Kyu Joong Ahn

Summary: Impaired immunity and changes in the microenvironment in patients with diabetes might influence the composition of the cutaneous microbiome. However, data on the cutaneous microbiome of these patients are scarce. This study compared the fungal and bacterial components of the skin microbiome between patients with type 2 diabetes mellitus (DM) and healthy individuals. We obtained skin swab samples from the plantar forefoot of 17 patients with DM and 18 healthy individuals to conduct a cross‐sectional study. The samples were profiled with culture‐independent sequencing of the V3 to V4 regions of the bacterial 16S rRNA gene and the fungal ITS2 region, followed by direct DNA extraction and molecular polymerase chain reaction (PCR). We observed a differential cutaneous microbiome, especially for fungi, in patients with type 2 diabetes compared to that in healthy controls. Trichophyton rubrum was more abundant in DM samples. The Shannon diversity index for fungi was lower in the DM patients. Principal coordinate analysis plots and permutational multivariate analysis of variance (PERMANOVA) tests based on Bray‐Curtis distances between samples supported the association of the fungal microbiome with DM at the species level. The results suggest that clinicians should pay attention to both fungi and bacteria and provide appropriate prevention and therapeutic strategies for diabetic cutaneous complications including diabetic foot ulcers. These data also contribute to future research associated with diabetes and cutaneous microbiomes.

Although oral antihistamines (H1-histamine receptor antagonists) are the main treatment option for pruritus in general skin dermatosis, their effect in treating pruritus of atopic dermatitis (AD) has not yet been established. We conducted a systematic review and meta-analysis to evaluate the effectiveness of combined therapy of H1-antihistamines and topical steroids. We systematically searched MEDLINE, Embase, and CENTRAL databases for articles published from 1967 to 2015. We identified 1,206 studies and assessed their titles, abstract, and full-text. Random effects meta-analysis was used to calculate mean differences (MD) with 95% confidence intervals (CI). Two studies satisfying the inclusion criteria of antihistamine therapy with mandatory topical steroid use were selected. Comparing antihistamine monotherapy with combination therapy, patients treated with the addition of antihistamine to topical corticosteroids showed a statistically significant clinical improvement (standard MD, −0.24; 95% CI, −0.42 to −0.05; p=0.01). H1-antihistamines may have a synergistic effect when combined with topical steroids by influencing various associative factors of chronic pruritus in AD.

Total serum immunoglobulin E level and specific allergens in adults with skin diseases

Han SH, et al. Ann Dermatol. 2018 Jun;30(3):296-303. https://doi.org/10.5021/ad.2018.30.3.296

Hydrogen peroxide (H2O2) is a reactive oxygen species (ROS) that induces numerous cellular events, including cellular senescence and inflammatory responses. Therefore, the aim of this study was to investigate the protective effect of Rosmarinic acid (RA) in H2O2‑induced oxidative stress in normal human dermal fibroblasts (NHDFs). Cytotoxicity assays were performed using a water‑soluble tetrazolium salt, and senescence‑associated β‑galactosidase activity was determined to investigate the proportion of senescent cells. Antioxidant capacities were evaluated via H2O2‑scavenging activity, reverse transcription‑quantitative polymerase chain reaction, NRF2 luciferase reporter gene activity and intracellular ROS scavenging assays. Cytokine‑coded gene expression analysis and nuclear factor‑κB luciferase activity were determined to verify the anti‑inflammatory effect of RA. As a result, the present study demonstrated that rosmarinic acid inhibited H2O2‑induced oxidative stress and inflammatory responses in normal human dermal fibroblasts. Initially, the doses of RA that exerted minimal cytotoxic effects in NHDFs were determined using a cytotoxicity assay. Subsequently, pretreatment with the appropriate doses of RA significantly reversed the H2O2‑induced decrease in NHDF cell viability and decreased cellular senescence of NHDFs. In addition, RA inhibited H2O2‑induced ROS production in NHDFs, as determined by a ROS scavenging assay. The protective effects of RA were mediated by the inhibition of nuclear factor erythroid‑derived 2‑like 2, a transcription factor that functions as a key regulator of redox sensitivity. Furthermore, RA suppressed H2O2‑induced inflammation in NHDFs and significantly rescued H2O2‑induced downregulation of sirtuin 1. RA also inhibited nuclear factor (NF)‑κB transcriptional activity and the expression of NF‑κB target genes, including tumor necrosis factor‑α and interleukin‑6, in H2O2‑exposed NHDFs. Taken together, these data indicate that RA inhibits H2O2‑induced cellular damage in NHDFs.

Han SH, et al. Ann Dermatol. 2017 Apr;29(2):206-209. https://doi.org/10.5021/ad.2017.29.2.206

An S, et al. Ann Dermatol. 2017 Feb;29(1):6-12. https://doi.org/10.5021/ad.2017.29.1.6

Recent literature has highlighted the possible role of vitamin D in atopic dermatitis (AD), and that vitamin D supplementation might help to treat AD. This study determined the relationship between vitamin D level and AD, and assessed the efficacy of vitamin D supplementation. We searched the MEDLINE, EMBASE, and Cochrane databases up to May 2015. Observational studies and randomized controlled trials were included based on the available data on the serum 25-hydroxyvitamin D (25(OH)D) level and quantified data available for severity assessed using the Scoring Atopic Dermatitis (SCORAD) index or Eczema Area and Severity Index (EASI) score. Compared with healthy controls, the serum 25(OH)D level was lower in the AD patients of all ages (standardized mean difference = −2.03 ng/mL; 95% confidence interval (CI) = −2.52 to −0.78), and predominantly in the pediatric AD patients (standardized mean difference = −3.03 ng/mL; 95% CI = −4.76 to −1.29). In addition, the SCORAD index and EASI score decreased after vitamin D supplementation (standardized mean difference = −5.85; 95% CI = −7.66 to −4.05). This meta-analysis showed that serum vitamin D level was lower in the AD patients and vitamin D supplementation could be a new therapeutic option for AD.