DISCUSSION

Psoriatic arthritis and psoriasis: classification, clinical features, pathophysiology, immunology, genetics

Discussion: Immunology, cellular pathology, genetics

C Ritchlin

Correspondence to:
Correspondence to:
Dr C Ritchlin
Clinical Immunology Research Center, University of Rochester Medical School, Rochester, NY, USA; christopher_ritchlin@urme.rochester.edu

Abbreviations: DC, dendritic cell; HLA, human leucocyte antigen; IL, interleukin; MHC, major histocompatibility complex; PsA, psoriatic arthritis; RA, rheumatoid arthritis; RANKL, receptor activator of nuclear factor B ligand; TNF, tumour necrosis factor

Keywords: Immunology; cellular pathology; psoriatic arthritis genetics

The first 150 words of the full text of this article appear below.

Much of the evidence supporting the genetic basis of PsA is derived from twin studies, family based investigations, and population based epidemiologic studies. Concordance rates of PsA in twins are unknown, but monozygotic twins have a threefold increased risk for psoriasis compared with fraternal twins. A population study conducted by Moll and Wright indicated the overall prevalence of PsA among first degree relatives was 5.5% and that the risk for affected first degree relatives (₁) is 55. This compares to a reported ₁ of 8 for psoriasis. One family study reported that if one sibling had PsA, the corresponding risk for another sibling to develop the disease was 0.10, 0.22, and 0.31 if no parent was affected, the mother was affected, or the father was affected, respectively.

The commonest approaches to identify specific genetic factors include positional cloning studies that . . . [Full text of this article]

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This article has been cited by other articles:

• Mease, P J, Antoni, C E (2005). Psoriatic arthritis treatment: biological response modifiers. Ann Rheum Dis 64: ii78-ii82 [Abstract] [Full Text]