Melasma is triggered by various factors including ultraviolet radiation and estrogen; however, its pathogenesis is unclear. To investigate the inflammatory features of melasma lesions as triggers for this disorder, 197 women with melasma who attended Asan Medical Center and Kangskin Clinic, Seoul, from June 2011 to October 2011 completed a questionnaire concerning triggering or aggravating factors. These cases were divided into "non-inflammatory" and "inflammatory" groups. Skin biopsies and immunostaining for CD68, CD117, and leukocyte common antigen (LCA) were performed in the lesional and peri-lesional skin of ten cases in the non-inflammatory group and nine cases in the inflammatory group. Among the 197 subjects (mean age, 41.5 years; mean age of melasma onset, 33.8 years), 50 patients (25.4%) were categorized into the inflammatory group. This group comprised cases that had inflammatory symptoms and events that triggered the melasma lesions. The lesional dermis contained more CD68(+) melanophages, CD117(+) mast cells, and LCA(+) leukocytes in the inflammatory group than in the non-inflammatory group. Inflammatory clinical features and an increased number of inflammatory cells in the lesion may be involved in the development of melasma in Asian skin.

Background: There has been a paucity of data about the difference in gene expression between melasma lesional skin and normal adjacent one. Objective: Our aim was to identify novel genes involved in the pathogenesis of melasma. Methods: We performed a microarray analysis and confirmed the results on quantitative real-time polymerase chain reaction (qRT-PCR) in Korean women with melasma. Results: There were 334 genes whose degree of expression showed a significant difference between melasma lesional skin and normal adjacent one. Of these, five were confirmed on qRT-PCR. In melasma lesional skin, there were down-regulation of genes involved in the PPAR signaling pathway and up-regulation of genes involved in neuronal component and the functions of stratum corneum barrier. Conclusion: This result suggests that the pathogenesis of melasma might be associated with novel genes involved in the above signaling pathway in Korean women.

An association between alopecia areata (AA) and other autoimmune diseases has been reported. We investigated the associations between AA and overt autoimmune thyroid diseases. A nationwide, population-based, cross-sectional study was performed using the Korea National Health Insurance claims database. We defined patients with AA as those whose records showed at least four physician contacts in which AA, alopecia totalis (AT) or alopecia universalis (AU) was the principal diagnosis. We also established an age- and sex-matched control group without AA. In a subgroup analysis, patients with AT or AU were classified into the severe AA group, and the remainder were classified into the mild to moderate AA group. Patients with AA were at an increased risk of Graves' disease (odds ratio [OR], 1.415; 95% confidence interval [CI], 1.317-1.520) and Hashimoto thyroiditis (OR, 1.157; 95% CI, 1.081-1.237), and the associations were stronger in the severe AA group (Graves' disease: OR, 1.714; 95% CI, 1.387-2.118; Hashimoto thyroiditis: OR, 1.398; 95% CI, 1.137-1.719). In conclusion, AA was significantly associated with overt autoimmune thyroid diseases. Furthermore, the risk was much higher in the severe AA group.