Psoriasis and its managementBMJ 2006; 333 doi: https://doi.org/10.1136/bmj.333.7564.380 (Published 17 August 2006) Cite this as: BMJ 2006;333:380
- Catherine H Smith (firstname.lastname@example.org), consultant dermatologist1,
- J N W N Barker, professor of clinical dermatology1
- 1 Skin Therapy Research Unit, St Johns Institute of Dermatology, Kings College London, St Thomas' Hospital, London SE1 7EH
- Correspondence to: C H Smith
- Accepted 30 June 2006
Behcet (1935) referred to the highly stigmatising and common inflammatory skin disease psoriasis (derived from the Greek word psora meaning itch) as “the antidote to a dermatologist's ego,” and although in some respects this is still true, major progress has been made in several important areas. Psoriasis occurs worldwide and affects about 2% of the population in the United Kingdom.
A great deal is known about the genetic and immunological mechanisms underlying the pathogenesis of psoriasis. Some of the new biological treatments recently licensed for psoriasis have been developed as a result of this improved understanding, whereas others have been contributory—for example, the profound efficacy of agents that block the actions of cytokine tumour necrosis factor highlighted the key role of tumour necrosis factor in the disease's pathogenesis. Evidence is also accumulating that psoriasis is not just associated with skin disease. Epidemiological studies have shown an increased standardised mortality in patients with psoriasis, particularly related to cancer and heart disease. Clinically relevant psychological and psychiatric comorbidity are also common and potentially amenable to therapeutic intervention. This article presents an overview of these developments and their implications for clinical practice.
What causes psoriasis?
Scans of the human genome reveal at least nine different loci with susceptibility to psoriasis (PSORS1-9). PSORS-1, a region of the major histocompatibility complex on chromosome 6p2, is the major genetic determinant of psoriasis, and accounts for up to 50% of genetic susceptibility to the disease,1 w1 although the definitive gene has not yet been identified.
Several of the implicated loci are shared by other autoimmune and inflammatory diseases such as inflammatory bowel disease, type1 diabetes, multiple sclerosis, and atopic dermatitis, suggesting that similar mechanisms underlie many common genetically complex inflammatory diseases.
Psoriasis is a common, disfiguring, and stigmatising skin disease associated with profound impaired quality of life
The gene …
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