Background Severity‐associated factors in atopic dermatitis (AD) have focussed on early onset, concomitant atopic diseases, markers of Th2‐shifted inflammation and filaggrin mutations. Objectives To investigate factors associated with severe AD in Finnish patients. Methods We conducted a single‐centre, cross‐sectional observational study with 502 AD patients aged 4.79 to 79.90 years (mean 32.08 years). Disease severity was assessed with the Rajka–Langeland severity score and EASI and associated clinical signs were evaluated. Data regarding onset, relatives, atopic and other comorbidities was gathered retrospectively. We investigated total serum IgE‐levels, a panel of filaggrin null mutations and functional variants of genes associated with skin barrier defects. Results Factors more frequent in severe AD included early onset (P = 0.004, 95%CI 0.000–0.024), male sex (P = 0.002, 95%CI 0.000–0.11), history of smoking (P = 0.012, 95%CI 0.000–0.024), concomitant asthma (P = 0.001, 95%CI 0.000–0.011), palmar hyperlinearity (P = 0.013, 95%CI 0.014–0.059), hand dermatitis (P = 0.020, 95%CI 0.000–0.029) and history of contact allergy (P = 0.042, 95%CI 0.037–0.096). Body mass indices (P < 0.000, 95%CI 0.000–0.011) and total serum IgE‐levels (P < 0.000, 95%CI 0.000–0.011) were higher in severe AD. No differences were observed for allergic rhinitis, allergic conjunctivitis, food allergy, peanut allergy, prick positivity, keratosis pilaris, history of herpes simplex infections, filaggrin null mutations and other gene variants. Conclusions Severity determinants in Finnish patients seem to be early‐onset, male sex, smoking, overweight, concomitant asthma, palmar hyperlinearity, hand dermatitis and high IgE‐levels. A sub‐typing of patients in relation to confirmed severity determinants may be useful for course prediction, prognosis and targeted AD management.
The burden of atopic dermatitis (AD) appears to be increasing in adult and elderly patients. The aim of this study was to analyse the nationwide database of the Finnish Institute for Health and Welfare regarding the number of patients with AD and of general practitioner consultations in Finland during 2018. The database comprised the main diagnoses of all visits to public primary healthcare. There were 2,094,673 primary care patients (males/females 43.19/56.81%) and 20,905 patients with AD (1.00%) and 24,180 consultations due to AD (0.45%). The highest numbers of patients with AD were in the age groups 0–14 years (9,922 patients, 47.46%) and 15–65 years (9,144 patients, 43.74%). A substantial proportion of patients with AD were aged > 50 years (3,515 patients, 16.81%) or >65 years (1,947 patients, 9.31%). Regression analysis indicated a statistically significant association of age group with patient numbers (p = 0.032) and number of consultations (p = 0.030). There were no differences between direct age group comparisons (p = 0.303), sex (p = 0.389), or number of consultations/patient (p = 0.235). Patients with AD are prevalent in all age groups in Finnish primary care. Patient numbers were also relatively high in groups other than childhood, indicating that age-related distribution in primary care may be shifting to older ages.
Background: Microbiome-targeted treatments have been investigated in atopic dermatitis (AD). We aimed to investigate the use of probiotic Lactococcus lactis lysate cream in AD. Methods: 13 patients with mild-to-moderate AD were treated with differently concentrated probiotic creams (3%, 10% and 30%) or placebo cream for 4 weeks. Disease severity (EASI, IGA), epidermal barrier function (TEWL) and patient-reported impact (DLQI, POEM, ADCT, pruritus and sleep disturbance VAS) were measured at baseline, 4 and 8 weeks. Comprehensive clinical data and laboratory values (blood eosinophil count, total serum IgE-levels and specific IgEs to aeroallergens) were obtained. Results: Comparison of the treatment groups showed no clear differences regarding AD severity (EASI, p=0.76, CI: 0.65-1.00), epidermal barrier dysfunction (TEWL, p=0.37, CI: 0.19-0.73) or patient-reported impact (DLQI, p=0.76, CI: 0.65-1.00; POEM, p=0.76, CI: 0.35-0.88; ADCT, p=0.72, CI: 0.65-1.00; pruritus VAS 0.67, CI: 0.55-1.00; sleep disturbance VAS, p=1.00, CI: 0.79-1.00) between different probiotic lysate concentrations and placebo. The probiotic lysate cream was well tolerated and there were no significant adverse effects. Limitations were a small and heterogenous patient groups and a relatively short follow-up with no evaluation of long-term effects. Conclusions: Topical probiotic L. lactis lysate cream showed no clear differences between the tratment groups in mild-to-moderate AD. Although topical probiotics have been reported effective in a limited number of studies, more placebo-controlled clinical studies are needed to explore their potential role in the treatment of AD.
Keratosis pilaris (KP) associates with epidermal barrier defects in atopic dermatitis (AD) but its role in disease severity and concomitant atopic diseases seems to vary between populations. We performed a cross‐sectional observational study with 502 randomly selected AD patients of a Finnish tertiary health care center. At a single clinical examination, disease severity (Rajka Langeland severity score and EASI), clinical signs and patient history were evaluated and total IgE levels and frequent filaggrin (FLG) loss‐of‐function mutations were investigated. There was no link with disease severity (p = 0.649, 95% CI 0.569–0.654), asthma (p = 0.230, 95% CI 0.206–0.281) or atopic sensitization (p = 0.351, 95% CI 0.309–0.392). Keratosis pilaris was significantly associated with palmar hyperlinearity (p < 0.000, 95% CI 0.000–0.006, OR 4.664, 95% CI 2.072–10.496) and the filaggrin loss‐of‐function mutation 2282del4 (p < 0.000, 95% CI 0.000–0.009, OR 4.917, 95%CI 1.961–12.330). The prevalence of KP in the cohort was generally low and KP seems to be infrequent in Finnish AD patients. This may be explained by the fact that the tested FLG loss‐of‐function mutations are rarer in the Finnish population compared for example, with central Europe or Asia. Mutations in other locations of the FLG gene or other genes of the epidermal barrier may play a more important role.
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