Psoriasis is a common, chronic skin condition that has a characteristic clinical and histologic appearance but has various clinical presentations.
The severity of psoriasis ranges from asymptomatic thin localized plaques that are an incidental finding, to widespread generalized plaques, or rarely, complete erythroderma.
Severity is often assessed as total-body surface area (BSA) affected, where the patient's palm = 1% BSA. Greater than 10% BSA is considered to be severe. However, less BSA involvement can still be severe if it significantly interferes with an individual's quality of life.
Lesions of psoriasis are characterized by well-demarcated pink papules or plaques with silvery-white scale.
Lesions tend to be remarkably symmetric in their distribution.
Psoriasis can present in various clinical forms (listed below) and a single patient may have multiple forms throughout his or her lifetime.
Those who have psoriasis commonly recognize the Köbner phenomenon in which new lesions appear at sites of injury or trauma to the skin.
Noxious stimuli, such as scratching and rubbing, or sunburn can elicit a Köbner reaction (Figs. 14.5 and 14.6).
Psoriasis can be a major blow to one's ego. It may stifle social activities and sexual spontaneity, interfere with job opportunities and inhibit participation in sports, and the use of beaches and public swimming pools.
The psychological ramifications of psoriasisanxiety, social isolation, alcoholism, depression, suicidal ideationare possible associations and outcomes of this essentially benign skin disease.
Factors that may adversely influence psoriasis include the following:
Stress. Stress has been implicated as a trigger in acute exacerbations and in progression of psoriasis.
Alcohol. Alcohol overindulgence has been reputed to exacerbate psoriasis.
Drugs. Antimalarials, beta-blockers, angiotensin-converting enzyme inhibitors, certain nonsteroidal anti-inflammatory drugs (e.g., indomethacin), systemic interferon, and lithium carbonate have been reported to worsen psoriasis; however, pre-existing psoriasis is not necessarily a contraindication to their use. Both systemic, and less likely, potent topical steroids have been known, albeit rarely, to trigger a severe, acute, potentially fatal pustular psoriasis (pustular psoriasis of von Zumbusch) that tends to occur after withdrawal of the medication.
Physical trauma. Surgery, thermal and chemical burns, and infections potentially exacerbate psoriasis. For example, an increase in psoriasis activity has been observed in patients who are, or become, infected with the human immunodeficiency virus (HIV).
Sunlight. A small minority of patients find that their psoriasis is worsened by strong sunlight, probably via the Köbner reaction (see Figs. 14.5 and 14.6), whereas the vast majority of patients generally discover that sunlight is beneficial.
Psoriasis is an erratic condition with an unpredictable, waxing- and-waning course. It has no known cure; however, there are numerous methods to keep it under control.
Many patients tend to improve during the summer and worsen during the colder periods of the year. This fluctuation is presumably the result of the positive influence of sunlight.
The diagnosis of psoriasis is usually made on clinical grounds.
A skin biopsy or fungal studies may be performed to rule in or rule out other possible diagnoses.
The differential diagnosis of psoriasis is extensive and varies, depending on the type and location of lesions. The differential diagnoses to consider for each clinical type of psoriasis will be discussed separately in this chapter. SEE PATIENT HANDOUT, Psoriasis IN THE COMPANION eBOOK EDITION. |
Psoriasis is an immunologically based inflammatory skin condition that results in abnormal epidermal differentiation and hyperproliferation.
Psoriasis is more likely to occur in persons with a genetic predisposition. Genome-wide association studies have revealed that psoriasis susceptibility genes have immune-related functions.
The inflammatory process is triggered and maintained by Th1, Th17, and Th22 cells and their corresponding proinflammatory cytokines, tumor necrosis factor alpha (TNF-) and IFN-, IL-17, and IL-22.
The lesions of psoriasis result from a dramatic activation of keratinocyte proliferation.
Such a turned-on epidermis, with a rapid accumulation of cells and no time for shedding, accounts for the characteristic lesion of psoriasis: a red papule or plaque (Fig. 14.1) with a buildup white or silvery (micaceous) scale (Figs. 14.2 and 14.3). Uncommonly, lesions may be very thick and verrucous (Fig. 14.4).
Ongoing vigorous investigation into the pathogenesis of psoriasis has resulted in a multitude of new, effective, targeted therapies.
The histopathologic findings demonstrate the altered cell kinetics of psoriasis (Illus. 14.1):
Marked thickening (acanthosis) as well as thinning of the epidermis with resultant elongation of the rete ridges
Dermal inflammation (lymphocytes and monocytes) and dilation of dermal blood vessels
Epidermal inflammation (polymorphonuclear cells) in the stratum corneum that may form the so-called microabscesses of Munro