ACE基因插入/缺失多态性与银屑病关系的研究

目的探讨血管紧张素转换酶(ACE)基因插入/缺失多态性与中国人群银屑病之间的关系。方法应用聚合酶链反应(PCR)对泰安地区88例银屑病患者及95例正常对照者的ACE基因插入/缺失多态性进行检测和分析。结果银屑病患者与正常对照者的II,ID,DD基因型及等位基因分布频率均无显著性差异(P>0.05),进一步分析显示ACE插入/缺失基因多态性与银屑病患者的性别及有无明确的家族史均无关联。结论ACE基因插入/缺失多态性可能不是中国人群银屑病发病的遗传学危险因素。     

N-乙酰基转移酶1基因多态性与染发皮炎的关系

目的探讨N-乙酰基转移酶1(NAT1)基因多态性与中国人染发皮炎的关系。方法应用聚合酶链反应(PCR)及限制性片段长度多态性(RFLP)技术检测和分析天津地区60例染发皮炎患者及73例正常对照者的NAT1基因多态分型,比较NAT1各等位基因及基因型频率在染发皮炎患者组与对照组间分布差异。结果病例组NAT1*10等位基因频率为35.80%,明显低于对照组(χ2=3.954,P0.05)。NAT1基因型NAT1*4/*4,NAT1*4/*10,NAT1*10/*10,NAT1*3/*10,NAT1*3/*4在病例组的频率分别是36.70%,40.00%,15.00%,1.70%,6.70%,在对照组为26.00%,42.50%,24.70%,4.10%,2.70%,两组相比差异无统计学意义。病例组基因型中含有NAT1*10者的表型(快型)频率为56.70%,略低于对照组的71.20%(χ2=3.058,P=0.08)。结论 NAT1*10可能是中国人染发皮炎发病的遗传学保护因素之一。     

银屑病与血管紧张素转化酶及血管紧张素Ⅱ

血管紧张素转化酶与血管紧张素Ⅱ是血管紧张素系统的两种重要成份,它们在血清及皮肤组织中均可表达,在银屑病患者的血清和皮损组织中均有不同程度的表达。血管紧张素转化酶与血管紧张素Ⅱ通过不同机制参与银屑病的相关发病过程。     

寻常型银屑病皮损中血管紧张素Ⅱ及血管紧张素转化酶的检测

目的:检测寻常型银屑病皮损中血管紧张素Ⅱ(AngⅡ)及血管紧张素转化酶(ACE)的水平变化。方法:应用荧光定量聚合酶链反应(FQ-PCR)和免疫组化技术检测30例寻常型银屑病患者(进行期17例,静止期13例)皮损AngⅡ和ACE mRNA及蛋白质的表达。结果:银屑病患者皮损中AngⅡ和ACE mRNA及蛋白质的表达明显高于正常人对照组(P0.001),且进行期高于静止期(P0.001)。结论:AngⅡ和ACE在银屑病皮损中表达上调,推测可能与银屑病皮损中新血管的形成有关。     

白癜风患者焦虑状态与血清中血管紧张素Ⅱ水平的研究

目的 探讨白癜风患者焦虑情绪与血清中血管紧张素Ⅱ水平的关系。方法 选择60例进展期白癜风患者和健康体检者30例,采用焦虑自评量表 （SAS）对两组进行情绪评分,并比较分析两组之间及焦虑与无焦虑患者血清中血管紧张素Ⅱ水平。结果 白癜风患者组SAS评分（46.13 ± 11.72）明显高于正常对照组（36.73 ± 12.59）,t = 3.50,P ＜ 0.01。白癜风患者焦虑情绪发生率为48.3%。女性患者SAS评分和焦虑发生率比男性患者显著增高（t = 2.47,χ2 = 4.58,P值均 ＜ 0.05）。未婚白癜风患者SAS评分和焦虑发生率比已婚患者显著增高（t = 2.59,P ＜ 0.01;χ2 = 6.17,P ＜ 0.05）。暴露部位白癜风患者SAS评分和焦虑发生率比非暴露部位患者显著增高（t = 3.60,P ＜ 0.01;χ2 = 5.84,P ＜ 0.05）。白癜风患者中具有焦虑情绪者血清中血管紧张素Ⅱ水平为（63.83 ± 10.92） ng/L,明显高于无焦虑情绪者（40.74 ± 8.70） ng/L,t =9.09,P < 0.01。结论 白癜风患者存在明显的焦虑情绪,且患者血清中血管紧张素Ⅱ水平与白癜风发病及焦虑状态关系密切,可能影响白癜风的发生与发展。     

心力衰竭患者体重指数与apelin、血管紧张素Ⅱ的关系

目的探讨充血性心力衰竭（CHF）患者的体重指数（BMI）与血浆apelin、血管紧张素11（Ang11）等因素的关系。方法41例心力衰竭患者，男20例，女21例，平均年龄（66±12．3）岁，按BMl分为正常体重组16例、超重组13例、肥胖组12例，按照心功能分级分为心功能Ⅲ级22列，心功能Ⅳ级19例。用酶联免疫吸附法测定各组的血浆apelin、AngⅡ水平。结果肥胖组apelin水平为（0．48±0．15）ng／ml，明显高于正常体重组[（0．18±0．15）ng／m1]及超重组（[O．27±0．06）ng／m1]，而超重组又明显高于正常体重组（P〈0．01）。心功能Ⅳ级患者的apelin水平为（0．35±0．16）ng／ml，显著高于心功能Ⅲ级的患者[（0．26±0．13）ng／ml，P〈0．05]。心功能Ⅳ级患者的Ang11水平为（0．34±0．15）ng／ml，显著高于心功能Ⅲ级的患者[（0．23±0．09）ng／ml，P〈0．05]。心力衰竭患者的血浆apelin水平与BMI成正相关、而Angll水平与BMI无关；血浆apelin、Angll水平之间无相关关系。结论肥胖的心力衰竭患者的血浆apelin水平较高，可能是其生存率提高的因素之一；心力衰竭患者测定apelin、Angll可作为判断病情的一个指标。     

人类皮肤:血管紧张素Ⅱ的起源和靶器官

<正>近10年来,在血管紧张素研究领域已有了新的发现。以往研究已证明血管紧张素Ⅱ(AngⅡ)不仅在调节血压和体液中起作用,而且在细胞增生和分化中也起作用。在这些进展中有几方面主要的突破;一方面,血管紧张素受体已被证实存在于心血管或肾脏之外的组织中;另一方面,至少4个不同血管紧张素受体亚型与血管紧张素相互作用的研究,包括非心血管领域。     

血管紧张素受体Ⅰ在某些皮肤肿瘤中的免疫组化研究

血管紧张素受体Ⅰ(angitotension type-1,AT1)是肾素血管紧张素Ⅱ的特异性受体之一,它可介导肾素血管紧张素调节血压和水盐平衡。近年来报道AT1亦与细胞增殖关系密切。在本实验中,我们采用免疫组化方法研究了AT1在皮肤基底细胞上皮瘤(BCE),鳞状细胞癌(SCC),角化棘皮瘤(KA)中的表达情况,探讨其在表皮肿瘤发生中的作用。     

白藜芦醇对A375人黑素瘤细胞株血管紧张素Ⅱ及其受体表达的影响

目的 探讨白藜芦醇对人恶性黑素瘤细胞血管紧张素Ⅱ(AngⅡ)2L其特异性受体-血管紧张素Ⅱ受体1(AT1R)表达的影响.方法 放免法检测白藜芦醇对人恶黑细胞株A375细胞培养上清液中AngⅡ表达水平的影响,逆转录聚合酶链式反应(RT-PCR)及Western印迹法检测白藜芦醇对A375细胞AT1R表达的影响.结果 100μmol/L白藜芦醇作用24h后,人恶性黑素瘤细胞株A375细胞培养上清液中AngⅡ表达水平较对照组差异无统计学意义(P>0.05);100μmol/L白藜芦醇作用24h后,AT1R在A375细胞mRNA及蛋白水平的表达较对照组明显降低,差异有显著性(P<0.05).结论 白藜芦醇参与对恶性黑素瘤局部肾素-血管紧张素系统的调控.其调控机制不是通过其血管紧张素转换酶抑制剂(ACEI)效应,而是通过抑制AT1R的表达来实现的.     

Association of insertion/deletion polymorphism of the angiotensin-converting enzyme gene with psoriasis

BACKGROUND: Genetic factors are likely to be of fundamental importance in the pathogenesis of psoriasis. There are reports concerning the induction or/and exacerbation of psoriasis by angiotensin-converting enzyme (ACE) inhibitors, which have been attributed to the ACE inhibitor-induced augmentation of kinin levels in skin. However, to the best of our knowledge there has been no molecular genetic study investigating whether ACE insertion/deletion (I/D) polymorphism may contribute to the genetic background in psoriasis. OBJECTIVES: To assess the role of ACE I/D polymorphism in psoriasis. METHODS: A group of 86 patients with psoriasis and 154 control subjects were analysed for ACE I/D polymorphism by polymerase chain reaction. RESULTS: The distribution of ACE I/D polymorphism and allele frequencies in psoriatic patients was not significantly different from controls. Further analyses of psoriasis patients showed that ACE I/D polymorphism was not associated with age at onset of disease, clinical type of psoriasis or gender. However, the frequency of the I allele was significantly higher in patients with a positive family history of psoriasis than in those with no family history (sporadic psoriasis) (48% vs. 32%; P =0.03). In addition, the I allele was found significantly more frequently in type I psoriasis patients (onset < 40 years and positive family history) than in type II psoriasis patients (onset >/= 40 years, no family history) (48% vs. 27%; P = 0.04). CONCLUSIONS: Our results suggest that the presence of the I allele may confer susceptibility to development of psoriasis in individuals from psoriatic families.     

An insertion/deletion polymorphism in the gene encoding angiotensin converting enzyme is not associated with generalised vitiligo in an English population

Vitiligo is an acquired hypomelanotic skin disorder characterised by circumscribed depigmented macules resulting from the loss of functional melanocytes from the cutaneous epidermis and autoimmunity has been suggested to play a role in the pathogenesis of the disease. Recently, an insertion/deletion (I/D) polymorphism of a 287-base pair repetitive sequence in intron 16 of the angiotensin converting enzyme (ACE) gene has been associated with autoimmune disease and with the development of vitiligo. In this study, the distribution of ACE gene I/D genotypes was investigated in a population of 106 English patients with generalised (non-segmental) vitiligo and 174 ethnically matched healthy controls using a restriction fragment length polymorphism-polymerase chain reaction genotyping method. No significant difference in the frequencies of II, ID and DD genotypes was detected between vitiligo patients and control subjects (P=0.35). The same result was evident for the genotype distribution in vitiligo patients with an autoimmune disease and for those without when compared with controls (P=0.33 and P=0.53, respectively). In addition, the results indicated that the D allele was not significantly over-represented in the group of patients with vitiligo compared with controls (P=0.42) and that this was also the case for patients with and without associated autoimmunity (P=0.40 and P=0.62, respectively).     

染发皮炎的病因探讨及预防

本文报告了多见于中年女性的染发皮炎39例,用1%对苯二胺对其中的19例进行斑贴试验,阳性率为94.7%,证实染发皮炎的致敏原主要是对苯二胺,以染过的头发作斑贴试验均为阴性。本文对染发剂的种类、染发原理及染发皮炎的病因进行了讨论,并在此基础上提出了预防措施。     

The angiotensin-converting enzyme insertion/deletion and the endothelin -134 3A/4A gene polymorphisms in patients with chronic plaque psoriasis

BACKGROUND: Psoriasis is a common chronic inflammatory skin disease. Vasoactive peptides such as endothelin-1 (ET-1) and bradykinin have previously been implicated in the pathogenesis of chronic plaque psoriasis. The angiotensin-converting enzyme (ACE) gene carries a 287-base pair insertion/deletion (I/D) gene polymorphism, which is associated with plasma concentrations of bradykinin-degrading ACE. A functional polymorphism (EDN1 -134 3A/4A) in the gene encoding ET-1 has been shown to affect ET-1 expression. The purpose of the present study was thus to investigate a hypothesized association between these gene polymorphisms and the presence of chronic plaque psoriasis. METHODS: The present case-control study comprised 207 patients with chronic plaque psoriasis (136 with early onset and 71 with late onset disease) and 182 control subjects. Genotypes of EDN1 and ACE were determined by a 5' exonuclease assay (Taqman). RESULTS: The prevalence of the homozygous ACE II genotype was significantly higher in patients with early-onset psoriasis than among control subjects (30.9% vs 19.2%, P = 0.016), yielding an odds ratio of 1.88 [95% confidence interval (CI): 1.12-3.15] for early-onset disease. For late-onset psoriasis, presence of the ACE II genotype was associated with a non-significant odds ratio 1.54 (95% CI: 0.81-2.92). As for the EDN1 -134 3A/4A gene polymorphism, no significant differences in genotype distributions were found between patients with either early- or late-onset psoriasis and control subjects (EDN1 -134 4A/4A: 9.6% in early-onset and 5.6% late-onset psoriasis vs 7.7% in controls; P > 0.05). CONCLUSIONS: Our data suggest that homozygosity for the ACE I allele may affect susceptibility to early-onset psoriasis.     

Association between the insertion/deletion polymorphism of the angiotensin I-converting enzyme gene and risk for psoriasis in a Chinese population in Taiwan

BACKGROUND: Genetic factors play an important role in susceptibility for psoriasis. The angiotensin I-converting enzyme (ACE) is expressed by keratinocytes. Administration of ACE inhibitors may induce or exacerbate psoriasis in clinical practice. Thus, ACE gene variants may contribute to the genetic background of psoriasis. OBJECTIVES: To assess the role of the ACE insertion/deletion (I/D) polymorphism in psoriasis among ethnically Chinese Taiwanese subjects. METHODS: In total, 312 patients with psoriasis and 615 control subjects were analysed for the ACE I/D polymorphism by polymerase chain reaction. RESULTS: A marginally significant difference (P=0 x 035) was found in the distribution of ACE I/D genotype frequencies between patients with psoriasis and controls. The frequency of the II genotype in patients with psoriasis was significantly higher than that in the control group (55 x 1% vs. 46 x 7%, respectively, P=0 x 015). Although the I allele frequency in patients with psoriasis (72 x 4%) was higher than that in the control group (68 x 2%), the difference was not significantly different (P=0 x 062). After adjusting for age and gender, carriers of the II genotype were 1 x 45 (95% confidence interval 1 x 09-1 x 92) times more likely than noncarriers to have psoriasis (P=0 x 010). CONCLUSIONS: Our results suggest that the presence of the I allele may confer susceptibility to development of psoriasis among ethnically Chinese Taiwanese individuals.     

Association of insertion/deletion polymorphism of the angiotensin-converting enzyme gene with angio-oedema accompanying chronic urticaria but not chronic urticaria without angio-oedema or the autologous serum skin test response

Background Chronic urticaria is defined as the daily or almost daily occurrence of weals for more than 6 weeks. The underlying pathophysiology is reported to be mast cell activation, with release of mast cell mediators, predominantly histamine. Substance P is a neuropeptide and has the capacity to provoke histamine release from skin mast cells. Angiotensin‐converting enzyme (ACE), widely expressed in skin, is one of the major peptidase for the degradation of substance P. An insertion/deletion polymorphism (I/D) in the ACE gene has been reported to be related to the levels of enzyme. Objective An increase in substance P levels due to a polymorphism in ACE gene might be related to the pathology. Thus, we aimed to investigate whether there is an association between ACE I/D polymorphism and chronic ordinary urticaria. Methods Ninety‐five patients with chronic ordinary urticaria were recruited and divided into two groups according to autologous serum skin test status and accompanying angio‐oedema. One hundred and sixty‐one healthy subjects were enrolled as control group. All participants were genotyped for I/D polymorphism in intron 16 of the ACE gene by polymerase chain reaction. Results A statistically significant association was not found between ACE I/D polymorphism and chronic ordinary urticaria. Further analyses of chronic ordinary urticaria patients showed that ACE I/D polymorphism was not associated with autologous serum skin test status of patients. However, the frequencies of II genotype and I allele were statistically significantly higher in chronic ordinary urticaria patients with accompanying angio‐oedema with regard to angio‐oedema‐negative patients (II genotype: 24% vs. 9%, P = 0.0002; I allele: 58% vs. 27%, P = 0.0001) and control group (II genotype: 24% vs. 19%, P = 0.01; I allele: 58% vs. 41%, P = 0.03). Conclusion The results of this study suggest no evidence of an association between ACE I/D polymorphism and risk of developing chronic ordinary urticaria. However, it can be a contributing factor to susceptibility of angio‐oedema in chronic ordinary urticaria.