Koebner phenomenon describes the appearance of psoriasis at skin areas affected by trauma.ĭefined as the presence of two or more chronic conditions, multimorbidity is common in individuals with psoriasis. In rare cases of severe uncontrolled disease, psoriasis causes a widespread erythematous rash (erythroderma) that is life-threatening due to potential complications including hypothermia, risk of infection, acute kidney injury and high-output cardiac failure. Patients with guttate psoriasis may later develop plaque psoriasis. Guttate psoriasis causes an acute symmetrical eruption of drop-like papules/plaques mainly involving the trunk and limbs, that is classically but not always preceded by streptococcal infection. Flexural psoriasis presents without much scaling and may affect the axillae, sub-mammary and genital areas. Bleeding points may be noted where scales have been removed (Auspitz sign). The most common form is plaque psoriasis, which presents as well-demarcated salmon pink plaques with silvery-white scale, typically in a symmetrical distribution and affecting the extensor surfaces (especially elbows and knees), trunk and scalp (Fig (Fig1). Psoriasis manifests in several ways: plaque, flexural, guttate, pustular or erythrodermic psoriasis. 7Īlthough there is a relative paucity of data, pustular psoriasis appears to be genetically distinct, with different susceptibility genes implicated ( I元6RN, AP1S3 in those of European descent and CARD14). ![]() 6 Environmental triggers have been known to exacerbate psoriasis such as obesity, stress, beta-blockers, smoking and lithium. 5 This suggests a complex interplay between T cells, dendritic cells and keratinocytes as the likely underlying the pathophysiology of psoriasis, with the IL-23/Th17 axis being the central driver of immune activation, chronic inflammation and keratinocyte proliferation. ![]() 5 Many of the candidate causal genes are involved in antigen presentation ( HLA-C and ERAP1), NF-kappa B signalling ( TNIP1), type 1 interferon pathway ( RNF113 and IFIH1), interleukin (IL)-23/Th17 axis ( IL23R, IL12B and TYK2) and skin barrier function ( LCE3). 5 More than 60 susceptibility loci have now been identified using genome-wide association studies. This was demonstrated by twin, family-based and large-scale population-level studies, with heritability estimated to be 60–90%. The pathogenesis of psoriasis is multifactorial, with genetics being a primary contributor especially in those with early-onset (<40 years) plaque psoriasis. ![]() Advances in the understanding of its pathophysiology have led to development of highly effective and targeted treatments. Psoriasis treatments include topical agents (vitamin D analogues and corticosteroids), phototherapy (narrowband ultraviolet B radiation (NB-UVB) and psoralen and ultraviolet A radiation (PUVA)), standard systemic (methotrexate, ciclosporin and acitretin), biologic (tumour necrosis factor (TNF), interleukin (IL)-17 and IL-23 inhibitors) or small molecule inhibitor (dimethyl fumarate and apremilast) therapies. Its association with psoriatic arthritis and increased rates of cardiometabolic, hepatic and psychological comorbidity requires a holistic and multidisciplinary care approach. An immune-mediated inflammatory disease, psoriasis has a major genetic component. An estimated 60 million people have psoriasis worldwide, with 1.52% of the general population affected in the UK. Psoriasis is a clinically heterogeneous lifelong skin disease that presents in multiple forms such as plaque, flexural, guttate, pustular or erythrodermic.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |