SeminarPsoriasis
Section snippets
Differential diagnosis
Seborrhoeic dermatitis is the most common condition that is difficult to distinguish from psoriasis. When only thin, diffuse, scaly, plaques are present, seborrhoeic dermatitis of the scalp, face, or intertriginous areas and mild psoriasis may be indistinguishable (figure 3). Chronic eczematous dermatitis may present as thick, well-demarcated plaques, which are usually more pruritic than psoriasis-related plaques. Also, chronic eczema generally lacks the discrete fine mica-like scaling
Clinical subtypes
More than 90% of patients who present with psoriasis have symmetrical discrete plaques, but clinical manifestations can vary greatly. The acute generalised onset of numerous small erythematous raindrop-like papules which are initially pink and become scaly characterise guttate psoriasis, the most common psoriasis variant. Pharyngeal streptococcal infection often triggers this eruption, perhaps as a result of superantigen stimulation of the immune system.5, 6 Presumptive antistreptococcal
Associated diseases and exacerbating factors
About 15% of patients with psoriasis develop a seronegative inflammatory arthritis that has many clinical features of rheumatoid arthritis.10 There have been many claims of an association between psoriasis and altered risk of other diseases, but these differences are likely to reflect associations in exposures and habits of patients with psoriasis rather than innate differences in susceptibility. Smoking and obesity are more frequent among patients with psoriasis than the general population.11,
Management
To give optimum treatment, the clinician must find out which aspects and to what extent the disease worries the patient and what type of improvement would substantially reduce this worry. In addition to cost and risk of treatment, time required for treatment and the patient's attitude towards risk should be considered. The chronic nature of the disease and the lack of treatments that induce very long-term remissions mean that treatment decisions should be viewed in the context of a lifelong
References (32)
- et al.
Role of the microcirculation in the treatment and pathogenesis of psoriasis
J Invest Dermatol
(1982) - et al.
Disease concomitance in psoriasis
J Am Acad Dermatol
(1995) - et al.
Psoriasis of early and late onset: characterization of two types of psoriasis vulgaris
J Am Acad Dermatol
(1985) - et al.
20-epi vitamin D3 analogues: a novel class of potent regulators of cell growth and immune responses
Biochem Pharmacol
(1991) - et al.
Action spectrum for phototherapy of psoriasis
J Invest Dermatol
(1981) - et al.
Effect of continued ultraviolet B phototherapy on the duration of remission of psoriasis: a randomized study
J Am Acad Dermatol
(1986) - et al.
Etretinate therapy for psoriasis: clinical responses, remission times, epidermal DNA and polyamine responses
J Am Acad Dermatol
(1983) - et al.
The safety of etretinate as long-term therapy for psoriasis: results of the etretinate follow-up study
J Am Acad Dermatol
(1995) - et al.
Psoriasis
- et al.
Intralesional T-lymphocyte activation as a mediator of psoriatic epidermal hyperplasia
J Invest Dermatol
(1995)
The Koebner (isomorphic) response in psoriasis: association with early age of onset and multiple previous therapies
Arch Dermatol
The role of streptococcal infection in the initiation of guttate psoriasis
Arch Dermatol
Evidence for streptococcal superantignen-driven process in acute guttate psoriasis
J Clin Invest
Erythrodermic psoriasis
J Am Acad Dermatol
Corticosteroids and pustular psoriasis. Br
J Dermatol
Acute generalized exanthematous pustulosis. Analysis of 63 cases
Arch Dermatol
Cited by (118)
miR124-3p/FGFR2 axis inhibits human keratinocyte proliferation and migration and improve the inflammatory microenvironment in psoriasis
2020, Molecular ImmunologyCitation Excerpt :More importantly, when co-transfected to HaCaT cells, FGFR2-overexpressing vector significantly attenuated the effects of miR-124-3p mimics on HaCaT cells. During psoriasis, defects in the normal cycle of epidermal development appear, resulting in epidermal excessive proliferation and hyperplasia, deregulation of skin cell maturation, vascular changes, and chronic inflammation (Stern, 1997). Previous studies have proposed evidence reporting the association between the hyperproliferative activity of keratinocytes and several growth factors.
In vitro models of psoriasis
2018, Skin Tissue ModelsThe Role of Fibroblast Growth Factor-Binding Protein 1 in Skin Carcinogenesis and Inflammation
2018, Journal of Investigative DermatologyCitation Excerpt :Fgf7 and Fgfr2 were not differentially expressed in the epidermis or dermis (Supplementary Figure S1b). Epidermal thickening observed in the Fgfbp1-KO model has been described in inflammatory pathologies of the skin such as psoriasis (Stern, 1997), and FGFR2 and FGF7 were found elevated in psoriatic skin (Guban et al., 2016). To assess FGFBP1 gene expression, we analyzed two previously published gene expression studies (Nair et al., 2009; Reischl et al., 2007) of paired samples of normal skin and psoriatic skin without and with lesions.
Characterization of human short chain dehydrogenase/reductase SDR16C family members related to retinol dehydrogenase 10
2017, Chemico-Biological InteractionsCitation Excerpt :Human RDHE2 was originally identified as a transcript highly upregulated in psoriasis [24]. Psoriasis vulgaris is a chronic autoimmune inflammatory skin disease characterized by hyperproliferation of keratinocytes [25]. It is well established that hyperproliferation of keratinocytes can be induced by elevated levels of RA [26].
In vitro models of psoriasis
2017, Skin Tissue Models