黄褐斑发病机制研究进展

黄褐斑是临床常见的获得性色素增加性疾病,多对称发生于面部曝光部位,不仅影响外观,对工作生活也带来一定困扰。黄褐斑确切病因及发病机制尚不完全明确,这也是治疗疗效欠佳的原因之一。近年来,国内外对黄褐斑的发病机制研究不断深入,主要认为与基因遗传、紫外线照射、性激素水平变化、屏障功能破坏及局部炎症反应等有关。本文综述近几年关于黄褐斑发病机制的文章,以期促进对黄褐斑的认识及对临床治疗提供帮助。     

联合治疗黄褐斑的研究进展

黄褐斑是一种常见的皮肤色素代谢障碍性疾病,因病因及发病机制复杂,单药治疗疗效不佳或不良反应较大,而联合治疗因疗效佳、不良反应小受到医生的亲睐。目前黄褐斑的治疗多样,主要有口服、外用药物,激光或光子疗法,多种方案联合治疗等。黄褐斑的治疗需根据患者病因、病程、临床分型、既往治疗情况等制定个性化治疗方案。多重治疗、序贯治疗或补充治疗应纳入黄褐斑治疗中。     

黄褐斑病因及发病机制的研究进展

黄褐斑是一种常见的获得性色素障碍性疾病,多发生于育龄期女性,表现为面部对称性色素沉着斑。该病治疗效果欠佳,给患者造成较大的精神、心理压力,严重影响患者生活质量。其病因及发病机制尚未完全明确,与日光照射、激素水平变化、遗传易感性、血管因素、营养水平及精神心理因素有关。现就目前黄褐斑病因及发病机制的研究作一综述。     

中国黄褐斑诊疗专家共识（2021版）

【摘要】 目前认为黄褐斑的发病与遗传、日光、性激素等有关，涉及黑素合成增加、皮损处血管增生、炎症反应及皮肤屏障受损等机制。诊断主要依据临床表现和无创检测技术。该指南结合近年研究新进展，全面阐述了黄褐斑的病因及发病机制、临床表现、分期与分型、诊断及治疗等，旨在提高中国皮肤科医师对黄褐斑的诊治水平。     

强脉冲光治疗黄褐斑的研究现状

近年来强脉冲光(intense pulsed light, IPL)在临床上应用广泛,也在黄褐斑的治疗上取得了很大的进展。由于多种机制参与黄褐斑的发病,现阶段,临床上常根据不同的病因采用IPL综合治疗的方法,其疗效显著,安全性高,患者依从性好。因此本文回顾了IPL在黄褐斑治疗方面的应用及不良反应等研究进展。     

女性黄褐斑中医辨证分型与微量元素之间的关系

黄褐斑是一种获得性色素沉着皮肤病，临床发病病因较为复杂，为了探讨其发病机制，我们观察了女性黄褐斑患者的中医辨证分型与微量元素之间的关系，现报道如下。     

黄褐斑病因及发病机制研究现状

黄褐斑是临床上常见而难治的色素障碍性疾病,其发病原因及机理尚不明确。传统医学认为黄褐斑与肝、情志、脾、肾、血瘀等有关,现代医学认为黄褐斑与紫外线、内分泌因素、遗传因素等有关。现将传统医学及现代医学对黄褐斑的病因及发病机制的研究进展作一综述。     

黄褐斑的药物治疗进展

黄褐斑是临床常见的获得性色素沉着性疾病，病因不明，尚元特效疗法，目前以药物治疗为主，抑制黑素生成是主要的作用机制，包括抑制酪氨酸酶合成、抑制黑素小体转运、加速表皮更新等，其中以酪氨酸酶抑制剂使用最为广泛；植物萃取物在治疗黄褐斑方面仍缺乏足够证据。应用明确有效的治疗及安全合适的维持治疗方案是主要治疗原则。随着对黄褐斑发病机制的进一步研究及基因工程药物的出现可能为本病的治疗带来新思路。     

黄褐斑的分型研究进展

黄褐斑是临床常见的一种获得性色素增加性疾病,常对称发生于面部曝光部位,不仅影响患者的外观,而且给患者带来了诸多生活及精神方面的痛苦.黄褐斑的治疗疗效欠佳,其确切病因及发病机制尚不清楚,目前认为,主要与激素及日光照射有关.近年来,国内外对黄褐斑的分型存在很多争议,且临床上尚未形成统一的标准,通过对近几年发表的有关黄褐斑分型的文章加以分析、归纳,对其中存在的一些问题进行探讨,希望能够对黄褐斑的治疗提供帮助.     

黄褐斑发病机制研究进展

黄褐斑是一种好发于颜面等暴露部位的色素增加性皮肤病,不仅影响外观,对工作生活也带来一定困拢。黄褐斑确切发病机制尚不完全明确。近年研究结果表明,表皮屏障破坏、炎症反应、血管改变、光老化、细胞自噬、非紫外线光热源及氧化应激因素在黄褐斑发病过程中也有重要意义。本文综述回顾近几年关于黄褐斑发病机制的文献,以期对黄褐斑的认识及治疗提供帮助。     

紫外线与黄褐斑的相关性

黄褐斑的发病与加重和日光暴晒有关,并具有夏重冬轻的特点.近年来研究发现,紫外线的直接作用及间接分子调节能增加皮肤黑素的生成,并且紫外线还可以通过促进自南基的生成而间接产生色斑.多种线索表明,紫外线与黄褐斑的发病存在联系,一般可见光引起的慢性光接触过敏可能也与黄褐斑发病有关.     

Histochemical and immunohistochemical study in melasma: evidence of damage in the basal membrane

The pathogenesis of melasma has not been clearly elucidated. Using Fontana Masson; diastase-resistant periodic acid-Schiff stains; and immunohistochemistry to stem cell factor (SCF), its receptor c-kit, anti-mast cell tryptase, and anti-collagen type IV antibody, we evaluated melasma lesions and compared them with perilesional skin and photoprotected skin. Samples were taken from lesional and photoprotected nonlesional skin in 24 patients. In other 24 patients, we took biopsies of lesional and perilesional skin. With Fontana Masson, we observed many pigmented basal cells protruding into the dermis of the melasma skin. Periodic acid-Schiff stain and anti-collagen type IV showed damage on the basal membrane in 95.5% and 83%, respectively, in melasma lesion. The immunoreactivity of SCF and the prevalence of mast cells were increased in the dermis of melasma compared with perilesional dermis. The expression of c-kit was significantly increased at lesional epidermis; a frequent protrusion of c-kit-positive basal cells into the dermis was evident in 70% versus that in 29% of perilesional skin. The expression of c-kit was increased at lesional dermis of melasma compared with perilesional skin. We found a low correlation between c-kit expression and prevalence of mast cells; these were increased in melasma skin. The results may suggest a role of SCF, c-kit, and mast cells in the pathogenesis of melasma. We were surprised by the unexpected evidence of damage to basal membrane (BM), which could facilitate the fall or the migration of active melanocytes and melanin into the dermis allowing the constant hyperpigmentation in melasma.     

An updated review of melasma pathogenesis

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.     

黄褐斑病因及发病机制的研究进展

黄褐斑是一种以面部或浅或深的棕黑色斑片为特征的色素性疾病.近年来研究发现,黄褐斑的发病机制涉及多个方面,基底膜结构受损、血管功能亢进、氧化应激.蛋白基因水平方面发现,黄褐斑皮损中脂类代谢相关基因的表达下调,非编码RNA H19基因显著低表达.分子生物学研究发现,多个信号转导通路如WNT通路、一氧化氮合酶与核因子κB通路在黄褐斑发病中起关键作用.另外神经调节也涉及黄褐斑的病理生理过程.     

黄褐斑病因及发病机制研究进展

黄褐斑是常见的色素代谢异常性疾病,多发生于中青年女性,不但影响容貌,而且给患者带来了诸多生活及精神方面的痛苦。但黄褐斑发病机理复杂,真正发病原因目前尚不十分清楚。本文就黄褐斑近年来在病因及发病机理方面的研究进展作一综述。     

What Should Be Considered in Treatment of Melasma

Melasma is a common acquired hyperpigmentary skin disorder characterized by light to dark brown macules and patches occurring in the sun-exposed areas of the face. Melasma lesional skin is characterized by epidermal hyperpigmentation through increased melanogenesis in epidermal melanocytes. Some patients have dermal melanin but its amount is not significant and its distribution is very heterogeneous in the whole melasma lesional skin. Melasma is not homogeneous disease and there are personal characteristics of patients with melasma. The pathogenesis of melasma is not fully understood, but several hypotheses have been suggested. Increased vascularity in melasma lesions has suggested the role of increased number of enlarged vessels in the development of melasma. Endogeneous and exogeneous stimuli such as sex hormones and ultraviolet irradiation respectively may stimulate the microenvironment leading to the release of various mediators that cause activation of melanocytes and/or these stimuli may directly activate the melanocytes. Melasma patients may have specialized melanocytes with an intrinsic sensitivity to these stimuli.     

The vascular characteristics of melasma

BACKGROUND: The pathogenesis of melasma is not yet fully understood. Previous studies indicate that dermal environment such as fibroblasts may have an important role in the development of melasma. Recently, it has been suggested that interactions between the cutaneous vasculature and melanocytes might have an influence on the development of pigmentation. OBJECTIVES: We investigated the vascular characteristics in melasma lesions. The expression of vascular endothelial growth factor (VEGF), a major angiogenic factor of the skin, was also investigated in melasma. METHODS: Erythema intensity was quantified by the increase of the a* parameter using a colorimeter. Skin samples were obtained from lesional and non-lesional facial skin of 50 Korean women with melasma. Immunohistochemistry was performed to determine the expression of factor VIIIa-related antigen and VEGF in melasma. RESULTS: The values of a* was significantly higher in the melasma lesion than that of perilesional normal skin. Computer-assisted image analyses of factor VIIIa-related antigen-stained sections revealed a significant increase of both the number and the size of dermal blood vessels in the lesional skin. There was significant relationship between the number of vessels and pigmentation in melasma. The expression of VEGF was significantly increased in melasma CONCLUSIONS: These data suggest that increased vascularity is one of the major findings in melasma. VEGF may be a major angiogenic factor for altered vessels in melasma.