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1 Party Criteria for the Definition of Atopic Dermatitis).
2 frequently associated with asthma and atopic dermatitis.
3 for the acute epidermal damage in radiation dermatitis.
4 matory diseases, including asthma and atopic dermatitis.
5 tion was investigated in two mouse models of dermatitis.
6 pful in preventing the development of atopic dermatitis.
7 sitization in patients suffering from atopic dermatitis.
8 ids in adults with moderate-to-severe atopic dermatitis.
9 d in the etiology and exacerbation of atopic dermatitis.
10 dels of atopic dermatitis and acute irritant dermatitis.
11 ular events are also seen in human radiation dermatitis.
12 allergic rhinitis, food allergy, and atopic dermatitis.
13 select aspects of AD, psoriasis, or contact dermatitis.
14 ectable cellular defects that lead to atopic dermatitis.
15 ation that may develop in humans with atopic dermatitis.
16 skin disorders including atopic eczema (AE)/dermatitis.
17 e management of chronic itch, notably atopic dermatitis.
18 ARN077, in a mouse model of allergic contact dermatitis.
19 tive strategy to reduce the burden of atopic dermatitis.
20 ; 79.5%), defined as children with no atopic dermatitis.
21 that this enzyme plays an important role in dermatitis.
22 d PBMCs from patients with asthma and atopic dermatitis.
23 ergic diseases ranging from asthma to atopic dermatitis.
24 the role of MCs in chronic allergic contact dermatitis.
25 ifferentiate from erythrodermic inflammatory dermatitis.
26 ed kallikrein 5 activity and ameliorated the dermatitis.
27 d to the development of spontaneous pruritic dermatitis.
28 pic status did not affect the risk of atopic dermatitis.
29 nd selection of the IgE repertoire in atopic dermatitis.
30 (94%) showed features of lichenoid interface dermatitis.
31 critical role in the pathogenesis of atopic dermatitis.
32 l as in an inducible mouse model of allergic dermatitis.
33 n other cases of anti-PD-1-induced lichenoid dermatitis.
34 rapeutic avenue in treating allergic contact dermatitis.
35 the development of IMQ-induced psoriasiform dermatitis.
36 as chronic sinusitis with polyps and atopic dermatitis.
37 rders, including acne, psoriasis, and atopic dermatitis.
38 risk of allergic diseases, including atopic dermatitis.
39 anism of acute epidermal damage in radiation dermatitis.
40 ly, when compared to children without atopic dermatitis.
41 treatment adherence of TCS phobia in atopic dermatitis.
42 luding asthma, allergic rhinitis, and atopic dermatitis.
43 dermatitis (atopic, contact, and seborrheic dermatitis), 0.29% for acne vulgaris, 0.19% for psoriasi
44 [1.2-4.3]) and doctor's diagnosis of atopic dermatitis (1.9 [1.0-3.4]) in childhood, and sensitizati
49 Atopic dermatitis (AD) and allergic contact dermatitis (ACD) have a dynamic relationship not yet ful
52 ted the effect of OA-NO2 on allergic contact dermatitis (ACD) using an established model of contact h
53 re commonly associated with allergic contact dermatitis (ACD), it is not known if they are mediated b
55 the following keywords: "psoriasis," "atopic dermatitis," "acne," "vitiligo," "seborrheic dermatitis,
56 he most common grade 3-4 adverse events were dermatitis acneiform (31 [14%] of 227 patients given dac
58 mation, particularly in patients with atopic dermatitis (AD) and AD-like congenital disorders, includ
61 icates a relevant association between atopic dermatitis (AD) and attention-deficit/hyperactivity diso
63 to determine the association between atopic dermatitis (AD) and cardiovascular events in the Nurses'
66 lls in lesional skin of patients with atopic dermatitis (AD) and psoriasis (PSO) might be directly ex
71 LC) in the epidermis of patients with atopic dermatitis (AD) carry the high-affinity receptor for IgE
72 ssic "allergic"/atopic comorbidities, atopic dermatitis (AD) emerges as systemic disease with increas
75 al influenza vaccine in patients with atopic dermatitis (AD) have not been carefully characterized.
76 ata (AA) and vitiligo associated with atopic dermatitis (AD) in a large cohort of US women, the Nurse
77 activity of IVM in a murine model of atopic dermatitis (AD) induced by repeated exposure to the alle
97 h pathway activation in patients with atopic dermatitis (AD) is fraught with the inability to precise
103 herapeutic armamentarium for treating atopic dermatitis (AD) was still primarily topical corticostero
104 estinal disease (EGID), patients with atopic dermatitis (AD), and nonatopic healthy control (NA) subj
106 red an efficient treatment option for atopic dermatitis (AD), but a global assessment of glucocortico
128 ; mean age, 44 years) who contracted unusual dermatitis after an occupational exposure in July and Au
129 B2(-/-) mice are more susceptible to contact dermatitis after topical application of dinitrofluoroben
130 dermatitis," "acne," "vitiligo," "seborrheic dermatitis," "alopecia areata," and "lichen planus." Div
131 icacy for patients with psoriasis and atopic dermatitis, although the biologic target and mechanism o
136 positive additive interaction between atopic dermatitis and allergic sensitization in their effects o
137 us aureus (S. aureus) is increased in atopic dermatitis and can result in increased severity of the d
139 tero exposures may affect the risk of atopic dermatitis and emphasize the importance of the early env
140 he association between emollient use, atopic dermatitis and FLG mutations, respectively, with urinary
141 udies, fresh blood from patients with atopic dermatitis and healthy control subjects was analyzed wit
142 ONOS), adults with moderate-to-severe atopic dermatitis and inadequate response to topical corticoste
143 d in human diseases, such as allergy, atopic dermatitis and nasal polyposis, but their function in hu
144 oviruses was identified in sows with porcine dermatitis and nephropathy syndrome (PDNS) and reproduct
146 of effective and safe treatments for atopic dermatitis and other inflammatory disorders of the skin.
148 topic march, with innate immunity initiating dermatitis and the adaptive immunity required for subseq
149 ortant in asthma, food allergies, and atopic dermatitis and their respectively developed antagonists.
150 uction of lesions in a mouse model of atopic dermatitis and to elucidate possible HOCl's mode of acti
153 been associated with risk of asthma, atopic dermatitis, and elevated total immunoglobulin E (IgE).
155 keratinocytes in the pathogenesis of atopic dermatitis, and the animals lacking BRAF and RAF1 in the
156 1.12 (95% CI 0.92-1.37, p = 0.27) for atopic dermatitis, and the effect size on log-transformed IgE l
157 ly reduced inflammation in imiquimod-induced dermatitis, and were resistant to induction of experimen
160 asthma, rhinitis, food allergies, and atopic dermatitis, are generally classified by the tissue rathe
161 ntact hypersensitivity and ovalbumin-induced dermatitis as models for TH2-mediated cutaneous inflamma
162 t mouse that spontaneously develops pruritic dermatitis as the result of an initial defect in skin ho
163 either atopic dermatitis or allergic contact dermatitis as well as in an inducible mouse model of all
164 UV exposure, to treatment-limiting radiation dermatitis associated with radiotherapy, to cutaneous ra
165 aried in size from 0.38% of total burden for dermatitis (atopic, contact, and seborrheic dermatitis),
166 skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are uncl
169 uring the past 30 years, only 3 outbreaks of dermatitis caused by Pyemotes ventricosus have been repo
170 dermatitis (AD), psoriasis (PS), and contact dermatitis (CD) are common skin diseases, characterized
171 ad inflammatory symptoms, including wasting, dermatitis, colitis, hypereosinophilia, and high IgE lev
172 pecia areata, vitiligo, psoriasis and atopic dermatitis, common variants have been identified that ar
175 treatment of aberrant cell proliferation in dermatitis, cutaneous T-cell lymphoma, and graft-versus-
178 a specific description of subtypes of atopic dermatitis depending on the timing of onset and progress
179 n, IgE transcripts from children with atopic dermatitis displayed a dominance of the otherwise scarce
181 march describes the progression from atopic dermatitis during infancy to asthma and allergic rhiniti
183 atory dendritic epidermal cells appearing in dermatitis/eczema lesions, LCs lack key monocyte-affilia
184 of more than 10 years, reported that atopic dermatitis, family asthma, early-life exposure to tobacc
185 ded grade 3 mucositis (12 patients), grade 3 dermatitis (five patients), grade 3 aminotransferase ele
187 hildren from this cohort with data on atopic dermatitis from birth to 6 years of age were included.
188 ts represented in the North American Contact Dermatitis Group (NACDG) series were conducted using Wil
190 esults obtained by uploading a recent atopic dermatitis GWAS meta-analysis to examine the genetic cor
192 h common FLG mutations, children with atopic dermatitis had significantly higher urinary levels of on
193 The role of MCs in chronic allergic contact dermatitis has not been investigated, in part because of
198 equency of as much as 11.1% in patients with dermatitis; however, few cohort studies in the US popula
199 relief of itch in human patients with atopic dermatitis; however, the specific antipruritic mechanism
200 ses in adults with moderate-to-severe atopic dermatitis in a dose-dependent manner, without significa
202 ysis was used to identify subtypes of atopic dermatitis in childhood based on the course of symptoms.
203 ASTURE data separated 4 phenotypes of atopic dermatitis in childhood: 2 early phenotypes with onset b
204 tic dog exposure affected the risk of atopic dermatitis in children during the first 3 years of life.
209 e management of asthma, rhinitis, and atopic dermatitis in the context of a better selection of treat
210 ative estimate of the annual costs of atopic dermatitis in the United States is $5.297 billion (in 20
211 iated with a strongly reduced risk of atopic dermatitis in two independent birth cohorts and in a dos
213 Thymic stromal lymphopoietin production and dermatitis induced by alkalinization of the skin could b
220 and dermal features of MC903-induced atopic dermatitis-like disease and suppresses the production of
222 istration of HOCl hydrogel (0.05%) on atopic dermatitis-like lesions in NC/Nga mice model as well as
223 wild-type mouse skin induces a human atopic dermatitis-like phenotype that is triggered by an increa
225 nduced skin damage characterized by clinical dermatitis, loss of barrier function, inflammation, and
227 stigation are targeted for psoriasis, atopic dermatitis, melanoma, hidradenitis suppurativa, and pemp
228 l keratinocytes, a DFE-induced murine atopic dermatitis model, and human atopic dermatitis lesions.
230 sed for chronic hepatic diseases and itching dermatitis, modulates the pathological processes of infl
231 stroenteritis, viral gastroenteritis, herpes dermatitis, multiple fractures, respiratory failure, and
234 childhood onset asthma (n = 15,008), atopic dermatitis (n = 40,835), and elevated IgE level (n = 12,
237 (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals, partl
238 is unclear if S. aureus is a cause of atopic dermatitis or a consequence of the abnormal epithelial e
239 sions of humans diagnosed with either atopic dermatitis or allergic contact dermatitis as well as in
244 were associated with risk of asthma, atopic dermatitis, or elevated serum IgE levels, using Mendelia
245 onferred an increased risk of asthma, atopic dermatitis, or elevated total serum IgE, suggesting that
246 (hay fever: OR: 5.50 [3.42-9.00] and atopic dermatitis: OR 3.76 [2.14-6.61]), and drug use (LABA + I
252 ch and in a transgenic mouse model of atopic dermatitis produced by overexpression of the TH2 cell-as
262 rate-to-severe AD (six area, six sign atopic dermatitis [SASSAD] score: geometric mean, 22.3 [95% CI,
264 rrelated with patient-reported global atopic dermatitis severity (Kendall tau = 0.336, P < 0.0001), n
265 ients with allergic disorders such as atopic dermatitis show a paucity of skin neutrophils and are pr
266 steroid treatment for 1 year improved atopic dermatitis signs and symptoms, with acceptable safety.
267 TLR1, TLR6, IL-25, and IL-33 in human atopic dermatitis skin lesions with high house dust mite sensit
268 molecules was investigated using an ex vivo dermatitis skin model with transient KLK5 expression and
269 ances were derived from the American Contact Dermatitis Society's Contact Allergen Management Program
270 s, 5 individuals (33%) demonstrated grade II dermatitis that was unresponsive to topical corticostero
271 a well-established model of allergic contact dermatitis, the absence of Mincle leads to a significant
272 genic skin phenotype, including pruritis and dermatitis, the number of tryptase-positive mast cells i
273 In a cohort of 14 dogs with canine atopic dermatitis, the skin microbiota were longitudinally eval
276 e an in vivo mouse model of allergic contact dermatitis to investigate how nanoparticles (NPs) may al
277 R1001 is also effective in alleviating acute dermatitis triggered by 12-O-tetradecanoylphorbol-13-ace
278 To identify different phenotypes of atopic dermatitis using a definition based on symptoms before a
279 ole of skin pH in the pathogenesis of atopic dermatitis using the NC/Tnd murine atopic dermatitis mod
280 ading to skin barrier dysfunction, itch, and dermatitis via the protease-activated receptor 2-thymic
286 Diagnosis of bronchial asthma and atopic dermatitis was made, but she rejected therapy except for
288 patient-level and societal burden of atopic dermatitis, we comprehensively reviewed the literature r
289 morphological appearance of several forms of dermatitis, we strongly suggest the use of a more specif
291 atent class analysis, 4 phenotypes of atopic dermatitis were identified depending on the onset and co
293 ns and symptoms of moderate-to-severe atopic dermatitis with acceptable safety, validating the crucia
295 were 5 times more at risk to develop atopic dermatitis with an early-persistent phenotype compared w
296 g on a cohort of patients with severe atopic dermatitis with and without comorbid infections, we foun
297 repertoire of preschool children with atopic dermatitis with regard to signs of superantigen-like act
298 In human subjects imiquimod induces contact dermatitis with the distinctive feature that pDCs are th
301 in treatment failure in patients with atopic dermatitis, yet it has been sparsely described in the li
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