Psoriasis is a common, chronic, relapsing, inflammatory skin disorder with a strong genetic basis. The plaque type is the most common, although several other distinctive clinical variants of psoriasis are recognized (eg,Guttate, Nails, Pustular). Plaque psoriasis is most typically characterized by circular-to-oval red plaques distributed over extensor body surfaces and the scalp. The plaques usually exhibit scaling as a result of epidermal hyperproliferation and dermal inflammation. The extent and duration of the disease is highly variable from patient to patient. Acute flares or relapses of plaque psoriasis may also evolve into more severe disease, such as pustular or erythrodermic psoriasis.
Up to 10-20% of patients with plaque psoriasis also experience Psoriatic Arthritis. A population-based study by Wilson et al that spanned more than 30 years reported that less than 10% of psoriasis patients develop clinically recognized psoriatic arthritis. The clinical features that were associated with an increased chance of leading to psoriatic arthritis were reported as being scalp lesions, nail dystrophy, and intergluteal or perianal psoriasis.1
The pathophysiology of psoriasis must be understood in terms of the prominent pathologies occurring in both major components of the skin—the epidermis and the dermis
Psoriasis is fundamentally an inflammatory skin condition with reactive abnormal epidermal differentiation and hyperproliferation. Current research suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained primarily by T cells in the dermis.
In this model, antigen-presenting cells in the skin, such as Langerhans cells, are believed to migrate from the skin to regional lymph nodes, where they interact with T cells. Presentation of an as yet unidentified antigen to the T cells, as well as a number of co-stimulatory signals, triggers an immune response, leading to T-cell activation and the release of cytokines. Co-stimulatory signals are initiated via the interaction of adhesion molecules on the antigen-presenting cells, such as lymphocyte function–associated antigen (LFA)–3 and intercellular adhesion molecule-1, with their respective receptors CD2 and LFA-1 on T cells. These T cells are released into the circulation and traffic back into the skin. Reactivation of T cells in the dermis and epidermis and the local effects of cytokines such as tumor necrosis factor lead to the inflammation, cell-mediated immune responses, and epidermal hyperproliferation observed in persons with psoriasis.
Both genetic and environmental factors have been implicated in the pathophysiology of psoriasis.
- Genetic factors: HLA-B13, -B17, and -Cw6 are all associated with plaque psoriasis. Multifactorial inheritance mechanisms and etiologies without any genetic component have not yet been excluded, although many families appear to exhibit autosomal dominant patterns of inheritance with decreased penetrance. Studies of twin siblings have shown concordant disease in 73% of monozygotic twins compared with 20% in dizygotic twins. Several putative genetic susceptibility loci have also been identified, including psoriasis susceptibility 1 (PSOR1) on chromosome 6, which is associated with up to 50% of cases. Six other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7) have been discovered, as well as the transcription factor RUNX1. While this certainly points to a genetic mechanism, the absence of 100% concordance among monozygotes suggests that environmental factors must play a role in the pathophysiology of this disease.
- Environmental factors: Infection and a number of physical agents (eg, HIV infection, alcoholism, smoking, UV light) all can affect the course, duration, and clinical appearance of plaque psoriasis. See for more details on the role of environmental factors.
One to 2% of the American population has plaque psoriasis. Family history has been shown to predict disease occurrence. When both parents are affected by psoriasis, the rate in siblings of probands is as high as 50%. When one parent is affected, the rate is 16.4%. When neither parent has psoriasis, only 7.8% of siblings of probands are affected. Other studies have shown that 36-71% of patients with psoriasis have one relative who is also affected by psoriasis.
Plaque psoriasis is universal in its occurrence and varies with race, geography, and environmental factors (eg, sun exposure).
- Pustular flares of disease may be provoked by systemic corticosteroid therapy. Such flares can be fatal. Other than this, disease-related mortality is exceedingly rare in psoriasis, and even then, the primary cause of mortality is related to its therapy. Adverse effects of systemic treatments (eg, hepatic fibrosis from methotrexate) and phototherapy (eg, psoralen plus UVA [PUVA]–induced skin cancers with metastases) are the primary disease-related causes of death.
- Morbidity is a much greater problem in patients with psoriasis and is often related to pruritus, dry and peeling skin, fissuring, and the adverse effects of therapy. By far, the patient's quality of life is most affected in plaque psoriasis, and studies have demonstrated patients with psoriasis have deficiencies in quality of life similar to those for persons with congestive heart failure. Self-consciousness and embarrassment about appearance, inconvenience, and the high cost of antipsoriatic treatment regimens all add to the morbidity of this chronic and relapsing disease.
Psoriasis can affect persons of any race; however, epidemiologic studies have shown a higher prevalence in western European and Scandinavian populations. In these groups, 1.5-3% of the population is affected by the disease.
- The highest documented disease prevalence is in Arctic Kasach'ye, with 12% of the population affected, followed by Norway, where 4.8% of the population has psoriasis.
- Lower prevalence rates for psoriasis have been reported among Japanese and Inuit populations.
- Psoriasis is thought to be rare in West Africans and African Americans and is nearly absent in North American Indians. Psoriasis was undetected in the Samoan population and in a study that examined 26,000 South American Indians.
Psoriasis affects adult males and females equally. Among children and adolescents, plaque psoriasis has been found to affect females more than males, but this observation may be due to the earlier age of onset in females.
Plaque psoriasis first appears during 2 peak age ranges.
- The first peak occurs in persons aged 16-22 years, and the second occurs in persons aged 57-60 years.
- Females develop plaque psoriasis earlier than males, and patients with a positive family history for psoriasis also tend to have an earlier age of onset.
- For siblings of patients whose psoriasis appeared before age 15 years, a 3-fold higher risk exists of developing disease compared with siblings of patients who first presented after age 30 years.
The typical history given by a patient with plaque psoriasis is relatively straightforward.
- Patients report prominent itchy, red areas with increased skin scaling and peeling.
- Patients are particularly aware of lesions on the scalp and extensor surfaces.
- Patients typically are self-conscious about their lesions and commonly report using clothing to cover affected sites and avoiding potentially embarrassing social activities.
- Patients commonly recognize that new lesions appear at sites of injury or trauma to the skin.
- This isomorphic phenomenon (Koebner reaction) typically occurs 7-14 days after the skin has been injured and has been found in 38-76% of patients with plaque psoriasis.
- In some patients, so-called reverse-Koebner reactions have also been noted in which preexisting psoriatic plaques actually clear after injury or trauma to the skin.
- Patients may report that their disease worsens in the winter and improves in the summer.
- Significant joint pain, stiffness, and deformity are reported in the 10-20% of patients with psoriasis who develop psoriatic arthritis.
The diagnosis of psoriasis is usually made on the basis of clinical findings, and ancillary laboratory tests are very rarely required.
- Several cardinal features of plaque psoriasis can be readily observed during the physical examination.
- Plaques: Psoriasis manifests as elevated lesions that vary in size from one to several centimeters. The thickened epidermis, expanded dermal vascular compartment, and infiltrate of neutrophils and lymphocytes account for the psoriatic lesions being raised and easily palpable. The number of lesions may range from few to many at any given time. The plaques are irregular to oval and are most often located on the scalp, trunk, and limbs, with a predilection for extensor surfaces such as the elbows and knees. Smaller plaques may coalesce into larger lesions, especially on the legs and sacral regions. Fissuring within plaques can occur when lesions are present over joint lines or on the palms and soles.
- Well-circumscribed margins: Psoriatic plaques are well defined and have sharply demarcated boundaries. Psoriatic plaques occasionally appear to be immediately encircled by a paler peripheral zone referred to as the halo or ring of Woronoff.
- Red color: The color of psoriatic lesions is a very distinctive rich, full, red color. When present on the legs, lesions sometimes carry a blue or violaceous tint.
- Scale: Psoriatic plaques typically have a dry, thin, silvery-white or micaceous scale; however, the amount and thickness of this scale is quite variable. Removing the scale reveals a smooth, red, glossy membrane with tiny punctate bleeding points. These points represent bleeding from enlarged dermal capillaries after removal of the overlying suprapapillary epithelium. This phenomenon is known as the Auspitz sign.
- Symmetry: Psoriatic plaques tend to be symmetrically distributed over the body. Lesions typically have a high degree of uniformity with few morphologic differences between the 2 sides.
Courtesy of University of British Columbia, Division of Dermatology.
Courtesy of University of British Columbia, Division of Dermatology.
- The following are psoriatic variations and associations that can be observed in persons with plaque psoriasis:
- Nail psoriasis: Nail changes are commonly observed in patients with plaque psoriasis. Nails may exhibit pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign. A proper assessment of any patient suspected of having psoriasis should include careful examination of the nails.
- Psoriasis in children: Plaque psoriasis manifests slightly differently in children. Plaques are not as thick, and the lesions are less scaly. Psoriasis may often appear in the diaper region in infancy and in flexural areas in children. The disease more commonly affects the face in children compared with adults.
- Inverse psoriasis: This is a variant of psoriasis that spares the typical extensor surfaces and affects intertriginous (ie, axillae, inguinal folds, inframammary creases) areas with minimal scale.
- Psoriatic arthritis: Red, warm, tender, and inflamed joints; joint deformity; dactylitis; and sausage digits may be observed in patients who also experience psoriatic arthritis.
Exacerbating causes of plaque psoriasis can be divided into local and systemic factors.
- Local factors
- Trauma: All types of trauma have been associated with the development of plaque psoriasis (eg, physical, chemical, electrical, surgical, infective, and inflammatory types of injury). Even excessive scratching can aggravate or precipitate localized psoriasis. The development of psoriatic plaques at a site of injury is known as the Koebner reaction or more details on the Koebner reaction.
- Sunlight: Most patients generally consider sunlight to be beneficial for their psoriasis. Most report a decrease in illness severity during the summer months or periods of increased sun exposure; however, a small minority find that their symptoms are aggravated by strong sunlight, and these individuals actually experience a worsening of their disease in the summer. A severe sunburn can lead to an exacerbation of plaque psoriasis via the Koebner reaction.
- Systemic factors
- Infection: Pharyngeal streptococcal infections have been shown to produce a clinically distinctive disease flare known as guttate psoriasis. Some evidence suggests that subclinical streptococcal colonization or overgrowth could be responsible for refractory plaque psoriasis.
- HIV: An increase in psoriasis activity has been observed in patients who are or become infected with HIV. The extent and severity of skin disease initially appears to parallel the disease stage. Psoriasis often becomes less active in advanced HIV infection.
- Drugs: A number of medications have been shown to cause an exacerbation of psoriasis. Lithium and withdrawal from systemic corticosteroids are well known to cause flares of disease. Beta-blockers, antimalarials, and nonsteroidal anti-inflammatory drugs (NSAIDs) have also been implicated.
- Psychogenic/emotional factors: Many patients report an increase in psoriasis severity with psychological stress. A clear cause-and-effect relationship between disease exacerbation and stress unfortunately has not been proven. Patients may show a decreased capacity to cope with their treatment regimen with higher levels of stress. Pruritus in the setting of increased anxiety or depression may promote scratching and a Koebner reaction.
- Smoking: An increased risk of chronic plaque psoriasis exists in persons who smoke cigarettes.
- Alcohol: Alcohol is considered a risk factor for psoriasis, particularly in young to middle-aged males.
- Endocrine: Psoriasis severity has been noted to fluctuate with hormonal changes. Disease incidence peaks at puberty and during menopause. Pregnant patients' symptoms are more likely to improve than worsen, if any changes occur at all. In contrast, the disease is more likely to flare in the postpartum period, again if any changes occur at all.