Discussion
There are many different clinical manifestations of psoriasis with plaque-type psoriasis being the most common. Plaque psoriasis also known as discoid psoriasis is presented with inflamed erythematous lesions covered by silvery scales that usually appear on the scalp, trunk and the extensor surfaces of the limbs [7]. In our second case, the patient had a solitary plaque on the concha of her left ear for 4 years without any similar lesions on other parts of the body. It was recurrent in the exact same spot and there were no other signs and symptoms supporting psoriasis. The most important differential diagnosis was discoid lupus erythematous (DLE). DLE is basically characterized by erythematous and violaceous scaly plaques that result in atrophy and scarring [8]. Typical histopathologic findings of DLE include vacuolar alteration of the basal layer, thickening of the basement membrane, follicular plugging, hyperkeratosis and atrophy of the dermis [9]. In our case the diagnosis of DLE was eliminated by inconsistent histopathology.
The first case report also presents an usual dermatomal psoriasis resistant to topical treatment. The most important differential diagnosis included lichenoid epidermal nevus, ILVEN (linear inflammatory verrucous epidermal nevus), Kaposi sarcoma, linear psoriasis, and linear lichen planus [10,11]. Linear psoriasis presents by linear distribution of psoriatic lesions along blaschko’s lines and may be confused with ILVEN. ILVEN however, develops during the first month of life and progresses slowly. ILVEN is often irresponsive to antipsoriatic drugs [10-13].
The pathogenesis of psoriasis is not fully understood. It is a multifactorial condition which is influenced by immunologic and genetic factors [2]. According to previous studies, psoriasis is associated with certain human leukocyte antigen (HLA) alleles including HLA-CW6, HLA-B27 and HLA-B13. Also, high levels of dermal and circulating TNF-αand increased activity of T-cells have been noted in previous studies [6, 14-20]. Pathogenesis of linear psoriasis could be explained by the concept of genetic mosaicism as Happle suggested that the loss of heterozygosity would occur in somatic cells during embryogenesis and it can be a good explanation for the non-hereditary linear distribution pattern of some skin diseases [21-23].
We reviewed the PubMed database (1950-present) and apparently this is the first report of dermatomal psoriasis. Further research need to be done to unravel the unknown pathogenesis of such conditions to get a better understanding of the disease and its potential treatment options.