usually follows overdose, such as accidental daily intake, or unrecognised severe renal insufficiency, so name the weekly dosing day on the prescription [16].
• Candidiasis is the distinguishing adverse effect of bimekizumab: 21.2% versus 4.6% with secukinumab over 48 weeks in BE RADIANT [16].
• When diagnosing latent tuberculosis, remember that IGRA accuracy during methotrexate may be reduced; this matters if a later switch to a biologic is likely [41].