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.