The Beneficial Effect of Korean Red Ginseng Extract on Atopic Dermatitis Patients: An 8 Weeks Open, Noncomparative Clinical Study

BACKGROUND: Atopic dermatitis (AD) is a chronic or chronically relapsing, eczematous, severely pruritic inflammatory skin disorder. Korean red ginseng (KRG) has been shown previously to exhibit diverse biological effects including anti-inflammatory and antipruritic effects in a murine model. OBJECTIVE: We aimed to investigate the beneficial effects of KRG on AD patients, to determine whether there was improvement in disease severity, skin barrier function, pruritus and sleep disturbance relief. METHODS: An open, noncomparative clinical study that utilized KRG tablets (500 mg/tablet) was conducted. This study included 41 patients with mild to moderate AD diagnosed by the Korean atopic dermatitis guidelines. Three visits to the hospital at days 1, 28±7, and 56±7 for evaluation were made. The effects of KRG were assessed by measuring eczema area and severity index (EASI) score, transepidermal water loss (TEWL), the visual analogue scale (VAS), total amount of topical agents used in recent 8 weeks and investigator global assessment (IGA). RESULTS: Patients taking KRG tablets showed significant decreases in EASI score and TEWL, and the VAS of pruritus and sleep disturbance were significantly reduced. The amount of topical agents used was reduced but not by a statistically significant amount. IGA at the third visit showed improvement of AD compared to the second visit, but the difference was not statistically significant. CONCLUSION: KRG can be safely used as a health food to achieve clinical improvement of AD as well as improving overall quality of life, and has potential for further development.

An Overview of the Package Insert and Contraindications of Filler Products in Korea / 대한피부과학회지

Filler injection is an extremely popular cosmetic procedure in Korea, but surprisingly few dermatologists are aware of the package inserts in filler products. In the era of legal dispute, it is important that we fully understand the indications, contraindications, and side effects of the individual filler products. The purpose of this paper is to provide a general overview of the contents of package inserts of filler products that are commercially available in Korea, especially in terms of the contraindications of filler injection. The authors emphasize that greater improvement in the Korean package inserts of filler products can be expected. Currently, practicing physicians are usually blamed for filler complications. We also found many significant translational errors. We hope that dermatologists take more interest in filler package inserts by reading this overview.

Multiple Epidermal Cysts in a Hepatocellular Carcinoma Patient Taking Nexavar® / 대한피부과학회지

An epidermal cyst is a keratin-filled lesion lined by an epidermis and presents as a single or multiple intradermal or subcutaneous mass. Sorafenib (Nexavar®, BAY 43-9006) is a tumor angiogenesis inhibitor that is used for treatment of hepatocellular and renal cell carcinomas. Sorafenib can cause a variety of cutaneous toxicities-hand-foot skin reaction (HFSR) and non-hand-foot skin reaction (non-HFSR). Symptoms of HFSR include paresthesia, tingling, burning or painful sensations of both palms and soles, and a decreased tolerance to hot objects. Non-HFSR cutaneous toxicities include yellow discoloration of the skin, alopecia, stomatitis, subungual splinter hemorrhages, facial swelling, keratoacanthomas, leukocytoclastic vasculitis, genital lesions, facial erythema, nevi, lentigenes, epidermal inclusion cysts, xerosis, etc. To our knowledge, the occurrence of epidermal cysts after sorafenib intake is very rare and has not yet been reported in Korea. Herein, we report a rare case of a hepatocellular carcinoma patient with multiple epidermal cysts following sorafenib intake.

Infundibulocystic Squamous Cell Carcinoma

Infundibulocystic squamous cell carcinoma was first reported in 2008 as a subset of squamous cell carcinoma arising from the infundibulum of the hair follicle and exhibiting infundibular differentiation. It has well-differentiated, less-differentiated, and infiltrative forms. It was thoroughly analyzed in a series of cases in 2011 by Misago et al. and has been redefined to include only the infiltrative form owing to its unique clinical and histological characteristics. Here, we report an interesting case of infundibulocystic squamous cell carcinoma in a 72-year-old man presenting with a mass on the left helix of the ear.

NDRG2-mediated Modulation of SOCS3 and STAT3 Activity Inhibits IL-10 Production

BACKGROUND: N-myc downstream regulated gene 2 (NDRG2) is a member of the NDRG gene family. Our previous report indicated a possible role for NDRG2 in regulating the cytokine, interleukin-10 (IL-10), which is an important immunosuppressive cytokine. Several pathways, including p38-MAPK, NF-kappaB, and JAK/STAT, are used for IL-10 production, and the JAK/STAT pathway can be inhibited in a negative feedback loop by the inducible protein, SOCS3. In the present study, we investigated the effect of NDRG2 gene expression on IL-10 signaling pathway that is modulated via SOCS3 and STAT3. METHODS: We generated NDRG2-overexpressing U937 cell line (U937-NDRG2) and treated the cells with PMA to investigate the role of NDRG2 in IL-10 production. U937 cells were also transfected with SOCS3- or NDRG2-specific siRNAs to examine whether the knockdown of SOCS3 or NDRG2 influenced IL-10 expression. Lastly, STAT3 and SOCS3 induction was measured to identify the signaling pathway that was associated with IL-10 production. RESULTS: RT-PCR and ELISA assays showed that IL-10 was increased in U937-mock cells upon stimulation with PMA, but IL-10 was inhibited by overexpression NDRG2. After PMA treatment, STAT3 phosphorylation was decreased in a time-dependent manner in U937-mock cells, whereas it was maintained in U937-NDRG2 cells. SOCS3 was markedly reduced in U937-NDRG2 cells compared with U937-mock cells. IL-10 production after PMA stimulation was reduced in U937 cells when SOCS3 was inhibited, but this effect was less severe when NDRG2 was inhibited. CONCLUSION: NDRG2 expression modulates SOCS3 and STAT3 activity, eventually leading to the inhibition of IL-10 production.