Psoriasis : Definition, Pathophysiology, Diagnosis And Treatment

Thursday, February 13th 2014. | Disease

Psoriasis : Definition, Pathophysiology, Diagnosis and Treatment

Psoriasis is a common chronic inflammatory disease characterized by recurrent exacerbations and remissions of thickened, erythematous, and scaling plaques.
Pathophysiology of Psoriasis :
  • Cell-mediated immune mechanisms play a central role in psoriasis. Cutaneous inflammatory T-cell-mediated immune activation requires two T-cell signals mediated via cell-cell interactions by surface proteins and antigen-presenting cells (APC) such as dendritic cells or macrophages. The first signal is the interaction of the T-cell receptor with antigen presented by APC. The second signal (called costimulation) is mediated through various surface interactions.
  • Once T cells are activated, they migrate from lymph nodes and the bloodstream into skin and secrete various cytokines (primarily interferon-Upsilon and interleukin-2) that induce the pathologic changes of psoriasis. Local keratinocytes and neutrophils are induced to produce other cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8).
  • As a result of pathogenic T-cell production and activation, psoriatic epidermal cells proliferate at a rate sevenfold faster than normal epidermal cells. Epidermal proliferation is also elevated in apparently normal skin of psoriatic patients.
  • There is a significant genetic component in psoriasis. Studies of histocompatibility antigens in psoriatic patients indicate a number of significant associations, especially with HLA-Cw6, where the relative likelihood for developing psoriasis is 9 to 15 times normal.
  • Climate, stress, alcohol, smoking, infection, trauma, and drugs may aggravate psoriasis. Warm seasons and sunlight improve psoriasis in 80% of patients, whereas 90% of patients worsen in cold weather. Psoriatic lesions may develop at the site of injury (e.g., rubbing, venipuncture, bites, surgery) on normal-appearing skin (Koebner response). Lithium carbonate, β-adrenergic blockers, some antimalarials, nonsteroidal anti-inflammatory drugs, ACE inhibitors, tetracyclines, and interferons have been reported to exacerbate psoriasis.
Diagnosis of Psoriasis :
  • The diagnosis is based on physical examination findings of the characteristic lesions of psoriasis.
  • The medical history of a patient with psoriasis should include information about the onset and duration of lesions, family history of psoriasis, presence of exacerbating factors, previous history of antipsoriatic treatment (if any) along with efficacy and adverse effect data, exposure to chemicals and toxins, and allergies (food, drugs, and environmental).
  • Skin biopsy of lesional skin is useful in confirming the diagnosis.
Treatment of Psoriasis :
  • Emollients (moisturizers) hydrate the stratum corneum and minimize water evaporation. They may enhance desquamation, eliminate scaling, and decrease pruritus. The lotions, creams, or ointments often need to be applied up to 4 times a day to achieve a beneficial response. Adverse effects include folliculitis and allergic or irritant contact dermatitis.
  • Balneotherapy (and climatotherapy) involves bathing in waters containing certain salts, often combined with natural sun exposure. The salts in certain waters (e.g., the Dead Sea) reduce activated T cells in skin and may be remittive for psoriasis.
  • Ultraviolet B (UV-B) light exposure (290 to 320 nm) is a beneficial intervention. Use of a “narrow-band” (NB) light sources, in which 83% of the UV-B emission is at 310 to 313 nm, focuses treatment within the most effective wavelength. NB-UVB has been demonstrated to be effective in plaque-type psoriasis. Many topical and systemic therapies (discussed below) are used adjunctively to hasten and improve the response to UV-B phototherapy (e.g., short-contact anthralin with UV-B, addition of topical calcipotriene, or adding systemic methotrexate or retinoids). Emollients enhance efficacy of UV-B and may be applied just prior to UV-B treatments.
  • Salicylic acid is one of the most commonly used keratolytics. It causes a disruption in corneocyte-to-corneocyte cohesion in the abnormal horny layer of psoriatic skin. This serves to remove scales, smooth the skin, and decrease hyperkeratosis. The keratolytic effect enhances penetration and efficacy of some other topical agents such as corticosteroids. It is applied as a 2% to 10% gel or lotion 2 or 3 times a day.
  • Topical corticosteroids may halt synthesis and mitosis of DNA in epidermal cells and appear to inhibit phospholipase A, lowering the amounts of arachidonic acid, prostaglandins, and leukotrienes in the skin. These effects, coupled with local vasoconstriction, reduce erythema, pruritus, and scaling. As antipsoriatic agents, they are best used adjunctively with a product that specifically functions to normalize epidermal hyperproliferation. Low-potency products (e.g., hydrocortisone 1%) have a weak anti-inflammatory effect and are safest for long-term application, for use on the face and intertriginous areas, for use with occlusion, and for use in infants and young children.
  • Vitamin D and its analogs inhibit keratinocyte differentiation and proliferation and have anti-inflammatory effects by reducing IL-8 and IL-2. Use of vitamin D itself is limited by its propensity to cause hypercalcemia.
  • Tazarotene (Tazorac) is a synthetic retinoid that is hydrolyzed to its active metabolite, tazarotenic acid, which modulates keratinocyte proliferation and differentiation. It is available as a 0.05% or 0.1% gel and cream and is applied once daily (usually in the evening) for mild to moderate plaque psoriasis. The 0.1% gel is somewhat more effective, but the 0.05% gel causes less irritation.
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