Ai-Young Lee

Dongguk University, Sŏul, Seoul, South Korea

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Publications (50)159.99 Total impact

  • PLoS ONE 06/2015; 10(6):e0129273. DOI:10.1371/journal.pone.0129273 · 3.23 Impact Factor
  • Chang-Hyun Kim · Ji-Young Kim · Ai-Young Lee
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    ABSTRACT: Although cyclosporine A (CsA) is a potent immunomodulating agent and is commonly used as a systemic agent for the management of psoriasis patients, current clinical treatments are not always effective due to the clinical inefficacy of low-doses and numerous harmful effects of higher doses. Currently, the combined use of two other systemic drugs often has better therapeutic efficacy and is safer than low or high dose of a single drug. Glucosamine (Glu) also has immunomodulatory properties for autoimmune diseases. The aims of our study were to investigate the therapeutic efficacy of Glu in combination with low-dose CsA on imiquimod (IMQ)-induced psoriasis-like dermatitis in mice and to determine its immunomodulatory mechanism. We found that combined treatment with Glu (300mg/kg) and low-dose (10 or 20mg/kg) CsA strongly ameliorated the development of psoriasis-like skin lesions and reduced the levels of Th1 cytokine (TNF-α) and Th17 cytokines (IL-17, IL-22, and IL-23) in the serum and dorsal skin. Histological findings also showed that the thickening of epidermis, stratum corneum, and inflammatory cell infiltration. Particularly, these combined treatments increased the number of CD4(+)CD25(+) regulatory T (Treg) cells in splenic. These results suggest that use of a combination of each drug might be used as an efficacious and safe alternative therapeutic strategy, as well as may provide an immunomodulatory approach for T cell-mediated autoimmune diseases, including psoriasis. Copyright © 2015. Published by Elsevier B.V.
    European journal of pharmacology 03/2015; 756. DOI:10.1016/j.ejphar.2015.03.010 · 2.68 Impact Factor
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    ABSTRACT: Allergic contact dermatitis (ACD) is a cell-mediated immune response that involves skin sensitization in response to contact with various allergens. Angiogenesis and lymphangiogenesis both play roles in the allergic sensitization process. Epidermal keratinocytes can produce vascular endothelial growth factor (VEGF) in response to UV irradiation and during wound healing. However, the effect of haptenic chemical allergens on the VEGF production of human keratinocytes, which is the primary contact site of toxic allergens, has not been thoroughly researched. We systematically investigated whether immune-regulatory cytokines and chemical allergens would lead to the production of VEGF in normal human keratinocytes (NHKs) in culture. VEGF production significantly increased when NHKs were treated with IFNγ, IL-1α, IL-4, IL-6, IL-17A, IL-22 or TNFα. Among the human sensitizers listed in the OECD Test Guideline (TG) 429, we found that CMI/MI, DNCB, 4-phenylenediamine, cobalt chloride, 2-mercaptobenzothiazole, citral, HCA, cinnamic alcohol, imidazolidinyl urea and nickel chloride all significantly upregulated VEGF production in NHKs. In addition, common human haptenic allergens such as avobenzone, formaldehyde and urushiol, also induced the keratinocyte-derived VEGF production. VEGF upregulation by pro-inflammatory stimuli, IFNγ, DNCB or formaldehyde is preceded by the production of IL-8, an acute inflammatory phase cytokine. Lymphangiogenic VEGF-C gene transcription was significantly increased when NHKs were treated with formaldehyde, DNCB or urushiol, while transcription of VEGF-A and VEGF-B did not change. Therefore, the chemical allergen-induced VEGF upregulation is mainly due to the increase in lymphangiogenic VEGF-C transcription in NHKs. These results suggest that keratinocyte-derived VEGF may regulate the lymphangiogenic process during the skin sensitization process of ACD.
    Toxicology and Applied Pharmacology 01/2015; 283(2). DOI:10.1016/j.taap.2015.01.008 · 3.63 Impact Factor
  • Ai-Young Lee
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    ABSTRACT: Melasma is a pigmentation disorder characterized by common clinical findings. However, the pathogenic mechanisms involved are heterogeneous in different individuals and ethnic groups. We have reviewed the pathophysiological mechanisms involved in melasma. Although the pathogenesis has not entirely been elucidated thus far, new findings are being identified by research groups. Epidemiologic studies may provide clues on the involvement of genetic factor(s), UV irradiation, or hormones in melasma. Some of the mechanisms of altered skin pigmentation, such as UV-induced pigmentation, may also be applicable to the pathogenesis of melasma. In fact, an increase in similar keratinocyte-derived melanogenic factors and their receptors occur in both UV-induced melanogenesis and melasma. Increased expression of female sex hormone receptors and the identification of the PDZ domain containing 1 (PDZK1) signaling mechanism provide insights to further our understanding of melasma. In addition to keratinocyte-derived paracrine factors, the role of paracrine factors from dermal fibroblasts, such as stem cell factor (SCF) and Wnt inhibitory factor-1 (WIF-1), is elucidated in melasma. Furthermore, the involvement of ion exchangers and microRNAs (miRNAs), such as H19 miRNA (miR-675), are also suggested.
    Dermatologica Sinica 11/2014; 32(4). DOI:10.1016/j.dsi.2014.09.006 · 0.57 Impact Factor
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    ABSTRACT: Many tissues of the human body encounter hyperosmotic stress. The effect of extracellular osmotic changes on melanin production has not yet been elucidated. In this study, we determined that hyperosmotic stress induced by organic osmolytes results in reduced melanin production in human melanoma MNT-1 cells. Under hyperosmotic stress, few pigmented mature melanosomes were detected, but there was an increase in swollen vacuoles. These vacuoles were stained with an anti-M6PR antibody that recognizes late endosomal components and with anti-TA99 and anti-HMB45 antibodies, implying that melanosome formation was affected by hyperosmotic stress. Electron microscopic analysis revealed that the M6PR-positive swollen vacuoles were multi-layered and contained melanized granules, and they produced melanin when L-DOPA was applied, indicating that these vacuoles were still capable of producing melanin, but the inner conditions were not compatible with melanin production. The vacuolation phenomenon induced by hyperosmotic conditions disappeared with treatment with the PI3K activator 740 Y-P, indicating that the PI3K pathway is affected by hyperosmotic conditions and is responsible for the proper formation and maturation of melanosomes. The microarray analysis showed alterations of the vesicle organization and transport under hyperosmotic stress. Our findings suggest that melanogenesis could be regulated by physiological conditions, such as osmotic pressure.
    PLoS ONE 08/2014; 9(8):e105965. DOI:10.1371/journal.pone.0105965 · 3.23 Impact Factor
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    ABSTRACT: Background Hydroquinone (HQ) with or without retinoic acid (RA) is routinely used for the treatment of hyperpigmented conditions. Skin irritation is a major problem with popular depigmenting agents, resulting in postinflammatory hyperpigmentation. Objective To examine the molecular mechanism associated with skin irritation by RA or HQ. Methods A genome-wide transcriptional profiling analysis was performed using monolayer cultures of human keratinocytes treated with or without irritant doses of RA, HQ, or sodium lauryl sulfate (SLS), a representative irritant. Differentially expressed genes (DEGs) were mapped on human chromosomes using a Manhattan plot. For the validation of candidate DEGs, the chemicals with different concentrations of varying irritation intensities were applied in vitro and in vivo and analyzed using real time-PCR and Western blotting. Results DEGs mapped to the 1q21 locus, which is composed of a cluster of genes encoding the cornified envelope precursors, showed an inverse expression pattern in response to HQ and RA. Concentrations of RA and HQ that induced a broad range of irritant responses in cultured cells or mice skin also induced inverse effects on the expression of cornified envelope-associated proteins. Conclusions Genetic modulation on cornified envelope-associated proteins by RA-induced irritation, which may be involved in physiological skin barrier disturbance, could be inverse to that by HQ- or SLS-induced irritation.
    Journal of Dermatological Science 08/2014; 76(2). DOI:10.1016/j.jdermsci.2014.08.003 · 3.34 Impact Factor
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    ABSTRACT: Hyper-pigmentation causes skin darkness and medical disorders, such as post-inflammatory melanoderma and melasma. Therefore, the development of anti-melanogenic agents is important for treating these conditions and for cosmetic production. In our previous paper, we demonstrated that the anti-diabetic drug voglibose, a valiolamine derivative, is a potent anti-melanogenic agent. In addition, we proposed an alternative screening strategy to identify valiolamine derivatives with high skin permeability that act as anti-melanogenic agents when applied topically. In this study, we synthesized several valiolamine derivatives with enhanced lipophilicity and examined their inhibitory effects in a human skin model. N-(2-hydroxycyclohexyl)valiolamine (HV) possesses a stronger inhibitory effect on melanin production than voglibose in a human skin model, suggesting that HV is a more potent anti-melanogenic agent for the skin.
    International Journal of Molecular Sciences 07/2014; 15(7):12188-95. DOI:10.3390/ijms150712188 · 2.86 Impact Factor
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    ABSTRACT: Vitiligo is a pigmentary disorder induced by a loss of melanocytes. In addition to replacement of pure melanocytes, cocultures of melanocytes with keratinocytes have been used to improve the repigmentation outcome in vitiligo treatment. We previously identified by in vitro studies, that adipose-derived stem cells (ADSCs) could be a potential substitute for keratinocytes in cocultures with melanocytes. In this study, the efficacy of pigmentation including durability of grafted melanocytes and short-term safety was examined in the nude mouse and Sprague-Dawley rat after grafting of primary cultured human melanocytes, with or without different ratios of primary cultured human ADSCs. Simultaneous grafting of melanocytes and ADSCs, which were separately cultured and mixed on grafting at the ratios of 1:1, 1:2, or 1:3, showed better efficacy than that of pure melanocytes. Grafting of melanocytes cocultured with ADSCs resulted in a similar outcome as the grafting of cell mixtures. Skin pigmentation by melanocytes : ADSCs at the ratios of 1:1 and 1:2 was better than at 1:3. No significant difference was observed between the 1-week and 2-week durations in coculturing. Time-course microscopic examination showed that the grafted melanocytes remained a little longer than 6-week post-grafting. No inflammatory cell infiltration was observed in the grafted skin and no melanocytes were detectable in other organs. Collectively, grafting of melanocytes and ADSCs was equally safe and more effective than grafting of melanocytes alone. Despite the absence of significant differences in efficacy between the group of 1:1 and that of 1:2 ratio, 1:2 ratio for 1-week coculturing may be better for clinical use from the cost-benefit viewpoint.
    Biomolecules and Therapeutics 07/2014; 22(4):328-33. DOI:10.4062/biomolther.2014.065 · 0.84 Impact Factor
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    ABSTRACT: Cadherin 11 (CDH11) was identified as a target of miR-675 by using a luciferase reporter assay. CDH11 expression and miR-675 expression were inversely correlated. CDH11 expression was not detected in melanocytes, but CDH11 expression in fibroblasts and keratinocytes positively influenced melanogenesis via the canonical Wnt and AKT activation pathways in cocultured melanocytes. CDH11 in fibroblasts or keratinocytes induced N-cadherin and Twist1 expression, while decreasing E-cadherin expression. This suggests a role for CDH11 in epithelial-mesenchymal transition. CDH11 in fibroblasts also induced the migration of cocultured melanocytes. N-cadherin knockdown abolished the tyrosinase expression that was induced in CDH11-overexpressing fibroblasts. Collectively, our data indicate that CDH11 in fibroblasts and keratinocytes is a target of miR-675, and could be involved in melanogenesis through the induction of N-cadherin during epithelial-mesenchymal transition.Journal of Investigative Dermatology accepted article preview online, 18 June 2014; doi:10.1038/jid.2014.257.
    Journal of Investigative Dermatology 06/2014; 134(12). DOI:10.1038/jid.2014.257 · 6.37 Impact Factor
  • Kyung Ah Cheong · Minsoo Noh · Chang-Hyun Kim · Ai-Young Lee
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    ABSTRACT: Skin irritation is one of the most common adverse reactions in hydroquinone (HQ) and retinoic acid (RA). Although melanocytes have rarely been considered to be involved in skin irritation, RA and particularly HQ could induce melanocyte toxicity, resulting in depigmentation. We chose S100B as a candidate gene for melanocytotoxicity from a genome-wide transcriptional profiling analysis after applying irritant doses of HQ, RA, and sodium lauryl sulfate (SLS) to cultures of keratinocytes and/or melanocytes. In this study, the role of S100B on melanocyte viability and cytotoxicity was examined. S100B was detected in melanocytes, but not in keratinocytes or fibroblasts. Melanocytes after treatment with increasing concentrations of HQ, RA, SLS, and urushiol showed significant increases in intracellular and extracellular S100B expression with reduced viable cell number and increased release of lactate dehydrogenase. No RAGE expression and no significant function of CD166/ALCAM in melanocyte survival and cytotoxicity favored the role of intracellular S100B in chemically irritated melanocytes. S100B knockdown increased apoptosis through inhibition of PI3K/AKT, NF-κB, and ERK activation, suggesting the increased intracellular S100B expression by chemical irritation as a compensatory reaction to reduce cytotoxicity. The numerical decrease in S100B/c-kit-double positive melanocytes was also examined in human skin epidermis irritated by HQ or RA with stronger staining intensities of S100B. Collectively, the decrease in viable cell number by reduced intracellular S100B levels in vitro and by chemical irritation in vivo suggests that S100B could be a potential biomarker for melanocytes cytotoxicity. This article is protected by copyright. All rights reserved.
    Experimental Dermatology 01/2014; 23(3). DOI:10.1111/exd.12332 · 4.12 Impact Factor
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    ABSTRACT: H19 non-coding RNA downregulation stimulates melanogenesis in melasma patients. However, its mechanism is unclear. In this study, the potential role of a H19 microRNA, miR-675, in melanogenesis was examined. Real-time PCR using cultured normal human skin keratinocytes, melanocytes, and fibroblasts with or without H19 knockdown showed accompanying changes between expression levels of H19 and those of miR-675 in keratinocytes. MiR-675 was also detected in concentrated culture supernatants and showed expression levels parallel with those of cell lysates. In addition to RNase resistance, FACS analysis showed anti-CD63-positive exosomes in culture supernatants, suggesting miR-675 could be released extracellularly and delivered to neighboring cells without degradation. In western blot analysis, the miR-675 mimic reduced the expression of microphthalmia-associated transcription factor (MITF) and phosphorylation of cAMP-responsive element-binding protein, extracellular signal-regulated kinase and apoptosis signal-regulating kinase, whereas these expressions were increased by the miR-675 inhibitor. Although H19 was not a miR-675 target, luciferase reporter assay showed a direct binding of miR-675 to 3'-untranslated region of MITF. In addition, localized in vivo miR-675 overexpression in mouse using a cationic polymer transfection reagent showed reduced mRNA expression levels of MITF, tyrosinase, tyrosine-related protein-1 (Trp-1), and Trp-2. Collectively, the results suggest that miR-675 derived from keratinocytes could be involved in H19-stimulated melanogenesis using MITF as a target of miR-675.Journal of Investigative Dermatology advance online publication, 12 December 2013; doi:10.1038/jid.2013.478.
    Journal of Investigative Dermatology 11/2013; 134(4). DOI:10.1038/jid.2013.478 · 6.37 Impact Factor
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    ABSTRACT: There exists a treatment challenge with periungual warts. Topical immunotherapy with diphenylcyclopropenone (DPCP) has recently been reported to be an effective treatment for recalcitrant warts, including periungual types. We aimed to evaluate the effectiveness and preference of topical immunotherapy with DPCP in treating periungual warts. Twenty-seven patients with periungual warts who were treated with DPCP immunotherapy (2007 through 2010; Dongguk University Ilsan Hospital, Goyang, Korea) were retrospectively recruited. Other treatment modalities were also used in some patients. Lesions were grouped into the types according to the following locations: proximal nail fold, lateral nail fold and hyponychium. Total and group clearance rates as well as treatment periods according to location and disease duration were evaluated. A patient questionnaire was performed to assess the satisfaction for the treatments in those who received multiple therapies. Total success rates were 85% (by subjects) and 91% (by individual lesions). Success rate and treatment period for proximal nail fold type seemed more desirable than other locations. Success rate decreased and treatment period increased as disease duration increased. The questionnaire revealed a significantly higher satisfaction rate for DPCP immunotherapy than for cryotherapy and pulsed-dye laser. Topical immunotherapy with DPCP is an effective and preferred method in the treatment of periungual warts.
    Annals of Dermatology 11/2013; 25(4):434-9. DOI:10.5021/ad.2013.25.4.434 · 0.95 Impact Factor
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    ABSTRACT: A fixed drug eruption (FDE) is not difficult to diagnose, given its clinical characteristics. However, the causative agent can be difficult to identify, particularly when the patient denies ingestion of any drugs. To the best of our knowledge, we present herein the first reported case of an FDE caused by antibiotics taken in food; doxycycline and erythromycin contained in pork and fish. A 57-year-old female experienced repeated episodes of well-demarcated erythematous patches covering her entire body. She denied taking any medications, but she thought that the lesions appeared after consuming pork and/or fish. An oral provocation test showed positive results for doxycycline and erythromycin, commonly used antibiotics in live-stock farming and in the fishing industry. Because of the antibiotics' thermostability, cooking does not guarantee the elimination of residual drugs. From the patient's history, we concluded that doxycycline and erythromycin contained in the pork and fish that she ate were the cause of the FDE.
    Allergy, asthma & immunology research 09/2013; 5(5):337-9. DOI:10.4168/aair.2013.5.5.337 · 3.08 Impact Factor
  • Chang-Hyun Kim · Kyung Ah Cheong · Ai-Young Lee
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    ABSTRACT: Light emitting diode (LED) phototherapy is an effective alternative for the treatment of inflammatory skin disorders. Tacrolimus (FK-506) is a potent immunomodulating agent, which has been used to treat AD. Combination therapy is often used in the treatment of AD to improve therapeutic efficacy or to reduce the dose of each drug. To investigate the therapeutic efficacy of monotherapy with either 850nm LED phototherapy or low-dose FK-506, and combination therapy in dermatophagoides farina (Df)-induced AD-like skin lesions in NC/Nga mice. The Df-induced NC/Nga mice with a clinical score of 7 were used for treatment with LED (10 and 25J/cm(2)) alone, low-dose FK-506 (1mg/kg) or in combination. The synergistic effects of combined therapy were evaluated by dermatitis scores, skin histology, skin barrier function, and immunological parameters, such as IgE, NO, Th2-mediated cytokines and chemokines. Combination therapy with 850nm (25J/cm(2)) LED and low-dose FK-506 showed a significant reduction in the severity of skin lesions. Combined therapy decreased in the serum level of IgE, NO, and in the splenic level of Th2-mediated cytokines and chemokines. Combination therapy significantly also reduced the inflammatory cellular infiltrate into the skin lesions. Moreover, combination therapy led to recovery of skin barrier function in the skin lesions. The use of combination of LED phototherapy and low-dose immunosuppressant improved Df-induced AD-like skin lesions in an NC/Nga mouse model by dominantly reducing IgE, NO, suppressing Th2-mediated immune responses, and inhibiting inflammatory cells, as well as improving skin barrier function.
    Journal of dermatological science 06/2013; 72. DOI:10.1016/j.jdermsci.2013.06.002 · 3.34 Impact Factor
  • Yunseok Choi · Won-Suk Lim · Ai-Young Lee · Seung-Ho Lee
    Indian journal of dermatology, venereology and leprology 05/2013; 79(3):435-6. DOI:10.4103/0378-6323.110793 · 1.33 Impact Factor
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    Kyung Ah Cheong · Nan-Hyung Kim · Minsoo Noh · Ai-Young Lee
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    ABSTRACT: Genetic susceptibility is involved in the pathogenesis of vitiligo. Association studies with a whole genome-based approach instead of a single or a few candidate genes may be useful for discovering new susceptible genes. Although the etiology of non-segmental and segmental types is different, the association between gene polymorphisms and vitiligo has been reported, without defining types or in non-segmental type. Whole genome-based single nucleotide polymorphisms (SNPs) were examined in patients with non-segmental and segmental types of vitiligo using the Affymetrix GeneChip 500K mapping array, and 10 functional classes of significant SNPs were selected. Genotyping and data analysis of selected 10 SNPs was performed using real-time PCR. Genotype and allele frequencies were significantly different between both types of vitiligo and three of the target SNPs, DNAH5 (rs2277046), STRN3 (rs2273171), and KIAA1005 (rs3213758). A stronger association was suggested between the mutation in KIAA1005 (rs3213758) and the segmental type compared to the non-segmental type of vitiligo. DNAH5 (rs2277046), STRN3 (rs2273171), and KIAA1005 (rs3213758) may be new vitiligo-related SNPs in Korean patients, either non-segmental or segmental type.
    Journal of Korean medical science 05/2013; 28(5):775-9. DOI:10.3346/jkms.2013.28.5.775 · 1.25 Impact Factor
  • Ai-Young Lee · Minsoo Noh
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    ABSTRACT: Abnormal pigmentation, particularly hyperpigmentation, is major issue of concern for people with colored skin. Several hypopigmenting agents, which exert their action by inhibiting tyrosinase activity and/or transcription, have been used for treatment. However, results have been discouraging. To manage abnormal pigmentation properly, the mechanisms of melanogenesis should be understood. Endogenous and exogenous factors affect melanogenesis via intracellular machineries. cAMP and PKC are critical factors of important transduction pathways and cross-talk between them could amplify the melanogenic effect. Here, factors involved in melanogenesis regulation via cAMP and/or PKC pathways are reviewed with their action mechanisms.
    Archives of Pharmacal Research 04/2013; 36(7). DOI:10.1007/s12272-013-0130-6 · 1.75 Impact Factor
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    ABSTRACT: Glucosamine (GlcN), like N-acetylglucosamine (GlcNAc), is salvaged into the hexosamine pathway and is converted to UDP-GlcNAc. Golgi N-glycan branching enzymes produce N-glycans, using UDP-GlcNAc as a substrate, which attach to the T cell receptor (TCR) and cytotoxic T lymphocyte antigen-4 (CTLA-4). These findings suggest that GlcN exerts the immunoregulation through TCR signaling, which could be involved not only in cytokine production but also activated T cell apoptosis. In fact, a preliminary study showed that GlcN reduced the number of CD3+ T cells of NC/Nga mice with AD-like skin lesions. Therefore, whether apoptosis of T cells would be one of the potential molecular mechanisms of GlcN-induced immunosuppression was investigated. Cultured human primary along with Jurkat T cells and purified T cells from NC/Nga mice with or without Df-induced AD-like skin lesion were used for the study. GlcN treatment increased the number of T cells expressing β1,6GlcNAc-branched N-glycans, with reduced ZAP-70 phosphorylation and enhanced CTLA-4 expression. GlcN treatment reduced the number of activated T cells from both the human primary and Jurkat cells and the dermatitis-induced mice. The expression of FasL and activated caspases, particulary caspase-3, was increased, whereas the phosphorylation of PI3K, Akt and NF-κB was decreased by GlcN treatment. Therefore, in addition to down-regulating TCR signaling and promoting CTLA-4 expression, GlcN may also suppress T cell function by enhancing apoptosis of activated T cells, through both extrinsic and intrinsic apoptotic signaling pathways, which were regulated by the inhibition of PI3K/Akt and NF-κB phosphorylation. This article is protected by copyright. All rights reserved.
    Scandinavian Journal of Immunology 04/2013; 78(1). DOI:10.1111/sji.12056 · 1.88 Impact Factor
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    Hyok Bu Kwon · Yunseok Choi · Hwa Jung Kim · Ai-Young Lee
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    ABSTRACT: Topical all-trans-retinoic acid (tretinoin) prevents skin atrophy induced by long-term use of topical corticosteroids, without abrogating their anti-inflammatory effects. The goal of this study was to determine the efficacy of tretinoin plus topical corticosteroids (tretinoin plus) for repigmentation in patients with vitiligo. A placebo-controlled, paired-comparison, left-right study was conducted for a period of 6 months on tretinoin plus and the vehicle plus the same topical corticosteroid (vehicle plus) treatment in 50 patients diagnosed with generalized vitiligo. Clinical responses were assessed using the computerized analysis, and the results were compared with the visual analysis. The percentage agreement between the 2 analyses was 91.8%. Among 49 participants who successfully completed this study, 27 (55%) showed a better response to tretinoin plus than to vehicle plus. The improved response was noted at an early stage of treatment, during the first 3 months in 60% of patients. Combined therapy with tretinoin plus topical corticosteroids is safe and effective and provides another option for treatment of patients with vitiligo. J Drugs Dermatol. 2013;12(4):e63-e67.
    Journal of drugs in dermatology: JDD 04/2013; 12(4):E63-e67. · 1.32 Impact Factor
  • Joon-Ho Lee · Byung-Jin Ahn · Minsoo Noh · Ai-Young Lee
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    ABSTRACT: Background Melanocytes involved in vitiligo may have inherent aberrations that make them vulnerable to extracellular insult. Allergic contact dermatitis (ACD) has been implicated in the development and progression of vitiligo. This study was conducted to investigate the association between ACD and vitiligo. Methods A total of 125 patients with vitiligo, who showed lesions in particular locations, onset at an older age, and/or pre-existing inflammation or pruritus, were included. Patch tests were performed using a Korean standard series. In order to investigate the association between avoidance of allergen and clinical improvement, 43 vitiligo patients who showed positive reactions to the patch test completed a questionnaire administered by telephone and self-assessed the status of their condition using a 10-point scale. Results A total of 98 (78.4%) of 125 patients with vitiligo showed positive patch test reactions to at least one antigen. Although a limited number of contact allergens may have specific predilection sites, a significant association (P = 0.002, odds ratio 3.06) was found between lesions distributed on the scalp and/or hairline and a positive patch test reaction to paraphenylenediamine (PPD). A positive correlation (P = 0.03) was also detected between avoidance of allergen and improvement of vitiligo lesions. Conclusions Causative allergens of ACD may play a role in the development and/or aggravation of vitiligo.
    International journal of dermatology 03/2013; 53(2). DOI:10.1111/j.1365-4632.2012.05666.x · 1.23 Impact Factor