BACKGROUND Complement overactivation is a major driver of lupus nephritis(LN).Impaired interactions of C-reactive protein(CRP)with complement factor H(CFH)have been shown as a pathogenic mechanism that contributes to ...BACKGROUND Complement overactivation is a major driver of lupus nephritis(LN).Impaired interactions of C-reactive protein(CRP)with complement factor H(CFH)have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN.However,genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.AIM To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.METHODS We genotyped six CRP single nucleotide polymorphisms(SNPs)(rs1205,rs3093062,rs2794521,rs1800947,rs3093077,and rs1130864)and three CFH SNPs(rs482934,rs1061170,and rs1061147)in 270 LN patients and 303 healthy subjects.RESULTS No linkage was found among CRP and CFH SNPs,indicating lack of genetic interactions between the two genes.Moreover,CRP and CFH SNPs,neither individually nor in combination,are associated with the risk or clinical manifestations of LN.Given the unambiguous pathogenic roles of the two genes.CONCLUSION These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.展开更多
AIM: Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world and complement factor H (CFH) polymorphism has been found to associate with the AMD. To investigate whether the Y402...AIM: Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world and complement factor H (CFH) polymorphism has been found to associate with the AMD. To investigate whether the Y402H variant in CFH is associated with AMD in Chinese populations, a systematic review and meta-analysis were performed to estimate the magnitude of the gene effect and the possible mode of action. METHODS: A meta-analysis was performed using data available from ten case-control studies assessing association between the CFH Y402H polymorphism and AMD in Chinese populations involving 1538 AMD. Data extraction and study quality assessment were performed in duplicate. Summary odds ratios (ORs) and 95% confidence intervals (CIs) an allele contrast and genotype contrast were estimated usingfixed- effects models. The Q-statistic test was used to assess heterogeneity, and Funnel plot was used to evaluate publication bias. RESULTS: Seven of ten case-control studies were neovascular AMD, and few studies came from west and north of China. There was strong evidence for association between CFH and AMD in Chinese population, with those having risk allele C 2.35 times more likely to have AMD than subjects with T allele. Evidence of publication bias was not observed in our meta-analysis. CONCLUSION: This meta-analysis summarizes the strong evidence for an association between CFH and AMD in Chinese and indicates each C allele increasing the odds of AMD by 2.33-fold. But more evidences about the relation between CFH polymorphism and different type of Chinese AMD from various district were needed.展开更多
Angiogenesis,the process of formation of new capillaries from existing blood vessels,is required for multiple physiological and pathological processes.Complement factorH(CFH)is a plasma protein that inhibits the alter...Angiogenesis,the process of formation of new capillaries from existing blood vessels,is required for multiple physiological and pathological processes.Complement factorH(CFH)is a plasma protein that inhibits the alternative pathway of the complement system.Loss of CFH enhances the alternative pathway and increases complement activation fragments with pro-angiogenic capacity,including complement 3a,complement 5a,and membrane attack complex.CFH protein contains binding sites for C-reactive protein,malondialdehyde,and endothelial heparan sulfates.Dysfunction of CFH prevents its interaction with these molecules and initiates pro-angiogenic events.Mutations in the CFH gene have been found in patients with age-related macular degeneration characterized by choroidal neovascularization.The Cfh-deficient mice show an increase in angiogenesis,which is decreased by administration of recombinant CFH protein.In this review,we summarize the molecular mechanisms of the anti-angiogenic effects of CFH and the regulatory mechanisms of CFH expression.The therapeutic potential of recombinant CFH protein in angiogenesisrelated diseases has also been discussed.展开更多
Age-related macular degeneration (AMD) is a leading cause of vision loss affecting tens of millions of elderly worldwide. Early AMD includes soft drusen and pigmentary changes in the retinal pigment epithelium (RPE). ...Age-related macular degeneration (AMD) is a leading cause of vision loss affecting tens of millions of elderly worldwide. Early AMD includes soft drusen and pigmentary changes in the retinal pigment epithelium (RPE). As people age, such soft confluent drusen can progress into two forms of advanced AMD, geographic atrophy (GA, or dry AMD) or choroidal neovascularization (CNV, or wet AMD) and result in the loss of central vision. The exact mechanism for developing early AMD and progressing to advanced stage of disease is still largely unknown. However, significant evidence exists demonstrating a complex interplay of genetic and environmental factors as the cause of AMD progression. Together, complement factor H (CFH) and HTRA1/ARMS polymorphisms contribute to more than 50% of the genetic risk for AMD. Environmentally, oxidative stress from activities such as smoking has also demonstrated a powerful contribution to AMD progression. To extend our previous finding that genetic polymorphisms in CFH results in OxPLs and the risk-form of CFH (CFH Y402H) has reduced affinity for oxidized phospholipids, and subsequent diminished capacity which subsequently diminishes the capability to attenuate the inflammatory effects of these molecules, we compared the binding properties of CFH and CFH related protein 1 (CFHR1), which is also associated with disease risk, to OxPLs and their effects on modulating inflammation and lipids uptake. As both CFH-402H and CFHR1 are associated with increased risk to AMD, we hypothesized that like CFH-402H, CFHR1 contribution to AMD risk may also be due to its diminished affinity for OxPLs. Interestingly, we found that association of CFHR1 with OxPLs was not statistically different than CFH. However, binding of CFHR1 did not elicit the same protective benefits as CFH in that both inflammation and lipid uptake are unaffected by CFHR1 association with OxPLs. These findings demonstrate a novel and interesting complexity to the potential interplay between the complement system and oxidative stress byproducts, such as OxPLs, in the mechanistic contribution to AMD. Future work will aim to identify the molecular distinctions between CFH and CFHR1 which confer protection by the former, but not latter molecules. Understanding the molecular domains necessary for protection could provide interventional insights in the generation of novel therapeutics for AMD and other diseases associated with oxidative stress.展开更多
Complement (C) activation-related hypersensitivity reactions (HSRs) represent an unsolved adverse immune effect of many i.v. administered “nanomedicines”, such as liposomal doxorubicin (Doxil/Caelyx). Because these ...Complement (C) activation-related hypersensitivity reactions (HSRs) represent an unsolved adverse immune effect of many i.v. administered “nanomedicines”, such as liposomal doxorubicin (Doxil/Caelyx). Because these pseudoallergic reactions can be severe or even lethal, it is an important clinical objective to find biomarkers for proneness for C activation by reactogenic nanoparticles that will allow the prediction of in vivo reactions by in vitro assays. With this goal in mind we identified a normal human blood donor who consistently showed high sensitivity to Caelyx-induced C activation in vitro, whose plasma (Caelyx sensitive plasma, CSP) was subjected to proteome profiling with a library of human plasma proteome specific mAbs. The chip (PlasmaScan-380TM) contained 380 non redundant (with respect to epitopes) mAbs. The analysis revealed 8 proteins that were differentially represented in CSP in comparison with Caelyx-insensitive control plasma. These proteins were identified by mass spectrometry and Western blot analyses to represent factor H (decreased in CSP), factor H related protein, serum amyloid P component, fibronectin, complement component C4, Apo B100, prothrombin and alpha-2-HS glycoprotein (all increased in CSP). Some of these protein changes are consistent with proneness for increased C activation, suggesting the potential use of this method in the search for biomarkers for liposome-induced or other types of nanomedicine-induced HSRs.展开更多
目的探讨血清半乳糖缺陷型IgA1(galactose-deficient IgA1,Gd-IgA1)、补体C4、补体因子H(complement factor H,CFH)和补体因子H相关蛋白(complement factor H related proteins,CFHRP)1、3、5在IgA肾病(IgA nephropathy,IgAN)中的诊断...目的探讨血清半乳糖缺陷型IgA1(galactose-deficient IgA1,Gd-IgA1)、补体C4、补体因子H(complement factor H,CFH)和补体因子H相关蛋白(complement factor H related proteins,CFHRP)1、3、5在IgA肾病(IgA nephropathy,IgAN)中的诊断价值。方法本研究为回顾性研究,收集2021年11月1日至2023年12月31日在雅安市人民医院行肾穿刺活检诊断为原发性IgAN的患者58例,同期其他肾小球疾病患者48例和健康志愿者20名作为对照,采用酶联免疫吸附分析法检测上述对象血清IgA、补体C4、Gd-IgA1、CFH、CFHRP1、3、5浓度并行组间比较,绘制受试者工作特征曲线评估血清Gd-IgA1、Gd-IgA1/CFH、CFHRP1/CFH、CFHRP5/CFH在IgAN中的诊断价值,筛选出受试者工作特征曲线的曲线下面积较大的指标Gd-IgA1、CFHRP1/CFH、CFHRP5/CFH,重点研究Gd-IgA1分别联合检测CFHRP1/CFH、CFHRP5/CFH对IgAN的诊断价值。结果原发性IgAN组患者血清IgA[1.568(1.344,1.705)g/L比1.177(0.618,1.893)g/L、0.538(0.433,0.732)g/L]、补体C4[0.547(0.494,0.643)g/L比0.396(0.312,0.515)g/L、0.289(0.186,0.356)g/L]、Gd-IgA1[0.003(0.002,0.004)g/L比0.002(0.001,0.003)g/L、0.0017(0.0010,0.0020)g/L]、CFHRP1[0.013(0.011,0.015)g/L比0.010(0.009,0.013)g/L、0.011(0.009,0.012)g/L]水平及Gd-IgA1/CFH[0.023(0.017,0.030)比0.012(0.009,0.021)mmol/L、0.005(0.004,0.007)mmol/L]、CFHRP1/CFH[0.115(0.091,0.161)比0.093(0.061,0.108)、0.038(0.028,0.043)]比值明显高于其他肾小球疾病组和健康组(P<0.05),血清CFH[0.000109(0.000089,0.000110)g/L比0.000285(0.000259,0.000347)g/L]浓度低于健康组(P<0.05);血清Gd-IgA1联合CFHRP1/CFH、CFHRP5/CFH诊断原发性IgAN的曲线下面积分别为0.946(95%CI:0.908~0.985)、0.926(95%CI:0.874~0.978),灵敏度分别为80%、90%,特异度分别为93.9%、86.3%。结论Gd-IgA1联合检测CFHRP1/CFH、CFHRP5/CFH对于诊断原发性IgAN具有较好价值,或可作为诊断IgAN的潜在无创性生物标志物。展开更多
AIM：To determine whether gene polymorphisms of the major genetic risk loci for age-related macular degeneration（AMD）：ARMS2（rs10490923）,the complement factor H（CFH）（rs1410996） and HTRA1（rs11200638） influenc...AIM：To determine whether gene polymorphisms of the major genetic risk loci for age-related macular degeneration（AMD）：ARMS2（rs10490923）,the complement factor H（CFH）（rs1410996） and HTRA1（rs11200638） influence the response to a treatment regimen with ranibizumab for exudative AMD.METHODS：This study included 100 patients（100 eyes）with exudative AMD.Patients underwent a treatment with ranibizumab injections monthly during three months.Reinjections were made when the best corrected visual acuity（BCVA） decrease five letters（ETDRS） or central subfield retinal thickness gained 100 pm in optical coherence tomography image.Genotypes（rs10490923,rs1410996 and rs11200638） were analyzed using TaqMan probes or polymerase chain reaction-restricted fragment length polymorphisms analysis.RESULTS：There were no statistically significant differences in allelic distribution of CFH（rs1410996）,ARMS2（rs10490923） and HTRA1（rs11200638）polymorphisms regarding to response to ranibizumab treatment.CONCLUSION：Ranibizumab treatment response is not related to CFH（rs1410996）,ARMS2（rs10490923） and HTRA1（rs11200638） poymorphisms.展开更多
目的研究血浆补体因子H(CFH)、超敏C反应蛋白(hsCRP)和胰岛素抵抗(IR)与冠心病(CAD)关系。方法采用JUdkins法行冠状动脉造影(CAG),排除冠心病(非冠心病组)204例,确诊冠心病155例。其中,冠脉病变血管1支组80例、2支组41例、3支组34例;按...目的研究血浆补体因子H(CFH)、超敏C反应蛋白(hsCRP)和胰岛素抵抗(IR)与冠心病(CAD)关系。方法采用JUdkins法行冠状动脉造影(CAG),排除冠心病(非冠心病组)204例,确诊冠心病155例。其中,冠脉病变血管1支组80例、2支组41例、3支组34例;按临床亚型可分稳定型心绞痛(SA)组62例、不稳定型心绞痛(UA)组69例和心肌梗死(MI)组24例。应用酶联免疫法测定血浆CFH浓度、Backman生化分析仪测定hsCRP、空腹血糖、胰岛素和血脂等指标。根据HOMA Model计算IR指数(IRI)。结果冠心病组IRI明显高于非冠心病组(3.89±1.89 vs 3.40±1.80)(P<0.05),MI组IRI(4.39±2.62)、UA组IRI(4.36±1.61)均明显高于SA组(3.19±1.14),(P<0.05);校正年龄、性别、吸烟史、高血压史和冠心病家族史后,hsCRP是冠心病的独立危险因素(OR:1.417,95%CI:1.236～1.625,P<0.05);IR与hsCRP的相关系数r为0.186,P<0.01。血浆CFH浓度在组间无差别。三个指标在不同病变血管支数组中没有差别。结论hsCRP为冠心病的独立危险因子,IR可以预测冠心病,CFH与冠心病无关。展开更多
文摘BACKGROUND Complement overactivation is a major driver of lupus nephritis(LN).Impaired interactions of C-reactive protein(CRP)with complement factor H(CFH)have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN.However,genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.AIM To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.METHODS We genotyped six CRP single nucleotide polymorphisms(SNPs)(rs1205,rs3093062,rs2794521,rs1800947,rs3093077,and rs1130864)and three CFH SNPs(rs482934,rs1061170,and rs1061147)in 270 LN patients and 303 healthy subjects.RESULTS No linkage was found among CRP and CFH SNPs,indicating lack of genetic interactions between the two genes.Moreover,CRP and CFH SNPs,neither individually nor in combination,are associated with the risk or clinical manifestations of LN.Given the unambiguous pathogenic roles of the two genes.CONCLUSION These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.
文摘AIM: Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world and complement factor H (CFH) polymorphism has been found to associate with the AMD. To investigate whether the Y402H variant in CFH is associated with AMD in Chinese populations, a systematic review and meta-analysis were performed to estimate the magnitude of the gene effect and the possible mode of action. METHODS: A meta-analysis was performed using data available from ten case-control studies assessing association between the CFH Y402H polymorphism and AMD in Chinese populations involving 1538 AMD. Data extraction and study quality assessment were performed in duplicate. Summary odds ratios (ORs) and 95% confidence intervals (CIs) an allele contrast and genotype contrast were estimated usingfixed- effects models. The Q-statistic test was used to assess heterogeneity, and Funnel plot was used to evaluate publication bias. RESULTS: Seven of ten case-control studies were neovascular AMD, and few studies came from west and north of China. There was strong evidence for association between CFH and AMD in Chinese population, with those having risk allele C 2.35 times more likely to have AMD than subjects with T allele. Evidence of publication bias was not observed in our meta-analysis. CONCLUSION: This meta-analysis summarizes the strong evidence for an association between CFH and AMD in Chinese and indicates each C allele increasing the odds of AMD by 2.33-fold. But more evidences about the relation between CFH polymorphism and different type of Chinese AMD from various district were needed.
基金supported by the National Nature Science Foundation of China (82171318,82241030,82011530024)the State Program of Scientific Research“Natural resources and the Environment” (3.01,2020–2021,Belarus)Academic Promotion Program of Shandong First Medical University (2019QL014)and Shandong Taishan Scholarship (J.L).
文摘Angiogenesis,the process of formation of new capillaries from existing blood vessels,is required for multiple physiological and pathological processes.Complement factorH(CFH)is a plasma protein that inhibits the alternative pathway of the complement system.Loss of CFH enhances the alternative pathway and increases complement activation fragments with pro-angiogenic capacity,including complement 3a,complement 5a,and membrane attack complex.CFH protein contains binding sites for C-reactive protein,malondialdehyde,and endothelial heparan sulfates.Dysfunction of CFH prevents its interaction with these molecules and initiates pro-angiogenic events.Mutations in the CFH gene have been found in patients with age-related macular degeneration characterized by choroidal neovascularization.The Cfh-deficient mice show an increase in angiogenesis,which is decreased by administration of recombinant CFH protein.In this review,we summarize the molecular mechanisms of the anti-angiogenic effects of CFH and the regulatory mechanisms of CFH expression.The therapeutic potential of recombinant CFH protein in angiogenesisrelated diseases has also been discussed.
文摘Age-related macular degeneration (AMD) is a leading cause of vision loss affecting tens of millions of elderly worldwide. Early AMD includes soft drusen and pigmentary changes in the retinal pigment epithelium (RPE). As people age, such soft confluent drusen can progress into two forms of advanced AMD, geographic atrophy (GA, or dry AMD) or choroidal neovascularization (CNV, or wet AMD) and result in the loss of central vision. The exact mechanism for developing early AMD and progressing to advanced stage of disease is still largely unknown. However, significant evidence exists demonstrating a complex interplay of genetic and environmental factors as the cause of AMD progression. Together, complement factor H (CFH) and HTRA1/ARMS polymorphisms contribute to more than 50% of the genetic risk for AMD. Environmentally, oxidative stress from activities such as smoking has also demonstrated a powerful contribution to AMD progression. To extend our previous finding that genetic polymorphisms in CFH results in OxPLs and the risk-form of CFH (CFH Y402H) has reduced affinity for oxidized phospholipids, and subsequent diminished capacity which subsequently diminishes the capability to attenuate the inflammatory effects of these molecules, we compared the binding properties of CFH and CFH related protein 1 (CFHR1), which is also associated with disease risk, to OxPLs and their effects on modulating inflammation and lipids uptake. As both CFH-402H and CFHR1 are associated with increased risk to AMD, we hypothesized that like CFH-402H, CFHR1 contribution to AMD risk may also be due to its diminished affinity for OxPLs. Interestingly, we found that association of CFHR1 with OxPLs was not statistically different than CFH. However, binding of CFHR1 did not elicit the same protective benefits as CFH in that both inflammation and lipid uptake are unaffected by CFHR1 association with OxPLs. These findings demonstrate a novel and interesting complexity to the potential interplay between the complement system and oxidative stress byproducts, such as OxPLs, in the mechanistic contribution to AMD. Future work will aim to identify the molecular distinctions between CFH and CFHR1 which confer protection by the former, but not latter molecules. Understanding the molecular domains necessary for protection could provide interventional insights in the generation of novel therapeutics for AMD and other diseases associated with oxidative stress.
文摘Complement (C) activation-related hypersensitivity reactions (HSRs) represent an unsolved adverse immune effect of many i.v. administered “nanomedicines”, such as liposomal doxorubicin (Doxil/Caelyx). Because these pseudoallergic reactions can be severe or even lethal, it is an important clinical objective to find biomarkers for proneness for C activation by reactogenic nanoparticles that will allow the prediction of in vivo reactions by in vitro assays. With this goal in mind we identified a normal human blood donor who consistently showed high sensitivity to Caelyx-induced C activation in vitro, whose plasma (Caelyx sensitive plasma, CSP) was subjected to proteome profiling with a library of human plasma proteome specific mAbs. The chip (PlasmaScan-380TM) contained 380 non redundant (with respect to epitopes) mAbs. The analysis revealed 8 proteins that were differentially represented in CSP in comparison with Caelyx-insensitive control plasma. These proteins were identified by mass spectrometry and Western blot analyses to represent factor H (decreased in CSP), factor H related protein, serum amyloid P component, fibronectin, complement component C4, Apo B100, prothrombin and alpha-2-HS glycoprotein (all increased in CSP). Some of these protein changes are consistent with proneness for increased C activation, suggesting the potential use of this method in the search for biomarkers for liposome-induced or other types of nanomedicine-induced HSRs.
文摘目的探讨血清半乳糖缺陷型IgA1(galactose-deficient IgA1,Gd-IgA1)、补体C4、补体因子H(complement factor H,CFH)和补体因子H相关蛋白(complement factor H related proteins,CFHRP)1、3、5在IgA肾病(IgA nephropathy,IgAN)中的诊断价值。方法本研究为回顾性研究,收集2021年11月1日至2023年12月31日在雅安市人民医院行肾穿刺活检诊断为原发性IgAN的患者58例,同期其他肾小球疾病患者48例和健康志愿者20名作为对照,采用酶联免疫吸附分析法检测上述对象血清IgA、补体C4、Gd-IgA1、CFH、CFHRP1、3、5浓度并行组间比较,绘制受试者工作特征曲线评估血清Gd-IgA1、Gd-IgA1/CFH、CFHRP1/CFH、CFHRP5/CFH在IgAN中的诊断价值,筛选出受试者工作特征曲线的曲线下面积较大的指标Gd-IgA1、CFHRP1/CFH、CFHRP5/CFH,重点研究Gd-IgA1分别联合检测CFHRP1/CFH、CFHRP5/CFH对IgAN的诊断价值。结果原发性IgAN组患者血清IgA[1.568(1.344,1.705)g/L比1.177(0.618,1.893)g/L、0.538(0.433,0.732)g/L]、补体C4[0.547(0.494,0.643)g/L比0.396(0.312,0.515)g/L、0.289(0.186,0.356)g/L]、Gd-IgA1[0.003(0.002,0.004)g/L比0.002(0.001,0.003)g/L、0.0017(0.0010,0.0020)g/L]、CFHRP1[0.013(0.011,0.015)g/L比0.010(0.009,0.013)g/L、0.011(0.009,0.012)g/L]水平及Gd-IgA1/CFH[0.023(0.017,0.030)比0.012(0.009,0.021)mmol/L、0.005(0.004,0.007)mmol/L]、CFHRP1/CFH[0.115(0.091,0.161)比0.093(0.061,0.108)、0.038(0.028,0.043)]比值明显高于其他肾小球疾病组和健康组(P<0.05),血清CFH[0.000109(0.000089,0.000110)g/L比0.000285(0.000259,0.000347)g/L]浓度低于健康组(P<0.05);血清Gd-IgA1联合CFHRP1/CFH、CFHRP5/CFH诊断原发性IgAN的曲线下面积分别为0.946(95%CI:0.908~0.985)、0.926(95%CI:0.874~0.978),灵敏度分别为80%、90%,特异度分别为93.9%、86.3%。结论Gd-IgA1联合检测CFHRP1/CFH、CFHRP5/CFH对于诊断原发性IgAN具有较好价值,或可作为诊断IgAN的潜在无创性生物标志物。
基金Supported by a Grant from Gerencia Regional de Salud de Castillay Leon GRS 957/A/14
文摘AIM：To determine whether gene polymorphisms of the major genetic risk loci for age-related macular degeneration（AMD）：ARMS2（rs10490923）,the complement factor H（CFH）（rs1410996） and HTRA1（rs11200638） influence the response to a treatment regimen with ranibizumab for exudative AMD.METHODS：This study included 100 patients（100 eyes）with exudative AMD.Patients underwent a treatment with ranibizumab injections monthly during three months.Reinjections were made when the best corrected visual acuity（BCVA） decrease five letters（ETDRS） or central subfield retinal thickness gained 100 pm in optical coherence tomography image.Genotypes（rs10490923,rs1410996 and rs11200638） were analyzed using TaqMan probes or polymerase chain reaction-restricted fragment length polymorphisms analysis.RESULTS：There were no statistically significant differences in allelic distribution of CFH（rs1410996）,ARMS2（rs10490923） and HTRA1（rs11200638）polymorphisms regarding to response to ranibizumab treatment.CONCLUSION：Ranibizumab treatment response is not related to CFH（rs1410996）,ARMS2（rs10490923） and HTRA1（rs11200638） poymorphisms.
文摘目的研究血浆补体因子H(CFH)、超敏C反应蛋白(hsCRP)和胰岛素抵抗(IR)与冠心病(CAD)关系。方法采用JUdkins法行冠状动脉造影(CAG),排除冠心病(非冠心病组)204例,确诊冠心病155例。其中,冠脉病变血管1支组80例、2支组41例、3支组34例;按临床亚型可分稳定型心绞痛(SA)组62例、不稳定型心绞痛(UA)组69例和心肌梗死(MI)组24例。应用酶联免疫法测定血浆CFH浓度、Backman生化分析仪测定hsCRP、空腹血糖、胰岛素和血脂等指标。根据HOMA Model计算IR指数(IRI)。结果冠心病组IRI明显高于非冠心病组(3.89±1.89 vs 3.40±1.80)(P<0.05),MI组IRI(4.39±2.62)、UA组IRI(4.36±1.61)均明显高于SA组(3.19±1.14),(P<0.05);校正年龄、性别、吸烟史、高血压史和冠心病家族史后,hsCRP是冠心病的独立危险因素(OR:1.417,95%CI:1.236～1.625,P<0.05);IR与hsCRP的相关系数r为0.186,P<0.01。血浆CFH浓度在组间无差别。三个指标在不同病变血管支数组中没有差别。结论hsCRP为冠心病的独立危险因子,IR可以预测冠心病,CFH与冠心病无关。
