Despite the advances in the last decades, the cause of psoriasis still remains unknown. It is considered a chronic skin and joint inflammatory disease, immunomediated, with polygenic predisposition. It is characterized by complex modifications of growth and epidermal differentiation and multiple biochemical, immune and vascular abnormalities. In addition, there seems to be an unexplained correlation with emotional episodes. In the past, the aetiopathogenic basis of psoriasis was thought to involve a primary disorder of keratinocytes; however, it is thought to be related to an immune affection mediated by a type Th1 response. Recently, new data have led to the conclusion that antigen-presenting cells are important, not only in the induction of psoriasis but also in its maintenance [1].

Considerable epidemiological evidence has been reported that certain genes have a key role in the pathogenesis of psoriasis [2]. The role played by genetic factors is underlined by the increased frequency of some human leucocyte antigens (HLA) haplotypes (HLA-Cw6, HLA-B13 and HLA-B17) and by concordance studies in twins [3]. The best evidence for a genetic basis for psoriasis comes from twin studies. Identical twins share all of their genes, and fraternal twins, like siblings, share only half their genes. Even if a disorder is caused by many genes, the disease should be present in both identical twins more often than in fraternal twins. Psoriasis is concordant about three times as often in identical twins as in fraternal twins [4]. Multiple genes are involved and psoriasis is clearly genetically heterogeneous. Interactions with the environment are also implicated in the development of psoriasis [2]. Initially, a number of genetic loci have been identified by genome-wide linkage scans and two loci have been replicated: PSORS1 on chromosome 6, within the major histocompatibility complex, and PSORS2 on chromosome 17q [2].

Genetic factors influence the pattern of psoriasis, severity and age of onset [3]. There remains controversy over the mode of inheritance. Swanbeck et al. [5] noted that the age of onset for psoriasis varied from early infancy to old age. They calculated the gene frequency for groups with different ages at onset. These data were consistent with the existence of three genetically distinct variants of psoriasis vulgaris. The risk for first-degree relatives of an isolated case is at least 10%. Children of two psoriatic parents have approximately a 50% risk [6].

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