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

 

The main abnormality is increased epidermal proliferation due to excessive division of cells in 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.

 

1-3 % of most populations has psoriasis. Common in Europe and North America. It may start at any age but is rare under 10 years and often seen between 15-40 years.

 

Aetiology

 

Basic defect

 

1.Genetic : Frequent genetic predisposition

A child with one affected parent has 15 % chance of developing the disease and this raises to 50 % if both parents are affected. If non-psoriatic parents have a a child with psoriasis the risk for subsequent children is about 10%. It is a heterogeneous but inheritance can be polygenic and others autosomal dominant with incomplete penetrance. Family studies in the USA identified susceptibility gene at the distal end of chromosome 17q. though marker appears to be independent of HLA CW6 and those antigens of histocompatibility complex linked with CW6 associated with psoriasis.

 

2.Biochemical. It is not known if this can cause it. There are increased levels of prostaglandins, leukotrienes and hydroxyeicosatetraenoic(HETE) acids in the epidermis. This may cause increased cellular proliferation and inflammatory changes. Increased activity of phospholipase A, appears to be primarily responsible.

Decreased cAMP and increased cGMP are found in lesions, beta-adrenoceptor antagonist drugs may exacerbate psoriasis by inhibiting cAMP formation.Polyamines are elevated in lesional skin, due to ornithine decarboxylase, which is associated with cellular proliferation. Plasminogen activator is increased in lesions of psoriasis and parellels epidermal mitotic rate.

Calmodulin levels , a calcium binding protein is also alevatged. This influences cell proliferation through phospholipase A2 and cAMP phosphodiesterase activity.

3.Immunopathological. Could be immunological response to unknown antigens. Immune complexes to epidermal antigens have been detected , thereby attracting neutrophils to the area. Certain interleukins )IL-1,2,6 and 8) and growth factors  are elevated. The dermal mononuclear infiltrate is mainly T lymphocytes, helper type.

 

4.Dermal. There is substantial evidence suggesting that the increased epidermal cell proliferation in psoriasis is related to increased replication and metabolism of dermal fibroblasts.