Psoriasis 

Psoriasis is a chronic, noncontagious, multisystem, inflammatory disorder. Patients with psoriasis have a genetic predisposition for the illness, which most commonly manifests itself on the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal clefts, and glans penis. The joints are also affected by psoriasis in up to 30% of patients with the disease. (See Pathophysiology and Etiology.)

Psoriasis has a tendency to wax and wane with flares related to systemic or environmental factors, including life stress events and infection. It impacts quality of life and potentially long-term survival. There should be a higher clinical suspicion for depression in the patient with psoriasis. (See Prognosis.)

Multiple types of psoriasis are identified, with plaque-type psoriasis, also known as discoid psoriasis, being the most common type. Plaque psoriasis usually presents with plaques on the scalp, trunk, and limbs (see the image below). These plaques appear as focal, raised, inflamed, edematous lesions covered with silvery-white “micaceous” scales. (See Clinical Presentation.)

Ocular signs occur in approximately 10% of psoriasis patients, and they are more common in men than in women. Patients with ocular findings almost always have psoriatic skin disease; however, it is rare for the eye to become involved before the skin.^{[1, 2, 3]}

The diagnosis of psoriasis is clinical. (See Workup.) Management of psoriasis may involve topical or systemic medications, light therapy, stress reduction, climatotherapy, and various adjuncts such as sunshine, moisturizers, and salicylic acid. (See Treatment and Management.)

For more information, see the following:

• Guttate Psoriasis
• Nail Psoriasis
• Plaque Psoriasis
• Pustular Psoriasis
• Psoriatic Arthritis
• Imaging of Psoriatic Arthritis
• Parapsoriasis

Psoriasis is a complex, multifactorial disease that appears to be influenced by genetic and immune-mediated components. This is supported by the successful treatment of psoriasis with immune-mediating, biologic medications.

The pathogenesis of this disease is not completely understood. Multiple theories exist regarding triggers of the disease process including an infectious episode, traumatic insult, and stressful life event. In many patients, no obvious trigger exists at all. However, once triggered, there appears to be substantial leukocyte recruitment to the dermis and epidermis resulting in the characteristic psoriatic plaques.

Specifically, the epidermis is infiltrated by a large number of activated T cells, which appear to be capable of inducing keratinocyte proliferation. This is supported by histologic examination and immunohistochemical staining of psoriatic plaques revealing large populations of T cells within the psoriasis lesions. One report calculated that a patient with 20% body surface area affected with psoriasis lesions has around 8 billion blood circulating T cells compared with approximately 20 billion T cells located in the dermis and epidermis of psoriasis plaques.^[4]

Ultimately, a ramped-up, deregulated inflammatory process ensues with a large production of various cytokines (eg, tumor necrosis factor-α [TNF-α], interferon-gamma, interleukin-12). Many of the clinical features of psoriasis are explained by the large production of such mediators. Interestingly, elevated levels of TNF-α specifically are found to correlate with flares of psoriasis.

One study adds further support that T-cell hyperactivity and the resulting proinflammatory mediators (in this case IL-17/23) play a major role in the pathogenesis of psoriasis.^[5]

Key findings in the affected skin of patients with psoriasis include vascular engorgement due to superficial blood vessel dilation and altered epidermal cell cycle. Epidermal hyperplasia leads to an accelerated cell turnover rate (from 23 d to 3-5 d), leading to improper cell maturation.

Cells that normally lose their nuclei in the stratum granulosum retain their nuclei, a condition known as parakeratosis. In addition to parakeratosis, affected epidermal cells fail to release adequate levels of lipids, which normally cement adhesions of corneocytes. Subsequently, poorly adherent stratum corneum is formed leading to the flaking, scaly presentation of psoriasis lesions, the surface of which often resembles silver scales.

Conjunctival impression cytology demonstrated a higher incidence of squamous metaplasia, neutrophil clumping, and nuclear chromatin changes in patients with psoriasis.^{[6, 7]}

Psoriasis involves hyperproliferation of the keratinocytes in the epidermis, with an increase in the epidermal cell turnover rate. (See Pathophysiology.) The cause of the loss of control of keratinocyte turnover is unknown. However, environmental, genetic, and immunologic factors appear to play a role.

Environmental factors

Many factors besides stress have also been observed to trigger exacerbations, including cold, trauma, infections (eg, streptococcal, staphylococcal, human immunodeficiency virus), alcohol, and drugs (eg, iodides, steroid withdrawal, aspirin, lithium, beta-blockers, botulinum A, antimalarials). Hot weather, sunlight, and pregnancy may be beneficial, although the latter is not universal. Perceived stress can exacerbate psoriasis. Some authors suggest that psoriasis is a stress-related disease and offer findings of increased concentrations of neurotransmitters in psoriatic plaques.

Genetic factors

Patients with psoriasis have a genetic predisposition for the disease. The gene locus is determined. The triggering event may be unknown in most cases, but it is likely immunologic. The first lesion commonly appears after an upper respiratory infection.

Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, particularly human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait.

A multicenter meta-analysis confirmed that deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor for susceptibility to psoriasis in different populations.^[8]

Obesity is another factor associated with psoriasis. Whether it is related to weight alone, genetic predisposition to obesity, or a combination of the 2 is not certain. Onset or worsening of psoriasis with weight gain and/or improvement with weight loss is observed.

Immunologic factors

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.

According to the National Institutes of Health (NIH), approximately 2.2% of the United States population has psoriasis. Internationally, the incidence of psoriasis varies dramatically. A study of 26,000 South American Indians did not reveal a single case of psoriasis, whereas in the Faeroe Islands, an incidence of 2.8% was observed. Overall, approximately 2-3% of people are affected by psoriasis worldwide. Psoriasis can begin at any age. Approximately 10-15% of new cases begin in children younger than 10 years. The median age at onset is 28 years.

Psoriasis appears to be slightly more prevalent among women than among men; however, men are thought to be more likely to experience the ocular disease. Psoriasis is slightly more common in women than in men.

The incidence of psoriasis is dependent on the climate and genetic heritage of the population. It is less common in the tropics and in dark-skinned persons. Psoriasis prevalence in African Americans is 1.3% compared with 2.5% in whites.^[9]

Although psoriasis is usually benign, it is a lifelong illness with remissions and exacerbations and is sometimes refractory to treatment. It progresses to arthritis in about 10% of cases. About 17-55% of patients experience remissions of varying lengths.

Mild psoriasis does not appear to increase risk of death.^[10] However, men with severe psoriasis died 3.5 years earlier compared with men without the disease. Women with severe psoriasis died 4.4 years earlier compared with women without the disease.^[10]

Psoriasis is associated with cardiovascular disease, smoking, alcohol, metabolic syndrome, lymphoma, depression, suicide, potentially harmful drug and light therapies, and possibly melanoma and nonmelanoma skin cancers.

A systematic review of 90 studies confirmed that patients with psoriasis had a higher risk of ischemic heart disease, stroke, and peripheral arterial disease but also a greater prevalence of risk factors for cardiovascular disease, compared with controls. The authors concluded that large prospective studies with long-term followup are required to determine whether psoriasis is an independent risk factor for vascular disease or is merely associated with known risk factors.^[11]

Psoriasis can significantly influence a person’s quality of life. One study suggests that the physical and mental disability experienced with this disease was comparable or in excess of that found in patients with other chronic illnesses such as cancer, arthritis, hypertension, heart disease, diabetes, and depression.^[12] A study by Kurd et al further supports the notion that psoriasis impacts quality of life and potentially long-term survival.^[13] There should be a higher clinical suspicion for depression in the patient with psoriasis.

Studies show that psoriasis of the palms and soles tend to have greater impact on the patient’s quality of life compared to those with more extensive psoriatic involvement not involving the palms and soles.^{[14, 15]}

Dry eye and its manifestations may be present. Avoiding drying conditions and using lubricants can be effective. Patient recognition of these symptoms is vital for effective early treatment of this disease. Most cases of psoriasis can be controlled at a tolerable level with the regular application of care measures.

For patient education resources, see the Psoriasis Center, as well as Psoriasis, What Is Psoriasis?, Types of Psoriasis, Nail Psoriasis, and Understanding Psoriasis Medications.