Psoriasis: Immune-Mediated Skin Disease

Reviewed by Dr C. J. Odike, MRCGP

Psoriasis is a chronic immune mediated disease that accelerates epidermal cell production and creates inflamed, scaly skin plaques. It is not contagious or caused by poor hygiene. Assessment includes skin, nails, joints, cardiovascular risk and psychological wellbeing because psoriasis can affect far more than appearance.

What psoriasis is Psoriasis is a chronic immune mediated disease affecting the skin and sometimes the nails and joints. Chronic means that the underlying tendency persists, although the visible disease can improve completely for long periods. Immune mediated means that altered immune signalling drives inflammation without an infection being the primary cause. Psoriasis is not contagious, and you cannot acquire it through touch, shared clothing, swimming or intimate contact. Psoriasis is not caused by poor hygiene Psoriasis does not develop because someone is dirty, careless or failing to wash their skin. Excessive washing and vigorous scale removal can irritate plaques and provoke further inflammation. Visible flakes can lead to unfair assumptions about cleanliness, particularly when scalp psoriasis falls onto clothing. Accurate explanation reduces stigma and prevents damaging cleaning routines that do not treat the underlying immune process. Skin renewal under normal conditions The epidermis continually replaces itself through cells called keratinocytes. New keratinocytes form near the lower epidermis, mature as they move upwards and eventually become part of the outer barrier. This organised process normally takes several weeks and produces a thin surface layer that sheds almost invisibly. Immune signals, growth factors and communication between skin cells regulate the speed and quality of this renewal. Accelerated keratinocyte turnover In psoriasis, inflammatory signals instruct keratinocytes to divide and move towards the surface much faster than usual. The cells reach the outer epidermis before completing normal maturation, so they retain features normally lost during development. These incompletely matured cells accumulate with inflammatory cells and create visible scale. Accelerated turnover explains scaling, but immune activation is the driver rather than skin cells simply growing too quickly by themselves. The immune pathways Dendritic cells, T lymphocytes, neutrophils and keratinocytes communicate through inflammatory cytokines. Tumour necrosis factor, interleukin 23 and interleukin 17 are particularly important within many psoriasis pathways. These signals increase keratinocyte proliferation, recruit additional immune cells and maintain chronic plaque inflammation. Modern targeted medicines work by blocking selected cytokines or their receptors rather than suppressing every immune function equally. The skin changes beneath a plaque Psoriatic epidermis becomes thickened and produces scale through incomplete keratinocyte maturation. Small blood vessels within the dermis become enlarged and more numerous, contributing to plaque colour and pinpoint bleeding after trauma. Inflammatory cells collect around vessels and within the epidermis. The visible plaque is therefore a combined product of immune inflammation, altered epidermal growth and vascular change. Genetics and environmental interaction Psoriasis often runs in families, showing that inherited susceptibility contributes. Many genes influence immune regulation and skin responses, and no single gene explains most cases. Some people inherit susceptibility but never develop psoriasis, while others have no recognised family history. Environmental exposures, medicines, infection, stress and skin injury can interact with genetic risk to trigger disease. Psoriasis can begin at any age Psoriasis can begin during childhood, adolescence or later adulthood. Earlier onset disease more often has a strong family history and certain immune genetic associations. Later onset psoriasis may follow a different course, but age alone does not predict future severity. A new rash in an older adult still requires diagnostic assessment because several other conditions can resemble psoriasis. Relapses and remissions Psoriasis usually follows a relapsing and remitting course. A flare means that existing plaques worsen or new lesions develop. A remission means that inflammation becomes minimal or disappears, sometimes for months or years. Treatment controls current disease and reduces future activity, but it does not permanently remove inherited and immune susceptibility. Plaque psoriasis Chronic plaque psoriasis is the commonest clinical pattern. It produces well defined raised plaques with a dry surface scale. Plaques are often symmetrical and commonly affect the elbows, knees, scalp, lower back, umbilicus and cleft between the buttocks. They may itch, burn, feel sore or crack, although some people have little discomfort despite extensive disease. Plaque borders and scale A plaque usually has a clear boundary separating inflamed skin from surrounding skin. The scale often appears silvery white on lighter skin and grey, cream or less conspicuous on darker skin. Removing scale forcibly can expose tiny bleeding points because superficial capillaries lie close beneath the abnormal epidermis. Scale appearance changes after bathing, moisturising or topical treatment and should not be used alone to judge activity. Psoriasis across different skin tones Inflammation may appear red or pink on lighter skin. On brown or black skin, plaques may appear violet, purple, dark brown, grey or only subtly different from surrounding skin. Scale, thickness, sharp borders, body distribution and the person's symptoms can be more informative than visible redness. Dark or light marks can remain after plaques settle and may cause substantial distress despite inactive inflammation. Scalp psoriasis Scalp psoriasis can produce thick adherent scale, itch and inflammation extending beyond the hairline. Common sites include behind the ears, the back of the scalp and the border around the forehead. Hair usually continues growing because ordinary psoriasis does not destroy follicles. Temporary shedding can occur through inflammation, scratching or forceful removal of scale, while permanent scarring suggests another diagnosis. Facial psoriasis Facial involvement can affect the eyebrows, hairline, eyelids, ears and creases beside the nose. The skin is thinner than on elbows or knees, so potent topical corticosteroids create greater local risk. Seborrhoeic dermatitis can overlap with psoriasis in oily facial and scalp areas. Treatment therefore uses site appropriate formulations and shorter anti inflammatory courses under a clear plan. Flexural or inverse psoriasis Flexural psoriasis affects folds such as the armpits, groin, under the breasts and between the buttocks. Plaques often appear smooth, shiny and well defined because moisture and friction reduce visible scale. Candida, bacterial intertrigo and contact irritation can coexist or mimic the condition. Thin folded skin is vulnerable to corticosteroid atrophy, so potent preparations are avoided at these sites. Genital psoriasis Genital psoriasis can cause smooth inflamed patches, soreness, fissures and discomfort during sexual activity. Scale may be minimal, and the appearance can resemble fungal infection, dermatitis or lichen sclerosus. The condition is not sexually transmitted and does not indicate poor hygiene. Sensitive explanation, appropriate examination and low risk site specific treatment can reduce physical symptoms and relationship anxiety. Palmoplantar psoriasis Psoriasis affecting palms and soles can cause thick scale, painful cracks and impaired walking or hand use. Even a small surface area can create severe functional disability. Palmoplantar pustulosis produces sterile pustules mainly on palms and soles and has a strong association with smoking. Fungal infection and contact dermatitis require consideration because they can resemble or coexist with palmoplantar disease. Guttate psoriasis Guttate psoriasis causes many small drop like scaly lesions across the trunk and limbs. It is more common in children and young adults and often follows a streptococcal throat infection. The eruption can clear within several months, recur after another infection or evolve into chronic plaque psoriasis. Widespread disease may require dermatology review and narrowband ultraviolet B treatment when topical therapy is impractical. Streptococcal infection and guttate disease A sore throat may precede guttate psoriasis by approximately two to three weeks. A throat swab or streptococcal antibody test can support evidence of recent infection in selected cases. Antibiotics treat active bacterial infection and reduce infectious complications. They do not reliably make an established guttate eruption disappear, so skin treatment follows its own pathway. Localised pustular psoriasis Pustular psoriasis produces visible collections of neutrophils that appear as white or yellow pustules. These pustules are usually sterile, meaning that bacteria are not the primary cause. Localised forms can affect palms, soles or the ends of fingers and toes. Infection can still coexist, so fever, spreading pain and systemic illness require clinical assessment rather than assuming every pustule is sterile. Generalised pustular psoriasis Generalised pustular psoriasis causes widespread waves of superficial pustules over tender inflamed skin. Fever, chills, weakness, dehydration, rapid heartbeat and laboratory abnormalities can develop. Pustules can merge into sheets and recur as earlier areas dry and peel. This unstable form can cause serious systemic complications and requires immediate same day hospital and dermatology assessment. Erythrodermic psoriasis Erythrodermic psoriasis causes widespread inflammation and scaling over most of the skin surface. The damaged barrier can lose fluid, protein and heat and can disturb normal temperature regulation. Complications include dehydration, infection, electrolyte disturbance, high output heart strain and circulatory instability. Rapidly generalising redness, scaling, shivering or systemic illness requires same day specialist assessment and often hospital treatment. Nail psoriasis Psoriasis can affect the nail matrix, nail bed or surrounding tissues. Changes include small pits, ridges, yellow red oil drop patches, crumbling, thickening beneath the nail and separation from the nail bed. Fingernails and toenails can both be affected, and severe disease can impair grip, footwear and fine tasks. Fungal infection can look similar and may require nail sampling before antifungal treatment. Nail pitting Nail pitting appears as multiple small depressions within the nail plate. It develops when psoriasis disrupts small areas of nail formation within the matrix. Pitting supports psoriasis but is not exclusive to it and can occur with alopecia areata or eczema. The number of pits does not reliably measure skin severity. Onycholysis Onycholysis means separation of the nail plate from the nail bed, usually beginning at the free edge. The detached area can appear white, yellow or discoloured. Debris and microorganisms can accumulate beneath the lifted nail and cause secondary changes. Avoid inserting sharp objects under the nail because trauma can worsen separation and introduce infection. Nail disease and joint risk Nail psoriasis is associated with an increased likelihood of psoriatic arthritis. The nail unit lies close to the tendon and ligament attachments around the end finger joints. This association does not mean that every person with pitting has arthritis. It does mean that new joint pain, stiffness, swelling or dactylitis deserves careful assessment. Psoriatic arthritis Psoriatic arthritis is an inflammatory musculoskeletal disease associated with psoriasis. It can affect peripheral joints, the spine, tendon insertions and entire fingers or toes. Skin disease usually begins first, but arthritis can appear before obvious plaques or with nail disease alone. Untreated inflammation can cause irreversible joint damage, functional loss and disability. Peripheral joint symptoms Psoriatic arthritis can cause joint pain, swelling, warmth and stiffness. Symptoms often worsen after rest and improve partly with movement, although patterns vary. The end joints of fingers, knees, ankles and other joints can be involved. Persistent morning stiffness, visible swelling or reduced function is more concerning than brief pain after an obvious mechanical strain. Dactylitis Dactylitis means diffuse inflammation of an entire finger or toe. The digit becomes swollen from base to tip, producing a sausage like appearance. Inflammation can involve joints, tendon sheaths and surrounding soft tissues simultaneously. Dactylitis strongly supports a spondyloarthritis pattern and should prompt rheumatology assessment. Enthesitis An enthesis is the site where a tendon or ligament attaches to bone. Psoriatic arthritis can inflame these sites, causing enthesitis. Common examples include heel pain at the Achilles tendon and pain beneath the foot at the plantar fascia attachment. Enthesitis can resemble overuse injury, so persistent symptoms with psoriasis require assessment of the complete inflammatory pattern. Axial psoriatic arthritis Axial disease affects the sacroiliac joints or spine. Clues include back pain beginning before age 45, morning stiffness, night pain and improvement with movement rather than rest. The PEST questionnaire does not detect axial arthritis reliably. A normal PEST result should not prevent referral when inflammatory back symptoms or other strong features are present. Screening for psoriatic arthritis NICE recommends annual assessment for psoriatic arthritis in people receiving treatment for psoriasis. A validated tool such as PEST can support screening in adults. PEST is not validated for children and does not identify every axial presentation. Screening is intended to trigger clinical assessment, not to diagnose arthritis through a questionnaire alone. Why early rheumatology referral matters NICE recommends rheumatology referral as soon as psoriatic arthritis is suspected. Early diagnosis allows disease modifying treatment before repeated inflammation causes permanent erosion, deformity or functional loss. Joint symptoms should not wait until the next routine dermatology review when they are persistent or progressive. Skin and joint treatment should be planned together because one medicine may benefit both conditions. Eye inflammation Psoriatic arthritis and related inflammatory disorders can be associated with uveitis. Symptoms include a painful red eye, light sensitivity and blurred vision. This differs from mild surface irritation and requires urgent ophthalmological assessment. Prompt treatment reduces the risk of complications affecting vision. Psoriasis is more than skin deep Psoriasis is associated with several physical and psychological conditions. These include psoriatic arthritis, cardiovascular disease, metabolic syndrome, depression, anxiety and inflammatory bowel disease. Shared immune pathways, genetic factors, treatment effects and lifestyle exposures contribute differently across these associations. Holistic care assesses these risks without implying that psoriasis has directly caused every additional diagnosis. Cardiovascular disease association Adults with severe psoriasis have an increased risk of cardiovascular disease. Chronic systemic inflammation may contribute alongside smoking, high blood pressure, diabetes, dyslipidaemia, obesity and reduced activity. NICE recommends cardiovascular risk assessment when severe psoriasis is diagnosed and at least every five years afterwards. A younger person can still benefit from blood pressure, weight, smoking and metabolic review even when a formal calculator is less informative. Metabolic syndrome Metabolic syndrome describes a cluster including central obesity, raised blood pressure, abnormal blood lipids and impaired glucose regulation. It occurs more frequently among people with psoriasis, particularly severe disease. The association is not a moral judgement about body weight, diet or motivation. Care should offer practical support and evidence based treatment for modifiable risk while also controlling inflammatory disease. Type 2 diabetes and fatty liver disease Psoriasis is associated with insulin resistance and type 2 diabetes. Obesity, alcohol, medicines and metabolic dysfunction can also increase fatty liver disease risk. These issues matter when choosing methotrexate, acitretin or another systemic treatment requiring liver monitoring. Abnormal liver tests require assessment rather than assuming psoriasis or body weight provides the complete explanation. Venous thromboembolism NICE advises that psoriasis, particularly severe disease, is associated with increased venous thromboembolism risk in adults. Risk becomes especially relevant during hospital admission, surgery and prolonged immobility. This does not justify routine anticoagulation for psoriasis alone. Ordinary VTE prevention assessment should account for psoriasis alongside other clinical factors. Psychological impact Visible plaques, scale and nail changes can affect self image, relationships, school, work and willingness to socialise. Itch, pain and treatment burden can disrupt sleep and concentration. Stigma can be intensified by the false belief that psoriasis is infectious or caused by poor cleanliness. Assessment should include emotional and social impact rather than judging severity only by skin surface area. Depression and anxiety Depression and anxiety occur more often in people with psoriasis than in the general population. The relationship includes inflammation, stigma, chronic symptoms, pain and treatment burden. NICE recommends assessing depression when reviewing psoriasis severity and escalating treatment. Thoughts of self harm or inability to remain safe require urgent mental health support, regardless of the visible skin severity. Common trigger factors A trigger is an exposure associated with disease onset or worsening. Recognised examples include infection, skin injury, stress, smoking, heavy alcohol exposure and selected medicines. Not every flare has an identifiable trigger, and removing one trigger does not guarantee permanent remission. Treatment should not be delayed while searching for one perfect explanation. The Koebner phenomenon The Koebner phenomenon means that new psoriasis lesions develop at sites of skin injury. Cuts, scratches, burns, tattoos, injections, surgical scars, friction and sunburn can provoke plaques. Lesions usually appear after the injury rather than immediately. The phenomenon explains why picking scale or repeatedly rubbing a plaque can worsen the affected area. Stress and flares Stress can influence immune signalling, sleep, scratching and treatment routines. A flare can then create further stress through discomfort, appearance concerns and social disruption. This interaction is genuine but does not mean that psoriasis is imaginary or caused by poor emotional control. Stress management support can complement medical treatment but should not replace anti inflammatory care. Medicines that can worsen psoriasis Lithium, beta blockers and antimalarial medicines can trigger or worsen psoriasis in susceptible people. Other possible contributors include interferons, some immune therapies and selected medicines with variable evidence. The reaction can begin weeks or months after treatment starts. Do not stop an important medicine independently. The prescriber must compare the dermatological effect with the reason for treatment and available alternatives. Systemic corticosteroid withdrawal Systemic corticosteroids are generally avoided as routine psoriasis treatment. Rapid reduction or withdrawal can sometimes trigger severe rebound, erythrodermic disease or generalised pustular psoriasis. People taking corticosteroids for another condition should not stop them suddenly. Any dose change should follow the prescribing clinician's plan, with dermatology advice when psoriasis becomes unstable. Smoking and alcohol Smoking is strongly associated with palmoplantar pustulosis and can worsen overall health risks. Higher alcohol intake is associated with more difficult psoriasis control in some people and can interact with systemic medicines. Dependence, stress and social circumstances may influence these behaviours. Support should be non judgemental and linked to the person's priorities rather than presented as punishment for having psoriasis. Obesity and psoriasis severity Obesity is associated with more severe psoriasis and can reduce the effectiveness of some systemic treatments. Adipose tissue produces inflammatory mediators, while painful joints and stigma can make activity difficult. Weight management may improve overall health and treatment response but is not a prerequisite for respectful or effective psoriasis care. Treatment of active disease can make movement and self care more achievable. Diagnosing psoriasis Psoriasis is usually diagnosed from the morphology and distribution of skin and nail changes. The clinician asks about duration, previous episodes, family history, infection, medicines and joint symptoms. The whole skin surface should be considered because small plaques can be hidden within the scalp, umbilicus or cleft. There is no routine blood test that confirms ordinary plaque psoriasis. When skin biopsy is used Skin biopsy is rarely necessary for typical plaque psoriasis. It can help when lymphoma, eczema, fungal infection, lichen planus, drug eruption or another inflammatory disorder remains possible. A local anaesthetic is used before a small skin sample is removed. Biopsy findings must be interpreted with the clinical pattern because treated or atypical lesions can be less specific. Fungal infection as a differential Tinea can produce scaly plaques with a more active advancing edge and partial central clearing. Topical corticosteroids can suppress redness while allowing fungal spread, producing tinea incognito. Skin scrapings can identify fungal elements when the diagnosis is uncertain. Fungal infection can coexist with psoriasis, particularly on feet, groins and nails. Eczema and contact dermatitis Eczema usually has less sharply defined borders and may show weeping, crusting or intense itch. Allergic contact dermatitis follows exposure to a sensitising substance and may affect hands, face or treatment sites. Psoriasis and eczema can overlap, and repeated topical products can cause contact allergy. Patch testing may be needed when treatment resistant disease follows an exposure pattern. Seborrhoeic dermatitis Seborrhoeic dermatitis produces flaky inflammation on the scalp, eyebrows, ears and creases beside the nose. Scale is often thinner and greasier than classic psoriasis. Sebopsoriasis describes an overlapping pattern with features of both conditions. Antifungal and anti inflammatory approaches may both be used when the diagnosis remains mixed. Pityriasis rosea and drug eruptions Pityriasis rosea can produce a sudden widespread scaly eruption, often beginning with one larger herald patch. Drug eruptions can create symmetrical red or scaly lesions after a new medicine. Guttate psoriasis, secondary syphilis and viral rashes can look similar. A sudden widespread eruption therefore requires history and examination rather than diagnosis from one photograph alone. Measuring severity Severity includes body surface area, plaque thickness, scale, inflammation, symptoms and response to previous treatment. Specialists often use the Psoriasis Area and Severity Index, called PASI. Quality of life tools such as the Dermatology Life Quality Index measure practical and psychological impact. These scores support decisions but should not override severe disease at a high impact site. High impact sites The face, scalp, genitals, palms, soles and nails are considered high impact or difficult to treat sites. Small areas here can impair walking, manual work, sleep, intimacy or social interaction. A low body surface measurement can therefore underestimate clinical severity. Treatment escalation and referral should consider function and distress alongside numerical scores. Treatment goals Treatment aims to clear or substantially reduce plaques, relieve symptoms and restore normal function. It should also protect joints, reduce treatment toxicity and address cardiovascular and psychological health. Complete clearance is possible with modern therapy but cannot be guaranteed permanently. The plan is stepped according to site, severity, impact, joint disease and previous response. Shared decision making Topical treatment can be time consuming, messy or difficult to apply to the scalp and back. Phototherapy requires repeated visits, while systemic medicines require monitoring and carry different risks. The clinician should discuss speed, convenience, pregnancy plans, comorbidities and personal treatment goals. Adherence improves when the formulation and schedule fit ordinary life. Emollients Emollients soften scale, reduce cracking and improve comfort. They are useful alongside active treatment but do not suppress the main immune pathways sufficiently by themselves. Ointments are often useful for thick dry plaques, while creams or lotions can be easier on hairy areas. Residue within clothing and bedding can increase fire risk, so treated fabrics must remain away from flames and cigarettes. Scale removal Thick scale can prevent active topical medicine reaching the inflamed skin beneath. Emollients, oils or salicylic acid preparations can soften and remove adherent scale. Forceful scraping causes trauma and can provoke Koebnerisation. Salicylic acid requires caution over large areas, in young children and with kidney impairment because systemic absorption can occur. Topical vitamin D analogues Calcipotriol and related vitamin D analogues regulate keratinocyte growth and immune activity. They are important treatments for plaque psoriasis on the trunk and limbs. Irritation can occur, particularly on the face or within folds. Excessive use over large areas can disturb calcium metabolism, so maximum quantities and product instructions matter. Topical corticosteroids Topical corticosteroids reduce inflammation and are effective components of psoriasis treatment. Potency and duration depend on site, age, plaque thickness and treatment history. Thin skin on the face, flexures and genitals is more vulnerable to atrophy. Continuous potent treatment without planned breaks can cause skin damage, reduced effectiveness and unstable rebound disease. Combination topical treatment For adults with trunk or limb psoriasis, NICE recommends an initial regimen combining a potent corticosteroid and vitamin D analogue. They may be applied separately at different times or provided as an authorised combination preparation. The corticosteroid controls inflammation quickly, while the vitamin D analogue supports longer term plaque control. The regimen needs review rather than continuous indefinite use without monitoring. Scalp treatment NICE recommends a potent topical corticosteroid once daily for up to four weeks as initial scalp treatment. Solutions, gels, foams, mousses and shampoos can reach hairy skin more easily than thick ointments. Adherent scale can be softened before the active treatment is applied. Poor response may reflect formulation difficulty, insufficient quantity, contact allergy, fungal overlap or an incorrect diagnosis. Face, flexure and genital treatment NICE recommends short term mild or moderate topical corticosteroid treatment for facial, flexural and genital psoriasis. Treatment is generally limited to brief courses because these areas absorb medicine readily. Potent and very potent corticosteroids should not be used on these sites. A topical calcineurin inhibitor can be considered by an experienced clinician when repeated steroid courses create unacceptable local risk. Topical treatment safety The product name and percentage alone do not reveal corticosteroid potency reliably. A clear plan should state where each product belongs, how often it is used and when it should stop. Very potent corticosteroids are reserved for specialist supervision and short treatment periods. Children using topical corticosteroids require age appropriate treatment and review for local adverse effects. Reviewing topical response Topical treatment should be reviewed after an agreed trial, commonly around four weeks for initial regimens. The review checks improvement, quantity used, application technique and practical barriers. Failure does not automatically mean that the disease is biologically resistant. Insufficient potency, small quantities, inaccessible sites and unacceptable formulations commonly explain poor control. Phototherapy Narrowband ultraviolet B phototherapy treats widespread plaque or guttate psoriasis uncontrolled by topical treatment. Treatment is usually delivered two or three times weekly within a supervised phototherapy unit. Ultraviolet exposure can cause redness, burns and cumulative skin ageing. A personal history of skin cancer, photosensitivity and previous ultraviolet exposure influence suitability. PUVA PUVA combines psoralen, a light sensitising medicine, with ultraviolet A radiation. It can treat selected difficult psoriasis patterns but carries a greater cumulative skin cancer risk than narrowband UVB. Eye protection and strict light precautions are required after psoralen exposure. PUVA is not routinely used in children and is avoided or limited in people with important skin cancer risk. When systemic treatment is considered Systemic treatment is considered when topical therapy cannot control psoriasis and the disease has substantial physical, psychological or social impact. Examples include extensive disease, severe high impact site involvement and rapid relapse after phototherapy. Systemic therapy can also be needed when psoriatic arthritis influences treatment choice. These medicines require specialist selection, baseline screening and continuing safety monitoring. Methotrexate NICE recommends methotrexate as the usual first choice conventional systemic treatment when systemic criteria are met. It reduces immune activity and can improve both skin psoriasis and peripheral psoriatic arthritis. Methotrexate is taken once weekly, never daily, and is commonly paired with folic acid. Blood counts, liver function and kidney function require monitoring because serious toxicity can occur. Methotrexate safety Pregnancy and conception plans must be discussed before methotrexate treatment. Liver disease, alcohol exposure, kidney impairment, infection and interacting medicines affect safety. Mouth ulcers, unusual bruising, severe sore throat, breathlessness or marked illness require prompt review. The medicine should not be stopped or restarted without advice when infection or laboratory abnormalities occur. Ciclosporin Ciclosporin suppresses T cell activity and can control psoriasis rapidly. NICE uses it as a first choice conventional option when rapid or short term control is needed or in selected conception circumstances. Kidney function and blood pressure require close monitoring. It is generally used for limited periods because cumulative kidney, hypertension and other toxicity increase with exposure. Acitretin Acitretin is an oral retinoid that regulates epidermal growth and differentiation. It can be useful for pustular psoriasis and when methotrexate or ciclosporin is unsuitable. Dry lips, skin dryness, lipid changes and liver abnormalities can occur. It is highly teratogenic and requires a prolonged pregnancy prevention programme after treatment ends. Systemic corticosteroids Oral or injected systemic corticosteroids are not routine treatments for chronic psoriasis. They can produce temporary improvement followed by severe rebound when reduced or stopped. Withdrawal has been associated with pustular or erythrodermic instability. When corticosteroids are essential for another illness, prescribing and withdrawal require coordination rather than abrupt self discontinuation. Biological medicines Biological medicines are targeted proteins given by injection or infusion. Available classes inhibit tumour necrosis factor, interleukin 17, interleukin 23 or the shared interleukin 12 and 23 pathway. They can produce major skin clearance and can treat selected psoriatic arthritis patterns. They are not permanent cures and require specialist assessment for infection, vaccination, comorbidities and treatment response. Targeted synthetic medicines Targeted synthetic medicines are oral drugs acting on selected intracellular or receptor pathways. Examples include apremilast and deucravacitinib within defined specialist pathways. Their adverse effect and monitoring profiles differ from biologics and conventional immune suppression. The least burdensome option is not automatically the safest for every person. Choosing advanced treatment Choice considers psoriasis pattern, joint disease, inflammatory bowel disease, previous infection, pregnancy plans and cardiovascular history. Some interleukin 17 inhibitors can worsen inflammatory bowel disease in susceptible people. Tumour necrosis factor inhibitors and several interleukin inhibitors have different benefits for joints, spine, entheses and skin. Dermatology and rheumatology should coordinate treatment when both skin and musculoskeletal disease are active. Treating psoriatic arthritis Joint inflammation requires disease modifying treatment rather than analgesia alone. Conventional medicines such as methotrexate can help selected peripheral joint disease. Biological and targeted synthetic treatments are chosen according to peripheral joints, spine, enthesitis, dactylitis and skin severity. Early treatment aims to achieve remission or low activity and prevent irreversible structural damage. Treating generalised pustular psoriasis Generalised pustular psoriasis requires hospital based supportive and specialist treatment. Fluid balance, temperature, infection, electrolytes and organ function require monitoring. Ciclosporin, acitretin, methotrexate or targeted therapy may be selected according to severity and circumstances. NICE now recommends spesolimab as an option for defined adult flares, reflecting the importance of interleukin 36 signalling in this disease. Treatment during pregnancy Pregnancy can improve, worsen or leave psoriasis unchanged. Topical treatment, phototherapy and systemic choices require review because fetal and maternal safety varies. Methotrexate and acitretin are contraindicated in pregnancy, while ciclosporin or selected biological treatment may be considered by specialists. Do not stop effective treatment when pregnancy is discovered without urgent advice, because uncontrolled disease and abrupt withdrawal can also create risk. Infection screening and vaccination Systemic immune treatments can increase susceptibility to selected infections. Baseline assessment can include tuberculosis, hepatitis and other infection testing according to the planned medicine. Routine vaccination should be updated before treatment where possible. Live vaccines may be unsuitable during certain immunosuppressive therapies, while non live vaccines remain important. Monitoring systemic treatment Monitoring depends on the medicine and includes blood counts, kidney function, liver tests, blood pressure, infection review and pregnancy precautions. Biological treatment is continued only when there is clear evidence of meaningful response. The review also asks whether joint activity, quality of life and high impact sites have improved. Adverse effects can emerge after the skin clears, so safety monitoring must continue. Complementary treatments Many supplements, restrictive diets and unregulated creams are promoted for psoriasis. Evidence is limited for most, and some products contain undeclared corticosteroids or irritants. Complementary treatment can interact with methotrexate, ciclosporin or anticoagulants. Tell the clinical team about everything being used so that toxicity and treatment failure can be interpreted accurately. Lifestyle and cardiovascular care Regular movement, nutritious eating, smoking cessation and moderation of alcohol support cardiovascular and general health. Advice should be practical and adapted when joint pain, poverty, work patterns or low mood limit choices. Blood pressure, cholesterol, glucose and weight require evidence based management when abnormal. Lifestyle support complements effective psoriasis treatment and should never be used as a reason to withhold it. School and work Scalp scale, visible plaques and treatment routines can affect confidence and attendance. Hand, foot and nail disease can impair manual work even when body surface involvement is small. Reasonable adjustments may include time for treatment, protective clothing and reduced exposure to repeated trauma or irritants. Colleagues and schools should understand that psoriasis is not infectious. Relationships and intimacy Genital plaques, scale and fear of rejection can affect intimacy. Partners may wrongly fear infection or sexual transmission. Clear explanation and sensitive treatment can reduce pain, embarrassment and avoidance. Sexual health assessment remains appropriate when symptoms or exposures suggest a separate infection. Prognosis Psoriasis varies greatly between people and across the lifespan. Guttate disease may resolve, while plaque psoriasis often follows a long relapsing course. Modern topical, ultraviolet and targeted systemic treatments can achieve excellent control or complete visible clearance. Joint and cardiometabolic risk still require review even when the skin is clear. Follow up Follow up records disease severity, treatment response, adverse effects and quality of life impact. People receiving treatment should be assessed annually for psoriatic arthritis. Adults with severe disease receive cardiovascular risk assessment at diagnosis and at least every five years. New widespread pustules, generalised redness, joint swelling or severe psychological distress require earlier review. The central safety message Psoriasis is an immune mediated systemic disease rather than a contagious hygiene problem. Plaque psoriasis is common, but pustular and erythrodermic forms can cause life threatening skin failure and systemic illness. Persistent joint pain, swelling, dactylitis, enthesitis or inflammatory back pain requires early rheumatology referral. Safe treatment is stepped from topical therapy to phototherapy and monitored systemic or targeted treatment according to disease impact.

Psoriasis is driven by immune signalling that accelerates keratinocyte turnover and sustains inflammation. Safe care treats the skin while screening for joint disease, cardiometabolic risk and psychological impact, with immediate escalation for generalised pustular or erythrodermic disease.

Medical words made simple

Psoriasis
A chronic immune-mediated disease causing inflamed, thickened and scaly skin, with possible nail and joint involvement.
Immune-mediated disease
A condition in which altered immune signalling drives inflammation and tissue changes.
Keratinocyte
The main cell of the epidermis, producing keratin and forming much of the skin barrier.
Epidermis
The outer cellular layer of the skin.
Keratinocyte turnover
The process through which epidermal cells are produced, mature, move to the surface and shed.
Cytokine
A signalling protein used by immune and other cells to coordinate inflammation.
Tumour necrosis factor
An inflammatory cytokine involved in psoriasis and targeted by several biological medicines.
Interleukin 17
A cytokine driving keratinocyte activation and inflammation within many psoriasis pathways.
Interleukin 23
A cytokine supporting inflammatory T-cell responses and targeted by several psoriasis treatments.
Plaque
A raised, well-defined area of abnormal skin larger than a small papule.
Plaque psoriasis
The commonest psoriasis pattern, producing persistent well-defined scaly plaques.
Scale
Visible flakes created when outer skin cells accumulate and shed abnormally.
Guttate psoriasis
A psoriasis pattern with many small drop-like lesions, often following streptococcal throat infection.
Pustular psoriasis
A psoriasis pattern producing visible sterile pustules, either locally or across large skin areas.
Generalised pustular psoriasis
A severe systemic psoriasis flare with widespread pustules, tender inflammation and possible fever or organ complications.
Erythrodermic psoriasis
Severe widespread psoriasis inflammation and scaling affecting most of the skin surface.
Flexural psoriasis
Psoriasis affecting skin folds and often appearing smooth and shiny with little scale.
Palmoplantar psoriasis
Psoriasis affecting the palms or soles, often causing thick scale, cracks and functional difficulty.
Koebner phenomenon
Development of new psoriasis lesions at sites of skin injury or repeated friction.
Nail pitting
Small depressions in the nail plate caused by disturbed nail formation.
Onycholysis
Separation of the nail plate from the nail bed.
Psoriatic arthritis
An inflammatory disease affecting joints, the spine, tendon attachments or entire digits in association with psoriasis.
Dactylitis
Inflammation causing an entire finger or toe to swell from base to tip.
Enthesitis
Inflammation where a tendon or ligament attaches to bone.
Axial arthritis
Inflammatory arthritis affecting the sacroiliac joints or spine.
PEST
The Psoriasis Epidemiological Screening Tool, a questionnaire supporting adult psoriatic arthritis screening.
Metabolic syndrome
A cluster involving central obesity, high blood pressure, abnormal lipids and impaired glucose regulation.
Body surface area
An estimate of how much skin is affected, often using the person's palm as approximately one percent.
PASI
The Psoriasis Area and Severity Index, combining affected area, thickness, scaling and inflammation.
Emollient
A moisturising treatment that softens scale, reduces cracking and improves skin comfort.
Vitamin D analogue
A topical medicine such as calcipotriol that regulates keratinocyte growth and skin inflammation.
Topical corticosteroid
An anti-inflammatory steroid medicine applied directly to affected skin.
Topical calcineurin inhibitor
A non-steroid topical anti-inflammatory medicine used at selected sensitive sites under experienced supervision.
Phototherapy
Controlled ultraviolet-light treatment delivered through a specialist service.
Narrowband ultraviolet B
A selected range of ultraviolet B wavelengths used to treat widespread plaque or guttate psoriasis.
PUVA
Treatment combining psoralen sensitisation with ultraviolet A radiation.
Systemic treatment
Medicine acting throughout the body rather than only where it is applied.
Methotrexate
A once-weekly immune-modifying medicine used for selected psoriasis and psoriatic arthritis.
Ciclosporin
A rapid-acting systemic immune medicine requiring kidney-function and blood-pressure monitoring.
Acitretin
An oral retinoid used for selected psoriasis, particularly pustular disease, with major pregnancy precautions.
Biological medicine
A targeted injected or infused treatment blocking a selected inflammatory molecule or receptor.
Targeted synthetic medicine
An oral medicine acting on a selected immune pathway rather than broadly suppressing every response.
Spesolimab
A targeted medicine blocking the interleukin 36 receptor and used for selected generalised pustular psoriasis flares.
Uveitis
Inflammation inside the eye causing pain, redness, light sensitivity or blurred vision.

Quick recap

  • Psoriasis is a chronic immune mediated disease and is not contagious.
  • It is not caused by poor hygiene, and excessive scrubbing can worsen plaques.
  • Immune cytokines accelerate keratinocyte turnover and create thickened scaly skin.
  • Plaque psoriasis is the commonest pattern and often affects elbows, knees, scalp and lower back.
  • Inflammation can appear purple, brown or grey rather than bright red on darker skin.
  • Scalp, nail, palm, sole, genital and facial disease can be severe despite limited surface area.
  • Guttate psoriasis causes small drop like lesions and often follows streptococcal throat infection.
  • Generalised pustular psoriasis causes widespread pustules and systemic illness and is a dermatological emergency.
  • Erythrodermic psoriasis inflames most skin and can disrupt fluid, protein and temperature balance.
  • Nail pitting and onycholysis support psoriasis but are not diagnostic by themselves.
  • Psoriatic arthritis can affect peripheral joints, the spine, entheses and entire digits.
  • Dactylitis produces swelling of a whole finger or toe.
  • PEST supports annual adult joint screening but does not detect every axial presentation.
  • NICE recommends rheumatology referral as soon as psoriatic arthritis is suspected.
  • Early disease modifying treatment reduces the risk of permanent joint damage.
  • Severe psoriasis is associated with increased cardiovascular disease and metabolic syndrome.
  • Adults with severe psoriasis should receive cardiovascular risk assessment at diagnosis and at least every five years.
  • Depression and anxiety should be assessed because psychological burden can exceed visible skin severity.
  • Skin trauma can produce new plaques through the Koebner phenomenon.
  • Lithium, beta blockers and antimalarial medicines can worsen psoriasis in susceptible people.
  • Do not stop prescribed medicines or systemic corticosteroids abruptly without clinical advice.
  • Psoriasis is usually diagnosed clinically, while biopsy is reserved for uncertain presentations.
  • Emollients soften scale and reduce cracking but do not replace active anti inflammatory treatment.
  • Vitamin D analogues regulate epidermal growth and are important topical treatments.
  • Topical corticosteroid potency and duration must match the body site and plaque thickness.
  • Narrowband UVB treats widespread plaque or guttate psoriasis uncontrolled with topical therapy.
  • Methotrexate is the usual first choice conventional systemic medicine when NICE systemic criteria are met.
  • Ciclosporin provides rapid control, while acitretin can help selected pustular disease.
  • Biologics target TNF, interleukin 17, interleukin 23 or related pathways.
  • Skin and joint treatment should be coordinated when psoriatic arthritis is present.
  • Systemic treatment requires infection screening, laboratory monitoring and pregnancy planning.
  • Modern treatment can achieve excellent control, but joint and cardiovascular review must continue.