Background and current state of research
Atopic eczema (AE), also known as atopic dermatitis (AD), is a chronic inflammation of the skin. With a prevalence of 10-20% in children and 5 % in adults it is widely spread [1, 2]. As a multifactorial disease, dysfunctions of the immune system and skin barrier, environmental exposures and genetic influences are discussed [3]. Prurigo nodularis (PN) is a possible manifestation of AE, but also linked to other diseases and, like the classical AE, characterized by itching [4-9]. Since the causes of classic AE, the PN manifestation of AE and non-AE-associated PN are still not clearly understood, the therapy is neither specific nor satisfactory [10].
1. Illi, S., et al., The natural course of atopic dermatitis from birth to age 7 years and the association with asthma. J Allergy Clin Immunol, 2004. 113(5): p. 925-31.
2. Worm, M., et al., Frequency of atopic dermatitis and relevance of food allergy in adults in Germany. Acta Derm Venereol, 2006. 86(2): p. 119-22.
3. Leung, D.Y. and T. Bieber, Atopic dermatitis. Lancet, 2003. 361(9352): p. 151-60.
4. Iijima, S., Prurigo nodularis. Tohoku J Exp Med, 1951. 54(1): p. 73-80.
5. Payne, E.R., et al., Nodular prurigo—a clinicopathological study of 46 patients. British Journal of Dermatology, 1985: p. 431-439.
6. McKenzie, A.W., D.G. Stubbing, and B.L. Elvy, Prurigo nodularis and gluten enteropathy. Br J Dermatol, 1976. 95(1): p. 89-92.
7. Suarez, C., et al., Prurigo nodularis associated with malabsorption. Dermatologica, 1984. 169(4): p. 211-4.
8. Fina, L., et al., Nodular prurigo associated with Hodgkin's disease. Dermatologica, 1991. 182(4): p. 243-6.
9. Berger, T.G., C. Hoffman, and M.D. Thieberg, Prurigo nodularis and photosensitivity in AIDS: treatment with thalidomide. J Am Acad Dermatol, 1995. 33(5 Pt 1): p. 837-8.
10. R. Fölster-Holst, T.Schwarz, E. Proksch, S. Weißmantel, Atopisches Ekzem- Grundlagen und Updates. UNI-MED, 2011.
Our goals
Since the quality of life of AE and PN patients is greatly reduced by itching and stigmatization, we aim to achieve a better understanding of the disease to be able to develop more effective therapeutic options. We will focus on investigating the immune system, skin barrier and microbiome. Furthermore, clinical examinations, anamnesis and questionnaires will be carried out to better classifyand understandpossible influences that cause skin disease.
How to get there
We will recruit patients with classic AE manifestation, AE patients with a PN manifestation, patients with non-AE-associated PN and healthy controls. After a detailed anamnesis, clinical examination and determination and documentation of the extent of the disease, the transepidermal water loss (TEWL) and hydration of the skin will be measured.
To better understand the immunologic influences, IgE and several cytokines will be measured in the blood and skin by means of molecular genetic methods. The skin barrier will be investigated using electron microscopy, an immuno-histochemical analysis of several cross-linking proteins of the skin, and screening the filaggrin gene for mutations. Furthermore, the microbiome will be sequenced.