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1 Working Party Criteria for the Definition of Atopic Dermatitis).
2 Working Party Criteria for the Definition of Atopic Dermatitis).
3 tokine frequently associated with asthma and atopic dermatitis.
4 asthma, allergic rhinitis, food allergy, and atopic dermatitis.
5 ly correctable cellular defects that lead to atopic dermatitis.
6 vaccination that may develop in humans with atopic dermatitis.
7 d in the management of chronic itch, notably atopic dermatitis.
8 reventative strategy to reduce the burden of atopic dermatitis.
9 n = 825; 79.5%), defined as children with no atopic dermatitis.
10 sets and PBMCs from patients with asthma and atopic dermatitis.
11 ous allergic diseases ranging from asthma to atopic dermatitis.
12 nal atopic status did not affect the risk of atopic dermatitis.
13 ation and selection of the IgE repertoire in atopic dermatitis.
14 play a critical role in the pathogenesis of atopic dermatitis.
15 practice and in future clinical research on atopic dermatitis.
16 rmatitis as a spontaneous nonrodent model of atopic dermatitis.
17 show that IL-4 and IL-13 are key drivers of atopic dermatitis.
18 ggered by microbes, such as in patients with atopic dermatitis.
19 as isolated from PBMCs of five children with atopic dermatitis.
20 y was determined by using the mouse model of atopic dermatitis.
21 /Tnd mice, which normally do not suffer from atopic dermatitis.
22 pathogenesis and microbiome modifications in atopic dermatitis.
23 his study used a spontaneous model of canine atopic dermatitis.
24 urface pH has been reported in patients with atopic dermatitis.
25 rently in human clinical trials for treating atopic dermatitis.
26 asthma, allergic rhinitis, food allergy, and atopic dermatitis.
27 b3a (mice) and SERPINB3/B4 (humans) early in atopic dermatitis.
28 ere associated with the persistent infantile atopic dermatitis.
29 es such as chronic sinusitis with polyps and atopic dermatitis.
30 us disorders, including acne, psoriasis, and atopic dermatitis.
31 uce the risk of allergic diseases, including atopic dermatitis.
32 pectively, when compared to children without atopic dermatitis.
33 fect on treatment adherence of TCS phobia in atopic dermatitis.
34 ses including asthma, allergic rhinitis, and atopic dermatitis.
35 inflammatory diseases, including asthma and atopic dermatitis.
36 lly helpful in preventing the development of atopic dermatitis.
37 IgE sensitization in patients suffering from atopic dermatitis.
38 costeroids in adults with moderate-to-severe atopic dermatitis.
39 plicated in the etiology and exacerbation of atopic dermatitis.
40 ms (2.2 [1.2-4.3]) and doctor's diagnosis of atopic dermatitis (1.9 [1.0-3.4]) in childhood, and sens
42 2.14-3.38); epithelial conditions, including atopic dermatitis (2.75, 1.23-6.16); and hypertension (1
45 ay a fundamental role in the pathogenesis of atopic dermatitis, a chronic relapsing inflammatory skin
46 using the following keywords: "psoriasis," "atopic dermatitis," "acne," "vitiligo," "seborrheic derm
48 inflammation, particularly in patients with atopic dermatitis (AD) and AD-like congenital disorders,
49 gen that colonizes the skin of patients with atopic dermatitis (AD) and aggravates their disease.
51 nce indicates a relevant association between atopic dermatitis (AD) and attention-deficit/hyperactivi
53 e aimed to determine the association between atopic dermatitis (AD) and cardiovascular events in the
56 ed T cells in lesional skin of patients with atopic dermatitis (AD) and psoriasis (PSO) might be dire
62 cells (LC) in the epidermis of patients with atopic dermatitis (AD) carry the high-affinity receptor
63 The lack of standardized nomenclature for atopic dermatitis (AD) creates unnecessary confusion for
65 ond classic "allergic"/atopic comorbidities, atopic dermatitis (AD) emerges as systemic disease with
68 seasonal influenza vaccine in patients with atopic dermatitis (AD) have not been carefully character
69 cia areata (AA) and vitiligo associated with atopic dermatitis (AD) in a large cohort of US women, th
70 ted the activity of IVM in a murine model of atopic dermatitis (AD) induced by repeated exposure to t
93 and itch pathway activation in patients with atopic dermatitis (AD) is fraught with the inability to
102 , our therapeutic armamentarium for treating atopic dermatitis (AD) was still primarily topical corti
103 n, less acidic skin, and fissured skin), and atopic dermatitis (AD) with a severe and persistent cour
104 cluding food allergy, drug hypersensitivity, atopic dermatitis (AD), allergic conjunctivitis, and air
105 strointestinal disease (EGID), patients with atopic dermatitis (AD), and nonatopic healthy control (N
106 from healthy control subjects, patients with atopic dermatitis (AD), and patients with psoriasis.
107 ammatory skin disease, such as psoriasis and atopic dermatitis (AD), another tryptophan metabolism en
108 considered an efficient treatment option for atopic dermatitis (AD), but a global assessment of gluco
109 Sleep disturbance is common in children with atopic dermatitis (AD), but effective clinical managemen
110 as been used for decades in the treatment of atopic dermatitis (AD), but evidence of its effectivenes
138 d five main atopic outcomes (asthma, wheeze, atopic dermatitis, allergic rhinitis and IgE) were asses
139 ted efficacy for patients with psoriasis and atopic dermatitis, although the biologic target and mech
144 also a positive additive interaction between atopic dermatitis and allergic sensitization in their ef
145 ylococcus aureus (S. aureus) is increased in atopic dermatitis and can result in increased severity o
147 er in utero exposures may affect the risk of atopic dermatitis and emphasize the importance of the ea
148 luate the association between emollient use, atopic dermatitis and FLG mutations, respectively, with
149 vivo studies, fresh blood from patients with atopic dermatitis and healthy control subjects was analy
150 AD CHRONOS), adults with moderate-to-severe atopic dermatitis and inadequate response to topical cor
151 involved in human diseases, such as allergy, atopic dermatitis and nasal polyposis, but their functio
153 lopment of effective and safe treatments for atopic dermatitis and other inflammatory disorders of th
154 l therapeutic approaches in the treatment of atopic dermatitis and psoriasis showed that promising su
156 are important in asthma, food allergies, and atopic dermatitis and their respectively developed antag
157 and reduction of lesions in a mouse model of atopic dermatitis and to elucidate possible HOCl's mode
162 ls have been associated with risk of asthma, atopic dermatitis, and elevated total immunoglobulin E (
165 d in lesional skin biopsies of patients with atopic dermatitis, and incubation of keratinocytes with
166 ed to treat skin diseases like psoriasis and atopic dermatitis, and is known to suppress contact hype
167 role of keratinocytes in the pathogenesis of atopic dermatitis, and the animals lacking BRAF and RAF1
168 a, and 1.12 (95% CI 0.92-1.37, p = 0.27) for atopic dermatitis, and the effect size on log-transforme
171 IgE transcripts from preschool children with atopic dermatitis are significantly less mutated, clonal
172 uch as asthma, rhinitis, food allergies, and atopic dermatitis, are generally classified by the tissu
174 robiome, and highlight the utility of canine atopic dermatitis as a spontaneous nonrodent model of at
175 ected with at least one of the conditions of atopic dermatitis, asthma, or allergic rhinoconjunctivit
176 tes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved a
179 keratinocytes cause a disease akin to human atopic dermatitis, characterized by IgE responses and lo
180 as alopecia areata, vitiligo, psoriasis and atopic dermatitis, common variants have been identified
185 wever, a specific description of subtypes of atopic dermatitis depending on the timing of onset and p
187 ribution, IgE transcripts from children with atopic dermatitis displayed a dominance of the otherwise
189 atopic march describes the progression from atopic dermatitis during infancy to asthma and allergic
191 ent knowledge on major asthma, rhinitis, and atopic dermatitis endotypes under the auspices of the PR
192 derable number of adults still suffered from atopic dermatitis evaluated both by questionnaire (17.1%
193 in (IL)-4 and IL-13 are requisite drivers of atopic dermatitis, evidenced by marked improvement after
194 the clinical observation that patients with atopic dermatitis experience increased sensitivity to mi
195 llow-up of more than 10 years, reported that atopic dermatitis, family asthma, early-life exposure to
197 t new results obtained by uploading a recent atopic dermatitis GWAS meta-analysis to examine the gene
199 ion with common FLG mutations, children with atopic dermatitis had significantly higher urinary level
201 ead to relief of itch in human patients with atopic dermatitis; however, the specific antipruritic me
202 opportunistically evaluated in patients with atopic dermatitis; however, they often failed to demonst
203 responses in adults with moderate-to-severe atopic dermatitis in a dose-dependent manner, without si
204 ss analysis was used to identify subtypes of atopic dermatitis in childhood based on the course of sy
205 it to PASTURE data separated 4 phenotypes of atopic dermatitis in childhood: 2 early phenotypes with
206 r domestic dog exposure affected the risk of atopic dermatitis in children during the first 3 years o
209 for the management of asthma, rhinitis, and atopic dermatitis in the context of a better selection o
210 conservative estimate of the annual costs of atopic dermatitis in the United States is $5.297 billion
211 s associated with a strongly reduced risk of atopic dermatitis in two independent birth cohorts and i
212 dupilumab in adults with moderate-to-severe atopic dermatitis inadequately controlled by topical tre
215 s as it was used in the PEER cohort to treat atopic dermatitis is associated with an increased risk o
223 idermal and dermal features of MC903-induced atopic dermatitis-like disease and suppresses the produc
224 VT transgenic mice that develop spontaneous atopic dermatitis-like disease that is dependent on T he
226 l administration of HOCl hydrogel (0.05%) on atopic dermatitis-like lesions in NC/Nga mice model as w
227 (RA) on wild-type mouse skin induces a human atopic dermatitis-like phenotype that is triggered by an
230 er investigation are targeted for psoriasis, atopic dermatitis, melanoma, hidradenitis suppurativa, a
231 pidermal keratinocytes, a DFE-induced murine atopic dermatitis model, and human atopic dermatitis les
234 6,761), childhood onset asthma (n = 15,008), atopic dermatitis (n = 40,835), and elevated IgE level (
236 fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals
237 er, it is unclear if S. aureus is a cause of atopic dermatitis or a consequence of the abnormal epith
238 skin lesions of humans diagnosed with either atopic dermatitis or allergic contact dermatitis as well
239 ing in the management of eczema (also called atopic dermatitis or atopic eczema) is poorly understood
242 owering alleles were associated with asthma, atopic dermatitis, or elevated IgE levels (p >/= 0.2).
243 levels were associated with risk of asthma, atopic dermatitis, or elevated serum IgE levels, using M
244 evels conferred an increased risk of asthma, atopic dermatitis, or elevated total serum IgE, suggesti
245 disease (hay fever: OR: 5.50 [3.42-9.00] and atopic dermatitis: OR 3.76 [2.14-6.61]), and drug use (L
246 y innocuous, it has strong associations with atopic dermatitis pathogenesis and has become the leadin
250 were used to analyze the association between atopic dermatitis phenotypes and other allergic diseases
251 cute itch and in a transgenic mouse model of atopic dermatitis produced by overexpression of the TH2
257 dies have identified 21 loci associated with atopic dermatitis risk predominantly in populations of E
259 th moderate-to-severe AD (six area, six sign atopic dermatitis [SASSAD] score: geometric mean, 22.3 [
261 se severity, such as the Severity Scoring of Atopic Dermatitis (SCORAD) index, or the incidence of AD
262 was AD severity evaluated using the Scoring Atopic Dermatitis (SCORAD) index, with scores ranging fr
263 best correlated with patient-reported global atopic dermatitis severity (Kendall tau = 0.336, P < 0.0
265 er, patients with allergic disorders such as atopic dermatitis show a paucity of skin neutrophils and
266 eous microbiome and skin barrier function in atopic dermatitis, show the impact of antimicrobial ther
267 corticosteroid treatment for 1 year improved atopic dermatitis signs and symptoms, with acceptable sa
268 ion of TLR1, TLR6, IL-25, and IL-33 in human atopic dermatitis skin lesions with high house dust mite
270 ier function and the cutaneous microbiota in atopic dermatitis, this study used a spontaneous model o
273 d the role of skin pH in the pathogenesis of atopic dermatitis using the NC/Tnd murine atopic dermati
274 diversity increased (P < 0.001) and scoring atopic dermatitis values decreased (P < 0.001) in all in
281 hly mutated (7.2%), somatic mutation rate in atopic dermatitis was less than half as high (3.4%).
283 PSAC2000 and COPSAC2010 cohorts, the risk of atopic dermatitis was significantly lower in children wi
286 ess the patient-level and societal burden of atopic dermatitis, we comprehensively reviewed the liter
289 , maternal asthma, infant bronchiolitis, and atopic dermatitis were associated with persistent wheeze
290 Using latent class analysis, 4 phenotypes of atopic dermatitis were identified depending on the onset
291 strated efficacy in patients with asthma and atopic dermatitis, which are both type 2 helper T-cell-m
293 ved signs and symptoms of moderate-to-severe atopic dermatitis with acceptable safety, validating the
295 lergies were 5 times more at risk to develop atopic dermatitis with an early-persistent phenotype com
296 quencing on a cohort of patients with severe atopic dermatitis with and without comorbid infections,
297 he IgE repertoire of preschool children with atopic dermatitis with regard to signs of superantigen-l
300 factor in treatment failure in patients with atopic dermatitis, yet it has been sparsely described in
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