COMPLETE CURE FOR PSORIASIS

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Treatment has to be continued for three months to avoid recurrence.

What is PSORIASIS ?

Psoriasis is a non-infectious, inflammatory disease of the skin, characterized by well-defined erythematous plaques with large, adherent, silvery scales.

The main abnormality in Psoriasis is increased epidermal proliferation due to excessive division of cells in the basal layers. The transit time of keratinocytes through the epidermis is shortened and the epidermal turnover time falls from 28 to 5 or 6 days.

Between 1% and 3% of most populations has Psoriasis. It is most common in Europe and North America. It may start at any age but is rare under 10 years and often seen between 15 and 40 years. The course of disease is unpredictable but is usually chronic with exacerbations and remissions.

Aetiology

Basic Defect
This remains unknown but the following factors are involved.

Genetic
There is frequently a genetic predisposition. A child with one affected parent has a 15% chance of developing the disease and this rises to 50% if both parents are affected. If non-psoriatic parents have a child with Psoriasis, the risk for subsequent children is about 10%. Psoriasis is a genetically complex disease trait. There is wide clinical and genetic heterogeneity. Linkages have been demonstrated to different loci, including chromosomes 6p(Cw6 region), 17q, 4q and 2q.

Biochemical
It is not known if biochemical abnormalities are the cause or result of increased epidermal proliferation. There are increased levels of prostaglandins, leukotrienes and hydroxyeicosatetraenoic (HETE) acids in the epidermis. These may cause both the increased cellular proliferation seen in Psoriasis and the inflammatory changes. Increased activity of phospholipase A₂ appears to be primarily responsible for these changes.

Decreased cyclic adenosine monophosphate (cAMP) and increased cyclic guanosine monophosphate (cGMP) are found in lesions, and Beta-adrenocepor antagonist drugs may exacerbate Psoriasis by inhibiting cAMP formation. Polyamines are elevated in lesional skin, due to increased activity of ornithine decarboxylase, and may be intimately associated with cellular proliferation. Plasminogen activator is greatly increased in the lesions of Psoriasis and its level parallels the epidermal mitotic rate.

The level of calmodulin, a calcium-binding protein, is also raised in lesions and falls with successful treatment. The calcium-calmodulin complex may regulate epidermal cell proliferation by influencing phospholipase A₂ and cAMP phosphodiesterase (catalyses cAMP conversion to AMP) activity.

Immunopathological
The inflammatory reaction may be part of an immunological reponse to as yet unknown antigens. Immune complexes to epidermal antigens have been detected in damaged skin and may activate complement, thereby attracting neutrophilis to the area. Certain interleukins (IL-1, IL-2, IL-6 and IL-8), interferon gamma, and growth factors (TNF alpha and TGF alpha) are elevated, and adhesion molecules are expressed or upregulated in lesions of Psoriasis. The mononuclear infiltrate is mainly of T lymphocytes, most of which are of the helper type (Th-1) in the dermis and of the cytotoxic type in the epidermis. The beneficial effect of cyclosporin A in Psoriasis may be due to its anti-T helper cell effect. Streptococcal superantigens, from the throat, appear to be responsible for the T-cell activation in guttate Psoriasis.

Dermal
There is substantial evidence to suggest that the increased epidermal cell prolifertaion of Psoriasis is also related to the increased replication and the metabolism of dermal fibroblasts. Both dermal and epidermal abnormalities appear to be necessary for the sustenance of Psoriasis.