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Cutivate, Betnovate, Dermovate, Eumovate

Disease background

Overview of steroid-responsive dermatoses

A range of different dermatological disorders respond to topical corticosteroid (TCS) treatment. These disorders are categorised as ‘steroid-responsive dermatoses’ and include: 1–4


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Atopic dermatitis

  • Atopic dermatitis/eczema
  • Allergic contact dermatitis
  • Irritant dermatitis
  • Hand and foot dermatitis
  • Lichen simplex chronicus
  • Nummular dermatitis
  • Prurigo nodularis
  • Seborrhoeic dermatitis
  • Recalcitrant eczemas (including scalp)

Psoriasis and scaling diseases

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Psoriasis of the hand

  • Psoriasis
  • Lichen planus
  • Scalp psoriasis

Other disorders

  • Discoid lupus erythematosus
  • Insect bite reactions
  • Inflammation associated with severe dandruff
    Miliaria (prickly heat)

Atopic dermatitis

Aetiology of atopic dermatitis

Atopic dermatitis (AD) is a multifactorial disease resulting from complex interactions between susceptibility genes, environmental factors, skin barrier dysfunction, immunology/allergy and pruritus. 5–7

AD is thought to be one symptom of a systemic atopic disorder that often leads to asthma and/or allergic rhinitis (a sequence of events known as the ‘atopic march’). 8

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Adapted from the, the LEAP Study, Evelina Children's Hospital, London 9

  • 50% of children who develop AD before age two will develop asthma 8

Pathophysiology of atopic dermatitis

The breakdown of the skin barrier due to environmental stimuli and/or filaggrin mutations is a key feature of AD pathogenesis. 510

Dry skin becomes itchy, and scratching exacerbates disruption of the skin barrier. Changes in the skin barrier result in cracks in the skin, allowing irritants and allergens to penetrate the skin, triggering an immune response.

Changes in the skin barrier with AD result in dry and itchy skin 10

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The pathogenesis of AD is now understood to be a complex process involving skin barrier dysfunction, allergy/immunological dysregulation, and pruritus, creating a positive feedback loop. 5 

The pathogenesis of AD involves a highly complex interplay between skin barrier disruption, allergy/immunology, and pruritus/scratching 5

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Epidemiology of atopic dermatitis

Prevalence 81112

  • At least 15% of children* and 2–10% of adults are affected by atopic dermatitis

*Data taken from a range of children worldwide, aged 5–16 years

Approximate % of atopic dermatitis cases which develop in childhood 8 12

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Although AD is commonly thought of as a childhood disease, it can persist into adulthood. Determining the exact prevalence of AD in adults is difficult due to the variable nature of the disease. 811

Prevalence of atopic dermatitis in children 13

  • Atopic dermatitis is the most common skin condition in the first four years of life
  • In 5–14 year olds warts are most common, and acne is most common in 15–24 year olds

Numerous studies have suggested that AD has been increasing in prevalence over the past 30–40 years. 14–16 However, the annual change in prevalence appears to be levelling off in many developed countries with previously high prevalence rates. Increases are still being observed in centres from many developing countries, particularly in younger children. 1718

A widespread survey performed over 5–10 years found: 17

  • In developing countries, such as Mexico, Chile, Kenya, Algeria and countries in Southeast Asia: the largest increase in prevalence of AD (an increase of ≥ 2 Eczema symptoms) was in children aged 6–7 and 13–14
  • In developed countries, such as the UK and New Zealand: there was the greatest reduction in AD prevalence (a reduction in ≥2 eczema symptoms) in 13–14 year olds

AD primarily affects children in urban areas or developed countries. 19 The increasing overall prevalence of childhood AD has been attributed to a large number of environmental factors, including:

  • Increased industrialisation 11
  • Pollution 11
  • Environmental changes which can increase antigen exposure, triggering the disease 11
  • Exposure to soaps and other harsh cleansing products 17
  • Changes to the home environment, including use of synthetic fabrics 11
  • Improved socioeconomic conditions and reduced family sizes
    • Children exposed to fewer infections, which can result in an increased incidence of AD and other allergic disorders 11 20
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Aetiology of psoriasis

The aetiology of psoriasis has been attributed to three key factors 21,22
1. Genetic predisposition
2. Immunological influence
3. Environmental triggers (e.g. infection)

The development and pathogenesis of psoriasis is strongly linked to genetic factors, with ten or more susceptibility loci contributing to disease predisposition. Psoriasis results from the interplay of susceptibility genes with various environmental factors that act on the skin and/or immune system. 23 24

The onset of psoriasis can be triggered by various factors in individuals with a genetic predisposition to the disease. 24Common triggers for psoriasis onset include: 2224

  • Alcohol consumption
  • Drugs such as lithium and beta-blockers
  • Emotional and physical (injury) stress
  • HIV
  • Obesity
  • Smoking
  • Streptococcal infections
  • Sunburn

Pathophysiology of psoriasis

Psoriasis is a chronic immune disease of the skin, associated with an activated cellular immune system.

Psoriatic skin lesions develop as a result of inflammation in the dermis and hyperproliferation of cells in the epidermis. Cells of the stratum corneum stack abnormally, leading to scale formation, which reduces the granular layer of the epidermis. Epidermal rete ridges (downward extensions of the epidermis) are elongated and blood vessels are enlarged, contributing to skin redness. The number of leukocytes increases and immune responses are activated. 23

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Adapted from Lowes, 2007 23

Psoriasis is associated with immune dysfunction involving both the innate and adaptive immune systems as well as abnormal keratinocyte proliferation and differentiation. Activation of antigen-presenting cells leads to the preferential development of Th1- and Th17-type T cells that migrate into, and proliferate within, the skin. Several mediators have been identified that orchestrate many of the changes typical of psoriasis, including IL-12 and IL-23, TNFα, and interferon γ (IFNγ). 24

Epidemiology of psoriasis

Psoriasis is one of the most frequent chronic inflammatory diseases worldwide. 24–28

  • Psoriasis affects 2–3% of the world’s population
  • The majority of psoriasis cases present before <35 years of age
    • Most people develop psoriasis between 15–30 years of age
    • Psoriasis is uncommon in children
  • Plaque psoriasis accounts for 80–90% of all psoriasis

Psoriasis is associated with a number of co-morbidities such as metabolic syndrome which can increase a patient’s cardiovascular risk, increasing their risk of mortality – the life expectancy for patients with severe psoriasis is ~3–4 years less than in healthy individuals. 24

At the 67th World Health Assembly meeting in 2014, the WHO recognised the seriousness of psoriasis, highlighting that it is a chronic, painful and disabling disease associated with substantial stigma and discrimination, for which there is no cure 29


  1. Stiefel: Betamethasone Global Data Sheet (13th September 2013)
  2. Stiefel: Clobetasol propionate Global Data Sheet (23rd August 2013)
  3. Stiefel: Flucticasone propionate Global Data Sheet (15th February 2011)
  4. Merck Manual: Hand and Foot dermatitis. Available at: d_foot_dermatitis.html (Last accessed August 2015)
  5. Kabashima K. J Dermatol Sci 2013;70:3–11
  6. Leung DY, et al. J Clin Invest 2004;113:651–7
  7. Berke R, Singh A, Guralnick M. Am Fam Physician 2012;86:35–42
  8. Watson W, Kapur S. Allergy Asthma Clin Immunol 2011;7(Suppl 1):54
  9. Allergy UK: The Allergic March. Available at: allergy/the-allergic-march (Last accessed August 2015)
  10. Cork MJ, Danby S. Br J Nurs. 2009;18:872, 874, 876–7
  11. Carroll CL, et al. Pediatr Dermatol 2005;22:192–9
  12. Akdis CA, et al. Allergy 2006;61:969–87
  13. Schofield J, et al. 2009, Skin conditions in the UK: a health care needs assessment. Centre of Evidence Based Dermatology, University of Nottingham
  14. Schulz Larsen F, Hanifin JM. Acta Derm Venereol Suppl (Stockh) 1992;176:7–12
  15. O’Connell EJ. Allergy 2004;59:7–11
  16. Sturgill S, Bernard LA. Curr Opin Pediatr 2004;16:396–401
  17. Williams H, et al. J Allergy Clin Immunol 2008;121:947–54
  18. Odhiambo JA et al. J Allergy Clin Immunol 2009;124:1251–8
  19. Merck Manuals: Atopic Dermatitis. Available at: ermatitis.html (Last accessed August 2015)
  20. Daley D. Curr Opin Allergy Clin Immunol 2014;14:390–6
  21. BMJ Best Practice: Psoriasis aetiology. Available at: (Last accessed September 2015)
  22. Merck Manual: Psoriasis. Available at: and-scaling-diseases/psoriasis (Last accessed September 2015)
  23. Lowes MA, Bowcock AM, Krueger JG. Nature 2007;445:866–73
  24. Pathirana D, et al. J Eur Acad Dermatol Venereol 2009;23:1–70
  25. Psoriasis statistics. Available at: (Last accessed September 2015)
  26. World psoriasis day: About psoriasis. Available at: (Last accessed September 2015)
  27. Psoriasis: Who gets and causes. Available at: to-z/diseases-and-treatments/m---p/psoriasis/who-gets-cause (Last accessed September 2015)
  28. Chronic plaque psoriasis. Available at: psoriasis (Last accessed September 2015)
  29. 67th World Health Assembly: Psoriasis. Available at:
    WHO psoriasis resolution: (Last accessed September 2015)

Cutivate, Betnovate, Dermovate and, Eumovate are registered trademarks of Stiefel, a GSK company.
Copyright © 2015 Stiefel, a GSK company