老年急性心肌梗死患者B型利钠肽和超敏C反应蛋白检测分析

Objective To explore the clinical significance of determination of the serum levels of brain (B-type) natriuretic peptide (BNP) and high-sensitivity C-reactive protein (hs-CRP) in patients with acute myocardial infarction (AMI).Methods The clinical data of 60 cases with AMI and 50healthy controls were analyzed retrospectively.The BNP and hs-CRP levels were analyzed in AMI and Killip class,and their relationship with prognosis was investigated.Results The serum levels of BNP,hs-CRP and creatine kinase (CK)-MB) were higher in AMI group than in control group (all P＜0.05),and the levels were lowered after treatment (P＜0.05).The correlation analysis indicated that BNP and hs-CRP had positive correlations with CK-MB (r=0.892 and 0.683,all P＜0.05),and increased along with the severity of Killip classification.The 8 cases (13.3 % ) died,and single factor analysis revealed that BNP (≥56.1 pmol/L),hs-CRP (≥9.0 mg/L),CK-MB (≥75.1 U/L) and Killip classification (grade Ⅲ and Ⅳ) were the poor prognostic factors (P＜0.05).Conclusions The elevation of BNP and hs-CRP level is correlated with the severity of AMI,and could be used to evaluate the AMI patients' diagnosis and prognosis.     

老年急性心肌梗死患者B型利钠肽和超敏C反应蛋白检测分析

Objective To explore the clinical significance of determination of the serum levels of brain (B-type) natriuretic peptide (BNP) and high-sensitivity C-reactive protein (hs-CRP) in patients with acute myocardial infarction (AMI).Methods The clinical data of 60 cases with AMI and 50healthy controls were analyzed retrospectively.The BNP and hs-CRP levels were analyzed in AMI and Killip class,and their relationship with prognosis was investigated.Results The serum levels of BNP,hs-CRP and creatine kinase (CK)-MB) were higher in AMI group than in control group (all P＜0.05),and the levels were lowered after treatment (P＜0.05).The correlation analysis indicated that BNP and hs-CRP had positive correlations with CK-MB (r=0.892 and 0.683,all P＜0.05),and increased along with the severity of Killip classification.The 8 cases (13.3 % ) died,and single factor analysis revealed that BNP (≥56.1 pmol/L),hs-CRP (≥9.0 mg/L),CK-MB (≥75.1 U/L) and Killip classification (grade Ⅲ and Ⅳ) were the poor prognostic factors (P＜0.05).Conclusions The elevation of BNP and hs-CRP level is correlated with the severity of AMI,and could be used to evaluate the AMI patients' diagnosis and prognosis.     

慢性肾脏病患者游离脂肪酸与细胞因子及颈动脉病变的关系

Objective To investigate the serum level of free fatty acid (FFA) and explore its relationship with cytokines and atherosclerosis (AS) in chronic kidney disease (CKD).Methods The serum level of FFA was determined with enzymatic colorimetry.IL-1 β, IL-6 and TNFα were determined with ELISA.High-sensitivity C-reactive protein (hsCRP) was measured with immunoturbidimetry.Prevalence of atherosclerosis was detected with carotid ultrasonography.We evaluated the relationship between serum levels of FFA and IL-1β,IL-6, TNFα, hsCRP as well as the renal function in 130 adult patients with CKD, stratified according to the GFR ( based on the National Kidney Foundation/Kidney Dialysis Outcomes Quality Initiatives) and in 58 hemodialytic (HD) patients.The relationship between FFA level and cardiac geometry incidence in CKD patients was analyzed with logistic regression model.Results The serum level of FFA was significantly higher in CKD patients as compared with that in the healthy controls [(492.63 ± 143.59)vs (302.65 ± 142.18) μ mol/L, P ＜ 0.01], even in the early stage of CKD.The level of FFA increased with the progression of renal dysfunction.In the non-dialytic CKD group, the level of FFA was negatively related to GFR and positively related to the proteinuria (P ＜ 0.05), while in the HD group, it was positively correlated with dialysis duration ( P ＜ 0.05 ).The serum levels of FFA were higher in CKD patients with carotid artery atherosclerosis than those in patients without ( P ＜ 0.05 or ＜ 0.01 ).However, in both groups with impairment of renal function, the levels of FFA were positively correlated with hsCRP, IL-1 β, IL-6,TNFα and TG( all P ＜ 0.05 ).A positive correlation between the level of FFA and the clinical manifestations such as carotid intimal medial thickness (IMT) and AS was also found.A negative correlation was found between the level of FFA and the serum level of albumin and GFR( P ＜ 0.05).Conclusion Serum levels of FFA are significantly higher either in non-dialytic CKD or in HD patients and it is related with hsCRP, IL-1 β, IL-6, TNFα as well as carotid artery atherosclerosis, indicating that FFA is an independent risk factor of AS in CKD.     

慢性肾脏病患者游离脂肪酸与细胞因子及颈动脉病变的关系

Objective To investigate the serum level of free fatty acid (FFA) and explore its relationship with cytokines and atherosclerosis (AS) in chronic kidney disease (CKD).Methods The serum level of FFA was determined with enzymatic colorimetry.IL-1 β, IL-6 and TNFα were determined with ELISA.High-sensitivity C-reactive protein (hsCRP) was measured with immunoturbidimetry.Prevalence of atherosclerosis was detected with carotid ultrasonography.We evaluated the relationship between serum levels of FFA and IL-1β,IL-6, TNFα, hsCRP as well as the renal function in 130 adult patients with CKD, stratified according to the GFR ( based on the National Kidney Foundation/Kidney Dialysis Outcomes Quality Initiatives) and in 58 hemodialytic (HD) patients.The relationship between FFA level and cardiac geometry incidence in CKD patients was analyzed with logistic regression model.Results The serum level of FFA was significantly higher in CKD patients as compared with that in the healthy controls [(492.63 ± 143.59)vs (302.65 ± 142.18) μ mol/L, P ＜ 0.01], even in the early stage of CKD.The level of FFA increased with the progression of renal dysfunction.In the non-dialytic CKD group, the level of FFA was negatively related to GFR and positively related to the proteinuria (P ＜ 0.05), while in the HD group, it was positively correlated with dialysis duration ( P ＜ 0.05 ).The serum levels of FFA were higher in CKD patients with carotid artery atherosclerosis than those in patients without ( P ＜ 0.05 or ＜ 0.01 ).However, in both groups with impairment of renal function, the levels of FFA were positively correlated with hsCRP, IL-1 β, IL-6,TNFα and TG( all P ＜ 0.05 ).A positive correlation between the level of FFA and the clinical manifestations such as carotid intimal medial thickness (IMT) and AS was also found.A negative correlation was found between the level of FFA and the serum level of albumin and GFR( P ＜ 0.05).Conclusion Serum levels of FFA are significantly higher either in non-dialytic CKD or in HD patients and it is related with hsCRP, IL-1 β, IL-6, TNFα as well as carotid artery atherosclerosis, indicating that FFA is an independent risk factor of AS in CKD.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

阿托伐他汀改善对比剂对肾功能的短期影响

Objective To study the effects of atorvastatin on contrast induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20 mg/qn, n = 60) or no atorvastatin (n =60) treatment 2 to 3 days before coronary angiography. Urinary α1-MG, TRF and mALB were checked for evidence of tubular or glomendar damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated according to Cockcroft-Ganh and GFR(ml/min) = 74. 835/Cys C1.333formulas basing on serum creatinine or cystatin C concentration. Results (1) In control group, comparison with the value before coronary angiography,urinary α1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography (P ＜ 0.01). In comparison to the levels at day 1 after angiography, urinary α1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P ＜ 0.01), but α1-MG, cystatin C still exceeded the values before coronary angiography, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline(P ＞0.05), hsCRP LeveL at day 2 after angiography had no significant change compared to that at day 1 after angiography (P ＞ 0.05) too. (2) In comparison with the value before coronary angiography in atorvastatin-treated group, the levels of urinary α1-MG, TRF and mALB or serum cystatin C at day 1 and day 2 after angiography had no significant change compared to baseline(P ＞0.05). Serum hsCRP significantly increased at day 1 after angiography compared to baseline(P ＜ 0.01), but it had no significant change compared to day 2 after angiography (P ＞ 0.05). (3)To compare to the atorvastatin-treated group, the values of urinary α1-MG, TRF and mALB or Cys C and hsCRP significantly increased at day 1 after angiography in control group (P ＜ 0.01), the values of urinary α1 -MG, cystatin C and hsCRP still significantly increased at day 2 (P ＜ 0.01) too, but those of TRF and mALB had no significantly change at day 1 or day 2 after angiography between the two groups (P ＞ 0.05). There was no significant change in BUN, Cr, Ccr levels before and after angiography between the two groups. Conclusions Low dose contrast induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients.     

Lipoprotein levels are associated with incident hypertension in older adults

OBJECTIVES: To determine the relationship between baseline measures of serum lipoproteins and incident hypertension in older adults. DESIGN: Prospective cohort study. SETTING: Pittsburgh, Pennsylvania, site of Systolic Hypertension in the Elderly Program (SHEP). PARTICIPANTS: One hundred eighty-seven men and women (mean age 71.3), normotensive (systolic blood pressure (SBP) <160 mmHg, diastolic blood pressure (DBP) <90 mmHg) at baseline, were followed annually over 8 years as an ancillary study to the SHEP. MEASUREMENTS: Hypertension development, defined as initiation of antihypertensive therapy or SBP greater than 160 mmHg or DBP greater than 90 mmHg. Lipoprotein measures included total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), HDL(2)-C, HDL(3)-C, triglycerides, and apolipoproteins 1, 2, and B. RESULTS: Over 8 years, 44 participants developed hypertension, for a Kaplan-Meier cumulative incidence rate of 31% (95% confidence interval (CI)=23-39%). Cumulative incidence rates were highly associated with baseline SBP, ranging from 8% in those with baseline SBP less than 120 mmHg to 70% in those with SBP of 140 to 159 mmHg. Other univariate associations included higher DBP, pulse pressure (P <.01 for both), triglycerides (P=.03), apolipoprotein B (P=.03), and lower HDL-C (P=.04) and HDL(3)-C (P=.02). In multivariate Cox regression analysis, higher baseline SBP (relative risk (RR)=1.8 per 10 mmHg, 95% CI=1.5-2.3) and lower HDL(3)-C (RR=0.8 per 5 mg/dL, 95% CI=0.42-1.0) remained significant independent predictors of time to hypertension. CONCLUSION: Older adults with abnormal serum lipoproteins are at increased risk of developing hypertension. Clinical trials exploring the effects of the modification of lipoprotein levels on hypertension incidence rates are needed.     

Relationship between plasma lipids and all-cause mortality in nondemented elderly

OBJECTIVES: To investigate the relationship between plasma lipids and risk of death from all causes in nondemented elderly. DESIGN: Prospective cohort study. SETTING: Community-based sample of Medicare recipients, aged 65 years and older, residing in northern Manhattan. PARTICIPANTS: Two thousand two hundred seventy-seven nondemented elderly, aged 65 to 98; 672 (29.5%) white/non-Hispanic, 699 (30.7%) black/non-Hispanic, 876 (38.5%) Hispanic, and 30 (1.3%) other. MEASUREMENTS: Anthropometric measures: fasting plasma total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and non-HDL-C, body mass index, and apolipoprotein E (APOE) genotype. clinical measures: neuropsychological, neurological, medical, and functional assessments; medical history of diabetes mellitus, heart disease, hypertension, stroke, and treatment with lipid-lowering drugs. Vital status measure: National Death Index date of death. Survival methods were used to examine the relationship between plasma lipids and subsequent mortality in younger and older nondemented elderly, adjusting for potential confounders. RESULTS: Nondemented elderly with levels of total cholesterol, non-HDL-C, and LDL-C in the lowest quartile were approximately twice as likely to die as those in the highest quartile (rate ratio (RR)=1.8, 95% confidence interval (CI)=1.3-2.4). These results did not vary when analyses were adjusted for body mass index, APOE genotype, diabetes mellitus, heart disease, hypertension, stroke, diagnosis of cancer, current smoking status, or demographic variables. The association between lipid levels and risk of death was attenuated when subjects with less than 1 year of follow-up were excluded (RR=1.4, 95% CI=1.0-2.1). The relationship between total cholesterol, non-HDL-C, HDL-C, and triglycerides and risk of death did not differ for older (>or=75) and younger participants (>75), whereas the relationship between LDL-C and risk of death was stronger in younger than older participants (RR=2.4, 95% CI=1.2-4.9 vs RR=1.6, 95% CI=1.02-2.6, respectively). Overall, women had higher mean lipid levels than men and lower mortality risk, but the risk of death was comparable for men and women with comparable low lipid levels. CONCLUSION: Low cholesterol level is a robust predictor of mortality in the nondemented elderly and may be a surrogate of frailty or subclinical disease. More research is needed to understand these associations.     

中老年人群血脂水平对新发颈动脉斑块的预测作用

目的 了解2002年至2007年中老年人群颈动脉斑块的变化情况,评价基线血脂水平对新发颈动脉斑块的预测作用.方法 研究样本来自中美队列中的石景山人群和多省市队列中的北京大学社区人群.2002年9月对这两个人群进行基线颈动脉超声检查和心血管病危险因素调查,2007年9至10月复查颈动脉超声.以两次颈动脉检查数据完整的2000名中老年人为研究对象,对基线血脂水平与颈动脉斑块的关系进行分析.结果 (1)2002年至2007年,颈动脉斑块患病率男性从30.3%增加到62.2%,女性从21.5%增加到51.5%;新发斑块率男性为41.8%,女性为34.1%.(2)男女两性颈动脉新发斑块率随着基线总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、非高密度脂蛋白胆固醇(non-HDL-C)及总胆固醇与HDL-C比值(TC/HDL-C)水平的增高而增加,其变化趋势差异均有统计学意义(P＜0.05或P＜0.01).(3)交叉分析显示,LDL-C,HDL-C,甘油三酯对斑块发生率有协同作用.(4)多因素分析显示,高LDL-C、高non-HDL-C和高TC/HDL-C是男女两性新发颈动脉斑块的独立影响因素(男性OR值分别为1.44、1.45、1.59,女性OR值分别为1.47、1.35、1.64,均P＜0.05).结论 2002年至2007年,中老年人群颈动脉斑块患病率在快速增长.高LDL-C、nonHDL-C和TC/HDL-C水平是中老年人群新发颈动脉斑块的独立预测指标.     

2型糖尿病患者应用吡格列酮治疗前后血清C反应蛋白的改变

目的观察盐酸吡格列酮治疗2型糖尿病(T2DM)前后血清高敏C反应蛋白(hsCRP)的变化及其影响因素,探讨糖脂代谢与炎症因子的关系。方法采用随机、双盲、安慰剂平行对照方法将130例已合用磺脲类和双胍类药物的T2DM患者随机分至盐酸吡格列酮组及安慰剂组,进行为期12周的临床观察。结果基线hsCRP水平与糖化血红蛋白(HbA1c)、高密度脂蛋白胆固醇(HDLC)、低密度脂蛋白胆固醇(LDLC)、甘油三酯(TG)水平、体质指数、性别均相关。吡格列酮治疗后患者hsCRP水平明显下降(P=0.0030)。而安慰剂组无改变。餐后血糖变化(P<0.01)及空腹血糖水平的变化(P<0.01)与hsCRP变化最相关,其次为LDLC(P<0.01)、HbA1c(P=0.033)及HDLC(P=0.047)的改变。结论T2DM患者慢性高血糖状态与炎症关系密切。吡格列酮治疗在改善糖脂代谢的同时,还具有明显的抗炎作用,使hsCRP水平明显下降。     

The relationship between high-sensitivity C-reactive protein and ApoB, ApoB/ApoA1 ratio in general population of China

Inflammatory biomarker high-sensitivity C-reactive protein (hsCRP) is considered as a major predictor of cardiovascular events. Apolipoprotein B (ApoB) directly reflects the number of plasma atherogenic lipoproteins, and may play a major role in vascular inflammation. We aimed to assess whether an association between ApoB and hsCRP exists and, furthermore, to examine whether ApoB is more predictive of the inflammatory status than other cardiovascular risk factors. This was a cross-sectional study, with 511 apparently healthy adult subjects enrolled. Waist circumference (WC), body mass index (BMI), and blood pressure (BP) were measured. Plasma glucose levels, hsCRP, lipid profile, and insulin were collected after 10-14 h fasting. From the lowest to the highest quartile of hsCRP, the values for BMI, WC, BP, HOMA-IR, insulin, glucose level, triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), ApoB and the ApoB/apolipoprotein A1 (ApoA1) ratio were increased as the hsCRP level increased (P < 0.01), and high-density lipoprotein cholesterol (HDL-C) and ApoA1 levels declined as hsCRP level increased (P < 0.0001). Pearson's correlation analysis demonstrated that hsCRP correlated with all variables (P < 0.01), except for total cholesterol (TC) (P = 0.154) and LDL-C (P = 0.087). According to forward stepwise regression analysis with hsCRP as the dependent variable, WC was the only variable entered the regression model. ApoB level correlated with hsCRP level but was not the major determinant of hsCRP. WC was stronger than other cardiovascular risk factors in the associations with hsCRP. Abdominal obesity rather than atherogenic dyslipidemia was the primary cause of chronic inflammatory status.     

Increased high-density lipoprotein cholesterol is associated with a high prevalence of pre-hypertension and hypertension in community-dwelling persons

The aim of this article was that high-density lipoprotein cholesterol (HDL-C) reduces blood vessel injury through its antioxidant and anti-inflammatory functions. However, the effect of HDL-C on blood pressure may be controversial. Therefore, the aim of this study was to address whether HDL-C level is associated with blood pressure, and we examined cross-sectional data from community-dwelling persons. A total of 859 men [58?±?15 (mean?±?standard deviation); 20-89 (range) (years) and 1,169 women (61?±?13; 19-88?years)] participants not on medication for hypertension were recruited from a single community at the time of their annual health examination. We examined the relationship between cardiovascular risk factors and blood pressure status. Multiple linear regression analysis using systolic blood pressure (SBP) and diastolic blood pressure (DBP) as an objective variable showed that HDL-C was significantly and independently associated with both SBP (β?=?0.138), and DBP (β?=?0.144). Compared to normotensive participants with the lowest quartile of HDL-C, multivariate-adjusted odds ratio (OR) for pre-hypertension was 1.72 (1.22-2.45) for the second quartile, 1.51 (1.07-2.15) for the third quartile, and 1.52 (1.04-2.22) for the highest quartile. Moreover, compared with normotensive participants with the lowest quartile, the multivariate-adjusted ORs for hypertension were 2.37 (1.63-3.45), 2.24 (1.54-3.28), 3.15 (2.10-4.74), respectively. There were no interactions between the two groups stratified by gender, age, BMI, drinking status, TG, FPG, and medication. Therefore, we concluded that HDL-C levels were positively associated with blood pressure in Japanese dwelling-community persons.     

Possible risk factors of carotid artery atherosclerosis in the Japanese population: a primary prevention study in non-diabetic subjects

OBJECTIVE: Hyperinsulinemia has been associated with the risk of coronary heart disease, stroke, and renal disease in nondiabetic subjects. However, direct evidence that hyperinsulinemia per se is directly associated with atherosclerosis has been conflicting. The present study was designed to investigate the cross-sectional association of carotid artery atherosclerosis with insulin, independent of well-known cardiovascular risk factors, in nondiabetic subjects. METHODS AND SUBJECTS: Between 1996 and 1997, 1,335 subjects (620 men and 715 women) were recruited from one Japanese community, interviewed, and examined. Clinical measurements in the study included intimal-medial thickness (IMT) of the carotid artery, fasting plasma insulin, serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting plasma glucose (FPG), hemoglobin type HbA1c, systolic blood pressure (SBP), diastolic blood pressure (DBP), and body mass index (BMI). We divided the subjects of both genders into three subgroups according to age (40-49 years of age; 50-59; and 60-69). RESULTS: Using simple regression analysis, we found that IMT was significantly correlated with at least one of TC, LDL-C, HbA1c, SBP, DBP, and BMI in each subgroup. The results of multivariate analysis showed that IMT was independently correlated with TC, HDL-C, LDL-C, SBP and BMI in males and with TC, TG, HDL-C, LDL-C, HbA1c, SBP, DBP, and BMI in females. Insulin levels showed no correlation with IMT in either males or females. CONCLUSION: Fasting hyperinsulinemia does not appear to be correlated with carotid artery atherosclerosis based on the present cross-sectional results.     

Evaluation of metalloproteinase 2 and 9 levels and their inhibitors in diabetic and healthy subjects

OBJECTIVES: We hypothesized that molecules active in vascular remodeling (i.e. MMPs and their TIMPs) could be modified in diabetic patients, as indirect markers of the diabetes related generalized abnormality of vascular activity. To test this hypothesis, we measured the plasma levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 in type 2 diabetic patients and in healthy subjects. METHODS: We enrolled 181 diabetic patients and 165 controls. We measured body mass index (BMI), glycosylated hemoglobin (HbA(1c)), fasting plasma glucose (FPG), fasting plasma insulin (FPI), homeostasis model assessment index (HOMA index), systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), triglycerides (Tg), lipoprotein(a) [Lp(a)], plasminogen activator inhibitor-1 (PAI-1), homocysteine (Hct) fibrinogen (Fg), high sensitivity C-reactive protein (hs-CRP), and plasma levels of MMP-2, MMP-9, TIMP-1, and TIMP-2. RESULTS: A significant increase (P<0.0001) of BMI, HbA(1c), FPG, FPI, HOMA index, SBP, DBP, TC, LDL-C, Tg, Lp(a), PAI-1, Hct, Fg, and hs-CRP was present in the diabetic group, with a significant decrease (P<0.0001) of HDL-C levels compared to healthy subjects. MMP-2 and MMP-9 levels were significantly higher (P<0.0001) in diabetic patients. Significant TIMP-1, and TIMP-2 increase was also observed (P<0.0001) in the diabetic group. CONCLUSION: Plasma levels of MMP-2, MMP-9, TIMP-1, and TIMP-2 are increased in diabetic patients which may reflect abnormal extracellular matrix (ECM) metabolism.     

糖尿病合并脑梗死的临床分析

目的探讨糖尿病合并急性脑梗死患者的临床特征及对预后的影响。方法通过回顾性分析60例糖尿病合并脑梗死患者与60例非糖尿病脑梗死患者的血糖、TC、TG、HDL-C、LDL-C的变化，对两组脑梗死的部位、面积与血糖的关系及两组的并发症、疗效及预后进行比较。结果糖尿病合并脑梗死组血糖、TC、TG、LDL-C较非糖尿病脑梗死组显著增高（P〈0．05），而HDL—C显著降低（P〈0．05），两组的梗死灶部位差异无统计学意义，糖尿病脑梗死组神经功能缺损程度、并发症及病死率显著高于非糖尿病脑梗死组，而疗效及预后低于非糖尿病脑梗死组。结论糖尿病合并脑梗死患者常因存在糖代谢紊乱而合并有脂代谢异常。当发生脑梗死时，梗死面积增大、症状加重，糖代谢紊乱加剧，糖尿病合并脑梗死患者预后差。     

老年人代谢综合征与良性前列腺增生的关系

目的 回顾性分析老年代谢综合征(MS)与良性前列腺增生(BPH)的关系.方法 老年男性859名,其中单纯MS患者8例,单纯BPH患者619例,两种疾病并存者192例,未患病者40例.检测空腹血糖(FBG)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C),并计算体质指数(BMI)、前列腺体积及前列腺年增长率(PG),分析代谢性危险因素与BPH的相关性.结果 BPH患者MS组与非MS组相比收缩压、舒张压、体质量、BMI、TG及FBG偏高(t=6.15、5.99、13.12、15.56、10.63、9.94,均P＜0.01),HDL-C浓度偏低(t=-7.57,P＜0.01);随着MS组分个数的增加,前列腺体积增加(F=2.98,P=0.031);随着年龄、体质量、BMI、收缩压、PG的增加,前列腺体积增大(t值分别为-6.39、-2.39、-2.36、-2.13、-25.85,均P＜0.05);前列腺体积与年龄、收缩压、体质量、BMI、血压升高呈正相关(r值分别为0.229、0.079、0.090、0.089、0.088,均P＜0.05);非条件Logistic回归分析校正混杂因素后,年龄、体质量和收缩压＞130 mm Hg(1 m Hg=0.133 kPa)为前列腺增生的独立相关因素(OR值分别为1.07、1.03、1.34,均P＜0.05).结论 老年患者BPH与MS有关,MS可能参与老年人BPH的发生发展过程,但其机制尚有待进一步研究.

Abstract：

Objective To retrospectively analyze the relationship between benign prostatic hyperplasia (BPH) and metabolic syndrome (MS) in senior patients. Methods The 859 male senior patients including 619 cases with BPH and 8 cases with MS were enrolled in this study, and there were 192 cases with both diseases and 40 controls. The levels of fasting blood glucose (FBG), total cholesterol (TC), triacylglycerol (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were measured. The body mass index (BMI), prostate volume and annual prostate growth rate were determined or calculated. The correlations of BPH with other metabolic risk factors were analyzed. Results The levels of systolic blood pressure (SBP), diastolic blood pressure (DBP), body weight, BMI, TG and FPG were higher (t=6.15, 5.99, 13.12, 15.56, 10.63 and 9.94, all P＜0.01), while serum HDL-C level was lower (t=-7.57,P＜0.01) in BPH patients with MS than without MS. As the number of components of MS was increased, the prostate volume was increased (F=2.98, P=0.031). As the age, body weight, BMI, SBP and PG were increased, the prostate volume was increased (t=-6.39,-2.39,-2.36,-2.13,-25.85,all P＜0.05). Spearman analysis showed that prostate volume was positively correlated with age, SBP, body weight, BMI and hypertension (r=0.229, 0.079, 0.090, 0.089 and 0.088, all P＜0.05). And age, body weight and SBP were the independent risk factors for BPH (OR=1.07, 1.03 and 1.34, all P＜0.05). Conclusions The present study demonstrates a relationship between BPH and MS in senior patients. Future studies are needed to confirm our results and to explain underlying mechanisms.