CASE #1: Plaque psoriasis
Plaque psoriasis, also known as psoriasis vulgaris, is quite common. The condition affects approximately 1% to 2% of whites, usually presenting in the third to fourth decade of life. Men with mycosis fungoides outnumber women by 2:1. Psoriatic lesions typically first appear on extensor surfaces and truncal skin. Psoriasis is a noncontagious, chronic, multisystem inflammatory disorder. Anywhere from 10% to 30% of those with the disease will also have a related form of arthritis called psoriatic arthropathy (PsA).
Psoriasis is a complex multifactorial condition that appears to be influenced primarily by genetic and immune-mediated factors. Environmental factors—especially stress, infection, and medications—seem to influence the course of the disease as well. In many patients, no trigger is ever identified, but once triggered, the disease appears to involve significant leukocyte recruitment to the dermis and epidermis, resulting in the formation of typical psoriatic lesions.1
The activated T-cells infiltrating the skin appear to be capable of inducing keratinocyte proliferation. Ultimately, this ramped-up, deregulated inflammatory process also promotes the production of such cytokines as tumor necrosis factor alpha and interleukin-12, which effectively mediate many of the features of plaque psoriasis.
In an individual with psoriasis, the turnover time for affected keratinocytes is reduced from 23 days to three to five days. This process greatly interferes with keratinocyte maturation and affects such functions as the adhesion of corneocytes that build up on the surface, accounting for the silvery lamellar scales seen with this disease.
Normally, these keratinocytes have time to gradually lose their nuclei as they migrate upward, a phenomenon known as orthokeratosis. In someone with psoriasis, however, the transit time is too short, and the cells retain their nuclei until they are shed. This microscopic finding is described as parakeratosis. Superficial vascular engorgement adds to the peculiar redness of the lesions.2 These theories are supported by voluminous research as well as by the positive response to immune-mediating biologic medications that are specifically designed for these functions.3
Histologically, all psoriasis is pustular,4 including spongioform intraepidermal pustules as well as Munro microabscesses within the stratum corneum. Neutrophilic microabscesses are generally seen above multiple small areas of parakeratosis. Cases of well-developed psoriasis feature regular epidermal acanthosis with long, bulbous rete ridges that thin over the dermal papillae but only scant spongiosis, except in the areas immediately surrounding collections of neutrophils.
For the most part, the diagnosis of psoriasis is clinical. In this case, the lesions and patient history were a near-perfect fit. The onset or flaring of psoriasis is related to stress, alcohol consumption, and obesity. Psoriasis takes a heavy toll on the patient in terms of stress and depression.5 At times, the diagnosis of psoriasis can be rendered difficult by clinical presentations in which the disease is relegated to inverse areas, nails, scalp, palms, soles or even the eyes.
Especially in early psoriasis, a biopsy can be less than helpful. This is particularly true in cases of chronic psoriasiform spongiotic dermatitis (a major item in the differential). Ideally, biopsy of psoriasis should show a lack of edema; the relative lack of spongiosis; tortuosity of capillary loops; and the presence of neutrophils above foci of parakeratosis, alternating in a rhythmic fashion with orthokeratosis.
The differential for psoriasis is extensive and includes such diagnoses as Bowen disease, nummular eczema, tinea corporis and mycosis fungoides (a form of cutaneous T-cell lymphoma). Early on, mycosis fungoides can manifest as what is termed large plaque parapsoriasis, with psoriasiform lesions ranging in size from 1 cm to 5 cm. These annular lesions feature faint scale, mild surface atrophy, mottled dyspigmentation and telangiectasia, and appear predominately on the lower abdomen, buttocks and breasts. Over a considerable amount of time, these lesions can evolve into infiltrative plaques, which, if left undiagnosed, can develop into a case of full-blown lymphoma. Biopsy and expert examination of the specimen are essential in making the diagnosis.4
Psoriasis can be difficult to treat. Options include topical calcipotriene (Dovonex), intralesional steroid injection, phototherapy and methotrexate (Rheumatrex, Trexall). Use of such injectible biologics as etanercept (Enbrel) and infliximab (Remicade) has revolutionized the treatment of this condition. The biologics have the potential to treat cutaneous psoriasis as well as PsA but are expensive and possess several potentially dangerous side effects.6
Other types of psoriasis that have been described include guttate, inverse, pustular and sebopsoriasis (an overlap between psoriasis and seborrheic dermatitis). Psoriatic arthritis is perhaps the most significant type of psoriasis. Left undiagnosed and untreated, PsA can lead to crippling destruction of the joint and must therefore be detected and treated early on. Unfortunately, there is no correlation between the severity or onset of psoriasis and the appearance of PsA. The sheer multiplicity of types of PsA makes diagnosis problematic, so this task is probably best left to a rheumatologist.4
Treatment of this patient’s psoriasis was relatively simple, employing the use of topical clobetasol spray and counseling for to reduce the patient’s weight and alcohol intake.