Psoriasis
Psoriasis is a relatively common dermatosis where there is an abnormally rapid epidermal cell proliferation resulting in scaling and erythematous plaques which can affect any area of the skin. Involvement of the vulva is usually bilateral and itch is comm
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Psoriasis Darion Rowan
25.1 Introduction
25.2 Pathogenesis
Psoriasis is a chronic inflammatory condition in which there is rapid proliferation of the epidermis (approximately 4 days compared with the normal 28 days) resulting in localized erythematous scaly plaques of skin [1–3]. It affects about 2–5% of the population and no ethnic group is spared. There is variance in incidence in different populations. Most commonly it develops in the second and third decades of life, but onset can be at any age. Psoriasis is familial in about 40% of those affected suggesting a genetic predisposition. Its onset may be triggered by infection such as measles and streptococcal throat infection, traumatic injury, some drugs or a stressful life event. However, in many affected individuals, it arises spontaneously. Inflammatory arthritis is present in approximately 10% of patients (estimates are from 7–42%) with psoriasis. It is also associated with signs of the metabolic syndrome which suggests that psoriasis is a multisystem chronic inflammatory disorder.
In the past it was thought that the pathogenesis was primarily related to changes in the keratinocytes stimulated to excessive proliferation by extravasation of neutrophils into the epidermis from dilated capillaries of the dermal papillae. However, that simplistic view is only a small part in the pathogenesis and the end result of dysregulation of the immune system. It is now thought to be a T-cell-driven disorder, and some consider it to be an autoimmune disorder. Both innate and adaptive immunity is altered in psoriasis. Interactions between cutaneous dendritic cells, T-cells, keratinocytes, neutrophils and the cytokines released from the immune cells contribute to the initiation and ongoing inflammation. Upregulation of interferon-alpha (IFNα) produced by plasmacytoid dendritic cells which are present in increased numbers in early psoriatic lesions stimulates the activation of myeloid dendritic cells. These cells produce cytokines including interleukin (IL)-23 and IL-12 that attract and activate T-cell differentiation, particularly Th17 and Th1 cells. These activated T-cells produce cytokines that stimulate keratinocytes to proliferate and produce proinflammatory antimicrobial peptides (AMPs). Other cytokines including tumour necrosis factor-alpha (TNFα) produced by immune cells and keratinocytes perpetuate the inflammatory process with the result that it becomes chronic. Biologic drugs which target specific cytokines
D. Rowan (*) Omnicare Women’s Health, Auckland, New Zealand
© Springer International Publishing AG, part of Springer Nature 2019 J. Bornstein (ed.), Vulvar Disease, https://doi.org/10.1007/978-3-319-61621-6_25
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help to support the current theories of pathogenesis of psoriasis [1].
25.3 Clinical Presentation There are many types of psoriasis and lesions. The most common is plaque psoriasis, but others include guttate psoriasis, flexural psoriasis, palmoplantar psoriasis, pustular psoriasis, keratoderma, erythrodermic psoriasis and na
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