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Consider obtaining the following baseline laboratory studies in patients being initiated on systemic therapies (eg, immunologic inhibitors):
Medications used in the management of psoriasis include the following:
The American Academy of Dermatology (AAD) guidelines recommend treatment with methotrexate, cyclosporine, and acitretin, with consideration of contraindications and drug interactions. 
A 2013 international consensus report on treatment optimization and transitioning for moderate-to-severe plaque psoriasis include the following recommendations :
Management of psoriasis may also involve the following nondrug therapies:
Ocular manifestations such as trichiasis and cicatricial ectropion usually require surgical treatment. Progression of corneal melting, inflammation, and vascularization may require lamellar or penetrating keratoplasty.
See Treatment and Medication for more detail.
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. 
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:
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. 
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. 
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. 
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.
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). One study showed an increased incidence of psoriasis in patients with chronic gingivitis. Satisfactory treatment of the gingivitis led to improved control of the psoriasis but did not influence longterm incidence, highlighting the multifactorial and genetic influences of this disease. 
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.
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 tract infection.
Psoriasis is associated with certain human leukocyte antigen (HLA) alleles, the strongest being human leukocyte antigen Cw6 (HLA-Cw6). In some families, psoriasis is an autosomal dominant trait. Additional HLA antigens that have shown associations with psoriasis and psoriatic subtypes include HLA-B27, HLA-B13, HLA-B17, and HLA-DR7. 
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. 
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.
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.