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Turkish Guideline for Atopic Dermatitis 2018

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Turkish Guideline for Atopic Dermatitis 2018 Review DOI: 10.6003/jtad.18122r1 Turkish Guideline for Atopic Dermatitis 2018 Burhan Engin,1 MD, Emel Bülbül Başkan,2 MD, Murat Borlu,3 MD, Selda Pelin Kartal,4 MD, Başak Yalçın,5 MD, Savaş Yaylı,6 MD, Server Serdaroğlu,1 MD Address: 1İstanbul Üniversitesi-Cerrahpaşa, Cerrahpaşa Tıp Fakültesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, İstanbul, 2Uludağ Üniversitesi Tıp Fakültesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, Bursa, 3Erciyes Üniversitesi Tıp Fakültesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, Bursa, 4Sağlık Bilimleri Üniversitesi, Ankara Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, Ankara, 5Ankara Yıldırım Beyazıt Üniversitesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, Ankara, 6Karadeniz Teknik Üniversitesi Tıp Fakültesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, Trabzon, Türkiye E-mail: [email protected] Corresponding Author: Dr. Burhan Engin, İstanbul Üniversitesi-Cerrahpaşa, Cerrahpaşa Tıp Fakültesi, Deri ve Zührevi Hastalıkları Anabilim Dalı, İstanbul, Türkiye Published: J Turk Acad Dermatol 2018; 12 (2): 18122r1. This article is available from: http://www.jtad.org/2018/2/jtad18122r1.pdf Keywords: Turkish guideline, Atopik dermatit Abstract Background: Atopic dermatitis (AD) is a common inflammatory skin disease worldwide and life-long prevalence thereof can exceed 20% in developed countries. The prevalence of the disease increases gradually in developing countries and in African and Asian countries with low income. AD affects quality of life unfavorably in a significant manner. The cost of AD is quite high both due to healthcare expenses required for treatment and causing labor loss. Patients receive long-term treatments owing to the fact that it is a disease with a chronic course and there is no curative treatment which also cause medicine expenses and a number of toxicities. This guideline covers etiology, clinic diagnosis, laboratory, complications and treatment approaches for atopic dermatitis in details. Atopic Dermatitis and in African and Asian countries with low income [1]. I. Epidemiology Generally, atopic dermatitis affects 25% of Atopic dermatitis (AD) is a common inflam- matory skin disease worldwide and life-long children and 2-3% of adults [2]. Data regar- prevalence thereof can exceed 20% in develo- ding the prevalence of atopic dermatitis in ped countries. The prevalence of the disease adults has been reported as variable with increases gradually in developing countries 0.3%-14.3% due to lack of multicenter stu- Page 1 of 37 (page number not for citation purposes) J Turk Acad Dermatol 2018; 12 (2): 18122r1. http://www.jtad.org/2018/1/jtad18122r1.pdf dies and well-established diagnostic criteria Overactivation of the immune system is con- [3]. ventionally predominanted by the profile of T- helper cell 2 (Th2) in atopic dermatitis. The age of onset of the disease is generally 3- Thymic stromal lymphopoietin (TSLP), inter- 6 months and clinical findings are observed leukin 25 (IL-25) and IL-33 are produced by in 45%, 60% and 85% of patients in the first keratinocytes damaged by the protease acti- 6 months, before the age of 1 and before the vation developing due to barrier impairment age of 5, respectively [4, 5]. Only in a patient in epidermis caused by genetic or environ- group as small as 2%, the symptoms appear mental factors. These cytokines initiate Th2 after the age of 20 [6]. Family history is ob- cell activation. Activated Th2 cells produce IL- served in 70% of the patients [7]. 4, IL-5, IL-13, IL-25 and IL-31. T2 cells, along with many other immune system cells and The course of the disease is mild in approxi- are responsible for increased levels of IL-4 mately 80% of children with atopic dermatitis and IL-13 in atopic dermatitis lesions. IL-4 [8]. In more than 70% of case, complaints do and IL-13 cause an increase in the inflamma- not continue in adulthood [8]. tory cell infiltration to skin and as aforeme II. Pathogenesis ntioned, cause a decrease in filaggrin expres- sion by keratinocytes hence an impairment in In the last decade, substantial developments skin barrier function. IL-4 induces IgE pro- have been recorded with the importance of fi- duction from B cells provides IL-5 eosinophil laggrin, immunologic changes in subtypes activation [4]. (Th17, Th22) of T-helper cells other than Th1 As the lesions become chronic, differences are and Th2 and identification of the effect of observed in cell infiltration; T2 cytokines do- many cytokines mainly IL-4 and IL-13 [9]. minant in the acute phase are replaced by Basically, two important events which are Th1-associated cytokines such as interferon- responsible for the pathogenesis of atopic gamma (IFN- γ) and IL-12 in the chronic dermatitis is skin barrier dysfunction and phase. In late lesions of atopic dermatitis, it overactivation of the immune system [4]. is acknowledged that Th2 cells are accompa- nied by Th22 cells producing IL-22. IL-22 is Pathogenetic mechanisms set forth in the responsible for keratinocyte proliferation and skin barrier dysfunction can be listed as im- acanthosis developing correspondingly. In ad- pairment in the proteins of various epidermal dition IL-22, along with IL-4 and IL-13, dec- differentiation complexes and filaggrin, dec- reases the expression of barrier-related rease in skin ceramides, impairments in the genes, such as filaggrin, loricrin and involuc- pH of stratum corneum and overexpression rin, decreasing the skin barrier function. It of chymotryptic enzyme [5]. Filaggrin is an es- plays a role in the late-stage tissue remodel- sential protein responsible for the prevention ling by increasing the expression of IL-17 pro- of transepidermal water loss and microbial fibrotic cytokines released from IL-13 and invasion ensuring the natural moisturization Th17 cells [4, 5]. of the skin by the breakdown products [10]. Reduction of filaggrin metabolites in the skin Increase in the density of nerve fibers in epi- causes skin barrier dysfunction also by cau- dermis and low stimulation threshold in ner- sing a decrease in skin acidification [11]. One ves are blamed for the pathogenesis of of the most well-known causes of skin barrier pruritus in atopic dermatitis. It is considered impairment observed in atopic dermatitis is that TSLP, IL-4, IL-13 and IL-31 are the cyto- the mutation in the filaggrin gene and is ob- kines playing a role in itching in atopic der- served in 10-30% of atopic dermatitis pati- matitis [4]. ents. Except the filaggrin gene mutations, in The role of microbial pathogens in the deve- almost all moderate-severe atopic dermatitis lopment of atopic dermatitis have been de- cases, there is an acquired defect in filaggrin monstrated. S. aureus, Malassezia species expression. This is explained by the fact that and Candida albicans are the microbial pat- overexpression of IL-4 and IL-13 causes a hogens which play a role in the pathogenesis decrease in filaggrin expression by kerati- of atopic dermatitis [13]. Bacterial coloniza- nocytes [12]. tion with S. aureus is associated with skin Page 2 of 37 (page number not for citation purposes) J Turk Acad Dermatol 2018; 12 (2): 18122r1. http://www.jtad.org/2018/1/jtad18122r1.pdf barrier dysfunction associated with the in- atopic eczema. In patients carrying filaggrin crease in protease activity in skin and basop- mutation, risk of early-onset severe atopic hil activation in skin and increase in the dermatitis and incidence of asthma have in- proinflammatory cytokine levels such as IL- creased [7]. In the genome-wide association 31 [14]. S. aureus density on lesional and analyses performed, common variants on non-lesional skin correlates with eczema se- 11q13 and 1q21 chromosomes have been ob- verity [15]. served. Hornerin, a protein that plays a piv otal role in the region keratinocyte differen- III. Histopathology tiation on 1q21 chromosome, encodes loricrin Histologic features of atopic dermatitis show and involucrin. The only nucleotide poly- similarity to a large extent with allergic con- morphism on the genetic region encoding tact dermatitis. In acute lesions, intercellular claudin-1 causes decreased gene expression edema in epidermis and marked perivascular of claudin functioning in the structure of tight T-cell infiltration accompanied by monocytes junctions between keratinocytes [11, 19]. A and macrophages in dermis are observed. relationship has been demonstrated between Lymphocytic infiltrate is formed of activated atopic eczema and mutations in SPINK5 gene memory T-cells carrying CD3, CD4, HLA-DR, encoding a serine protease inhibitor. The mu- CD25 and CD45RO. In acute lesions, eosi- tation in this gene impairs the protease-an- nophils and mast cells are observed whereas tiprotease balance that is necessary to ensure basophils and neutrophils are sporadic. Epi- skin barrier function. It is suggested that, in dermal hyperplasia, elongation of the rete rid- the genetic studies, the variants detected in ges, hyperkeratosis and minimal spongiosis the genes encoding IL-4, IL-4 receptor and IL- are observed in acute lichenified lesions. In- 13, play a role in the development of eczema crease in the count of dendritic cells in epi- [20]. dermis and monocyte-rich infiltration in ii. Environmental Factors dermis occur. Elevated count of eosinophils are detected in dermis with the immunoche- The fact that the prevalence of atopic derma- mical stain of eosinophil products such as eo- titis varies within the same country, higher sinophil major basic protein, eosinophil incidence of atopic dermatitis is observed in cationic protein, and eosinophil-derived neu- people migrating from the countries with low rotoxin [5, 16]. prevalence to developed countries and the IV. Etiology prevalence increases correspondingly with urbanization demonstrates the importance of I. Genetic Factors environmental factors in etiopathogenesis [1]. Environmental factors causing an increase in Genetic factors play a role in predisposition the risk of atopic dermatitis are summarized to atopic dermatitis. Familial history is posi- in (Table 1).
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