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Psoriasis: Epidemiology, clinical manifestations, and diagnosis

Psoriasis: Epidemiology, clinical manifestations, and diagnosis
Literature review current through: Aug 2023.
This topic last updated: Sep 12, 2022.

INTRODUCTION — Psoriasis is a common chronic inflammatory skin disease that may exhibit a variety of clinical manifestations. Chronic plaque psoriasis, the most common subtype of psoriasis, is characterized by well-demarcated, erythematous plaques with overlying, coarse scale (picture 1A-I). Other major subtypes of psoriasis include guttate psoriasis, which typically presents as the acute onset of numerous small, inflammatory plaques (picture 2A-C); pustular psoriasis, which may present as an acute, subacute, or chronic pustular eruption (picture 3A-B); and erythrodermic psoriasis (picture 4A-B), which exhibits cutaneous erythema and scale involving most or all of the body surface area. (See 'Clinical subtypes' below.)

Psoriasis has also been identified as a multisystem chronic inflammatory disorder associated with multiple comorbidities. Psoriatic arthritis is a common comorbidity that should be screened for in all patients. Examples of other comorbidities that are more common in individuals with psoriasis and may warrant intervention include obesity, metabolic syndrome, hypertension, diabetes, and atherosclerotic disease. (See "Comorbid disease in psoriasis".)

The epidemiology, clinical manifestations, and diagnosis of psoriatic skin disease will be reviewed here. In-depth discussions of specific aspects of psoriasis are provided separately.

General principles:

(See "Pathophysiology of plaque psoriasis".)

(See "Treatment of psoriasis in adults".)

(See "Comorbid disease in psoriasis".)

Clinical variants:

(See "Nail psoriasis".)

(See "Guttate psoriasis".)

(See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis".)

(See "Pustular psoriasis: Management".)

(See "Erythrodermic psoriasis in adults".)

Special populations:

(See "Treatment selection for moderate to severe plaque psoriasis in special populations".)

(See "Management of psoriasis in pregnancy".)

(See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis".)

(See "Psoriasis in children: Management of chronic plaque psoriasis".)

Psoriatic arthritis:

(See "Clinical manifestations and diagnosis of psoriatic arthritis".)

(See "Treatment of psoriatic arthritis".)

(See "Psoriatic juvenile idiopathic arthritis: Pathogenesis, clinical manifestations, and diagnosis".)

(See "Psoriatic juvenile idiopathic arthritis: Management and prognosis".)

EPIDEMIOLOGY — Psoriasis is a relatively common disorder that occurs in children and adults worldwide, though the prevalence varies among populations. A systematic, worldwide review found the prevalence of psoriasis ranged from 0.5 to 11.4 percent in adults and 0 to 1.4 percent in children [1]. The prevalence of psoriasis tends to increase with increasing distance from the equator.

There is no clear sex predilection for psoriasis [2,3]. In addition, psoriasis can begin at any age, though it is less common in children than adults. Peak ages for the onset of psoriasis are between 30 and 39 years and between 50 and 69 years [2].

The incidence of psoriasis may be increasing. A population-based study in the United States found an increase in the incidence of psoriasis between the years 1970 to 1974 (50.8 cases per 100,000) and 1995 to 1999 (100.5 cases per 100,000) [4]. A rise in incidence was also detected among children, increasing from 29.6 cases per 100,000 to 62.7 cases per 100,000 during the same time periods [5]. However, changes in diagnostic patterns over time may also contribute to increasing rates of diagnosis [4].

RISK FACTORS — There are multiple proposed risk factors for psoriasis. Genetic predisposition is considered a key contributor, and environmental and behavioral factors may also play roles [6]. In particular, elevated rates of smoking, obesity, and alcohol use are found among individuals with psoriasis. Medications and infections have also been identified as potential triggering or exacerbating factors for psoriasis. (See 'Genetic factors' below and 'Other factors' below.)

Genetic factors — Support for a genetic contribution to psoriasis comes from the observation that approximately 40 percent of individuals with psoriasis or psoriatic arthritis have a family history of the disease [7], as well as the observation that the disease is more frequently concordant among monozygotic twins than dizygotic twins [8-10]. Moreover, genome-wide association studies have identified multiple susceptibility loci for psoriasis, many of which contain genes involved in regulation of the immune system [11-17].

MHC genes — The psoriasis-susceptibility (PSORS1) locus within the major histocompatibility complex (MHC) on chromosome 6p21 (location of the HLA genes) is considered a major genetic determinant of psoriasis [18,19]. Among other MHC genes that have been associated with psoriasis, HLA-Cw6 is the most important allele for susceptibility to early-onset psoriasis [20]. HLA-Cw6 also has a strong association with guttate psoriasis. HLA-B17 may be associated with a propensity for psoriasis and more severe psoriatic arthritis [21,22]. (See "Guttate psoriasis", section on 'Pathogenesis'.)

Other genes — MHC and HLA associations explain only a portion of genetic susceptibility to psoriasis. Interleukin (IL) 23-related genes have been implicated in psoriasis, and this pathway, which involves Th17 cells, has been a target for drug development. (See "Pathophysiology of plaque psoriasis", section on 'Interleukin-23'.)

Genes that encode the shared subunit of the receptor for IL-12 and IL-23 have been identified as susceptibility loci for psoriasis [16,23,24]. Certain receptor polymorphisms appear to predispose to, or protect from, psoriasis [23,24]. In addition, the IL12B gene, which encodes the p40 subunit of IL-12 and IL-23, as well as the IL23A gene, which encodes the p19 subunit of IL-23 and IL-39 [25], are strongly associated with psoriasis [16].

Additional examples of genes involved in immune regulation that are linked to psoriasis include TNIP1 and TNFAIP3, whose gene products act downstream of tumor necrosis factor (TNF)-alpha and regulate nuclear factor kappa-B (NFkB) signaling [16]. Genes encoding IL-4 and IL-13, which modulate Th2 responses, and beta defensins, which are involved in innate immunity, are also implicated [16,26].

Multiple other genes involved in the innate or adaptive immune systems may be associated with psoriasis [17]. As an example, late-onset psoriasis (psoriasis with onset after age 40) may be associated with polymorphisms in the IL1B gene [27]. Highly penetrant gain-of-function mutations in CARD14 can also lead to psoriasis and psoriatic arthritis [28].

In addition, the LCE gene cluster on chromosome 1q21, which encodes cornified envelope proteins that are important for epidermal cell differentiation, is a susceptibility locus for psoriasis [29]. A genome-wide scan revealed that deletions of LCE3B and LCE3C, genes located within the LCE cluster, are associated with an increased risk of psoriasis [30].

The generalized pustular psoriasis variant of psoriasis has been associated with distinct genetic mutations. The role of genetics in generalized pustular psoriasis is reviewed separately. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Genetics'.)

Pharmacogenomic studies have been done to identify genes associated with response to psoriasis treatments [31]. Additional study is necessary to determine the role of pharmacogenomics in the treatment of psoriasis.

Other factors — In addition to genetics, a variety of medical conditions, behavioral conditions, and environmental exposures have been proposed as risk factors or exacerbating factors for psoriasis.

Examples of medical and behavioral risk factors linked to psoriasis include smoking, obesity, and alcohol use. The relationship between psoriasis and these and other medical or behavioral conditions is reviewed in detail separately. (See "Comorbid disease in psoriasis".)

Multiple drugs are associated with worsening psoriasis or psoriasis-like drug eruptions (table 1). The most common implicated drugs are beta blockers, lithium, and antimalarial drugs. Immune checkpoint inhibitors are a newer class of drugs that can cause or exacerbate psoriasis [32,33]. Paradoxically, TNF inhibitors, drugs used for the treatment of psoriasis, are occasionally linked to the development of psoriasis-like eruptions [34-37]. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects", section on 'Cutaneous reactions'.)

Infections, both bacterial and viral, may be associated with worsening of psoriasis. Poststreptococcal flares of guttate psoriasis and the onset or worsening of psoriasis in association with HIV infection are recognized contributors. (See "Guttate psoriasis", section on 'Streptococcal infection' and 'HIV-infected patients' below.)

The role of vitamin D status in psoriasis is uncertain, but low vitamin D levels have been observed in patients with psoriasis [38]. A case-control study that compared 43 patients with psoriasis and 43 matched controls with other nonphotosensitive dermatologic diseases found that serum levels of 25-hydroxyvitamin D were lower in the patients with psoriasis even after adjusting for factors such as Fitzpatrick skin phototype (table 2) and estimated sun exposure [39]. (See "Vitamin D and extraskeletal health", section on 'Immune system'.)

Stress is often cited as an inciting or exacerbating factor for psoriasis. However, a systematic review and meta-analysis of studies evaluating the relationship between antecedent psychologic stress and onset or exacerbation of psoriasis found insufficient data to confirm an association [40]. The included studies were primarily retrospective, had significant limitations, and yielded conflicting results. Further study is necessary to clarify the impact of stress on the course of psoriasis.

PATHOPHYSIOLOGY — Historically, psoriasis was viewed as primarily a disease of hyperproliferation; however, it is now known that psoriasis is a complex immune-mediated disease in which T lymphocytes, dendritic cells, and cytokines (interleukin [IL] 23, IL-17, and tumor necrosis factor [TNF]) play a central role. A pathogenic role for observed differences in the skin microbiota of psoriatic skin compared with normal skin remains to be confirmed [41,42]. (See "Pathophysiology of plaque psoriasis".)

The typical clinical findings of scaling, induration, and erythema are the result of hyperproliferation and abnormal differentiation of the epidermis, inflammatory cell infiltrates, and vascular dilatation. When compared with a normal epidermis, this hyperproliferative state is characterized by:

Increased numbers of epidermal stem cells

Increased numbers of cells undergoing DNA synthesis

A shortened cell cycle time for keratinocytes (36 hours compared with 311 hours in normal skin)

A decreased turnover time of the epidermis (4 days from basal cell layer to stratum corneum compared with 27 days in normal skin)

Abnormal differentiation in psoriatic skin is evidenced by a delay in the expression of keratins 1 and 10 (seen in normal skin) and an overexpression of keratins 6 and 16 (seen in reactive and healing skin).

The body of evidence demonstrating the importance of the immune system in the pathogenesis of psoriasis is contributing to the development of new therapies for the disease. The availability of biologic agents that work through targeted interference with specific cytokines has revolutionized psoriasis therapy and has confirmed the critical role of these components of the immune system in the pathogenesis of psoriasis. In addition, new treatments are contributing to our understanding of the immune pathogenesis of the disease. The role of the immune system in psoriasis is discussed in greater detail separately. (See "Pathophysiology of plaque psoriasis" and "Treatment of psoriasis in adults", section on 'Biologic agents' and "Treatment of psoriasis in adults", section on 'Emerging therapies'.)

CLINICAL MANIFESTATIONS — Psoriasis occurs in a variety of clinical forms and may exhibit varying features based upon the affected body area.

Clinical subtypes — The major subtypes of psoriasis include:

Chronic plaque psoriasis

Guttate psoriasis

Pustular psoriasis

Erythrodermic psoriasis

Chronic plaque psoriasis is the most common subtype. A population-based study of 1633 patients with adult-onset psoriasis and 357 patients with pediatric-onset psoriasis found that chronic plaque psoriasis accounted for 79 and 74 percent of cases of psoriasis, respectively [5]. A questionnaire study of 3179 women and 646 men in the Nurses' Health Study (NHS) and Health Professionals Follow-up Study (HPFS) with physician-diagnosed psoriasis found that 55 to 60 percent reported plaque psoriasis [43].

Chronic plaque psoriasis — Patients with chronic plaque-type psoriasis usually present with symmetrically distributed, cutaneous plaques (picture 1A-I). The scalp, extensor elbows, knees, and gluteal cleft are common sites for involvement. The extent of involvement can range from limited, localized disease to involvement of the majority of the body surface area. Involvement of intertriginous areas (inverse psoriasis), the ear canal, umbilicus, palms, soles, or nails may also be present (picture 5A-B). (See 'Special sites' below.)

Psoriasis plaques are erythematous with sharply defined margins (picture 1A-I). In patients with highly pigmented skin, postinflammatory hyperpigmentation may be prominent and may obscure erythema. The plaques can range from less than 1 to more than 10 cm in diameter. A thick, silvery scale is usually present, although bathing may remove the scale, and applications of emollients may make the scale temporarily invisible.

The plaques may be asymptomatic, but pruritus is common. Palm or sole involvement can include painful fissures (picture 6A-B). (See 'Palmoplantar psoriasis' below.)

Guttate psoriasis — Guttate psoriasis is characterized by the abrupt appearance of multiple small, psoriatic papules and plaques (picture 2A-C). The papules and plaques are usually less than 1 cm in diameter (giving rise to the name "guttate," which means "drop-like"). The trunk and proximal extremities are the primary sites of involvement. (See "Guttate psoriasis".)

Guttate psoriasis typically occurs as an acute eruption in a child or young adult with no previous history of psoriasis. Less commonly, a guttate psoriasis flare occurs in a patient with pre-existing psoriasis. There is a strong association between recent infection (usually streptococcal pharyngitis) and guttate psoriasis. (See "Guttate psoriasis", section on 'Streptococcal infection'.)

Pustular psoriasis — Pustular psoriasis is a form of psoriasis that can have life-threatening complications. The most severe variant (the von Zumbusch-type of generalized pustular psoriasis) presents with the acute onset of widespread erythema, scaling, and sheets of superficial pustules (picture 3A-B). This form of psoriasis can be associated with malaise, fever, diarrhea, leukocytosis, and hypocalcemia. Renal, hepatic, or respiratory abnormalities and sepsis are potential complications. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis".)

Reported causes of pustular psoriasis include pregnancy, infection, and the withdrawal of oral glucocorticoids. The term "impetigo herpetiformis" has been used to refer to pustular psoriasis of pregnancy. (See "Dermatoses of pregnancy", section on 'Pustular psoriasis of pregnancy' and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Precipitating factors'.)

Acrodermatitis continua of Hallopeau is a localized version of pustular psoriasis in which disease involves the distal digits (picture 7). (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Acrodermatitis continua of Hallopeau'.)

The categorization of palmoplantar pustulosis as a localized form of pustular psoriasis or as a distinct entity is controversial (picture 8A-B). (See "Palmoplantar pustulosis: Epidemiology, clinical features, and diagnosis".)

Erythrodermic psoriasis — Erythrodermic psoriasis is an uncommon manifestation that may be acute or chronic. It is characterized by generalized erythema and scaling involving most or all of the body surface area (picture 4A-B). Affected patients are at high risk for complications related to loss of adequate barrier protection, such as infection (including sepsis) and electrolyte abnormalities secondary to fluid loss [44]. (See "Erythrodermic psoriasis in adults".)

Special sites — Psoriasis involving intertriginous skin (inverse psoriasis), nails, and palms or soles can exhibit unique features.

Inverse (intertriginous) psoriasis — "Inverse psoriasis" refers to a presentation involving the intertriginous areas, including the inguinal, perineal, genital, intergluteal, axillary, or inframammary regions. This presentation is called "inverse" since it is the reverse of the typical presentation of plaque psoriasis on extensor surfaces.

Characteristic findings of inverse psoriasis include well-demarcated, smooth, shiny plaques with absent or minimal scale that are often misdiagnosed as intertriginous fungal or bacterial infections (picture 9A-E). Genital involvement, in particular, may have a significant negative effect on patient quality of life (picture 10A-B) [45]. (See "Approach to the patient with an intertriginous skin disorder".)

Nail psoriasis — Nail psoriasis is most often noted after the onset of psoriatic skin lesions but also may occur concurrently or prior to the onset of psoriasis in other areas [46,47]. Nail disease is particularly common in patients with psoriatic arthritis [46,48,49]. Occasionally, nail involvement is the only manifestation of psoriasis [47,48]. (See "Nail psoriasis" and "Overview of nail disorders".)

The typical nail abnormality associated with nail matrix disease is pitting, consisting of a few to multiple tiny pits scattered over the nail plate (picture 11). Other nail matrix findings include leukonychia, red spots on the lunula, and crumbling of the nail plate.

When the nail bed is involved, a localized color change in the nail may occur that resembles the tan-brown color of new motor oil, referred to as the "oil drop sign" (picture 12). Other nail bed findings reported to occur in patients with psoriasis include onycholysis, subungual hyperkeratosis, and splinter hemorrhages. [46,47,49]. Subungual hyperkeratosis and nail plate thickening can be confused with onychomycosis (picture 13). (See "Overview of nail disorders".)

Nail psoriasis is reviewed in detail separately. (See "Nail psoriasis".)

Palmoplantar psoriasis — Palmoplantar psoriasis is psoriasis involving the palms or soles. The classic presentation consists of erythematous, hyperkeratotic plaques that may have associated fissures (picture 6A-D). Fissures are often painful and may be disabling. Concomitant nail psoriasis is common.

It is controversial whether palmoplantar pustulosis, a condition characterized by recurrent, pustular eruptions on the palms or soles, is a variant of psoriasis or a distinct disease entity. Palmoplantar pustulosis is reviewed separately. (See "Palmoplantar pustulosis: Epidemiology, clinical features, and diagnosis".)

Classic signs — The Koebner phenomenon and Auspitz sign are common findings in chronic plaque psoriasis. However, the presence or absence of these signs does not confirm or exclude a diagnosis of psoriasis [50].

Koebner phenomenon — The Koebner phenomenon describes the development of skin disease in sites of skin trauma. This finding may also occur in other skin diseases, such as lichen planus and vitiligo.

Auspitz sign — The Auspitz sign refers to the visualization of pinpoint bleeding after removal of scale overlying a psoriatic plaque.

SPECIAL POPULATIONS — The characteristics of psoriasis may differ in certain populations, such as HIV-infected individuals, children, and pregnant individuals.

HIV-infected patients — Psoriasis may be the presenting sign of HIV infection or can develop after the diagnosis. Psoriasis associated with HIV infection is often severe, with palmar and plantar involvement, nail disease, arthritis, and widespread, nearly erythrodermic disease (picture 14). Considerable clinical overlap among HIV-associated psoriasis, psoriatic arthritis with HLA-B27 positivity, and reactive arthritis has led some authors to view these entities as a disease continuum [51]. (See "Pathogenesis of spondyloarthritis".)

Children — Although psoriasis in adults and children can present similarly, there are characteristic features in the pediatric population. (See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis".)

Psoriasis in infants often presents with involvement of the diaper area. Infants with diaper-area involvement typically develop symmetrical, well-demarcated, erythematous patches with little scale (picture 15A-B). Maceration may be present. Unlike irritant diaper dermatitis, the inguinal folds are usually involved. Affected infants may also have psoriatic plaques in other body areas. These plaques are often smaller and thinner than the psoriatic plaques in adult patients [52]. (See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis", section on 'Special sites'.)

The frequencies of specific features of the subtypes of psoriasis are notable in children. Scalp involvement is a common and often initial presentation of chronic plaque psoriasis in children (picture 16) [53]. In addition, children with chronic plaque psoriasis are more likely to have facial involvement than adults. The most common presentation of generalized pustular psoriasis in children is the annular pustular psoriasis variant [54]. Patients with generalized annular pustular psoriasis develop a recurring, subacute eruption of annular or figurate, erythematous plaques with peripheral pustules and scale. (See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical presentation'.)

Pregnant individuals — Pregnant individuals with psoriasis may experience improvement, worsening, or stability of psoriasis during pregnancy. Pregnant individuals may also develop pustular psoriasis of pregnancy (formerly called impetigo herpetiformis), a rare form of generalized pustular psoriasis that usually occurs during the third trimester of pregnancy. (See "Management of psoriasis in pregnancy", section on 'Special considerations' and "Dermatoses of pregnancy", section on 'Pustular psoriasis of pregnancy'.)

ASSOCIATED DISORDERS — Patients with psoriasis are at risk for psoriatic arthritis, an inflammatory musculoskeletal disease. A wide variety of other conditions have also been associated with psoriasis, including systemic disorders, psychiatric and psychosocial disorders, and ocular disease. (See "Comorbid disease in psoriasis".)

Psoriatic arthritis — Psoriatic arthritis is common in patients with psoriasis, though reported prevalence estimates vary widely. Most patients with psoriatic arthritis have coincidental skin involvement, although arthritis precedes the skin disease in a minority of cases. Associated nail involvement is common [46]. (See "Clinical manifestations and diagnosis of psoriatic arthritis" and 'Nail psoriasis' above.)

Common symptoms of psoriatic arthritis include joint pain, joint stiffness (particularly morning stiffness), and back pain [55]. Several clinical patterns of joint involvement have been identified [56]:

Distal arthritis, characterized by involvement of the distal interphalangeal (DIP) joints (picture 17)

Asymmetric oligoarthritis in which less than five small and/or large joints are affected in an asymmetric distribution

Symmetric polyarthritis, similar and at times indistinguishable from rheumatoid arthritis

Arthritis mutilans, characterized by deforming and destructive arthritis (picture 18 and image 1)

Spondyloarthropathy, including both sacroiliitis and spondylitis

Soft tissue inflammation manifesting as enthesitis (inflammation at the site of tendon insertion into bone), tenosynovitis, and dactylitis ("sausage digits") are additional common findings in psoriatic arthritis. Psoriatic arthritis is discussed in greater detail separately. (See "Clinical manifestations and diagnosis of psoriatic arthritis".)

Other comorbidities — Understanding of the prevalence of various comorbid conditions in individuals with psoriasis is increasing. Examples of diseases reported to occur at a higher frequency in patients with psoriasis include cardiovascular disease, malignancy, diabetes, hypertension, metabolic syndrome, inflammatory bowel disease, serious infections, and autoimmune disorders [57-67].

The reasons for these associations are not well understood; both genetic and environmental causes are postulated. Examples of factors that may contribute to the occurrence of comorbid disease in patients with psoriasis include the effects of immune-mediated chronic inflammation, lifestyle factors, and the adverse effects of systemic therapies. The comorbidities of psoriasis are reviewed separately. (See "Comorbid disease in psoriasis".)

Ocular findings — Disorders of the eye, such as blepharitis, conjunctivitis, xerosis, corneal lesions, and uveitis, may occur with increased frequency in patients with psoriasis. Symptoms of eye involvement include ocular discomfort, flaking or crusting within the eyelashes, swollen eyelids, red eyes, visual changes, and psoriatic lesions on the lids or lid margins [68].

CLINICAL COURSE — The clinical course of psoriasis for an individual patient is unpredictable. Plaque psoriasis tends to be a chronic disease [69]. However, there may be marked variability in severity over time [70]. Guttate psoriasis may spontaneously remit, recur, or progress into chronic plaque psoriasis. Generalized pustular psoriasis often runs an unstable and prolonged course without treatment. (See "Guttate psoriasis", section on 'Clinical course' and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical course'.)

Psoriasis is a rare cause of mortality (eg, with widespread pustular or erythrodermic psoriasis), but there were at least a few dozen deaths due to psoriasis in the United States annually before the introduction of biologic medications [71]. In addition to mortality from severe disease, psoriasis is associated with increased overall mortality [72,73]. Some deaths may be due to adverse effects from systemic therapies. Psoriasis may contribute to more deaths through an increased risk of comorbid cardiovascular disease or other disease. (See "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical course' and "Comorbid disease in psoriasis".)

HISTOPATHOLOGY — Classic histologic findings of psoriasis include:

Epidermal hyperplasia that is regular or uniform in degree

Parakeratosis (retention of nuclei in the stratum corneum)

Neutrophils in the stratum corneum and epidermis (microabscesses may be present in the stratum corneum)

Thinned or absent granular cell layer of the epidermis

Thinning of the suprapapillary dermal plates

Tortuous, dilated dermal papillary capillaries

Early lesions differ from established plaques and may only possess superficial, perivascular, lymphocytic infiltrates and dilated, tortuous capillaries. Additionally, atypical cases and partially treated cases of psoriasis can have histologic findings that are suggestive but not diagnostic.

Histologic features similar to psoriasis may be present in superficial fungal skin infections. Special stains for fungal organisms aid with distinguishing psoriasis from fungal infections.

DIAGNOSIS — A diagnosis of chronic plaque psoriasis can be made by physical examination in the vast majority of patients. A skin biopsy can be helpful for challenging cases but is not usually necessary. There are no other laboratory tests that confirm the diagnosis. Genetic testing is not used for the diagnosis of psoriasis.

The diagnostic approach for guttate, pustular, erythrodermic, and nail psoriasis is reviewed separately. (See "Guttate psoriasis", section on 'Diagnosis' and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Diagnosis' and "Erythrodermic psoriasis in adults", section on 'Diagnosis' and "Nail psoriasis", section on 'Differential diagnosis'.)

History and physical examination – A full skin examination that includes examination of the scalp, nails, and anogenital skin should be offered to patients with suspected chronic plaque psoriasis. Supportive examination findings include chronic, well-demarcated, inflamed plaques with coarse scale, particularly when involvement of the scalp, ears, elbows, knees, and umbilicus is present. The recognition of characteristic nail disease or inverse psoriasis in the intergluteal cleft or other sites can support a diagnosis of psoriasis in difficult cases.

Helpful patient history questions may include inquiries regarding a family history of psoriasis and exposure to medications that may induce or exacerbate psoriasis (table 1). (See 'Risk factors' above.)

Skin biopsy – A skin biopsy may be performed if the diagnosis remains uncertain after the history and physical examination. Typically, a 4 mm punch biopsy from involved skin is performed, though a shave biopsy through the mid-dermis may also be adequate. A periodic acid-Schiff-diastase (PAS-D) stain of the specimen may help distinguish psoriasis from a superficial fungal infection. (See "Skin biopsy techniques", section on 'Punch biopsy' and 'Histopathology' above.)

ADDITIONAL EVALUATION — In addition to the evaluation above, patients with psoriasis should be assessed for signs or symptoms of psoriatic arthritis and other comorbidities [74]. (See 'Associated disorders' above.)

Joint guidelines from the American Academy of Dermatology and the National Psoriasis Foundation recommend routine screening for signs and symptoms of psoriatic arthritis to facilitate the earliest possible detection [74]. Screening questions can include asking about the presence of joint pain, joint stiffness (particularly morning stiffness), and back pain (which patients may not recognize as a manifestation of joint pain) [55]. (See "Clinical manifestations and diagnosis of psoriatic arthritis", section on 'Diagnosis'.)

Assessment for other comorbidities is reviewed separately. (See "Comorbid disease in psoriasis", section on 'Evaluation and management'.)

The proportion of patients with psoriasis and ocular disorders is not definitively known, and guidelines for screening for ocular involvement in patients with psoriasis have not been established. Asking patients about ocular symptoms at each follow-up visit may help to identify patients with ocular involvement. In addition, some authors have suggested routine ophthalmic examinations every one to two years in patients with severe psoriasis [68]. (See 'Ocular findings' above.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of chronic plaque psoriasis varies according to the clinical presentation. Key disorders that may be mistaken for chronic plaque psoriasis include seborrheic dermatitis, lichen simplex chronicus, atopic dermatitis, and nummular eczema. The differential diagnoses for guttate, pustular, erythrodermic, and nail psoriasis are reviewed separately. (See "Guttate psoriasis", section on 'Differential diagnosis' and "Pustular psoriasis: Pathogenesis, clinical manifestations, and diagnosis", section on 'Differential diagnosis' and "Erythrodermic psoriasis in adults", section on 'Differential diagnosis' and "Nail psoriasis", section on 'Differential diagnosis'.)

Seborrheic dermatitis – Seborrheic dermatitis usually presents with erythematous patches with overlying scale (picture 19A-C). In individuals with dark skin, the erythema may be less visible (picture 19B, 19D). Both psoriasis and seborrheic dermatitis commonly involve the scalp, ears, and intertriginous areas. Features that support a diagnosis of seborrheic dermatitis include the characteristic fine, greasy scale typically evident in nonintertriginous locations and involvement of classic areas such as the eyebrows, nasolabial folds, central chest, or postauricular area. The presence of nail changes or characteristic changes of psoriasis in other areas helps distinguish psoriasis from seborrheic dermatitis. (See "Seborrheic dermatitis in adolescents and adults" and "Cradle cap and seborrheic dermatitis in infants".)

Lichen simplex chronicus – Lichen simplex chronicus describes skin changes that occur secondary to excessive scratching of the skin. An underlying cause of pruritus or scratching (eg, atopic dermatitis, arthropod bite, or psychologic disorder) is often present. Patients develop plaques of thickened skin that exhibit accentuated skin markings (picture 20). Overlying scale or hyperpigmentation may be present. Sites where the patient cannot reach are unaffected. Lichen simplex chronicus can occur in combination with psoriasis when psoriasis lesions are very itchy. (See "Pruritus: Etiology and patient evaluation", section on 'Secondary skin disorders'.)

Atopic dermatitis – Atopic dermatitis is a common skin disorder associated with the development of pruritus and often excoriated papules and patches that may exhibit erythema, hyperpigmentation, or scale (picture 21A-B). Localized areas of skin lichenification (thickening) are common. The characteristic thick, coarse scale and sharp, raised, well-defined borders of psoriasis are typically absent. In older children and adults, atopic dermatitis tends to involve skin flexures. Infants often have facial or scalp involvement (picture 22). Unlike psoriasis, the diaper area is typically spared. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

Nummular eczema – Nummular eczema (also known as nummular dermatitis) typically presents with well-demarcated, round plaques 1 to 10 cm in diameter (picture 23A-C). The plaques are often erythematous with overlying scale, crust, or small fissures and have indistinct borders, unlike psoriasis. The trunk and extremities are the usual sites of involvement. The face and scalp are spared. (See "Nummular eczema".)

Superficial fungal infections – Superficial fungal infections (eg, tinea corporis, tinea pedis, cutaneous candidiasis) may present with erythematous plaques (with or without pustules) that may be mistaken for psoriasis (picture 24A-B). Nail changes related to onychomycosis can also be confused with nail psoriasis (picture 25). A potassium hydroxide (KOH) preparation or biopsy can be useful for confirming fungal infection. (See "Dermatophyte (tinea) infections" and "Onychomycosis: Epidemiology, clinical features, and diagnosis".)

Other less common disorders that should be considered in the differential diagnosis of chronic plaque psoriasis include subacute cutaneous lupus erythematosus, pityriasis rubra pilaris, crusted scabies, and cutaneous T cell lymphoma.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Psoriasis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Psoriasis (The Basics)")

Beyond the Basics topics (see "Patient education: Psoriasis (Beyond the Basics)" and "Patient education: Psoriatic arthritis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Overview – Psoriasis is a common chronic inflammatory skin disease that has also been identified as a multisystem inflammatory disorder associated with multiple comorbidities.

Epidemiology – Psoriasis affects males and females equally. Psoriasis can begin at any age; however, onset during adulthood is most frequent. (See 'Epidemiology' above.)

Pathophysiology – Psoriasis is a complex immune-mediated disease. Genetic factors play an important role, and multiple genes have been associated with susceptibility to psoriasis. The psoriasis-susceptibility (PSORS1) locus within the major histocompatibility complex (MHC) on chromosome 6p21 is considered a major genetic determinant of this disease. (See 'Pathophysiology' above and "Pathophysiology of plaque psoriasis".)

Clinical manifestations – There are multiple clinical subtypes of psoriasis. Chronic plaque psoriasis, the most common form of psoriasis, most often presents with sharply defined, erythematous plaques with overlying, coarse scale (picture 1A-I). The scalp, extensor elbows, knees, and gluteal cleft are common locations for chronic plaque psoriasis. Other major subtypes include guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. (See 'Clinical manifestations' above.)

Associated disorders – Individuals with psoriasis are at risk for psoriatic arthritis and multiple other comorbidities. Examples of other comorbidities linked to psoriasis include obesity, metabolic syndrome, hypertension, diabetes, and atherosclerotic disease. (See 'Associated disorders' above and "Comorbid disease in psoriasis".)

Diagnosis – A diagnosis of psoriasis can be made by physical examination in the vast majority of patients. Occasionally, a skin biopsy is needed to rule out other conditions. (See 'Diagnosis' above.)

  1. Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol 2017; 31:205.
  2. Parisi R, Symmons DP, Griffiths CE, et al. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J Invest Dermatol 2013; 133:377.
  3. Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol 2014; 70:512.
  4. Icen M, Crowson CS, McEvoy MT, et al. Trends in incidence of adult-onset psoriasis over three decades: a population-based study. J Am Acad Dermatol 2009; 60:394.
  5. Tollefson MM, Crowson CS, McEvoy MT, Maradit Kremers H. Incidence of psoriasis in children: a population-based study. J Am Acad Dermatol 2010; 62:979.
  6. O'Rielly DD, Jani M, Rahman P, Elder JT. The Genetics of Psoriasis and Psoriatic Arthritis. J Rheumatol Suppl 2019; 95:46.
  7. López-Estebaranz JL, Sánchez-Carazo JL, Sulleiro S. Effect of a family history of psoriasis and age on comorbidities and quality of life in patients with moderate to severe psoriasis: Results from the ARIZONA study. J Dermatol 2016; 43:395.
  8. Farber EM, Nall ML, Watson W. Natural history of psoriasis in 61 twin pairs. Arch Dermatol 1974; 109:207.
  9. Duffy DL, Spelman LS, Martin NG. Psoriasis in Australian twins. J Am Acad Dermatol 1993; 29:428.
  10. Brandrup F, Holm N, Grunnet N, et al. Psoriasis in monozygotic twins: variations in expression in individuals with identical genetic constitution. Acta Derm Venereol 1982; 62:229.
  11. Genetic Analysis of Psoriasis Consortium & the Wellcome Trust Case Control Consortium 2, Strange A, Capon F, et al. A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1. Nat Genet 2010; 42:985.
  12. Ellinghaus E, Ellinghaus D, Stuart PE, et al. Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2. Nat Genet 2010; 42:991.
  13. Hüffmeier U, Uebe S, Ekici AB, et al. Common variants at TRAF3IP2 are associated with susceptibility to psoriatic arthritis and psoriasis. Nat Genet 2010; 42:996.
  14. Stuart PE, Nair RP, Ellinghaus E, et al. Genome-wide association analysis identifies three psoriasis susceptibility loci. Nat Genet 2010; 42:1000.
  15. Tsoi LC, Spain SL, Knight J, et al. Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity. Nat Genet 2012; 44:1341.
  16. Nair RP, Duffin KC, Helms C, et al. Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways. Nat Genet 2009; 41:199.
  17. Mahil SK, Capon F, Barker JN. Genetics of psoriasis. Dermatol Clin 2015; 33:1.
  18. Trembath RC, Clough RL, Rosbotham JL, et al. Identification of a major susceptibility locus on chromosome 6p and evidence for further disease loci revealed by a two stage genome-wide search in psoriasis. Hum Mol Genet 1997; 6:813.
  19. Sagoo GS, Tazi-Ahnini R, Barker JW, et al. Meta-analysis of genome-wide studies of psoriasis susceptibility reveals linkage to chromosomes 6p21 and 4q28-q31 in Caucasian and Chinese Hans population. J Invest Dermatol 2004; 122:1401.
  20. Chen L, Tsai TF. HLA-Cw6 and psoriasis. Br J Dermatol 2018; 178:854.
  21. Alenius GM, Jidell E, Nordmark L, Rantapää Dahlqvist S. Disease manifestations and HLA antigens in psoriatic arthritis in northern Sweden. Clin Rheumatol 2002; 21:357.
  22. Umapathy S, Pawar A, Mitra R, et al. Hla-a and hla-B alleles associated in psoriasis patients from mumbai, Western India. Indian J Dermatol 2011; 56:497.
  23. Cargill M, Schrodi SJ, Chang M, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet 2007; 80:273.
  24. Garcia VE, Chang M, Brandon R, et al. Detailed genetic characterization of the interleukin-23 receptor in psoriasis. Genes Immun 2008; 9:546.
  25. Hasegawa H, Mizoguchi I, Chiba Y, et al. Expanding Diversity in Molecular Structures and Functions of the IL-6/IL-12 Heterodimeric Cytokine Family. Front Immunol 2016; 7:479.
  26. Hollox EJ, Huffmeier U, Zeeuwen PL, et al. Psoriasis is associated with increased beta-defensin genomic copy number. Nat Genet 2008; 40:23.
  27. Hébert HL, Bowes J, Smith RL, et al. Polymorphisms in IL-1B distinguish between psoriasis of early and late onset. J Invest Dermatol 2014; 134:1459.
  28. Sundberg JP, Pratt CH, Silva KA, et al. Gain of function p.E138A alteration in Card14 leads to psoriasiform skin inflammation and implicates genetic modifiers in disease severity. Exp Mol Pathol 2019; 110:104286.
  29. Zhang XJ, Huang W, Yang S, et al. Psoriasis genome-wide association study identifies susceptibility variants within LCE gene cluster at 1q21. Nat Genet 2009; 41:205.
  30. de Cid R, Riveira-Munoz E, Zeeuwen PL, et al. Deletion of the late cornified envelope LCE3B and LCE3C genes as a susceptibility factor for psoriasis. Nat Genet 2009; 41:211.
  31. Caputo V, Strafella C, Cosio T, et al. Pharmacogenomics: An Update on Biologics and Small-Molecule Drugs in the Treatment of Psoriasis. Genes (Basel) 2021; 12.
  32. Mullangi S, Ponnam S, Lekkala MR, Koya S. A Case of De Novo Psoriasis Secondary to Nivolumab in a Patient With Metastatic Renal Cell Carcinoma. Cureus 2021; 13:e15703.
  33. Cutroneo P, Ingrasciotta Y, Isgrò V, et al. Psoriasis and psoriasiform reactions secondary to immune checkpoint inhibitors. Dermatol Ther 2021; 34:e14830.
  34. Cullen G, Kroshinsky D, Cheifetz AS, Korzenik JR. Psoriasis associated with anti-tumour necrosis factor therapy in inflammatory bowel disease: a new series and a review of 120 cases from the literature. Aliment Pharmacol Ther 2011; 34:1318.
  35. Pugliese D, Guidi L, Ferraro PM, et al. Paradoxical psoriasis in a large cohort of patients with inflammatory bowel disease receiving treatment with anti-TNF alpha: 5-year follow-up study. Aliment Pharmacol Ther 2015; 42:880.
  36. Eickstaedt JB, Killpack L, Tung J, et al. Psoriasis and Psoriasiform Eruptions in Pediatric Patients with Inflammatory Bowel Disease Treated with Anti-Tumor Necrosis Factor Alpha Agents. Pediatr Dermatol 2017; 34:253.
  37. Famenini S, Wu JJ. Infliximab-induced psoriasis in treatment of Crohn's disease-associated ankylosing spondylitis: case report and review of 142 cases. J Drugs Dermatol 2013; 12:939.
  38. Filoni A, Vestita M, Congedo M, et al. Association between psoriasis and vitamin D: Duration of disease correlates with decreased vitamin D serum levels: An observational case-control study. Medicine (Baltimore) 2018; 97:e11185.
  39. Orgaz-Molina J, Buendía-Eisman A, Arrabal-Polo MA, et al. Deficiency of serum concentration of 25-hydroxyvitamin D in psoriatic patients: a case-control study. J Am Acad Dermatol 2012; 67:931.
  40. Snast I, Reiter O, Atzmony L, et al. Psychological stress and psoriasis: a systematic review and meta-analysis. Br J Dermatol 2018; 178:1044.
  41. Benhadou F, Mintoff D, Schnebert B, Thio HB. Psoriasis and Microbiota: A Systematic Review. Diseases 2018; 6.
  42. Fyhrquist N, Muirhead G, Prast-Nielsen S, et al. Microbe-host interplay in atopic dermatitis and psoriasis. Nat Commun 2019; 10:4703.
  43. Merola JF, Li T, Li WQ, et al. Prevalence of psoriasis phenotypes among men and women in the USA. Clin Exp Dermatol 2016; 41:486.
  44. Boyd AS, Menter A. Erythrodermic psoriasis. Precipitating factors, course, and prognosis in 50 patients. J Am Acad Dermatol 1989; 21:985.
  45. Larsabal M, Ly S, Sbidian E, et al. GENIPSO: a French prospective study assessing instantaneous prevalence, clinical features and impact on quality of life of genital psoriasis among patients consulting for psoriasis. Br J Dermatol 2019; 180:647.
  46. Klaassen KM, van de Kerkhof PC, Pasch MC. Nail psoriasis: a questionnaire-based survey. Br J Dermatol 2013; 169:314.
  47. van der Velden HM, Klaassen KM, van de Kerkhof PC, Pasch MC. Fingernail psoriasis reconsidered: a case-control study. J Am Acad Dermatol 2013; 69:245.
  48. Grover C, Reddy BS, Uma Chaturvedi K. Diagnosis of nail psoriasis: importance of biopsy and histopathology. Br J Dermatol 2005; 153:1153.
  49. Brazzelli V, Carugno A, Alborghetti A, et al. Prevalence, severity and clinical features of psoriasis in fingernails and toenails in adult patients: Italian experience. J Eur Acad Dermatol Venereol 2012; 26:1354.
  50. Bernhard JD. Auspitz sign is not sensitive or specific for psoriasis. J Am Acad Dermatol 1990; 22:1079.
  51. Reveille JD, Conant MA, Duvic M. Human immunodeficiency virus-associated psoriasis, psoriatic arthritis, and Reiter's syndrome: a disease continuum? Arthritis Rheum 1990; 33:1574.
  52. Tollefson MM. Diagnosis and management of psoriasis in children. Pediatr Clin North Am 2014; 61:261.
  53. Shah KN. Diagnosis and treatment of pediatric psoriasis: current and future. Am J Clin Dermatol 2013; 14:195.
  54. Liao PB, Rubinson R, Howard R, et al. Annular pustular psoriasis--most common form of pustular psoriasis in children: report of three cases and review of the literature. Pediatr Dermatol 2002; 19:19.
  55. Taylor SL, Petrie M, O'Rourke KS, Feldman SR. Rheumatologists' recommendations on what to do in the dermatology office to evaluate and manage psoriasis patients' joint symptoms. J Dermatolog Treat 2009; 20:350.
  56. Garg A, Gladman D. Recognizing psoriatic arthritis in the dermatology clinic. J Am Acad Dermatol 2010; 63:733.
  57. Gelfand JM, Neimann AL, Shin DB, et al. Risk of myocardial infarction in patients with psoriasis. JAMA 2006; 296:1735.
  58. Gisondi P, Tessari G, Conti A, et al. Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case-control study. Br J Dermatol 2007; 157:68.
  59. Neimann AL, Shin DB, Wang X, et al. Prevalence of cardiovascular risk factors in patients with psoriasis. J Am Acad Dermatol 2006; 55:829.
  60. Bernstein CN, Wajda A, Blanchard JF. The clustering of other chronic inflammatory diseases in inflammatory bowel disease: a population-based study. Gastroenterology 2005; 129:827.
  61. Pearce DJ, Morrison AE, Higgins KB, et al. The comorbid state of psoriasis patients in a university dermatology practice. J Dermatolog Treat 2005; 16:319.
  62. Makredes M, Robinson D Jr, Bala M, Kimball AB. The burden of autoimmune disease: a comparison of prevalence ratios in patients with psoriatic arthritis and psoriasis. J Am Acad Dermatol 2009; 61:405.
  63. Brauchli YB, Jick SS, Miret M, Meier CR. Psoriasis and risk of incident cancer: an inception cohort study with a nested case-control analysis. J Invest Dermatol 2009; 129:2604.
  64. Patel RV, Shelling ML, Prodanovich S, et al. Psoriasis and vascular disease-risk factors and outcomes: a systematic review of the literature. J Gen Intern Med 2011; 26:1036.
  65. Qureshi AA, Choi HK, Setty AR, Curhan GC. Psoriasis and the risk of diabetes and hypertension: a prospective study of US female nurses. Arch Dermatol 2009; 145:379.
  66. Wakkee M, de Vries E, van den Haak P, Nijsten T. Increased risk of infectious disease requiring hospitalization among patients with psoriasis: a population-based cohort. J Am Acad Dermatol 2011; 65:1135.
  67. Wu JJ, Nguyen TU, Poon KY, Herrinton LJ. The association of psoriasis with autoimmune diseases. J Am Acad Dermatol 2012; 67:924.
  68. Rehal B, Modjtahedi BS, Morse LS, et al. Ocular psoriasis. J Am Acad Dermatol 2011; 65:1202.
  69. Nijsten T, Looman CW, Stern RS. Clinical severity of psoriasis in last 20 years of PUVA study. Arch Dermatol 2007; 143:1113.
  70. Nevitt GJ, Hutchinson PE. Psoriasis in the community: prevalence, severity and patients' beliefs and attitudes towards the disease. Br J Dermatol 1996; 135:533.
  71. Pearce DJ, Lucas J, Wood B, et al. Death from psoriasis: representative US data. J Dermatolog Treat 2006; 17:302.
  72. Springate DA, Parisi R, Kontopantelis E, et al. Incidence, prevalence and mortality of patients with psoriasis: a U.K. population-based cohort study. Br J Dermatol 2017; 176:650.
  73. Noe MH, Shin DB, Wan MT, Gelfand JM. Objective Measures of Psoriasis Severity Predict Mortality: A Prospective Population-Based Cohort Study. J Invest Dermatol 2018; 138:228.
  74. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol 2019; 80:1073.
Topic 5664 Version 39.0

References

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