Q.

Briefly outline the clinical manifestations and

management of psoriasis.
INTRODUCTION :-
•The main abnormality in psoriasis is the increased
epidermal proliferation due to excessive division of cells in
the stratum basale and a shorter cell cycle. In association
with the basal cell hyperplasia, there is enhanced
metabolism and accelerated synthesis and degradation of
nucleoproteins, resulting in hyperuricaemia. There is
proliferation of the subepidermal vasculature, which is
responsible for the "Auspitz's sign". T lymphocytes are
important in the pathogenesis.
•Commonly presents before the age of 35 years. It is
equally common in both males and females.
•May be a presenting sign of HIV infection.
CLINICAL FEATURES :-
•The characteristic lesions are pink-red, sharply
demarcated papules and rounded plaques, and are
covered by silvery scales (plaque psoriasis).
•The most common areas of involvement are the extensor
body areas (elbows and knees), gluteal cleft and the scalp.
Trunk is also commonly involved.
PATHOPHYSIOLOGY:-
Traumatised areas are often involved (Koebner or
isomorphic phenomenon) and this explains common
involvement of elbows and knees.
•Besides typical lesions described above, the skin lesions
can range from small drop-shaped papules (guttate
psoriasis,- frequently affect children and adolescents
following a streptococcal infection or an upper respiratory
tract infection) to pustules (pustular psoriasis,-multiple
tender sterile pustules with an underlying, blotchy, and
erythematous base), to generalised erythema and scales
(erythroderrnic psoriasis,--develops if existing psoriasis is
poorly controlled, systemic medication are withdrawn
suddenly, reaction to a drug such as lithium, or presence
of an underlying systemic infection).
INVESTIGATIONS :-
•On scrapping .a psoriatic lesion with a microscopic slide,
silvery scales come out first. After that, pin-point bleeding
appears at the base of the lesion. The latter is known as
Auspitz's sign.
•Psoriatic arthritis is seen in 5-10% of psoriatic patients
and usually occurs several years after appearance of skin
lesions. It is a form of seronegative spondyloarthropathy.
•Medical co-morbidities: Some of the co-morbidities
associated with psoriasis include ulcerative colitis, Crohn 's
disease, coronary artery disease, metabolic syndrome and
lymphoma.
MANAGEMENT AND PREVENTION
•Most patients with psoriasis have skin lesions limited to
localised areas. For these patients, topical therapy remains
a part of their therapeutic regimen.
Local Treatment
•Local measures include application of emollients, coal tar
preparations, dithranol, topical steroids, and ultraviolet
radiation (narrowband UVB and PUVA). Topical steroids
range in strength from weak steroids such as 1 % hydrocor-
tisone to superpotent corticosteroids, such as clobetasol
propionate and betamethasone dipropionate. Side effects
of topical corticosteroids, especially those that carry the
superpotent categorisation include cutaneous atrophy,
devel-opment of striae and formation of telangiectasia.
Hypothalamic-pituitary-adrenal axis suppression can occur
with prolonged use.
•Other local agents include vitamin D analogues that inhibit
keratinocyte growth, promote keratinocyte differentiation,
and decrease inflammation in psoriatic lesions via vitamin
D receptors on keratinocytes and T lymphocytes. These
include calcipotriol, calcitriol and tacalcitol.
•Local retinoid, tazarotene, is also useful.
•Calcineurin inhibitors (tacrolimus and pimecrolimus)
improve symptoms with less skin atrophy than topical
corticoste-roids and are considered first-line treatments for
facial and flexural psoriasis.