Atopic dermatitis (AD) is a complex disease with multifactorial pathogenesis and variable clinical presentation. Up to one-fifth of patients with AD develop moderate to severe disease that is often refractory to classical therapies and can compromise quality of life. This review summarizes recent clinical evidence on biological agents and small-molecule immunotherapies for the treatment of AD.

Atopic dermatitis (AD) is a complex disease with multifactorial pathogenesis and variable clinical presentation. Up to one-fifth of patients with AD develop moderate to severe disease that is often refractory to classical therapies and can compromise quality of life. This review summarizes recent clinical evidence on biological agents and small-molecule immunotherapies for the treatment of AD.

Atopic dermatitis (AD) is a complex disease with multifactorial pathogenesis and variable clinical presentation. Up to one-fifth of patients with AD develop moderate to severe disease that is often refractory to classical therapies and can compromise quality of life. This review summarizes recent clinical evidence on biological agents and small-molecule immunotherapies for the treatment of AD.

Atopic dermatitis (AD) is a complex disease with multifactorial pathogenesis and variable clinical presentation. Up to one-fifth of patients with AD develop moderate to severe disease that is often refractory to classical therapies and can compromise quality of life. This review summarizes recent clinical evidence on biological agents and small-molecule immunotherapies for the treatment of AD.

Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disease driven by immune dysregulation and skin barrier dysfunction. Currently, we are experiencing a new era of understanding of the pathogenesis of AD and, as a consequence, a new era of innovation in therapeutics, including small molecules and biologic therapy. In contrast to biologics, small molecules are similar to conventional pharmacologic chemical agents used as drugs and are generally prepared by chemical synthesis. Unlike biologics, these drugs often are taken orally or formulated for topical use. The purpose of this review is to summarize the efficacy and safety of the current topical and systemic new therapies in AD by reviewing recently published papers on therapies currently in phase 2 or 3 clinical trials. In this review, it is important to note the characteristics of the study population, the primary endpoints, and whether or not there was concomitant topical therapy allowed. These study design elements may significantly alter the results of studies and should be taken into account. Targeted therapy help push AD treatment into a new era of personalized medicine.

Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disease driven by immune dysregulation and skin barrier dysfunction. We are currently experiencing a new era of understanding of the pathogenesis of AD and, as a consequence, a new era of innovation in therapeutics, including small molecules and biologic therapy. Recently, advances in translational research have challenged the traditional AD pathogenesis paradigm of AD being solely a Th2-dominant disease. Other immune pathways seem to play a role in the complex AD pathophysiology, although the clinical relevance of these additional immune pathway abnormalities is unclear. Type 1, type 22, and type 17 pathway activation (with related cytokines/chemokines) have been demonstrated in the skin and blood of AD patients. Type 2 (interleukin [IL]-4, IL-13), IL-31, and type 22 (IL-22) pathway cytokines are increased in AD acute lesions. IL-22 induces both an epidermal hyperplasia at the onset of acute AD and a marked increase in the terminal differentiation S100 genes.This understanding of pathogenesis corresponds to a historic increase in therapeutic development in AD. The extreme clinical heterogeneity and the chronic progression of AD establish the need for newer, safer, and more effective treatments, control the disease, and improve the quality of life of affected patients.

Cancer metastasis to the skin, especially epidermotropic metastasis, is uncommon. Sometimes it is difficult to find the primary lesion; immunohistochemical (IHC) staining of cutaneous metastasis is used to determine the origin, but diagnosis may occasionally prove difficult. A 77-year-old man visited our hospital with a 1-month diagnostic history of multiple nodules in the right axilla. The patient had undergone surgery for gastric adenocarcinoma (T3N3M0) 21 years ago, and was diagnosed with lung adenocarcinoma 1 year previously; however, no treatment was ongoing. Biopsy of the lesions revealed atypical cells surrounding the papillary projections of the epidermis and tumor nests of the upper dermis. IHC staining was positive for CK7 and CEA and negative for CK5/6, CK20, napsin A, TTF-1, GCDFP 15, and p63. The tissues revealed glandular structures and tested negative for p63 and CK5/6 on IHC staining. The patient was diagnosed with epidermotropic metastasis of lung adenocarcinoma.

Prurigo nodularis (PN) is a disease characterized by chronic itch and presence of firm nodules or papules on the skin. The underlying pathophysiology of PN is still under debate, but it has been reported to be due to synergistic neural- and immune-mediated mechanisms. In this review, the authors summarize the etiology, epidemiology, clinical characteristics, and diagnosis of PN and suggest management protocols for patients with PN despite the absence of local guidelines for PN in Korea. The prevalence of PN in Korea was reported as 0.036%, similar to that in other countries. The various etiologies of PN are known to be associated with neural sensitization and inflammation, and the related treatment targets being studied for PN include interleukin-4, 13, 31, and transient receptor potential vanilloid 1 (TRPV1). Understanding of predisposing factors or concomitant diseases is beneficial towards targeted management of patients with PN. In addition, it has been reported that PN is more frequently accompanied by metabolic diseases, or renal disorders compared to other inflammatory skin diseases characterized by itchiness such as atopic dermatitis or psoriasis. The clinical diagnosis of PN is generally based on three core symptoms; chronic pruritus over six weeks, firm lesions, and repeated scratching. To evaluate the severity of PN, the following objective and subjective assessments can be used: Investigator’s Global Assessment for PN or Peak Pruritus Numerical Rating Scale. We propose a localized work-up algorithm for PN. It is expected that the increased awareness of PN can facilitate its diagnosis, thereby reducing the disease burden of patients with PN.

omega6 and omega3 fatty acids are important cellular components and known to be involved in disease processes. However, few studies have focused on mucosa fatty acid in human gastric cancer. The purpose of this study was to investigate how fatty acid patterns of mucosa are altered in gastric cancer. Fatty acids were analyzed by gas chromatography and their relative compositions (%) were determined and evaluated both in mucosa total-fatty acids and in phospholipid-fatty acids in paired cancerous and non-cancerous gastric cancer tissues (n = 18). The level of arachidonic acid (20:4omega6, AA) appeared significantly higher both in phospholipid-fatty acids (p < 0.05) and in total-fatty acids (p < 0.001) in cancerous mucosa compared to non-cancerous mucosa. The omega6/omega3 fatty acid ratio of phospholipid-fatty acids was also significantly higher in cancerous mucosa. The higher level of AA in cancerous tissue can be partially explained by the higher ratio of 20:4omega 6/20:3omega6 (desaturation index) and the lower ratio of 22:4omega6/20:4 omega6 (elongation index). The change in the relative composition of arachidonic acid may influence the production of prostaglandins and related metabolites, which regulate cell differentiation and proliferation. The findings of this study with respect to fatty acid changes, especially in terms of arachidonic acid metabolism, may be of relevance in the understanding of the roles of specific fatty acids and possibly of eicosanoids in gastric cancer.
Adult ; Aged ; Arachidonic Acid/metabolism ; Fatty Acids/metabolism* ; Female ; Gastric Mucosa/metabolism* ; Human ; Male ; Middle Age ; Phospholipids/metabolism ; Stomach Neoplasms/metabolism*

BACKGROUND: Rapid and sensitive detection of transfusion adverse reaction is fundamental to reducing transfusion-related morbidity and mortality. The aim of this study was to develop an effective system for reporting of transfusion adverse reaction. METHODS: Inpatient lists with transfusion adverse reaction on a nurse electronic medical records (EMR) from December 4th, 2014 to May 21st, 2015 were automatically selected and displayed to the computer screen of the blood bank data management system. After review of clinical and laboratory data of suspected patients with transfusion reaction, frequency of transfusion adverse reaction according to blood components was calculated. RESULTS: The frequency of transfusion adverse reactions according to blood components was, in decreasing order, red blood cells (RBC) 0.91% (58/6,404), frozen fresh plasma (FFP) 0.20% (5/2,549), and platelets 0.10% (6/5,728). Of 47 allergic reactions, the relative ratio by blood components was RBC 76.6%, platelets 12.8%, and FFP 10.6%. All of 22 febrile nonhemolytic transfusion reactions were RBC related reactions. CONCLUSION: The online transfusion adverse reaction reporting system based on a nurse EMR is helpful in easy and accurate estimation of transfusion adverse reaction incidence.
Blood Banks ; Blood Group Incompatibility ; Electronic Health Records* ; Erythrocytes ; Humans ; Hypersensitivity ; Incidence ; Inpatients ; Mortality ; Plasma