白癜风中西医治疗研究进展

白癜风是一种色素生成障碍性皮肤病,好发于暴露部位而影响美观,症状为皮肤出现局限性或泛发性色素脱失斑,皮损处黑素的生成减少或消失,亦称＂白驳风＂。全世界患病率为0.5%～4.0%,我国患病率0.1%～2.7%[1],且呈逐年上升的趋势。可发生于任何年龄,10～30岁为发病高峰,无性别差异[2]。其发病机制尚不明确,治疗仍较困难[3]。下面就其发病机制、治疗方法和治疗药物的研究现状综述如下,以期对临床治疗白癜风有所帮助。     

白癜风相关细胞因子的研究进展

白癜风的发病机制尚不十分清楚 ,主要有自身免疫学说、黑素细胞 (ＭＣ)自体破坏学说和神经发病学说 ,近年来研究多集中在自身免疫方面。细胞分子生物学的新进展揭示机体的免疫效应大部分通过细胞因子介导。皮肤作为一个器官 ,含有多种细胞 ,既可产生大量细胞因子 ,同时也在分化、增殖等方面受这些细胞因子的调节。细胞因子与疾病的关系受到重视 ,本文旨在综述相关细胞因子对白癜风影响的研究进展。一、细胞因子对ＭＣ分化、增殖及色素生成的影响Ｐｉｎｃｅｌｌｉ等[1] 报告 ,角质形成细胞 (ＫＣ)产生的神经生长因子(ＮＧＦ)在活体上对ＭＣ的…     

白癜风与遗传因素

白癜风是一种常见的色素脱失性皮肤病,几乎世界上所有的种族都可能发病,但发病率有所不同。一般肤色越深的人发病率越高,其中有色人种的发病率高于白色人种,黄种人的发病率介于黑种人和白种人之间。如美国发病率不足1.0%,印度为4.0%,我国人群中发病率约为0.17%～1.00%。白癜风的发病在性别间无明显差异,各年龄组均可发病,但青少年多发,约50%的患者其发病年龄在20岁以内。近年来发现白癜风发病率有增加趋势,这可能与环境的污染加重有关。白癜风的发病机制至今尚不十分清楚,但研究证明与遗传、自身免疫、精神创伤及日光中的紫外线等多种因素有…     

氧化应激与白癜风

白癜风病因复杂，尚未明确。目前学术界关于其发病机制的讨论大致有两派观点：一方认为白癜风是一种原发性的自身免疫性疾病，另一方认为它本质上是一个氧化应激相关的皮肤病。本综述旨在从氧化应激这一方面回顾、总结白癜风发病机制的最新研究及相关的治疗进展。     

骨免疫学研究进展

骨重塑主要通过成骨细胞和破骨细胞之间相互作用而进行,其中RANKL-RANK-OPG系统在骨吸收和骨形成的耦联中起着关键作用。巨噬细胞集落刺激因子与其受体结合对破骨细胞发展是必须的。近年发现,成骨细胞还可与破骨细胞直接通过ephrin-Eph途径双向促进骨形成。免疫细胞和骨细胞共同起源于骨髓,从起始、成熟到活化,存在着相互影响。免疫细胞和骨细胞间通过许多细胞因子及其受体相互作用,调节骨代谢平衡,存在共同的骨代谢转录因子和信号转导途径。脂肪因子作为骨骼、免疫、脂肪系统的共同交叉机制,通过影响免疫细胞、成骨细胞或破骨细胞,进一步影响骨重塑方向。越来越多研究证实,骨免疫参予许多骨科疾病的发生与发展,揭示免疫系统对骨代谢的重要调节作用,有助于有效地预防和治疗骨科相关疾病。     

骨免疫学研究进展

骨重塑主要通过成骨细胞和破骨细胞之间相互作用而进行,其中RANKL-RANK-OPG系统在骨吸收和骨形成的耦联中起着关键作用.巨噬细胞集落刺激因子与其受体结合对破骨细胞发展是必须的.近年发现,成骨细胞还可与破骨细胞直接通过ephrin-Eph途径双向促进骨形成.免疫细胞和骨细胞共同起源于骨髓,从起始、成熟到活化,存在着相互影响.免疫细胞和骨细胞间通过许多细胞因子及其受体相互作用,调节骨代谢平衡,存在共同的骨代谢转录因子和信号转导途径.脂肪因子作为骨骼、免疫、脂肪系统的共同交叉机制,通过影响免疫细胞、成骨细胞或破骨细胞,进一步影响骨重塑方向.越来越多研究证实,骨免疫参予许多骨科疾病的发生与发展,揭示免疫系统对骨代谢的重要调节作用,有助于有效地预防和治疗骨科相关疾病.     

白癜风与自身免疫研究进展

白癜风是一种常见的获得性的以局部或全身色素脱失为特征的皮肤病,人群中的患病率小于2%。通常青少年发病,10～30岁为发病高峰期,各种族均可发生,无明显性别差异。目前发病机制尚不明确,主要有遗传学说,自身免疫学说,氧化应激学说,神经精神学说和病毒学说等[1]。近年来,多数学者认为白癜风是一种多基因遗传的自身免疫性疾病,体液免疫和细胞免疫对黑素细胞的破坏在白癜风形成中起重要作用。现就白癜风与自身免疫相关的研究进展综述如下。     

白癜风的鉴别诊断

白癜风是一种原发性、局限性或泛发性皮肤色素脱失症。有关白癜风的发病机制尚不十分清楚,但一般认为,其发病是具有遗传素质的个体在多种内外因子的激发下表现为免疫功能、神经精神及内分泌、代谢功能等各方面的紊乱,导致酶系统的抑制或黑素细胞的破坏或使黑素体的生成或黑化过     

白斑美容霜治疗白癜风的临床观察

融治疗和美容为一体研制了白斑美容霜,用于治疗颜面手背部白癜风161例,取得了较好的疗效.用药时间(?)=46.55,SD=49.49(天),增加色素的有效率占75.2%。     

自体表皮移植联合308nm准分子激光治疗白癜风疗效观察

白癜风是一常见的色素脱失性皮肤病,以表皮和毛囊黑素细胞破坏为特征,临床易诊断,但治疗时间长,见效慢。2005年8月～2006年2月,我们采用自体表皮移植联合308nm准分子激光治疗白癜风取得满意疗效,现报道如下。     

Advances in transplantation immunology

Although there have been dramatic advances in clinical organ transplantation over the past 20 years, rejection, both acute and chronic, and the complications of immunosuppression remain major problems. Nevertheless as our understanding of the immune response to a vascularized organ allograft develops, so too will our ability to develop more specific immunosuppression. In any strategy for more specific immunosuppression compatibility for the major histocompatibility complex of antigens (HLA in man) is likely to be important. Monoclonal antibodies to T cell subpopulations, or even to T cells specifically activated by the graft, provide methods of suppressing the immune response at a more specific level. The recognition that stable grafts are maintained, at least in experimental rodent models, by T suppressor cells may allow development of precise methods of inducing the generation of such cells in clinical practice. The induction of tolerance in the adult animal can be achieved in a number of ways, the most promising of which for clinical application, is antigen pretreatment. If tolerance could be achieved in clinical practice within the not too distant future, then this would represent the attainment of the ultimate goal of transplantation. Members of the department who contributed to the work described in this lecture were M. Dallman, S. Fuggle, J. Madsen, G. Tellides, A. Ting and K. Wood This paper is based on a lecture given at the 87th Annual Congress of the Japanese Surgical Society, Tokyo, Japan, 1987.     

Advances in transplantation immunology

Although there have been dramatic advances in clinical organ transplantation over the past 20 years, rejection, both acute and chronic, and the complications of immunosuppression remain major problems. Nevertheless as our understanding of the immune response to a vascularized organ allograft develops, so too will our ability to develop more specific immunosuppression. In any strategy for more specific immunosuppression compatibility for the major histocompatibility complex of antigens (HLA in man) is likely to be important. Monoclonal antibodies to T cell subpopulations, or even to T cells specifically activated by the graft, provide methods of suppressing the immune response at a more specific level. The recognition that stable grafts are maintained, at least in experimental rodent models, by T suppressor cells may allow development of precise methods of inducing the generation of such cells in clinical practice. The induction of tolerance in the adult animal can be achieved in a number of ways, the most promising of which for clinical application, is antigen pretreatment. If tolerance could be achieved in clinical practice within the not too distant future, then this would represent the attainment of the ultimate goal of transplantation.     

Transplant immunology

The immune response to an allogeneic transplanted organ is T-cell dependent. It is governed partially by the context in which the T-cell encounters the antigen and can range from apoptosis, anergy, and neglect to full activation. The current armamentarium of immunosuppressive agents acts to inhibit the various steps of this T-cell activation pathway; at the level of the T-cell receptor (monoclonal antibodies such as OKT3), intracellular signally (calcineurine-inhibitors), DNA synthesis (azathioprine), or to cause lymphocyte depletion (ATG, ALG). Most protocols use a combination of agents for induction and maintenance immunosuppression. Although successful in preventing and treating allograft rejection, they are not without side effects. With improved patient and graft survival rates, adverse events such as hypertension, nephrotoxicity, hyperglycaemia, and lymphoproliferative disease become increasingly important issues. Newer drugs (IL-2 receptor antagonists, mycophenolate mofetil, rapamycin) have been introduced in an attempt to spare or avoid these adverse effects. Inducing graft tolerance and long-term drug-free survival is the goal of transplant immunologists. Postulated mechanisms include clonal deletion, anergy, and immunoredirection. Although a number of methods have been tested experimentally, none has been proven to induce tolerance for routine clinical use. Immunosuppression remains the cornerstone of the success of organ transplantation. Until investigators are able to induce tolerance in their transplant recipients or develop a tolerance assay, they would need to continue to tailor their immunosuppressive therapy according to the risk profile of the individual recipient.