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PubMed2001

The ACVD task force on canine atopic dermatitis (III): the role of antibodies in canine atopic dermatitis.

Although an important pathogenic role for IgE is established in the case of allergic asthma and rhinitis in man, its role in atopic dermatitis is less clear. There are many studies where allergists and immunologists have provided evidence in favour of such a role, whereas dermatologists are less than convinced. In dogs, however, there is an abundance of clinical evidence implying that atopic dermatitis is antigen driven, and recent studies suggest that there may be a role for IgE, not only in the effector pathway, but also in antigen capture. Although an IgG response often accompanies an IgE response in dogs with atopic dermatitis, there is little evidence in support of a pathogenic role in respect of the former isotype.

Allergens↗

PubMed2002

Dichotomic nature of atopic dermatitis reflected by combined analysis of monocyte immunophenotyping and single nucleotide polymorphisms of the interleukin-4/interleukin-13 receptor gene: the dichotomy of extrinsic and intrinsic atopic dermatitis.

Patients with atopic dermatitis display substantial immunologic abnormalities, among which elevated total IgE is considered as a hallmark; however, a subgroup of atopic dermatitis patients exhibits normal IgE levels, but mechanisms contributing to the so-called "intrinsic" or "nonallergic" form of atopic dermatitis are obscure. In order to unravel similarities and differences of both atopic dermatitis subtypes, the phenotype of monocytes, total serum IgE levels, and serum levels of cytokines regulating the IgE production from nonatopic individuals and patients with allergic rhinitis, and extrinsic and intrinsic atopic dermatitis were measured. Concomitantly, genomic DNA probes of all subjects were analyzed for single nucleotide polymorphisms of candidate genes of structures involved in the regulation of the IgE synthesis, such as interleukin-4 and the interleukin-4R/interleukin-13R. Our data show that the surface expression of the high- and low-affinity receptor for IgE (FcepsilonRI and FcepsilonRII/CD23) and the interleukin-4Ralpha chain were significantly elevated in monocytes from patients with extrinsic atopic dermatitis. Furthermore, serum levels of interleukin-13 were significantly increased in patients with intrinsic atopic dermatitis. In addition, the frequency of the interleukin-4Ralpha polymorphism C3223T and the interleukin-4 polymorphism C590T tended to be higher in extrinsic atopic dermatitis than in intrinsic atopic dermatitis. Altogether our findings indicate that intrinsic atopic dermatitis patients exhibit phenotypic and immunologic features, which differ from those of patients with extrinsic atopic dermatitis or other atopic disorders.

Adolescent↗

PubMed1994

The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. II. Observer variation of clinical diagnosis and signs of atopic dermatitis.

The level of agreement between 14 physicians as to what constitutes a case of atopic dermatitis was tested on 15 selected patients with a range of diagnoses. Between-observer agreement was good, with a mean pair agreement index (P0) of 0.94, and a chance corrected index (kappa) of 0.78. Between-observer agreement in the recording of 18 separate physical signs of atopic dermatitis was then tested by asking the 14 physicians to note the presence or absence of each sign in a different group of patients to those seen in the first part of the exercise. Substantial between-observer agreement (kappa > 0.61) was only present for truncal dermatitis. Most signs showed only fair to moderate agreement (kappa 0.21-0.60), and some signs, such as keratosis pilaris, xerosis, orbital pigmentation, fine hair, and extensor dermatitis, showed poor agreement (kappa 0.01-0.20). The findings were similar when the responses of two independent observers from the national study outlined in Paper I were compared for each sign. Within-observer variation for the recording of physical signs was substantially better than between-observer variation. Physicians interested in atopic dermatitis agree reasonably well on what constitutes a typical case of atopic dermatitis. Between-observer variation with regard to some physical signs of atopic dermatitis is of a magnitude which argues against their continued use in clinical and epidemiological studies.

Dermatitis, Atopic↗

PubMed1992

Topical corticosteroids and Staphylococcus aureus in atopic dermatitis.

BACKGROUND: Atopic dermatitis is commonly colonized with Staphylococcus aureus in high densities. OBJECTIVE: Our purpose was to study the effect of topical corticosteroids on the colonization of S. aureus in atopic dermatitis. METHODS: Sixty-six patients were treated with moderately potent, or very potent corticosteroids. Quantification of S. aureus and evaluation of the severity of the eczema was performed before, after 1 week, and after 2 weeks of treatment. RESULTS: Fifty-three patients carried S. aureus in the most pronounced lesion before treatment. The colonization was significantly correlated with the severity of the eczema. The density of S. aureus was reduced by topical corticosteroids. The reduction increased with the potency of the corticosteroid and was most pronounced during the first week. S. aureus was eliminated after a successful 2-week treatment with a very potent corticosteroid. Propylene glycol 25% added to a moderately potent corticosteroid did not significantly increase the reduction of S. aureus. CONCLUSION: Topical corticosteroids of sufficient potency reduce the density of S. aureus in atopic dermatitis.

Administration, Cutaneous↗

PubMed1998

Linkage between atopy and the IgE high-affinity receptor gene at 11q13 in atopic dermatitis families.

Atopic dermatitis is a common skin disease frequently associated with allergic disorders such as allergic rhinitis and asthma. Controversial linkage findings between atopy and markers at chromosome 11q13 led us to search chromosome 11 for genes conferring susceptibility to atopic dermatitis and atopy. Twelve families were investigated using highly polymorphic markers and a powerful model-free linkage test. Two markers gave evidence for linkage, D11S903 (P = 0.02) and FCER1B (P = 0.005). A two-point lod-score analysis between these two markers revealed significant evidence for linkage (zmax = 4.02 at (theta = 0.0). In regard to model-dependent lod-score analyses between atopic disorders and FCER1B, two-point analysis gave a lod score of z = 0.78 whereas two-locus analysis using a recessive-dominant mode of inheritance displayed a significant lod score of z = 3.55. Only 2 of 12 families showed evidence for linkage using the latter oligogenic model. In conclusion, the results of our study map the FCER1B gene in close proximity to D11S903, support the finding of Cookson et al. implicating the IgE high-affinity receptor gene (FCER1B) at 11q13, and furthermore suggest an oligogenic mode of inheritance as well as heterogeneity in the genetic susceptibility to atopy and atopic dermatitis.

Adolescent↗

PubMed2004

[Role of immediate hypersensitivity to airborne allergens in the pathogenesis of atopic dermatitis].

UNLABELLED: Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with hyperproduction of immunoglobulin E directed against common environmental allergens. OBJECTIVES: The aim of the study was to evaluate the immediate type of immunological reaction indicated by airborne allergens in the pathomechanism of atopic dermatitis. MATERIAL AND METHODS: 529 patients with AD aged (0.5-60 years) who fulfilled basic Hanifin and Rajka criterias and 60 healthy volunteers in the control group were investigated. In order to evaluate IgE-mediated allergy to common airborne and alimentary allergens skin prick tests (SPT) were performed (26 airborne and 7 basic alimentary allergens) and concentration of serum antigen specific IgE (asigE) was measured. RESULTS: Our results indicated airborne allergy in case of 405 patients (76.6%) and food allergy only in 67 cases (12.7%). In the group of children aged 0.5-4 years food allergy was predominant but later on the predominance of airborne allergy was observed. CONCLUSIONS: We conclude that airborne allergy plays an important and predominant role in the pathomechanism of atopic dermatitis.

Adolescent↗

PubMedDate not supplied

[New concepts about atopic dermatitis].

The atopic dermatitis is a chronic inflammatory skin illness, with remissions and exacerbations, itch, and association with allergic rhinitis and asthma. There is a complex interrelationship of genetic, environmental, pharmacological and psychological factors that contribute to the development and severity of the illness: Different manifestations of immunological disorders are an increment in the number of IgE antibodies toward common antigens, an increment in the liberation of proinflammatory mediators by basophils and mast cells, peripheral and local eosinophilia, biphasic activity Th1/Th2 with the liberation of cytokines (IL-4, IL-5, IL-13), GM-CSF and the IFN-gamma caused by the cells Th1. an increment in the liberation of major basic protein, eosinophil cationic protein besides the expression of chemotactic factors by the monocytes (RANTES, eotaxin, vasoactive intestinal peptide, etc.). In 1980, Hanifin and Rajka made public the diagnostic criteria for the atopic dermatitis and it has been universally accepted as an standard for the diagnosis. Leung reported that a knowledge about the immunopathological bases of the atopic dermatitis has important clinical implications for the diagnosis and possible treatment there are multiple choices for a treatment because of the complexity of the illness. Among these are thalidomide and transfer factor as an immunomodulator treatment with acceptable safety and clinical efficacy.

Adjuvants, Immunologic↗

PubMed2000

An open study of efficacy and safety of long-term treatment with mometasone furoate fatty cream in the treatment of adult patients with atopic dermatitis.

BACKGROUND: Atopic dermatitis is a severe chronic skin disease often deteriorated by the presence of microorganisms and often responds well to treatment with potent corticosteroids. However, the long-term use of potent topical corticosteroids are accompanied by side-effects such as skin atrophy. OBJECTIVE: To study the effect and safety of prophylactic treatment with mometasone furoate fatty cream (contains hexylene glycol) for 6 months in patients with atopic dermatitis. RESULTS: Sixty-one of 68 (90%) patients were still free of their disease after 6 months of twice weekly treatment and only one showed possible treatment related signs of skin atrophy. The number of Staphylococcus aureus and Pityrosporum ovale were significantly reduced in cleared patients. CONCLUSIONS: Mometasone furoate fatty cream is effective and safe both for treatment and as a prophylaxis in patients with atopic dermatitis.

Administration, Topical↗

PubMed1978

Immunofluorescence of the skin in allergic diseases: an investigation of patients with contact dermatitis, allergic vasculitis and atopic dermatitis.

Skin biopsies for immunofluorescent studies were taken from patients with contact dermatitis (positive patch tests), atopic dermatitis and allergic vasculitis for comparison with normal-appearing skin from the same patients, and from healthy controls. A variety of deposits of immunoglobulins, complement components and fibrinogen were demonstrated in 6 out of 20 patients with contact dermatitis, 7 out of 10 with atopic dermatitis, 8 out of 10 with allergic vasculitis, and in 4 out of 20 control individuals. No diagnostic pattern of deposits was found. Elevated serum IgE and eosinophilic counts were found in patients with atopic dermatitis, and high serum IgA and fibrinogen levels were found in the allergic vasculitis group.

Adolescent↗

PubMed2005

Analysis of T cell receptor (TCR) BV-gene clonotypes in NC/Nga mice developing dermatitis resembling human atopic dermatitis.

BACKGROUND: Our previous study showed that T cells in skin lesions of human atopic dermatitis (AD) had oligoclonal accumulation, indicating the involvement of antigen-specific immune reactions at those sites. Recently, NC/Nga mice, which develop skin lesions similar to AD, have been proposed as a model for that disease. OBJECTIVE: To clarify whether NC/Nga mice are suitable as a model for human AD from the viewpoint of their antigen-specific immune responses. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and single strand conformation polymorphism (SSCP) analyses were conducted to detect TCR BV genes of clonally expanded T cells derived from NC/Nga mice at an early phase of the AD-like dermatitis, at a late phase of the dermatitis, and with no AD-like dermatitis. RESULTS: (1) T cells with TCR BV 7, 10 and 17 reside in the skin of NC/Nga mice without the AD-like dermatitis. (2) T cells with these BV genes contain oligoclonal accumulations, however, expanded T cell clonotypes are also detected in the spleen and exist constantly during the course of the AD-like dermatitis. (3) Development of the AD-like dermatitis is associated with additional oligoclonal expansion/accumulation of T cells with TCR BV 2, 4 and 6 genes. (4) Progression of the AD-like dermatitis is associated with further oligoclonal expansion/accumulation of T cells with the TCR BV 14 gene. (5) Some of the expanded TCR clonotypes are common between the individual mice and between early and late phases. CONCLUSIONS: Taking these data together with the previous human AD studies, NC/Nga mice seem to be an appropriate model for human AD.

Animals↗

PubMed1990

[Langerhans cells in the physiopathology of atopic dermatitis].

INTRODUCTION. Atopic dermatitis (AD), allergic rhino-conjunctivities and allergic asthma constitute the classical triad of atopic diathesis attended, in many cases, by high serum IgE levels. While the pathophysiology of IgE-mediated allergic respiratory diseases is now better understood, the pathophysiological significance of atopic phenomena in the genesis and control of AD is still far from being clear. Numerous clinical and laboratory data point to a pathophysiological relation between IgE-mediated reactions and AD, but no one yet knows by which mechanism this interaction takes place. Some recent studies suggest that Langerhans cells might well be the missing link. THE LANGERHANS CELLS. Langerhans cells (LC) are dendritic epidermal cells originating in the bone marrow and supposedly belonging to the monocyte lineage. Their circulating precursors, the mechanism of their migration into the epidermis and their relationship with other dendritic cells, such as the interdigitating follicular cells, are controverted. LC express numerous surface markers, such as class I and II HLA, CD1a, CD4 and receptors for complement and IgE Fc fragments. Under normal conditions, LC do not express IgE receptors. Ultrastructurally, LC are characterized by the presence of Birbeck granules in their cytoplasm. Among the presumed functions of LC in the skin, the best documented is the presentation of antigens to T lymphocytes in allergic contact dermatitis. LANGERHANS CELLS IN ATOPIC DERMATITIS. Quantitative studies. Modern immunohistological methods based on the reactivity of monoclonal anti-CD1a antibodies have given results that are sometimes conflicting due to differences in the quantification techniques utilized. However, morphometric enumeration of LC on cryostat sections have shown that their number is about the same in AD and in normal skin. PRESENCE OF IgE BEARING LANGERHANS CELLS IN ATOPIC DERMATITIS. The presence of IgE molecules on the LC surface has been demonstrated in subjects with AD. It must be noted that in atopic subjects IgE bearing Lc are only found in patients with high serum IgE levels. They are absent in asthma patients without eczema, irrespective of their serum IgE levels. Daily applications of corticosteroids on AD lesions result in a decrease of anti-IgE markers on LC after one week and in their complete disappearance after 2 weeks. IN ATOPIC DERMATITIS LANGERHANS CELLS EXPRESS A RECEPTOR SPECIFIC TO Fc FRAGMENTS OF IgE. The exact nature of the receptor for IgE expressed in situ in AD patients is still conjectural. Some authors have been able to demonstrate that the binding of IgE molecules by LC isolated from the skin of atopic patients is inhibited by a monoclonal antibody directed against the low affinity receptor (Fc epsilon R2) of eosinophils and macrophages. This strongly suggests that certain factors induce the expression by LC of an Fc epsilon R2 receptor. IN VITRO INDUCTION OF IgE RECEPTORS ON NORMAL LANGERHANS CELLS...

Dermatitis, Atopic↗

PubMed1994

The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. I. Derivation of a minimum set of discriminators for atopic dermatitis.

A working party of 13 dermatologists, two family practitioners and a paediatrician was assembled, with the aim of developing a minimum list of reliable discriminators for atopic dermatitis. Each physician was asked to select 10 consecutive new cases of unequivocal mild to moderate atopic dermatitis and 10 controls with other inflammatory dermatoses. Each subject was examined by two independent observers, who were blind to the clinical diagnosis and study aim, with regard to 31 clinically useful diagnostic features for atopic dermatitis. Two hundred and twenty-four patients were studied (120 cases and 102 controls). Using the key physician's clinical diagnosis as a gold standard, the sensitivity and specificity of each of the 31 diagnostic criteria were tested. Using multiple logistic regression techniques, a minimum set of diagnostic criteria for atopic dermatitis was derived. These were: history of flexural involvement, history of a dry skin, onset under the age of 2, personal history of asthma, history of a pruritic skin condition, and visible flexural dermatitis. Adjustment for age, sex, region, social class and ethnic group did not alter the choice of final criteria. The discriminatory value of these criteria was also satisfactory when tested against a further sample of 150 patients drawn from the community, who did not have skin disease.

Adolescent↗

PubMed2003

Atopic dermatitis and the atopic march.

Atopic dermatitis (AD), one of the most common skin disorders seen in infants and children, usually has its onset during the first 6 months of life. The prevalence of AD is similar in the United States, Europe, and Japan and is increasing, similar to that of other atopic disorders, particularly asthma. AD has been classified into 3 sequential phases: infantile, childhood, and adult, each with characteristic physical findings. AD has a tremendously negative effect on the quality of life of patients as well as family, most commonly disturbing sleep. The condition also creates a great financial burden for both the family and society. The cutaneous manifestations of atopy often represent the beginning of the atopic march. On the basis of several longitudinal studies, approximately half of AD patients will develop asthma, particularly with severe AD, and two thirds will develop allergic rhinitis. Epicutaneous sensitization has been thought to be responsible, with subsequent migration of sensitized T cells into the nose and airways, causing upper and lower airway disease. Animal models and human observation concur with this theory. Preliminary prevention studies with oral antihistamines provide evidence that early intervention might slow the atopic march.

Asthma↗

PubMedDate not supplied

[The time of manifestation of atopic dermatitis in children with atopic family anamnesis].

Studies about the time of first manifestation of atopic dermatitis in children with atopic family history. Children with atopic family history were followed prospectively during their first year of life and the time of the first manifestation of an atopic dermatitis was noted. 241 children were observed during their first six months, 197 out of these during the whole first year of life. The weekly rate of first manifestation of atopic dermatitis was nearly the same during the whole first year.

Age Factors↗

PubMed2026

Single-cell transcriptome revealed the aberrant keratinocytes activation in antigen presentation in atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD), a common chronic inflammatory skin disease, has been extensively studied using single-cell genomics. However, keratinocytes, as key effector cells in AD, have underlying mechanisms remain incompletely understood and require further investigation. METHODS: We integrated single-cell transcriptomic data from skin tissues of healthy controls, chronic active AD patients, spontaneously healed AD (SHAD) patients, and an ovalbumin-induced AD mouse model. The study particularly emphasized the gene expression and cellular dynamics of keratinocytes across the different groups, as well as their interactions with immune cells. RESULTS: Compared to healthy controls, we observed significant changes in the keratinocyte transcriptome, cellular state, and keratinocyte-immune cell ligand-receptor interactions in AD skin, particularly the marked activation of genes involved in antigen processing and presentation. Interestingly, such gene activation was not observed in keratinocytes from the ovalbumin-induced AD mouse model, despite its phenotype closely resembling human AD. Furthermore, in SHAD, we identified a recovery of both the ligand-receptor interaction patterns and antigen processing and presentation genes, accompanied by a notable shift in the transcriptome. This involved a significant downregulation of genes related to cytoplasmic transcription and oxidative phosphorylation. Notably, this pattern was not observed in the self-healing mouse model following the removal of ovalbumin stimulation. CONCLUSION: Our results suggest that the persistent activation of antigen processing and presentation pathways in keratinocytes may be a key driver of chronic inflammation in AD. Therefore, redirecting anti-allergic therapeutic strategies from solely targeting immune cells to targeting of keratinocyte-mediated antigen presentation may offer a more effective approach. Furthermore, we raise concerns about the use of ovalbumin-induced mouse models to recapitulate human chronic AD, as the underlying mechanisms may differ significantly.

Dermatitis, Atopic↗

PubMed2000

Pilot study of IFN-gamma-induced specific hyposensitization for house dust mites in atopic dermatitis: IFN-gamma-induced immune deviation as a new therapeutic concept for atopic dermatitis.

IFN-gamma/IL-4 imbalance is a central immunologic defect which is responsible for increased IgE antibody response in atopic dermatitis. Effects of hyposensitization were controversial in atopic dermatitis. Reversed IFN-gamma/IL-4 balance was induced using IFN-gamma in atopic dermatitis and specific hyposensitization with house dust mites (HDM) was tried in the status of IFN-gamma-induced immune deviation. A total of 58 atopic dermatitis patients who had obvious allergy to HDM were selected in this study. IFN-gamma-induced hyposensitization for HDM was tried in 10 patients. Twenty-two patients received IFN-gamma therapy and six were treated by simple hyposensitization. Twenty were enrolled as control subjects. The clinical severity scores decreased effectively only by IFN-gamma-induced hyposensitization for HDM. Specific hyposensitization for HDM in the status of IFN-gamma-induced immune deviation successfully improved atopic dermatitis. HDM might play a pathogenic role in subpopulation of atopic dermatitis.

Adolescent↗

PubMed2004

Impaired responses of peripheral blood mononuclear cells to nickel in patients with nickel-allergic contact dermatitis and concomitant atopic dermatitis.

BACKGROUND: Allergic contact dermatitis (ACD) is pathogenetically dependent on cell-mediated immune responses mediated by type 1 T lymphocytes. Atopic dermatitis (AD), in contrast, occurs as a result of sustained activation of type 2 subsets of T cells. Although atopic patients may become sensitized to various contact allergens, little is known about the influence of atopy on delayed-type hypersensitivity. OBJECTIVES: To investigate the in vitro responses of peripheral blood mononuclear cells (PBMC) to nickel stimulation in groups of atopic and nonatopic patients with patch test-verified nickel ACD. METHODS: Ten nonatopic patients with nickel ACD, 10 patients with nickel ACD and concomitant AD, 10 patients with AD but with no contact allergy, and 10 healthy persons participated in the study. PBMC were cultured in the presence or absence of nickel sulphate, phytohaemagglutinin (PHA) or tetanus toxoid (TT). [(3)H]thymidine incorporation was used to measure the rate of antigen-induced DNA synthesis and enzyme-linked immunosorbent assay was used to measure the production of interleukin (IL)-2 (type 1 cytokine) and IL-5 (type 2 cytokine). RESULTS: Nickel-stimulated PBMC of nickel-allergic patients with AD proliferated significantly less and secreted significantly lower amounts of IL-2 than cells of nonatopic nickel-allergic patients. IL-5 production was also lower in the former group, although the difference was nonsignificant. Moreover, neither the nickel-specific DNA synthesis nor the cytokine production by PBMC of atopic nickel-allergic patients differed significantly from those of healthy control persons and AD patients without contact allergy. Proliferative and secretory responses of PBMC to PHA or TT stimulation differed nonsignificantly between the groups. Nickel-induced IL-2 production correlated well with IL-5 production in nickel-allergic patients regardless of their atopic status. CONCLUSIONS: Our results indicate that PBMC of nickel-allergic patients with concomitant AD are characterized by impaired in vitro proliferative and secretory responses to the contact allergen nickel but not to the mitogen PHA or the recall antigen TT. The type 2 cytokine IL-5 may play a role in the development of ACD.

Adolescent↗

PubMed2006

Nocturnal wrist movements are correlated with objective clinical scores and plasma chemokine levels in children with atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD) is a distressing disease associated with pruritus and sleep disturbance. Scratching due to pruritus is an important mechanism in the exacerbation of AD but is difficult to document in the home environment. OBJECTIVES: To evaluate whether nocturnal wrist activities, defined as average acceleration in the early hours of sleep, were correlated with components of the SCORing Atopic Dermatitis (SCORAD) index and various AD-associated chemokine markers. METHODS: Patients with AD aged under 18 years were recruited and the severity of eczema was assessed with the SCORAD index. Concentrations of plasma AD-associated chemokines [cutaneous T-cell attracting cytokine (CTACK); macrophage-derived chemokine (MDC); thymus and activation regulated chemokine (TARC)], interleukin (IL)-18, serum total IgE, and eosinophil counts were measured in these patients. Healthy children with noninflammatory and nonitchy skin conditions as well as healthy children of staff volunteers were recruited as controls. All children were instructed to wear the DigiTrac monitor on their dominant wrist before sleeping. The monitor was programmed to record limb motion between 22.00 and 08.00 h the following morning. RESULTS: Twenty-four Chinese children with AD (mean +/- SD age 12.6 +/- 3.7 years) and 15 normal children (mean +/- SD age 11.9 +/- 3.4 years) were recruited. The median (interquartile range) SCORAD was 54.8 (32.8-70.2). Plasma concentrations in pg mL(-1) of CTACK, MDC, TARC and IL-18 in the patients were 105 (92-172), 1648 (973-4214), 258 (100-850) and 415 (304-539), respectively. When compared with controls, most wrist activities occurred at frequencies between 1 and 3 Hz. These activities were most consistent over the first 3 h of sleeping and correlated significantly with disease severity, extent, intensity, and AD-associated chemokine markers CTACK, MDC and TARC. However, there was no significant correlation between wrist activities and the subjective symptom of pruritus or sleep loss. CONCLUSIONS: This is the first study to demonstrate that wrist activities, nonintrusively measured by the DigiTrac monitor at home, are closely correlated with the objective clinical scores and levels of peripheral blood chemokine markers for AD but not with the reported symptoms of pruritus or sleep loss. We propose that wrist activities between 1 and 3 Hz for the first 3 h are a good indicator of AD severity in children and should substitute for the pruritus and sleep-loss components of the SCORAD.

Adolescent↗