Introduction and Epidemiology
Psoriasis is a chronic dermatitis of the skin, a consistent hyperactive growth of cells appearing on the integumentary system. Psoriasis is an inflammatory autoimmune disease that alters the life cycle of skin cells, shortening them from a month to a week of cell production. These dead cells are thick, dry and silvery with overlapping flaky scales that can resemble dandruff. The condition is not contagious and can range from mild to severe cases of inflammation of skin. The disease is thought to be the result of genetic susceptibility with environmental influences.
The five main manifestations of psoriasis include erythrodermic, pustular, guttate, inverse and plaque psoriasis (see table 1). Plaque psoriasis is seen in approximately 90% of cases as patches of white scales under which there is a red area, it is also known as psoriasis vulgaris. Pustular psoriasis can be seen as pus-filled blisters. The gluttate form presents as ovular lesions and the inverse form describes the red patches seen in skin folds. Erythrodermic is an advanced from where the psoriasis is affecting most of the body sites including the face, likely as multiple forms. Typically the area affected are the forearms, shins and around the midriff but 50% of those diagnosed have scalp psoriasis perhaps solely or as an addition. For the purpose of this piece the psoriasis mentioned will assumed to be psoriasis vulgaris of the scalp.
There is often a mild to severe pruritus that comes with psoriasis, along with the visibility this can cause emotional distress, anxiety and low self-esteem to certain individuals. There has not yet been a cure for psoriasis but there are over counter medications and prescriptions that could be used to alleviate the disease symptoms. Three quarters of cases can be managed with creams. The disease affects 2-4% of the western population with no particular preference between men and woman, it can begin at any age but 33% will be diagnosed before twenty.
The function of the immune system is to recognise and neutralise non-self antigens, but autoimmunity occurs when there if a failure in supressing self-antigens, leading the targeting of a tissue type. This is what occurs in psoriasis, and the cells that have been implicated are T cells, they are believed to mediate an immune response against living skin tissue, but only in restricted areas. The life cycle of cell production should last between three to four weeks under normal circumstances but this process is reduced by three to seven days, due to the inflammatory environment, which includes a lot of death inducing molecules as well as offensive attack by immune cells. There is an increased development of cells in order to repair the dead cells. This results in an excessive proliferation of cells that quickly die, thus they accumulate in layers of dry scales on the surface of the skin. Psoriasis can be triggered by anything that has an impact on the immune system like stress, skin injury, certain infections like throat infection, some medications like antimalarial and excessive intake of alcohol and smoking. HIV patients are prone to be affected by psoriasis due to their immune impairment.
As previously mentioned, the disease is thought to be the result of genetic susceptibility with environmental influences. Genome wide association studies is a technique that attempts to find similarities within the genomes of patients suffering from a disease, similarities that don’t exist when compared to unaffected individuals. These areas, named loci are said to be linked to the disease. There have been nine such loci found for psoriasis and they have been named ‘psoriasis susceptibility’ PSORS 1-9. Within these areas are genes known to be part of the inflammation pathway and some of the genes are known to be involved in other autoimmune conditions. Interestingly the HLA genes (human leukocyte antigen) have been seen to have strong linkage with the disease, and these are the self-antigens on body cells that interact with T-cells in order to communicate that they are infected, leading to a T-cell mediated immune response that leads to the death of that cell.