Psoriasis

Psoriasis is a chronic, immune-mediated inflammatory disease of the skin, and in many patients also of the joints and other organs. Its hallmark is the erythematous, thickened, silvery-scaled plaque, which forms when T cells and cytokines drive keratinocytes to multiply far faster than normal and the skin's inflammatory circuits stay switched on. Estimates put its global frequency at roughly 2% to 5% of people, and it is now treated as a systemic condition rather than a purely cutaneous one. Although it is not contagious, it is classed among autoimmune diseases because the immune system is misdirected against the body's own tissue.

The disease matters for several reasons. It is lifelong and relapsing, it can damage joints, and it is linked to cardiometabolic, psychiatric and other comorbidities that affect life expectancy and quality of life. The past two decades have changed its management: understanding of the IL-23/IL-17 immunologic pathway led to biologic drugs that clear skin in most patients with moderate-to-severe disease, and this has reshaped how clinicians think about treatment targets.

This entry covers the disease from several angles: its clinical forms and diagnosis, its genetic and environmental causes, the immune and tissue mechanisms behind the plaques, the associated joint and systemic disease, the full range of treatments from topical agents to biologics, and the open questions about relapse and long-term control.

Clinical Features and Presentation

Typical plaques

The classic lesion is a sharply demarcated, erythematous plaque covered by thick, silvery-white scale. When the scale is lifted, pinpoint bleeding points appear on the plaque surface. This is the Auspitz sign, named after the Viennese dermatologist Paul Gustav Auspitz. Plaques are usually symmetrical and favour the extensor surfaces of the elbows and knees, the scalp, the lumbosacral region and the natal cleft. Scalp lesions often extend past the hairline onto the forehead, neck or ears, which helps separate them from seborrhoeic dermatitis.

Symptoms

Itching is the most frequently reported symptom, but many patients also describe burning, soreness and cracking. Fissuring is most common in flexural areas and on the fingertips, where skin movement stresses the plaques. Lesions can disrupt sleep, cause discomfort when they rub against clothing, and limit everyday tasks such as gripping objects, washing or dressing. The degree of distress often does not correspond precisely to the visible extent of the disease, which is relevant to how symptoms are assessed in clinical practice.

Nail involvement

Nail changes are common and may appear with or without skin lesions on the same person. Typical findings include pitting, which consists of small depressions in the nail plate; onycholysis, in which the nail separates from the nail bed; oil-drop discoloration, a yellow-brown patch beneath the nail that reflects abnormal accumulation of scale; and subungual hyperkeratosis, a crumbling thickening of debris under the nail. Nail disease is more frequent in people who also have joint involvement, and the presence of nail changes is therefore often used as a prompt to check the joints.

Koebner phenomenon

The Koebner phenomenon describes the appearance of new lesions at sites of skin trauma. Scratches, surgical incisions, abrasions, sunburn, insect bites and tattoos can all serve as the trigger, typically appearing a few days to several weeks after the injury. In diagnosis, the phenomenon helps explain why plaques sometimes occur in linear or unusual patterns and can support the distinction from other conditions. In treatment, it is a reason for caution with invasive procedures, and it is considered when planning interventions that would traumatise the skin.

Course

The condition is chronic and generally lifelong, although no cure exists. It typically follows a relapsing and remitting course, with flares that may be linked to infection, stress, skin injury or medication, and periods of partial or near-complete clearance. The extent of disease varies widely. Many people have a few small plaques confined to limited areas, while others develop extensive involvement that covers large portions of the body. The disease reflects underlying inflammation of the skin, and its severity is usually judged by how much of the body surface is affected and by how much it limits function.

Epidemiology and Global Distribution

Estimates of how many people have psoriasis depend heavily on the data source and method. In the Global Burden of Disease (GBD) 2021 analysis, prevalent cases rose by roughly 86%, from about 23 million in 1990 to about 43 million in 2021, and the number of new cases grew by about 80% over the same period (From 1990 to 2021, global psoriasis prevalence increased from 23.06 million to 42.98 million (an 86% rise), and incidence grew by 80% from 2.85 million to 5.10 million cases.). Much of this growth reflects population ageing and better access to care in high-income regions, where the largest burden is concentrated (The global psoriasis burden continues to increase, particularly in high-SDI regions, where aging populations and greater healthcare access coexist.). The Global Psoriasis Atlas, which relies partly on self-reported cases, gives a much wider range: about 102 million people, with a plausible span of 65 million to 218 million (An estimated 102 million (from 65 million to 218 million) people have psoriasis based on self-report cases provided by individuals.). Data remain sparse, since general-population epidemiological data exist for only about 41 of more than 220 countries and territories (Only 41 of over 220 countries and territories in the world have epidemiological data on psoriasis in the general population).

Regional differences are large. Age-standardized prevalence in GBD-based analyses varies about fourteenfold, from 0.14% in East Asia to 1.99% in Australasia (age-standardized prevalence rates that vary 14-fold between low-prevalence regions like East Asia (0.14%) and high-prevalence regions like Australasia (1.99%)). Physician-diagnosed prevalence in the Atlas ranges from 0.15% in Eastern Sub-Saharan Africa to 3.68% in Australasia (In adults, prevalence of psoriasis varies between 0.15% in Eastern Sub-Saharan Africa to 3.68% in Australasia). A 20-country study that applied one methodology throughout found a different ordering, with the highest prevalence in East Asia and no significant difference between Australia, Europe and the Middle East (our study, applying the same methodology across all 20 countries, surprisingly revealed that prevalence is highest in East Asia., with no significant difference in prevalence between Australia, Europe, and the Middle East.). The conflict likely reflects differences in case definition, since self-report, modelled estimates and physician-confirmed diagnoses do not measure the same thing. Explanations for geographic variation linked to latitude and urban living have been proposed, including differences in sunlight exposure, lifestyle and diagnostic access, but these associations are confounded and are not consistently replicated.

Age of onset follows a bimodal pattern. Henseler and Christophers separated disease into type I, beginning before age 40 with a peak at 16–22 years, and type II, beginning after 40 with a peak at 57–60 years (Type I psoriasis manifests before age 40 with peak onset at 16–22 years, and Type II psoriasis begins after age 40 with peak onset at 57–60 years). Family history is strongly tied to the early-onset group: Type I psoriasis has a stronger genetic basis as a greater proportion of patients had a family history of psoriasis, and has stronger HLA-C∗06 associations; however, Type II psoriasis is negative in family history. Relative risk for first-degree relatives was about 10 for type I, compared with 1 to 2 for type II (The risk ratio for first degree relatives for type I psoriasis was 10, compared with 1 or 2 for those with type II psoriasis.). Early-onset disease also tends to be more severe, and one Spanish study found it more likely to be unstable and to carry a greater psychosocial burden (early onset psoriasis, defined as onset below 30 years of age, was more likely to be unstable, more severe, and associated with a positive family history of psoriasis.).

The sex distribution of onset is also informative. In one analysis of 2147 case histories, the peak age was about 16 in women and about 22 in men in roughly two-thirds of cases (the age of onset for psoriasis is bimodally distributed; in approximately two thirds of the cases the peak age of onset was determined to be 16 (female) to 22 (male) years of age). Overall prevalence shows little difference between the sexes. Women's rates rise more steeply in youth, but after about the early twenties the prevalence in men and women is similar (Whilst the prevalence increases more rapidly with age in young female patients (i.e., age <20 years) compared with young male patients, thereafter, the prevalence of psoriasis is similar in both sexes.).

Sex differences are clearer in severity than in frequency. A Swedish registry study of 5438 patients receiving systemic treatment found that, after adjustment, women had less severe disease in all body areas except the head (Analysis showed that women have less severe psoriasis compared with men, after controlling for several possible confounders, such as age, smoking habits etc. Importantly, this difference between sexes was true for all body areas, except the head, where the PASI scores were equal.). Women typically present earlier and with milder disease, while men are more likely to develop severe disease and to receive systemic treatment (Female patients typically experience an earlier age of onset and milder disease severity, whereas male patients are more likely to develop severe psoriasis and have higher rates of systemic treatment use). The evidence has limits. Most epidemiological studies include only patients receiving systemic therapy (most epidemiological studies include selected patients undergoing systemic therapies only), so treatment-based comparisons may reflect who is referred rather than who is affected. Whether the male predominance in biologic prescribing reflects disease activity or unequal access is also debated (The asymmetry in allocation of biologic therapy thereby probably reflects the differing disease activity between the sexes, and is not a discrimination against women per se.).

Incidence trends and their measurement pose methodological challenges. The GBD estimates are model-based, using Bayesian meta-regression to combine multiple data sources, because direct registry coverage is incomplete (Data from GBD 2021, covering 204 countries and regions, were used to estimate psoriasis incidence, prevalence, and DALYs through the DisMod-MR 2.1 model with Bayesian meta-regression to integrate multiple data sources.). Registry and claims-based studies capture different populations: dermatology registries tend to include patients on systemic treatment, while administrative claims depend on diagnostic coding and miss the many mild cases managed without specialist input. Underdiagnosis in primary care means that both approaches may undercount, and changes in coding practice can create apparent trends.

Paediatric psoriasis shares the adult types but has distinct features. Onset of non-pustular disease is most common between about 15 and 25 years (the peak age of onset for nonpustular psoriasis, especially the chronic stationary form of the disease, is between 15 and 25 years of age.), and guttate forms are associated with younger onset and nail involvement (guttate-type psoriasis was associated with younger age of onset and with nail involvement.). Commonly cited estimates place roughly a third of cases before adulthood, but childhood-specific prevalence data are less consistent across studies, and children are under-represented in most adult-focused cohorts.

Genetics and Environmental Triggers

Polygenic inheritance and the MHC region

Psoriasis is best understood as a polygenic condition, in which many common variants each add a modest amount of risk. The first strong genetic signal came from linkage analysis, which placed the psoriasis susceptibility 1 (PSORS1) interval on the short arm of chromosome 6, inside the major histocompatibility complex (MHC). Genome-wide association studies have repeatedly placed their most significant signal in this same region. Within it, the HLA-C*06:02 allele is the strongest single risk factor. HLA-C is a class I molecule that presents peptides to CD8+ T cells, and HLA-C06:02 is associated with early-onset disease, with greater severity, and with familial clustering. Its mechanism is still incompletely understood, and no HLA-C06:02-specific antigen has been firmly identified. The PSORS1 interval also contains other genes, such as CDSN and CCHCR1, and some variants there show associations independent of HLA-C*06:02. One Polish case-control study reported that some of these effects differed between men and women, and this finding has yet to be validated in larger and more diverse populations. Outside the MHC, genome-wide studies have identified dozens of further loci. Many of these affect the cytokine signalling pathways that drive the IL-23/IL-17 axis, type I interferon responses, and innate immune sensing. The CARD14 gene, which encodes a signalling protein expressed in keratinocytes, is one example and appears to be especially relevant to pustular forms.

Heritability from twin and family studies

Twin and family data support a strong genetic component. In a population-based sample of 10,725 Danish twin pairs, the proband-wise concordance was 0.33 in monozygotic pairs and 0.17 in dizygotic pairs, and genetic factors accounted for about 68% of the variation in susceptibility. Earlier twin studies reported heritability estimates between 66% and 90%, and heritability estimates vary with study design and population. Family data show a similar pattern: in a Swedish survey, 6.4% of relatives of patients were affected, compared with 1.96% of the general population, and in the closed Faroe Islands community, 91% of patients had a family history. Concordance in monozygotic twins is well below 100%, which indicates that the genotype does not fully determine the phenotype. Twin studies also suggest that clinical type, age of onset, course and severity are influenced to a large extent by genetic factors.

Environmental triggers

Several environmental exposures are repeatedly linked to onset or flares. Streptococcal throat infection is the most closely studied. Patients often report a sore throat about two weeks before a guttate eruption, and the association with guttate psoriasis is considerably stronger than with chronic plaque disease. Skin trauma produces the Koebner phenomenon, in which new lesions appear at the site of a scratch or abrasion. Psychological stress is among the best-supported triggers for both the onset and aggravation of existing disease. Several medications are also implicated. Lithium can precipitate or worsen psoriasis, and its lesions are often resistant to standard treatment but may remit after the drug is stopped. Beta-blockers, including propranolol, antimalarials, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors have also been associated with flares. Rebound flares can follow withdrawal of systemic corticosteroids. Other factors, such as smoking, alcohol, obesity and low humidity, have been proposed, but their effects are less well established.

Gene–environment interaction

Genetic susceptibility and environmental exposure appear to act together. Disease onset before about age 40 is associated with a combination of HLA-Cw6 carriage and early streptococcal infection. Age also modifies the genetic effects: some PSORS1 associations are strongest in very early-onset disease and weakest after age 40. Although more than 80 genes have been linked to psoriasis, only about 2–3% of the population develops it. Many people who carry risk variants therefore never develop the disease, most likely because they lack the particular combination of variants or do not encounter the relevant triggers. Such penetrance is incomplete, and this explains why family members of an affected person often remain unaffected.

Epigenetic and regulatory mechanisms

Epigenetic mechanisms are thought to amplify genetic predisposition by changing gene expression without altering the DNA sequence. Abnormal DNA methylation patterns in immune-related genes, histone modifications that change chromatin accessibility, and dysregulated non-coding RNAs, such as the long non-coding RNA MEG3, have been reported to influence keratinocyte differentiation and immune cell activation in lesions. Some of these changes may be inherited, while others may be induced by environmental insults, and either route could sustain chronic inflammation. Comparisons of gene expression between lesional and non-lesional skin, and in circulating immune cells, form a major part of current research into how these regulatory differences arise and persist.

Immunopathogenesis: The IL-23/Th17 Axis

Dendritic cells, IL-23 and Th17 cells

Psoriatic inflammation is organised around dendritic cells (DCs) in the skin. In the dermis, IL-23, secreted by dermal dendritic cells, can induce Th17 lymphocyte activation. Once stimulated, skin DCs secrete IL-23 and IL-12 that engage several resident T-cell populations. IL-23 signals through JAK2 and STAT3 (IL-23 binding to its receptor complex results in Jak2-mediated phosphorylation of tyrosine residues, and phosphorylated residues serve as a docking site for STAT3). The cells that respond to it export IL-17A, IL-17F and IL-22. Within lesions, both CD4+ and CD8+ T cells produce IL-17A and IL-17F on ex vivo stimulation, and the populations have been termed Th17 and Tc17, respectively. Dermal Th17 cells are therefore one part of a broader IL-17-producing T-cell pool.

The model has shifted over time. Until recently, interferon-γ (IFN-γ)-producing Th1 cells were considered to be the main pathogenic cells in psoriasis. Later work showed that IL-23 stimulates and promotes differentiation in a subset of memory-activated CD4+ T-cells known as Th17 cells. TNF-α was also part of the earlier picture, and it still appears in lesional cytokine profiles alongside IL-17 and IL-22 (psoriasis is driven by T cell activation associated with the secretion of proinflammatory cytokines, including TNF-α, IL-17A, IL-22, and IFN-γ). Th1 and Th17 signals therefore coexist, with the IL-23/Th17 arm now regarded as central.

IL-17 actions on keratinocytes and other tissue cells

IL-17A and IL-17F act through a receptor complex on keratinocytes. Once engaged, the complex recruits the adaptor protein Act1, which leads to numerous proinflammatory cytokines, chemokines, and antimicrobial peptides that drive the lesion. IL-22 has a complementary role: it induces proliferation of keratinocytes, while IL-22 synergizes with IL-17A and IL-17F to enhance the KC expression of antimicrobial peptides. IL-17A also drives neutrophil recruitment by inducing the chemokines CXCL1 and CXCL8 in keratinocytes. These cytokines are not restricted to keratinocytes; within the skin and joints, IL-17A acts on keratinocytes, neutrophils, endothelial cells, fibroblasts, osteoclasts, chondrocytes, and osteoblasts.

Neutrophils and self-sustaining loops

Neutrophils are both targets and sources of IL-17 in lesions. In one proposed sequence, LTB4 accumulates at the subcorneal portion and attracts neutrophils, and infiltrated neutrophils secrete IL-17A, which acts on keratinocytes to express CCL20. CCL20 then recruits CCR6-expressing T cells into the epidermis, and IL-23 is produced by keratinocytes perturbed by neutrophil infiltration, and recruited cells expand in the presence of IL-23 and IL-1β and secrete IL-17A, completing the positive feedback loop. The authors of that work suggested this loop is one reason why psoriasis is a recalcitrant disease. Neutrophil extracellular traps add to the loop, since NETs further supply IL-17 and induce Th17 cells to release more IL-17. Persistence is also visible in tissue: even after successful treatment, IL-17-producing αβ T cell clones remain present in asymptomatic psoriatic skin.

LL-37, self-DNA and plasmacytoid dendritic cells

The antimicrobial peptide LL-37, encoded by the CAMP gene and also known as cathelicidin, is a central autoantigen-related trigger. LL-37 is overexpressed in inflamed skin in psoriasis, binds to extracellular self-DNA released from dying cells and converts self-DNA into a potent stimulus for plasmacytoid dendritic cells (pDCs). Normally, whereas pDCs normally sense microbial DNA in a Toll-like receptor 9 (TLR9)-dependent fashion, in psoriatic lesions pDCs respond to self-DNA and secrete interferon-α. The complexes are internalised and reach the relevant receptor: LL-37 formed aggregated complexes with DNA, and these complexes entered pDCs and were localized to early endosomes, where TLR9 is found. Activated pDCs then produce type I interferon, which, along with TNFα, IL-6 and IL-1β, activates local myeloid DCs, thus promoting T cell-mediated inflammation.

Triggers such as injury and infection feed this process. Triggers such as trauma and infections lead to the release of self-DNA and self-RNA, which form complexes with LL37 and activate plasmacytoid dendritic cells (pDCs) and myeloid dendritic cells (mDCs), respectively. LL-37 also has an adaptive role. Complexes of self-DNA with LL-37 can also be presented by HLA-C*06:02 molecules and specifically activate T cells through their TCR. In this way LL-37 is described as a T-cell autoantigen that acts for pathogenic Th17 cells. The picture is not uniformly pro-inflammatory, however: LL-37 has been described as playing contrasting roles in skin inflammation in psoriasis, and this dual character is still under study.

Keratinocyte Hyperproliferation and Tissue Changes

The epidermal changes in psoriasis begin with altered keratinocyte kinetics. In normal skin, a cell formed in the basal layer needs about four weeks to reach the outer stratum corneum. In psoriatic lesions, this transit time falls from 28 days to about 4–7 days. The result is an epidermis that thickens (acanthosis) because cells are produced faster than they can mature. Maturation is also incomplete. Underexpression of keratinocyte differentiation markers leads to incomplete differentiation, which is seen as parakeratosis. Histologically, nuclei are retained in the stratum corneum, and the epidermis as a whole becomes thicker. The granular layer is typically absent, and the rete ridges are regularly elongated, creating a thickened appearance that, in some descriptions, looks club-shaped toward the tips.

Basal keratinocytes divide more often than normal. The mitotic rate of basal keratinocytes in psoriatic lesions is significantly increased compared with normal skin. Part of this is driven by immune signals. Infiltrating Th17 cells increase production of IL-17A and IL-22 in psoriatic lesions. These cytokines bind keratinocyte receptors, pull basal cells out of a quiescent state, and slow their terminal differentiation. IL-17A activates keratinocytes and recruits neutrophils, while IL-22 promotes excessive proliferation and abnormal differentiation. At the level of the cell cycle, keratinocytes in lesions show a shortened mitotic cycle and shortened epidermal passage time, together with delayed differentiation. Expansion of the transit-amplifying cell compartment is a distinctive morphological feature of psoriatic epidermal hyperplasia. Work in an imiquimod-induced mouse model found both perpendicular and parallel division patterns in dividing stem cells within inflamed epidermis. Metabolic competition may also contribute. Highly proliferative basal keratinocytes in psoriasis outcompete other cells for glucose uptake, which impairs their differentiation.

Neutrophils accumulate within the epidermis, forming the histological structures long used for diagnosis. Munro's microabscesses, filled with neutrophils, were first described in 1898 and are considered one of the major histopathological hallmarks of psoriasis. These collections sit in the stratum corneum. Spongiform pustules of Kogoj, which are epidermal spongiotic pustules with neutrophilic infiltration, are also described. Neutrophils reach these sites by migrating through the epidermis. In psoriasis, neutrophils move through the epidermis into the stratum corneum, which produces the pallor seen in the upper epidermal layers. Their presence is useful in practice. On volar skin, where psoriasis can resemble allergic contact or dyshidrotic dermatitis, the pathologist looks for tortuous dermal capillaries and neutrophils in the epidermis.

The dermal vasculature changes early. Dermal papillary capillaries become more tortuous, dilated and permeable, and show marked elongation. These vascular alterations are regarded as the earliest detectable histological changes in psoriasis, and they precede visible epidermal proliferation. VEGF plays a role. Dilated and prominent dermal blood vessels arise in part from upregulation of vascular endothelial growth factor. The new vessels are thought to support the lesion. Increased vascular permeability and angiogenesis nourish proliferative keratinocytes, facilitate inflammatory cell migration, and contribute to the onset and persistence of psoriasis. The dense capillary network is also linked to the visible redness and warmth of plaques. Psoriatic skin biopsies show a high capillary density in the dermal papilla and increased blood flow. Vascular changes also outlast clinical improvement. In treated lesions, dilated, tortuous capillaries emerged as the most reliable sign of psoriasis at all stages and in all forms.

Clinically cleared skin is not fully normal at the molecular level. After successful treatment the macroscopic pathology normalizes and scarring is not apparent, but local immune cell populations still differ from non-lesional skin, and clear molecular differences are observed in resolved psoriasis. Treatment studies illustrate this. After anti-TNF therapy, keratinocyte hyperproliferation and Th17-related gene expression fell quickly, within one week. Yet a residual disease genomic profile was defined as psoriasis-associated genes that improved by less than 75%, and it comprised about 250 transcripts across inflammatory and structural gene groups. Some structural abnormalities of the skin were not fully reversed. Even non-lesional skin is affected. Levels of inflammatory molecules in non-lesional skin can distinguish mild from severe psoriasis.

Clinical Subtypes

Classifications of psoriasis differ between sources. Most list plaque, guttate, inverse, pustular and erythrodermic forms as the main phenotypes, although the number of named types varies from five to six depending on whether pustular and inverse forms are counted separately. The subtypes below overlap: a person may have plaque disease alongside a guttate, pustular or erythrodermic flare.

Plaque psoriasis

Plaque psoriasis, also called psoriasis vulgaris, is the commonest form. Estimates of its share range from around 90% of cases in one review to 80–90% of cases in another. It is the reference type used in clinical trials and in classification, so most evidence on efficacy and safety comes from this group.

Guttate psoriasis

Guttate psoriasis produces a sudden crop of small, drop-shaped lesions, mainly on the trunk and proximal limbs. Sources disagree on lesion size: one describes papules of 1–10 mm, while another gives 0.3–0.5 cm in diameter. The form is more common in children and adolescents than adults, and it accounts for less than 2% of psoriasis cases. A preceding strep throat infection is a frequent trigger, although it is not always identified.

Pustular psoriasis

Pustular psoriasis is marked by white sterile pustules, either in generalized or localized distribution. Localized forms include palmoplantar pustular psoriasis and acrodermatitis continua of Hallopeau. Generalized pustular psoriasis (GPP) is described as a neutrophilic autoinflammatory skin disease, and it can occur with or without a history of plaque disease. Its genetic basis is distinct from that of plaque psoriasis. Loss-of-function variants in the gene IL36RN, which encodes the interleukin-36 receptor antagonist, dysregulate the proinflammatory interleukin-36 pathway and are found in some patients. Such mutations have not been detected in patients with plaque psoriasis alone. Variants in CARD14 and AP1S1 have also been implicated. Triggers include infections, drugs, pregnancy, and sudden withdrawal of glucocorticoids. Infantile cases are rare, and they are estimated to account for 3.5%–16% of childhood psoriasis. Treatment has moved toward IL-36 blockade: spesolimab selectively inhibits interleukin-36, and in adults with GPP flares a single intravenous dose has been described as effective and safe.

Erythrodermic psoriasis

Erythrodermic psoriasis is the most severe form, and it is also among the least frequent. Its frequency is reported as 1-2% of those who already have psoriasis in one source and as less than 3% of people with psoriasis in another. Thresholds for the extent of involvement also vary; one review cites erythema and scaling over more than 75% of body surface area, while another uses usually 90% or more.

The systemic burden follows from the loss of the skin barrier. Sequelae include thermoregulatory dysfunction, cardiovascular strain, fluid imbalance, secondary infection, metabolic derangement, and protein loss. Some patients develop high-output cardiac failure, and hospitalization and prompt multidisciplinary care are often required. For this reason it is regarded as a medical emergency. Common precipitants include infection, abrupt withdrawal of systemic corticosteroids, stress, or certain medications. Pathogenesis involves the IL-23–Th17 axis, with aberrant activation of dendritic cells driving the response. Historically, systemic therapies such as ciclosporin or low doses of methotrexate or acitretin were used, and biologics are now also employed.

Inverse, scalp and nail psoriasis

Inverse (flexural) psoriasis affects skin folds such as the axillae, the area under the breasts and the genital region. It presents without much scaling, which is one reason it is easily missed. Moist, macerated folds can resemble candidal intertrigo, and this overlap is a common diagnostic difficulty in practice.

Scalp and nail disease are both classed among the high-impact and difficult-to-treat psoriasis sites. Scalp plaques can be thick and hard to separate from seborrhoeic dermatitis, and nail involvement often needs assessment alongside any coexisting joint symptoms. These two sites are also discussed in the clinical features and psoriatic arthritis sections.

Psoriatic Arthritis

Prevalence and timing relative to skin disease

Estimates of how many people with psoriasis develop joint disease vary widely. A systematic review and meta-analysis of 266 studies, covering close to a million patients with psoriasis, put the pooled prevalence at 19.7%, or roughly one in four to five (prevalence). Higher estimates were found in patients with moderate-to-severe psoriasis than in patients with mild psoriasis. Individual studies report figures from about 4% to 30%, and different disease definitions and geography contribute to that spread. Regional differences have also been recorded, with one meta-analysis giving 22.7% for European patients and 14.0% for Asian patients. These differences are partly attributed to differences in HLA-B27 allele expression, methodological approaches, and underdiagnosis (allele).

Skin disease usually comes first. In one pooled description, in 60–70 % of patients Pso precedes PsA, while in 15–20 % arthritis precedes the onset of Pso. The two can also appear together, and PsA may precede, co-occur with, or follow the skin manifestations. Underdiagnosis is a significant problem: In Europe and North America, the diagnosis of PsA is missed in more than one-third of patients with psoriasis.

Patterns of joint involvement

The classic framework of five joint patterns was set out by Moll and Wright in the 1970s, covering distal interphalangeal (DIP) predominant arthritis, arthritis mutilans, symmetrical polyarthritis, asymmetrical oligoarthritis or monoarthritis, and spondylitis-predominant disease. Asymmetrical oligoarthritis is the most frequent clinical joint pattern of PsA. Oligoarthritis often involves larger joints—knees, ankles, or elbows, and the pattern can change over time, with a large proportion of individuals with monoarthritis or oligoarthritis progressing to polyarthritis.

Symmetrical polyarthritis is a rheumatoidlike pattern. Clinicians separate it from rheumatoid arthritis by looking for distal joint involvement, some asymmetry, the absence of subcutaneous nodules and a negative rheumatoid factor. DIP-predominant disease is considered a classic feature of PsA, but it occurs in only 5-10% of patients, primarily men, and it is usually accompanied by nail changes.

Arthritis mutilans is the most severe form. Fewer than 5 percent of individuals with psoriatic arthritis have this form of the disorder, and it produces resorption of bone (osteolysis), with dissolution of the joint, seen radiographically as a "pencil-in-cup" appearance. Spinal disease is distinct from ankylosing spondylitis in its pattern, though spondylitis may occur and result in fusion similar to AS. Axial involvement is more prominent in male patients with positive HLA-B27 and typically asymmetric at the sacroiliac joints.

Enthesitis and dactylitis

Enthesitis, inflammation where tendons and ligaments insert into bone, is a characteristic feature. It commonly affects where the Achilles tendon and the plantar fascia attach to the calcaneus, and clinically produces tenderness, soreness, and pain at entheses on palpation (enthesitis). Dactylitis, in which swelling of an entire digit is apparent, is not characteristic of rheumatoid arthritis, is fairly common and asymmetric in psoriatic arthritis (dactylitis). It affects the feet more often than the hands. Both features are built into the CASPAR (Classification criteria for Psoriatic Arthritis) criteria (caspar-criteria) and are often among the earliest signs of PsA and can precede the development of overt synovitis. Imaging helps here: ultrasound is optimal for detecting enthesitis, which is often the initial manifestation of musculoskeletal psoriatic disease.

Radiographic damage and the case for early diagnosis

Structural damage can progress quickly. Irreversible joint damage may be observed if patients are not treated promptly and appropriately. Dactylitis has been consistently linked to radiographic damage, particularly erosions in small joints of the hands and feet. Typical radiographic findings include erosions of distal interphalangeal joints, unilateral or bilateral sacroiliac joint changes, and spondylitis. Delay matters: diagnostic delays of even 6 months from symptom onset can lead to poor radiographic and functional outcomes, and in particular this delay carries a 10-fold increased risk of the most devastating form of PsA, arthritis mutilans. Ultrasound and MRI can detect joint damage earlier than plain radiographs (diagnosis).

Screening and classification

PsA is diagnosed using the CASPAR criteria, which were developed to replace earlier, less consistent definitions. Because dermatologists often see patients first, these professionals need to be trained to diagnose this comorbidity and treat it, together with rheumatologists. Practical screening relies on symptom questions and examination: physicians are advised to look for peripheral inflammatory pain, axial inflammatory pain, dactylitis, and buttock and sciatic pain. Nail involvement is a notable marker; in one cohort it was present in 25 (52.1%) of PsA patients, and a family history of PsA was a significant predictor of disease in the same study (biomarker).

Comorbidities and Systemic Burden

Psoriasis is now generally regarded as a systemic inflammatory condition rather than a disease confined to the skin, and several organ systems show measurable excess risk. The strongest evidence concerns the cardiovascular system. A systematic review and meta-analysis of observational studies found that mild psoriasis was associated with a modest rise in myocardial infarction (relative risk about 1.29) and stroke (about 1.12), while severe psoriasis carried higher risks for myocardial infarction (about 1.70), stroke (about 1.56) and cardiovascular death (about 1.39). The authors noted that covariate adjustment differed between studies, so residual confounding could not be excluded. Later cohort meta-analyses reported smaller but still significant pooled risks, and the excess is most evident in people with moderate-to-severe disease. Proposed explanations centre on shared inflammatory pathways, including T helper 1-type inflammation, altered angiogenesis and endothelial dysfunction, which may partly operate independently of conventional risk factors. Conventional 10-year risk calculators appear to underestimate risk in this group, which has practical consequences for prevention, and observational data suggest that biologic therapy is associated with fewer myocardial infarctions than topical treatment, although this cannot establish causation.

Metabolic disorders form a second cluster. People with psoriasis show higher rates of hypertension, type 2 diabetes and dyslipidaemia than comparison groups, and obesity is both more frequent and linked to more active skin disease. Adipose tissue is itself an inflammatory source, which provides one plausible connection between weight and cutaneous inflammation, and the relationship appears to run in both directions. Insulin resistance has been examined as a shared feature of the metabolic and inflammatory pathways, but the evidence on whether it actively drives skin severity remains less settled than the associations themselves.

Non-alcoholic fatty liver disease (NAFLD) is one of the most frequently reported hepatic comorbidities. Estimates of NAFLD among people with psoriasis have ranged widely across studies, from about 44% to 66% in some reports, compared with substantially lower rates in controls, and pooled odds ratios in some analyses exceed 2. Risk appears to be higher in men and in those with obesity, hyperglycaemia or hypertension, and the association has been reported across Asian, European and North American populations. Inflammatory bowel disease (IBD) is also more common among people with psoriasis: in a large population-based analysis, about 2.4% of adults with psoriasis had IBD compared with 1.6% of those without, and the association was stronger for more severe disease. Conversely, psoriasis is found more often among people with IBD, particularly Crohn's disease. Uveitis is another recognised extra-cutaneous inflammatory feature. Its incidence appears higher in people with psoriatic arthritis than in those with skin disease alone, and the effect of joint involvement on IBD and uveitis risk is discussed further under psoriatic-arthritis in the relevant section.

Psychiatric comorbidity is substantial and has been studied extensively. A large meta-analysis of studies in adults with psoriasis estimated pooled prevalences of about 20% for depression and 21% for anxiety, with suicide reported in under 1%. Pooled odds ratios for depression have been reported around 1.5, and anxiety odds ratios have been higher in some analyses. The association with severity is less consistent than the association with the disease itself. Moderate-to-severe psoriasis has been linked to anxiety in pooled observational data, but not clearly to depression, and individual studies have reported correlations between skin severity scores and depressive or anxiety scales as well as null findings. Psoriatic arthritis, female sex, and younger age at onset have repeatedly been associated with worse psychological outcomes, and longitudinal studies suggest that the skin disease often precedes the psychiatric diagnosis. Both the direction of effect and the role of stigma and quality-of-life burden remain under investigation, which is why psychological screening is widely recommended.

Other associations, including osteoporosis and bone loss, are reported less consistently and have been studied with smaller samples. The practical implication across all these conditions is the same: because comorbidities cluster, routine assessment should extend beyond the skin to blood pressure, glycaemic and lipid status, liver enzymes, joint symptoms, mood and cardiovascular risk. Multidisciplinary coordination with cardiology, endocrinology, gastroenterology, ophthalmology and mental health services is therefore a recurring theme in clinical guidance, and the choice of systemic therapy may itself be influenced by these comorbid conditions.

Diagnosis and Assessment

Clinical diagnosis

Psoriasis is diagnosed mainly by clinical examination. No single laboratory test confirms it, so the diagnosis rests on the morphology and distribution of lesions. Typical plaques are sharply demarcated, erythematous and covered with silvery scale, and they favour the extensor surfaces, scalp, umbilicus, lumbosacral area and natal cleft. The Auspitz sign, in which pinpoint bleeding appears when scale is removed, supports the diagnosis, but it is not specific. Nail pitting, onycholysis and oil-drop discoloration, a history of chronic relapsing skin lesions, and a family history of the condition add further weight. Scalp and intertriginous (inverse) disease are harder to recognise, and they are often confused with seborrhoeic dermatitis, eczema and fungal infection.

Dermoscopy helps separate psoriasis from look-alike conditions. In psoriasis it typically shows regularly distributed dotted vessels on a red or pink background, with whitish-silver scale. Eczema generally lacks such regular dotted vessels and instead shows features of spongiosis and scale. Tinea tends to show irregular or comma-shaped vessels and a scaling pattern that differs from psoriatic scale. Lichen planus is characterised by white reticular lines (Wickham striae) that are absent in psoriasis. A bedside potassium hydroxide (KOH) examination of scale is the standard way to exclude a fungal cause.

Histopathology and biopsy

Histological findings include parakeratosis, acanthosis, regular elongation of the rete ridges with club-shaped or bowling-pin ends, and thinning of the suprapapillary epidermis over the dermal papillae. The papillary dermis shows dilated, tortuous capillaries. Histopathological features can also include neutrophilic microabscesses in the stratum corneum (Munro microabscesses) and spongiform pustules in the spinous layer (Kogoj). The granular layer is usually absent over the lesions. These features are not unique to psoriasis, and the overlap with lichenoid and other inflammatory dermatoses means that histology complements rather than replaces clinical judgement.

A skin biopsy is indicated when the diagnosis is uncertain, when lesions are atypical or treatment-resistant, when a palmoplantar or pustular presentation is unclear, or when lymphoma-like conditions such as mycosis fungoides or lichen planus need to be excluded. It is generally not required for typical plaque disease in a patient with a classic presentation.

Severity scoring

The Psoriasis Area and Severity Index (PASI) divides the body into four regions: head, upper limbs, trunk and lower limbs. In each region the extent of involvement is graded from 0 to 6 by percentage area, and erythema, induration and desquamation are each graded from 0 to 4. The total ranges from 0 to 72. Because the score requires training and time, inter-rater variability is a recognised limitation.

Body surface area (BSA) is a simpler measure. The patient's palm, including the fingers, is commonly taken to approximate 1% of BSA, and many guidelines use BSA thresholds, often above 10%, to classify disease as moderate to severe. Patient-reported measures capture the burden that physician scores do not. The Dermatology Life Quality Index (DLQI) consists of 10 questions, each scored from 0 to 3, giving a total from 0 to 30. Higher scores indicate a greater effect on quality of life, and the scores are conventionally banded from no effect to extremely large effect.

Screening for comorbidity

Guidelines increasingly recommend that every assessment include screening for psoriatic arthritis. This involves asking about joint pain, stiffness, dactylitis and enthesitis, and examining the joints, entheses and nails. Questionnaires such as the Psoriatic Arthritis Screening and Evaluation (PASE) can support this process in busy dermatology and primary care settings. The CASPAR criteria are used for classification in research and rheumatology practice, and they require inflammatory articular disease together with a set of supporting features, including current or past psoriasis.

Cardiometabolic risk should be assessed at the same time. This includes measurement of body mass index or waist circumference, blood pressure, fasting glucose or HbA1c, and lipid profile, because these factors relate to cardiovascular risk, metabolic status and the choice of systemic therapy. Screening for depressive symptoms and psychological distress is also part of routine assessment.

Trials versus routine practice

Clinical trials use standardised outcome measures, such as PASI, the static Physician's Global Assessment (sPGA) or the Investigator's Global Assessment, and the proportion of patients achieving clear or almost clear skin. Trials usually apply minimum severity thresholds for entry, use trained assessors and exclude many patients with comorbidities. These conditions limit the generalisability of the results to routine practice. In everyday care, BSA, DLQI and simple global judgements are more common because PASI is time-consuming. Patient-reported measures of itch and symptoms are increasingly included alongside them, so that treatment decisions reflect how the patient experiences the disease as well as its visible extent.

Topical and Phototherapy Treatments

Topical therapy is usually the first step for limited plaque disease, and topical corticosteroids remain the most effective topical class for plaques. They are rated by potency into seven classes, with class 1 being the most potent and class 7 being the least potent. Trial evidence favours the middle of the range: initial treatment with class 2 to 5 agents has the best evidence of benefit. Potency is matched to the site. Lower-potency products are best used on the face, forearms, and intertriginous areas to avoid adverse effects, while higher-potency agents are reserved for thick, chronic plaques. Choice also depends on severity, patient preference and age, as the disease severity, disease location, patient preference, and the age of the patient all shape the decision.

The main local hazards are atrophy-related. These include skin atrophy, telangiectasia, striae distensae, acne, folliculitis, and purpura. Guidance on duration is conservative for strong agents: very potent corticosteroids are not used on any one site for more than 4 weeks at a time with a 4 week break in between courses. Daily use of the strongest classes for up to four weeks is generally regarded as low risk for atrophy, and adults and children should be reviewed annually for skin atrophy and 'other side effects' if a combination or monotherapy corticosteroid is regularly used. Rebound is the other recognised problem. It is disease that recurs and is more severe than before treatment, which can follow abrupt withdrawal of topical corticosteroids, although the frequency and severity of this phenomenon are unknown.

Calcipotriol, a vitamin D analogue, is paired with betamethasone dipropionate in most modern topical regimens. The two components act on different targets: calcipotriol affects keratinocyte differentiation, while betamethasone influences inflammatory processes and minimizes skin irritation (e.g., pruritus) after calcipotriol application. The pairing is also a formulation challenge, because calcipotriol is stable in alkaline solutions with pH above 8, whereas betamethasone dipropionate requires an acidic environment with pH between 4 and 6. Therefore, the presence of both substances in an aqueous environment leads to interactions and to their decomposition. Fixed-dose products were designed to avoid this. In comparative data, the proportion of patients whose psoriasis improved was always significantly higher in the two-compound group compared to the group treated with the individual substances, and the fixed combination was generally associated with a lower risk of adverse events. Vitamin D analogues, calcineurin inhibitors and tazarotene are also options that can limit chronic topical corticosteroid use.

Coal tar, salicylic acid and emollients are adjunctive rather than primary agents. Coal tar has long been used for its antiproliferative and anti-inflammatory effects, but its odour, staining and safety concerns restrict its use. Salicylic acid is a keratolytic that softens thick scale, which can help other topical agents penetrate. Emollients support the skin barrier, reduce dryness and itch, and are used to maintain control between active courses, while scale removal is most useful before applying active treatment.

Phototherapy uses ultraviolet light, and the main options differ in efficacy, convenience and risk. Narrowband UVB is often considered first-line: in one paired comparison, narrowband UV-B is comparably as effective as PUVA in many patients, and given the lack of photosensitizer-related adverse reactions and the possibly lower long-term cancer risk, can be considered as first-line treatment. Broadband UVB is less effective, and broadband UV-B phototherapy is primarily indicated in patients with mild to moderate psoriasis, whereas for severe forms of PUVA is indicated. PUVA combines oral or bath psoralen with UVA. In a systematic review, the response rate defined by 75% or more improvement in PASI was 80% with PUVA vs. 70% with NB-UVB, and the meta-analysis of the three comparative studies found a higher probability of remission at 6 months with PUVA than with NB-UVB. PUVA is also reserved for particular situations, such as when NB-UVB fails, there is rapid relapse following NB-UVB or in specific indications, such as pustular or erythrodermic psoriasis.

The Goeckerman regimen pairs broadband UVB with crude coal tar. Its evidence base is mainly retrospective. In one Turkish cohort of 65 patients, PASI-75 responses in the NB-UVB, retinoid+NB-UVB (re-NB), Goeckerman and retinoid+Goeckerman (re-Goeckerman) groups were achieved for 12 of 31 patients (39%), 13 of 21 patients (62%), 15 of 17 patients (88%) and 10 of 12 patients, and the authors concluded that Goeckerman therapy was more effective. That study was retrospective, the patients were not randomized and the number of patients in the treatment groups were dissimilar. Its speed and cost are often cited, but the regimen involves messy application and staining, and UV exposure carries cumulative skin-cancer risk for all UV-based approaches.

Practical factors often decide whether phototherapy works in routine care. Treatment typically runs several times a week, and in comparative trials treatment was performed 3 times weekly until complete or almost complete clearing with one or both regimens or over a maximum period of 18 exposures. Adherence to topical and light-based regimens depends on therapeutic efficacy, patient satisfaction, patient treatment preferences and ease of application, and simpler schedules are thought to help, since the combination therapy rapid onset of action, coupled with a simplified dosing regimen, has been identified as crucial for improving long-term adherence and patient outcomes. Clinic travel, time off work and access to equipment are therefore part of the treatment decision.

Systemic Conventional Therapies

Methotrexate

Methotrexate is a folate antagonist with antiproliferative and immunomodulatory effects. In psoriasis it is given once weekly rather than daily. Guidelines commonly describe starting doses of 7.5 to 15 mg and escalation toward a maximum of 25 to 30 mg per week, guided by response. Recommendations differ across guidelines, and few are supported by controlled dose-comparison data. Most guidance favours low starting doses with gradual titration, and does not endorse a routine test dose. Efficacy is usually judged after about 12 weeks at the maximum tolerated dose.

Monitoring centres on liver and blood toxicity, with regular blood counts, renal and liver tests. The frequency of laboratory testing differs between dermatology and rheumatology guidelines, and a 2018 Dutch retrospective cohort reported that dermatological monitoring schedules were associated with shorter drug survival, without evidence of higher risk in psoriasis patients. Because methotrexate suppresses the immune system, it raises the risk of infection, reactivation of latent tuberculosis and hepatitis, and lymphoma. It is also teratogenic, which restricts its use in pregnancy. Its role in long-term management is limited by cumulative toxicity, although it remains a widely used low-cost option.

Cyclosporine

Cyclosporine is a calcineurin inhibitor that acts quickly and is generally reserved for crisis control rather than indefinite use. Clinical practice typically uses 2.5 to 5 mg/kg/day for remission induction, in short intermittent courses of about 3 to 6 months. Doses above 5 mg/kg/day add little efficacy but increase adverse effects, and a starting dose of around 3 mg/kg/day is often considered to offer a better benefit-risk balance. Maximal effect is usually reached after 2 to 3 months, and benefit can persist after stopping.

Nephrotoxicity and hypertension are the principal dose-related risks. In one series of patients with psoriasis, renal tubular atrophy and interstitial fibrosis were observed in about a fifth of those treated, with an average exposure of roughly 23 months. Blood pressure is checked every two weeks during the first three months, and dosage is reduced by 25 to 50 percent if hypertension develops or serum creatinine rises by 25 percent or more above baseline. Manufacturers do not recommend continuous treatment beyond one year, and reviews suggest cumulative use of about two years or less. Older age, obesity, pre-existing hypertension and raised creatinine increase the risk of toxicity. Prior PUVA or other immunosuppressive treatment raises the risk of skin malignancy during cyclosporine therapy, and relapse usually follows withdrawal.

Acitretin and other retinoids

Acitretin is the active metabolite of etretinate and an oral vitamin A derivative. It was approved for psoriasis in the United States in 1997, and it replaced etretinate because of a shorter half-life, although its teratogenic effects persist for a prolonged period after stopping. Acitretin has no direct immunosuppressive action; instead it normalises keratinocyte differentiation, slows epidermal proliferation and reduces certain inflammatory mediators. Its main role is in pustular psoriasis, especially generalised and palmoplantar forms, and in erythrodermic disease. In generalised pustular psoriasis, doses of 0.5 to 1 mg/kg/day often clear lesions within about 10 days, after which the dose is tapered. Relapse is common within a few months of discontinuation, so maintenance dosing is frequently required.

Dose-dependent mucocutaneous effects such as cheilitis and hair loss are the most common adverse events, and hepatotoxicity, pancreatitis and lipid abnormalities are reported less often. Triglycerides may rise and HDL cholesterol may fall, so lipid monitoring and dietary advice are part of management. Alcohol is avoided because it can be converted into etretinate, which has a much longer half-life. Strict pregnancy prevention is required in people who could become pregnant.

Apremilast and other oral small molecules

Apremilast is an oral phosphodiesterase-4 inhibitor. By raising intracellular cyclic AMP, it modulates the production of pro-inflammatory and anti-inflammatory mediators without broad cytotoxicity. It is used for plaque psoriasis and psoriatic arthritis. Its efficacy is generally lower than that of biologics, and its most frequent adverse effects are gastrointestinal, such as diarrhoea and nausea. Weight loss and psychiatric warnings are also included in its labelling. Its major practical advantage is that it does not require routine laboratory monitoring. Apremilast occupies an intermediate position between conventional drugs and biologics, and it is often considered for patients in whom methotrexate or cyclosporine are unsuitable, or who prefer an oral agent without the burden of injections or infusions. More recently, the oral TYK2 inhibitor deucravacitinib has been incorporated into European guidance, further expanding the oral options.

Choosing among systemic drugs

Selection depends on several factors. Comorbidities are central: renal function and blood pressure constrain cyclosporine, liver disease and alcohol use constrain methotrexate and acitretin, and lipid disorders are relevant to retinoid therapy. Pregnancy potential excludes or restricts teratogenic agents such as methotrexate and retinoids, and requires contraception planning. Cost and access influence the use of conventional drugs in many health systems, while infection risk determines whether tuberculosis and hepatitis screening are needed before immunosuppressive therapy. Patient preference and shared decision-making, which current guidelines emphasise, shape the final choice. Conventional agents are often used for induction, bridging or rotation, with cyclosporine offering rapid control for short periods, while combination and sequential strategies are recommended to limit long-term exposure to any single drug.

Biologic Therapies

TNF-α inhibitors

Five TNF-α antagonists are used in psoriasis. Infliximab, a chimeric antibody, binds and neutralises TNF Infliximab is a chimeric monoclonal antibody which binds and neutralizes TNF. Among TNF-class agents, infliximab stands out for speed: it is one of the few TNF inhibitors that performs well in early response, while the other members generally act more slowly. A Bayesian network meta-analysis of 53 phase 2b and 3 trials found that TNF-alpha inhibitors, except infliximab, generally showed slower responses. At PASI 90, the most efficacious treatments were the IL-17 inhibitors (brodalumab, ixekizumab, secukinumab), IL-23 inhibitors (guselkumab and risankizumab), and infliximab. Across a 77-trial network, however, IL-17 inhibitors, guselkumab and risankizumab were found to be more efficacious than tildrakizumab, ustekinumab, all TNF inhibitors and non-biologic systemic treatments at inducing all levels of PASI response. Anti-TNF agents are also used in psoriatic arthritis. Paradoxical psoriasiform eruptions during anti-TNF therapy, usually given for other conditions, are a recognised problem.

IL-12/23 and IL-23 inhibitors

Ustekinumab acts on the shared p40 subunit, so it blocks both IL-12 and IL-23 Ustekinumab is a monoclonal antibody against the p40 subunit of the IL-12 and IL-23 cytokines which are involved in inflammatory and immune responses. The newer agents guselkumab, tildrakizumab and risankizumab instead target the p19 subunit unique to IL-23. In the same 77-trial network, guselkumab and risankizumab were significantly more effective than ustekinumab and tildrakizumab, and they showed the greatest benefit ... for PASI 90 and PASI 100 response. Their onset is somewhat slower than that of IL-17 blockade. The evidence for durable clearance is strongest for the IL-23 agents and the IL-17 agents: a one-year network analysis found that Interleukin (IL)-17 and IL-23 inhibitors demonstrated greater cumulative clinical benefits for both PASI 100 and PASI 90 versus IL-12/23 and tumor necrosis factor inhibitors. IL-23 blockade has also been reported to help patients with coexisting Crohn's disease, which is relevant to the gut safety issues discussed below.

IL-17 inhibitors

Secukinumab is an anti-IL-17A antibody that is approved for psoriasis, psoriatic arthritis and ankylosing spondylitis Secukinumab is an anti-interleukin (IL)-17A IgG1-κ monoclonal antibody approved for psoriasis, psoriatic arthritis, and ankylosing spondylitis. Brodalumab and ixekizumab are in the same class, and bimekizumab neutralises both IL-17A and IL-17F. The rapid onset is the most distinctive feature of this class. In a 2024 analysis, IL-17 inhibitors had the shortest time to achieve PASI75 and PASI90 followed by risankizumab in the weighted mean analysis. Bimekizumab was significantly faster in time to PASI75 among the remaining therapeutics.

The main safety concerns are infections and gut inflammation. IL-17 inhibitors increase the risk of infections, especially respiratory tract infections and candidiasis, and inflammatory bowel disease. A US claims-based cohort reported that IL-17A users had a 3-fold increase in the risk of oral candidiasis (RR = 3.43; 1.48-7.84), a 19% increase in the risk of outpatient infections, and no meaningful increase in major adverse cardiac events or malignancy compared with other biologics. Baseline oral colonisation with <i>Candida albicans</i> without symptoms was associated with later oral candidiasis, with none observed in an adalimumab comparison group Baseline oral Candida albicans colonization with no clinical symptoms was associated with an increased risk of oral candidiasis during the first year of interleukin-17 inhibitor therapy. Regarding bowel disease, the US regulator has advised caution in patients with a history of, or risk for, IBD the Federal Drug Administration (FDA) to encourage caution when prescribing to patients with a history or risk of IBD. Observational studies have reported new-onset or flaring IBD, but a 2025 retrospective analysis concluded there was no causal relationship and noted that IL-17's protective role in the gut may be involved The study found no causal relationship between IL-17 inhibitors and IBD, but IL-17's protective role in the gut may be involved.

Comparisons and sequencing

Network meta-analyses have ranked the biologics fairly consistently, but differences within classes remain. The 77-trial analysis, covering 34,816 patients, found that brodalumab, ixekizumab and risankizumab were significantly more efficacious than secukinumab; no significant difference was found in the comparison with guselkumab. Most patients still do not reach complete clearance with these agents, and the same authors note that in the majority of patients they do not provide complete skin clearance. Many of the comparative data predate newer drugs; one 2024 analysis observed that most were published before the approval of bimekizumab. Direct evidence on sequencing after failure is therefore limited, and the guidance rests largely on modelling. A cost-effectiveness model favoured a sequence beginning with an adalimumab biosimilar, followed by ustekinumab, then secukinumab, and then best supportive care the optimal sequence (having the lowest incremental cost per quality-adjusted life-years without incorporating an estimated discount)—adalimumab biosimilar → ustekinumab originator → secukinumab → best supportive care—with a total quality-adjusted life-year of 14.74 and a total cost of £78,731.

Access, costs and biosimilars

Cost is a major barrier to biologic use. In a US analysis of 2014 wholesale prices, the cost of one year of induction and maintenance treatment was highest for ustekinumab ($53,909), followed by etanercept ($46,395), and adalimumab ($39,041). Sales-based costs were also rising steeply over the period studied. Biosimilars have partly addressed this. Adalimumab biosimilars have the ability to reduce the costs of biologics and to expand access, and in one European model, using an adalimumab biosimilar first-line provided £2530 of cost savings per patient treated without loss of effect. Reported savings vary by setting and by discount assumptions; one review reports that adalimumab biosimilars showed cost reductions of approximately 30% to 40% compared with the originator product while maintaining comparable clinical outcomes. Recent international recognition has followed, as these 2 biologics were added to the WHO EML for psoriasis, referring to the adalimumab and ustekinumab biosimilars.

Treatment Goals, Monitoring and Relapse

Treat-to-target and response endpoints

Trials have historically measured efficacy with the Psoriasis Area and Severity Index (PASI), and the 75% reduction threshold has served as the main benchmark. PASI 75 response is currently considered the gold standard for assessing treatment efficacy in moderate-to-severe psoriatic patients. A 90% reduction is generally taken to reflect a larger clinical gain. Some protocols also add the Investigator Global Assessment as a co-primary measure, with the proportion achieving IGA 0 (clear) or 1 (almost clear) as the outcome. In practice, the aim is to achieve almost clear or clear skin and maintain disease control, regardless of baseline disease severity.

Because relative PASI changes depend on the starting score, an absolute target has been proposed. Analysis of the British BADBIR registry, which used receiver operating characteristic curves, found that PGA clear/almost clear was concordant with PASI ≤ 2 in 90% of cases, and the authors concluded that an absolute PASI ≤ 2 and PGA clear/almost clear represent relevant disease end points to inform treat‐to‐target management strategies in psoriasis. The quality-of-life rationale is also cited: a meta-analysis estimated that the Dermatology Life Quality Index improved by about 90% (95% CrI: 88-93%) in PASI 90 responders, compared with 78% (95% CrI: 75-82%) in PASI 75–89 responders.

Relapse after withdrawal

Remission achieved with biologics or other systemic agents is usually not permanent. After treatment is stopped, the disease returns over the course of months, with lesions reappearing in the same locations as prior lesional activity. Local recurrence is common and unpredictable, which complicates clinical management of psoriasis. In real-world data, the cumulative probability of remaining relapse-free after biologic discontinuation was 35.6%, 19%, 11.6%, and 9.1% at 6, 12, 18, and 24 months, respectively. Median times to relapse, defined as loss of PASI 50 in the studies cited, varied by agent, from about 16 to 28 weeks.

Tissue-resident memory T cells (TRM) are proposed as a key cellular basis for this memory. Lesional skin contains TRM that are profusely infiltrated in the lesions observed during psoriasis relapse. CD8⁺ TRM are located mainly in the epidermis, whereas CD4⁺ TRM are found in the dermis, and since IL-23 can activate Trm, neutralizing antibodies against IL-23 are suggested to be more effective in clinical treatment. A 2025 study examining skin from patients who had stopped ustekinumab described a TRM population that persisted after clinical response and sat close to LAMP3⁺ dendritic cells and FOXP3⁺ regulatory T cells at the dermal-epidermal interface. Relapse-related evidence remains partly indirect, and the mechanisms are not fully established. One consequence is that visible clearance and biological stability should not be considered interchangeable.

Pre-treatment infection screening

Infection is regarded as the main safety concern. A patient's risk of developing a serious infection remains the biggest concern. Baseline laboratory work usually includes complete blood cell count, comprehensive metabolic panel, and latent tuberculosis screening is recommended before immunosuppressive therapy. Interferon-gamma release assays have largely replaced the tuberculin skin test, and the latter being preferred for its higher sensitivity and specificity. If latent infection is found and the patient has no active disease on chest radiography, guidelines advise at least one month of LTB treatment before initiation of a biologic medication.

Hepatitis screening is also standard. Screening for hepatitis B virus (HBV) and hepatitis C virus (HCV) should be performed prior to initiation of any biologic therapy. Risk differs by class: TNF inhibitors and ustekinumab are associated with an increased risk of latent tuberculosis and hepatitis B virus reactivation, whereas IL-17 and IL-23 inhibitors are considered to carry no significant infection risk. For patients with documented tuberculosis, IL-17 or IL-23 inhibitors should be prioritized when available as first-line options.

Toxicity monitoring and shared care

Laboratory monitoring during treatment is less well supported by evidence than pre-treatment screening. One systematic review noted that there was insufficient evidence to support complete blood cell count screening, and, given the low grade evidence on monitoring hepatic function, the authors suggested this should be performed at the clinician's discretion, particularly among patients treated with infliximab. Conventional agents carry more defined monitoring needs. Methotrexate and cyclosporine require periodic liver and kidney function tests, and hepatitis screening is advised before both. Because these drugs cross specialty boundaries, dermatologists typically coordinate with hepatology, rheumatology, nephrology or infectious disease colleagues when comorbidities or abnormal results arise.

Maintenance and tapering

Maintenance strategies involve a balance between sustained control and treatment burden. Because psoriasis tends to recur after withdrawal, patients tend to continue receiving costly treatment indefinitely. Tapering or intermittent dosing can reduce exposure, but it carries the risk of earlier recurrence. Decisions therefore weigh the expected time to relapse against the cost, infection risk and inconvenience of continued therapy, and these trade-offs are individualized rather than fixed by a single protocol.

Quality of Life, Mental Health and Social Impact

Psoriasis imposes a burden that extends well beyond the skin. Itch, burning, soreness and cracking can disrupt sleep, and the resulting fatigue reduces daytime function. Lesions on visible sites also interfere with choice of clothing and with ordinary daily activities such as bathing, exercise and intimate contact. Many patients describe the chronic, relapsing course as a source of hopelessness about a cure, and the unpredictability of flares as a constant concern about future plans. Qualitative and survey studies repeatedly identify a sense of lacking control over the disease as one of its most distressing aspects, and this feeling appears to compound the physical symptoms. Severity matters: quality-of-life impairment rises with the extent of skin involvement, and patients with psoriatic arthritis tend to report greater impairment than those with skin disease alone.

Psoriasis is also socially isolating. Visible scaling and erythema can provoke stigma from others, and many patients avoid situations such as swimming, sport, close physical contact or job interviews to limit exposure to unwanted attention. Children and adolescents are particularly affected; teasing and exclusion at school can shape peer relationships and self-esteem during formative years, and the consequences may persist into adulthood. Because the stigma is tied to appearance rather than to any infectious or dangerous feature of the disease, it often persists even when the skin is mild.

Depression is among the best-documented psychiatric comorbidities. Estimates vary with the population studied and the instruments used, but one review cited in the literature suggests that around 30% of patients develop clinically significant depression, and in one study about 9.5% expressed a wish to be dead. A 2024 systematic review of treatment studies found that biologic agents such as guselkumab, brodalumab and bimekizumab were associated with reductions in depressive symptoms, which the authors attributed at least partly to improved skin clearance and quality of life. Evidence on suicidality is more mixed. Some cohort and meta-analytic studies report raised odds of suicidal ideation relative to people without psoriasis, whereas the British BADBIR register found that suicide rates among patients with moderate to severe disease were not significantly higher than in the general population. Suicidal ideation was reported in some patients receiving brodalumab, and the drug carries a labelled warning, although a causal relationship has not been established. Proposed explanations for the link include shared systemic inflammatory pathways, and current guidance favours routine screening for psychological distress, with referral to mental health services where indicated.

The economic consequences are substantial and fall on patients, employers and health systems. A widely cited US analysis estimated the total annual burden of psoriasis in 2013 at USD 35.2 billion, with about one-third from incremental medical costs, about one-third from reduced health-related quality of life and about one-third from productivity losses. Work impairment increases with disease severity: in a 2017 analysis of patient-reported data, adults with mild disease lost about 137 hours of work per year, compared with about 310 hours for moderate disease and 551 hours for severe disease. Presenteeism, meaning working while impaired, accounts for a large share of this loss. Costs are further increased by comorbidities, and a 2024 international analysis by a patient federation estimated that comorbidity-related costs alone are considerable across several countries. A 2021 global analysis put the economic burden of psoriasis at about USD 148.85 billion, with high-income countries bearing most healthcare costs while lower-income countries bore a larger proportion of productivity losses.

Non-pharmacological support forms a complementary part of care. Patient education helps people understand the chronic relapsing course, the purpose of each treatment and the warning signs of comorbidity, which can reduce anxiety and improve engagement with therapy. Peer support groups provide practical advice and reduce the sense of isolation, and psychological interventions such as cognitive behavioural approaches may be offered to patients whose distress is affecting daily life. Integrating these approaches with dermatological treatment, rather than treating them as separate concerns, is widely regarded as the appropriate model for managing the psychosocial dimension of the disease.

Special Populations and Pregnancy

Paediatric patients

Treatment in children rests on a thinner evidence base than in adults. Treatment of paediatric psoriasis is complicated by limited data on efficacy and safety. Among biologics, etanercept has the longest paediatric record, having been first approved by the FDA for children aged 4 and older with plaque psoriasis in November 2016. Dosing is weight-based. Adalimumab is given at 0.8 mg/kg, to a maximum of 40 mg, at weeks 0 and 1 and then every two weeks, and ustekinumab is dosed by body weight, with doses given at week 0, 4, and 16 and then every 12 weeks. Secukinumab received approval from both the FDA and EMA in 2020 for moderate-to-severe plaque psoriasis in children aged 6 and older. Paediatric trial data for biologics have been largely placebo-controlled, and all biologics showed improved PASI responses over control arms. Real-world paediatric series report that no specific severe adverse effects necessitating treatment discontinuation were observed in pediatric patients, but long-term safety data remain limited. Topical corticosteroids, vitamin D analogues and narrowband UVB are used in children, with dose and site limits that reflect the greater skin absorption and growth concerns of younger patients.

Pregnancy and breastfeeding

Management follows a stepwise pattern. The first line of therapy for treating psoriasis in pregnant and breastfeeding women should be topical treatment with moisturizers and emollients, such as petroleum jelly, because these products cause no known adverse effects. If these fail, low to moderate doses of topical corticosteroids may be tried, followed by high-potency topical corticosteroids used only as needed in the second and third trimesters of pregnancy. Narrowband UVB is the usual second-line option. Vitamin D analogues are a notable exception to topical safety: manufacturers of vitamin D analogues such as calcipotriol advise that these agents should be avoided in pregnancy, and tazarotene is avoided in pregnancy and while trying to conceive.

Systemic options are more restricted. Acitretin is contraindicated: patients of reproductive age treated with acitretin need to use effective contraception for at least one month before treatment initiation, as well as during treatment and for three years after discontinuation. Among biologics, certolizumab pegol is the biological treatment of choice throughout pregnancy and lactation in one German guideline, while other sources advise that biologics be stopped or reviewed in the third trimester. The Spanish consensus, for example, recommends that biologic therapy be maintained during the first and second trimesters, with the third trimester decided case by case. Guidance on TNF inhibitors and cyclosporine differs: some sources allow cautious use only from the second trimester. Planning before conception is therefore emphasised, because potential pregnancy should always be considered when deciding on a specific treatment option in these patients.

Breastfeeding guidance is generally more restrictive about systemic drugs. The US National Psoriasis Foundation generally advises against taking systemic or biologic drugs while breastfeeding, "unless there is a clear medical need." PUVA is a notable concern, since psoralen in breast milk could cause light sensitivity in the infant, and topical PUVA is not recommended during breastfeeding, whereas narrowband UV-B phototherapy can be used.

Older adults

Older patients usually carry a heavier burden of cardiovascular, metabolic and renal comorbidity, and often take several other drugs. This shapes choices among systemic agents. Cyclosporine requires attention to kidney function and blood pressure, and methotrexate dosing must account for renal clearance. Retinoids such as acitretin are non-immunosuppressive, which may be relevant in older patients with infection or malignancy risk, while biologic agents such as adalimumab, infliximab, etanercept, and ustekinumab are classed as systemic immunosuppressive therapies. Drug interactions with antihypertensives and other chronic medications need review at each step.

HIV and other immunosuppression

Psoriasis in people living with HIV is often difficult to control. The clinical course often is progressive and refractory; therefore, first- and second-line therapies including topical agents, phototherapy, and oral retinoids often are inadequate. Most systemic options suppress immunity further, which complicates management. Evidence is limited: specific guidelines for management and treatment of HIV-infected psoriasis patients are still lacking as most evidence is limited to case reports, and small series of patients, lacking randomized clinical trials. Methotrexate has been used, but it is hepatotoxic and can cause leucopenia and opportunistic infections, hence it should be used with caution. Short cyclosporine courses have been reported to clear disease, with cyclosporine recommended for short intermittent courses of up to 12 weeks. Biologics have been reported to help, and may have a positive effect on CD4 and viral counts when used in combination with highly active antiretroviral therapy. Among biologics, IL-23 inhibition is considered comparatively favourable, since selective inhibition of IL-23, particularly through its unique p19 subunit, provides a more favourable safety profile when compared with inhibiting other inflammatory cytokines such as IL-17 and TNF. Antiretroviral therapy itself is often the first step in patients with deep immunosuppression.

Skin of colour and under-studied groups

Clinical features are not uniform across skin types. On darker skin, erythema is less visually obvious, so plaques may appear grey, violaceous or brown, and post-inflammatory hyperpigmentation or hypopigmentation can dominate the picture. This can delay diagnosis and complicate assessment with scoring tools that rely heavily on redness. Historically, many trials and pivotal studies have enrolled predominantly lighter-skinned participants, limiting the data on efficacy and safety in patients with skin of colour. Similar gaps apply to people with limited access to specialist care, to certain ethnic groups in low- and middle-income settings, and to people with other under-represented characteristics. Greater representation in research and training is needed to improve recognition and treatment across these populations.

Research History

For most of recorded history, scaly skin eruptions were not separated from psoriasis as a disease of their own. Physicians of the eighteenth century described skin conditions in general terms, and the names used for psoriasis overlapped with those for leprosy, a confusion that carried social consequences because people with skin lesions were often isolated. The English physician Robert Willan, in On Cutaneous Diseases (published 1808–1809), grouped skin disorders by the morphology of their primary lesions and gave the first clear descriptions of several forms of psoriasis, including guttate, scalp and palmar varieties. Willan still used the term lepra vulgaris for the disease, and his student and successor Thomas Bateman sharpened the separation from leprosy by stressing that psoriatic patches have irregular outlines and neither raised nor inflamed borders. The name psoriasis became standard only around 1840.

Ferdinand von Hebra, working in Vienna, extended Willan's approach in 1841 by adding microscopic description to the morphological classification. His histological vocabulary, including parakeratosis, is still used for the characteristic changes of the disease. Clinical associations were also recorded in this period: the French dermatologist Jean Louis Alibert noted a link with a form of arthritis in 1818, and Ernest Bazin later coined the term "arthritic psoriasis" in 1860. Through the nineteenth century, the main clinical variants were defined and the basis for today's classification was laid, although the cause and mechanism of the disease remained unknown.

Several bedside signs were named during this period. The Auspitz sign, the pinpoint bleeding that appears when the scale is removed, is attributed to the Austrian dermatologist Heinrich Auspitz, who described it in 1885, although earlier observations by Devergie (1860) and von Hebra (1845) have been cited. The sign is useful but not specific, because it can be absent in psoriasis and can appear in other scaling disorders. The Koebner phenomenon, the appearance of new lesions at sites of trauma, was described by Heinrich Koebner, a Berlin dermatologist who reported it in the 1870s. Sources differ on the exact year (1872, 1876 and 1877 all appear), and Koebner's observations included lesions at scratches, tattoos and bite sites. Over time, the phenomenon became a practical tool: it supports the diagnosis when lesions appear in new locations, and it influences decisions about procedures and injuries in patients.

The first major twentieth-century treatments were topical and light-based. Before this, remedies such as arsenic and mercury had been used. Crude coal tar had long been applied to psoriatic skin, and in 1925 the American dermatologist William H. Goeckerman combined tar application with ultraviolet irradiation. This Goeckerman regimen became a standard treatment for severe disease and remains in use, including as the basic hospital regimen for severely affected patients at the Mayo Clinic. Later studies tried to isolate the contribution of each component: one controlled comparison found that ultraviolet exposure alone improved the disease but did not clear it unless combined with a tar preparation or a lubricating base. Phototherapy was later extended by the development of PUVA, which pairs a psoralen with UVA light.

Systemic drugs followed. Methotrexate, first used in the 1950s, and cyclosporine, adopted from the 1980s onward, were tested in trials that established their role for severe disease. Their use was limited by toxicity, particularly to the liver, kidneys and blood, which made long-term management a central problem.

The biologic era began in the early 2000s. In 2003, alefacept and efalizumab became the first biologic agents approved for psoriasis in the United States. Etanercept followed in 2004 as a TNF-α blocker, and later TNF inhibitors were approved for the disease. The later approvals shaped scientific understanding as much as treatment. TNF inhibitors confirmed that cytokine blockade could rapidly clear skin, while ustekinumab (2009), which targets the p40 subunit shared by IL-12 and IL-23, prompted the separation of these two pathways. Subsequent IL-23 and IL-17 inhibitors, many of them monoclonal antibodies approved from 2015 onward, supported the view that the IL-23/Th17 axis is central to the disease and replaced earlier Th1-centred models.

Unresolved Questions and Future Directions

Genetic risk does not translate directly into disease. Psoriasis affects roughly 2–3% of the global population, yet the strongest known susceptibility factor, HLA-C06:02, is linked to a roughly 9- to 23-fold rise in risk. Most carriers therefore remain unaffected, and the reasons are still unclear. Current explanations focus on additional genes that add to the risk, the environmental triggers that must act on susceptible individuals, and the immune tolerance that normally holds autoreactive responses in check. Whether a reliable predictive biomarker can be found, whether for disease onset or for treatment response, remains an open question. So far, the most advanced predictive tools use clinical variables rather than molecular markers. One model, built from clinical parameters, achieved an area under the curve of about 0.80 for predicting relapse after biologic discontinuation. Pharmacogenetic work is also at an early stage. In one ustekinumab program, carriers of HLA-C06:02 showed a modest increase in the likelihood of response, especially at early time points, but the biological basis of this association is not understood.

Relapse after biologic withdrawal

Relapse after stopping biologic therapy is one of the most practical unresolved problems. Studies consistently show that more than half of patients who achieved clearance relapse within six months of stopping treatment. In a Taiwanese cohort of 874 relapses, the cumulative proportion of patients still relapse-free was about 53% at six months but only about 6% at two years. Time to relapse was shorter in patients who had withdrawn from biologics more often, and in those who had received more agents. Whether relapse can be prevented, delayed, or ultimately avoided through durable remission or cure remains uncertain. Tissue-level studies suggest a biological explanation. Genes encoding inflammatory mediators and skin structural proteins in visually resolved lesions still differ from those in healthy skin, and T cells of the tissue-resident memory type persist in these lesions while retaining the capacity to produce IL-17A and IL-22. The mechanisms that keep these cells in place, and the reasons some patients are more prone to relapse than others, have not been fully resolved.

The gut and skin microbiome

Several studies have described altered microbial communities in psoriasis. Patients often show reduced microbial diversity compared with controls, with shifts in butyrate-producing bacteria, and some investigators have reported increased intestinal permeability, with raised plasma levels of markers of barrier damage. Results remain inconsistent, however, and reports disagree about which genera change. The central question is directional. Investigators do not yet know whether gut bacteria initiate inflammation, respond to it, or simply modify its course. Animal work points in several directions. Germ-free mice developed milder imiquimod-induced skin inflammation than conventional mice, which supports a pathogenic role for the gut. Other experiments showed that colonization with particular bacteria could worsen skin inflammation. Some authors have proposed a bidirectional loop in which skin inflammation selects for certain gut bacteria that in turn sustain systemic inflammation. Human causal inference is harder, and Mendelian randomization analyses have produced associations for specific taxa that require replication.

Precision medicine and long-term safety

The aim of precision medicine in psoriasis is to match patients to drug classes using clinical, genetic, or molecular information before treatment begins. Progress has been limited by the heterogeneity of the disease and by the lack of validated markers that predict response to a particular mechanism. Clinical predictors, genotype data, and tissue signatures are each being studied, but no marker has yet been validated for routine use.

Long-term safety is another open area. Biologics and oral small molecules have been studied for limited periods in trials, and longer exposure in diverse populations is needed to clarify rare adverse events, infection risk, and effects on comorbidities. Real-world registries and cohorts that include women, older adults, and patients from diverse ancestries are central to answering these questions, because trial populations have historically been narrow.

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