Temporal variation of Staphylococcus aureus clonal complexes in atopic dermatitis: a follow-up study.

BACKGROUND: A strong link between disease severity and Staphylococcus aureus colonization of the skin has been reported in patients with atopic dermatitis (AD). OBJECTIVES: To examine temporal variations in S. aureus colonization and S. aureus CC type in patients with AD, and to investigate links to disease severity, skin barrier properties and filaggrin gene (FLG) mutations. METHODS: This was a follow-up study of a cohort of 101 adult patients with AD recruited from an outpatient clinic. Bacterial swabs were taken at baseline and follow-up from lesional skin, nonlesional skin and the nose. Swabs positive for S. aureus were characterized by spa and the respective clonal complex (CC) type was assigned. Patients were characterized with respect to disease severity [Scoring Atopic Dermatitis (SCORAD)], skin barrier properties [transepidermal water loss (TEWL), pH] and FLG mutations. RESULTS: In total, 63 patients participated in a follow-up visit. Twenty-seven patients (43%) were colonized at both visits, 27 were colonized at only one visit and nine (14%) were not colonized at either visit. Of patients colonized at both visits, 52% remained colonized with the same CC type at follow-up. Change in CC type was related to an increase in SCORAD of 10·7 points; patients who carried the same CC type had a reduction in SCORAD of 4·4 points. Significantly higher skin pH was found in patients colonized at both visits, while change in CC type was not related to TEWL, pH or FLG mutations. CONCLUSIONS: The data indicate that temporal variation in S. aureus CC type is linked to flares of the disease.

Staphylococcus aureus colonization in atopic eczema and its association with filaggrin gene mutations.

BACKGROUND: Atopic dermatitis (AD) is a prevalent disease with significant impact on physical health and quality of life. Staphylococcus aureus has been directly correlated to disease severity, and may also be a contributing causal factor in the pathogenesis of AD. OBJECTIVES: The primary aim was to assess differences in S. aureus colonization in patients with AD with and without filaggrin gene mutations. The secondary aim was to assess disease severity in relation to S. aureus colonization. Exploratory analyses were performed to investigate S. aureus genetic lineages in relation to filaggrin gene (FLG) mutations and disease severity. METHODS: Adult patients with AD (n = 101) were included in the study. Bacterial swabs were taken from lesional skin, nonlesional skin and the nose. Swabs positive for S. aureus were characterized by spa and the respective clonal complex (CC) type assigned. Patients were characterized with respect to disease severity (Scoring Atopic Dermatitis) and FLG mutations (n = 88). Fisher's exact test was used to analyse differences in S. aureus colonization in relation to FLG mutations. RESULTS: Of the 101 patients included, 74 (73%) were colonized with S. aureus. Of the colonized patients, 70 (95%) carried only one CC type in all three different sampling sites. In lesional skin, S. aureus was found in 24 of 31 patients with FLG mutations vs. 24 of 54 wild-type patients (P = 0·0004). Staphylococcus aureusCC1 clonal lineage was more prevalent in patients with FLG mutations (n = 10) than in wild-type patients (n = 2) (P = 0·003). No specific bacterial lineage was linked to disease severity. CONCLUSIONS: Increased S. aureus colonization in patients with AD with FLG mutations, and increased prevalence of CC1 in patients with FLG mutations, suggest that host-microbe interactions and clonal differences in S. aureus are important for colonization of AD skin.

Quality of life and disease severity in patients with atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD) affects quality of life (QoL) negatively in patients and their families. We examined the relationship between disease severity and QoL in patients with AD. METHODS: Consecutive, newly referred outpatients with AD, 4 years of age or older, were assessed from January 2012 onwards by means of the dermatology life quality index (DLQI, range 0-30), the Scoring of AD (SCORAD) disease severity score (range 0-103), filaggrin gene (FLG) mutation status and paraclinical tests related to allergy. RESULTS: A total of 250 patients with a mean age of 26.0 years were identified with complete data on DLQI; 148 (59.2%) females and 102 (40.8%) males. Of these 45.6% had asthma, 46.8% had hay fever, 22.7% had a loss-of-function mutation in FLG, and 61.9% had one or more inhalant allergic sensitizations. The correlation between SCORAD and DLQI was 0.42 (P < 0.001). After multivariate adjustment there was an increasing mean DLQI score with increasing disease severity measured by SCORAD (DLQI in mild = 5.30, moderate = 8.59 and severe = 11.94 AD), P-value for difference between groups <0.001; a higher mean DLQI among females than males (9.73 vs. 8.34), P = 0.028; and among patients reporting facial eczema (9.88 vs. 6.24), P = 0.012. No statistically significant influence on DLQI was found for hand or foot eczema, age, blood eosinophil count, allergic sensitization, asthma, hay fever, FLG mutation status and smoking. FLG null mutation status was not significantly associated with SCORAD. CONCLUSION: AD impacts negatively on the QoL, proportional to the severity of the disease. Furthermore, female sex and facial eczema are associated with low QoL. Positive FLG null mutation status is not associated with QoL or disease severity.

Human ß-defensin-2 as a marker for disease severity and skin barrier properties in atopic dermatitis.

BACKGROUND: Skin infections related to disrupted antimicrobial defence are a common problem in atopic dermatitis (AD). Altered levels of antimicrobial peptides, including human ß-defensin (hBD)-2, have been reported in AD skin, and a link to impaired barrier function has been suggested. OBJECTIVES: To study hBD-2 in relation to skin barrier function in patients with AD and controls, and to study hBD-2 in relation to disease severity. METHODS: Twenty-five patients with AD and 11 controls were enrolled. hBD-2 peptide concentration was determined in stratum corneum samples collected by a minimally invasive tape-stripping method. Disease severity was assessed by SCORing Atopic Dermatitis (SCORAD), and skin barrier function was evaluated by measurement of transepidermal water loss (TEWL) and skin pH. Patients with AD were characterized according to filaggrin mutations. RESULTS: hBD-2 concentrations in the stratum corneum were found to differ between lesional and nonlesional AD skin and controls, with the highest values in lesional skin (P < 0·001). SCORAD and TEWL were significantly increased in participants with measureable hBD-2 (P < 0·018 and P < 0·007, respectively). Significant correlations between hBD-2 in lesional skin, and TEWL and SCORAD were observed (R = 0·55 and R = 0·44, respectively). No correlations with skin pH were found. hBD-2 was not found to relate to filaggrin mutations. CONCLUSIONS: A significant correlation was found between hBD-2, disturbed skin barrier function and disease severity. The minimally invasive skin sample technique enables evaluation of the stratum corneum and its proteins over time and provides the possibility of relating these findings to treatment, infections and physiological variations.