2型糖尿病患者GFR相关因素分析
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摘要
目的:2型糖尿病患者伴有肾小球滤过率、内生肌酐清除率、糖化血红蛋白、尿微量白蛋白、甘油三酯等的变化,现就2型糖尿病患者的肾小球滤过率、内生肌酐清除率、糖化血红蛋白、尿微量白蛋白等指标进行分析,并探讨测量肾小球滤过率和内生肌酐清除率对糖尿病肾病的临床指导意义。方法:对72例2型糖尿病住院患者测量收缩压(SBP)、舒张压(DBP)、肾小球滤过率(GFR)、内生肌酐清除率(Ccr)、总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、脂蛋白a、血清肌酐(Scr)、血清尿素氮(BUN)、空腹血糖(FPG)、糖化血红蛋白(HbA1c)、血尿酸(UA)、尿微量白蛋白(mA1b)等指标。根据GFR的大小分组进行各项指标的比较,并分析GFR与Ccr、DM病程的相关性;将HbA1c分组来评价各项指标;按mA1b分组比较各项指标;对合并高血压和未合并高血压的患者进行分组比较;根据患者的糖尿病病程将其分组来比较各项指标。采用t检验、方差分析和线性回归分析评价2型糖尿病患者GFR、Ccr、DM病程等指标的相关情况。结果:①DM病程、SBP、Scr、mA1b、UA、Ccr在不同GFR组之间具有统计学差异(p<0.05);(r =-0.416,回归系数为-0.416,P<0.0001),GFR与Ccr呈正相关(r =0.578,回归系数为0.464,P<0.001)。②除了空腹血糖在不同HbA1c组之间有统计学意义外(p<0.05),其它各项指标均显示无统计学意义。③SBP、GFR、Scr、Ccr在mA1b正常组和升高组之间具有统计学差异(p<0.05),在mA1b升高时,患者的SBP升高、GFR减少、Scr升高、Ccr减低。④合并高血压组的GFR低于未合并高血压组(p<0.05)。⑤在不同DM病程组,组间GFR、Scr、Ccr值具有统计学差异(P<0.05)。结论:2型糖尿病患者GFR变化与糖尿病病程的相关性大于Ccr与DM病程的相关性,且GFR与SBP、Scr、mA1b,UA、Ccr都密切相关。
Objective: Type 2 diabetes with glomerular filtration rate(GFR)、glycosylated hemoglobin(HbA1c)、urinary microalbumin(mA1b), triglyceride(TG) and other changes.The aim of this study was to discuss the relationship between them and to compare the clinical guiding significance of GFR and Ccr . Methods: From 2007 to 2008,72 diabetic patients were assayed renal glomerulus filtering coefficient(GFR)、endogenous creatinine clearance rate(Ccr)、glycosylated hemoglobin(HbA1c)、systolic blood pressure(SBP)、diastolic blood pressure(DBP)、total cholesterol(TC)、triglyceride(TG)、low density lipoprotein(LDL-C)、high density lipoprotein(HDL)、lipoprotein-a、blood serum creatinine(Scr)、fasting blood glucose(FPG)、blood uric acid(UA)、urinary microalbumin(mA1b) and so on. According to the detection results of GFR,the patients were divided into different groups to research clinical indicators,and analyze the dependability among GFR、Ccr and the course of diabetes. According to the results of HbA1c,the patients were divided into two groups.According to the results of mA1b, the patients were divided into the normal microalbuminuria group(mA1c<20mg/L)and the microalbuminuria group(20≤mA1c<200mg/L). According to the patients whether or not with the hypertention,we divided the patients into two groups. At last, we divided the patients by the course of diabetes.Then,we analyzed the association between different groups of other indicators. Result:①The course of disease、SBP、Scr、mA1c、Ccr、UA were significantly different in groups of GFR (P<0.05);The correlation analysis indicated that the course of diabetes was negatively correlatied with GFR(r=-0.416,coefficient b=-0.416,P<0.0001).And Ccr was positively correlatied with GFR(r=0.578, b=0.464,P<0.001).②FPG was significantly different in HbA1c groups (P<0.05).③In microalbuminuria group,SBP、Scr were higher and GFR、Ccr were lower than the normal group(P<0.05).④GFR in the group of T2DM combined with hypertention was significantly lower and SBP was significantly higher than the group without hypertention(P<0.05).⑤In different group of the course of disease, ANOVA indicated that GFR、Ccr and Scr had statistically significance (P<0.05).With the extension of duration of diabetes,GFR values and Ccr values gradually reduced and Scr values gradually increased. Conclusion: The dependability between GFR and diabetic duration was greater than the dependability between GFR and Ccr,and GFR、SBP、Scr、Ccr、UA、mA1c had a close correlation.
引文
[1] Drury PL, Watkins PJ. Diabeticrenal disease and its prevention [J]. Clin Endocrinol, 1993,38(5):445-50.
    [2]刘新明.糖尿病肾病的发病机制与治疗现状[J].肠外与场内营养,2003(3):170-173.
    [3] Vincent Rigalleau,Catherine Lasseur,Christelle Raffaitin,Carolineperlemoine,Nicole Barthe,Philippe Chauveau,Christian Combe,Henri Gin:Glucose control influences Glomerular Filtration Rate and Its Prediction in Diabetic Subject. [J]Diabetes Care29:1491-1495,2006.
    [4] Mogensen CE: Early glomerular hyperfiltration in insulin-dependent diabetics and late nephropathy. Scand J Clin Lab Invest 46:201–206, 1986
    [5] Silveiro SP, Friedman R, de Azevedo MJ,Canani LH, Gross JL: Five-year prospective study of glomerular filtration rate and albumin excretion rate in normofiltering and hyperfiltering normoalbuminuric NIDDM patients. [J] Diabetes Care 19:171–174, 1996
    [6] Vora JP, Dolben J, Williams JD, Peters JR,Owens DR: Impact of initial treatment on renal function in newly-diagnosed type 2(non-insulin-dependent) diabetes mellitus. [J]Diabetologia 36:734–740, 1993
    [7] Ahmad J, Singh M, Kumar S: Kidney functions in newly diagnosed type 2 diabetic patients: role of glycemic control. J Assoc Physicians India 50:882– 886, 2002
    [8] Remuzzi A, Viberti G, Ruggenenti P, Battaglia C, Pagni R, Remuzzi G: Glomerular response to hyperglycemia in human diabetic nephropathy. [J] Am J Physiol 259:F545–F552, 1990
    [9] Soper CP, Barron JL, Hyer SL: Long-term glycaemic control directly correlates with glomerular filtration rate in early type 1diabetes mellitus before the onset of microalbuminuria. [J]Diabet Med 15:1010–1014, 1998
    [10] Klahr S, Levey AS, Beck GJ, Caggiula AW,Hunsicker L, Kusek JW, Striker G: The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease: Modification of Diet in Renal Disease Study Group. [J]N Engl J Med 330:877–884, 1994
    [11] Romano Nosadini,Giancarlo Tonolo: Relationship between Blood Glucose Control, Pathogenesis and Progression of Diabetic Nephropathy. [J]J Am Soc Nephrol 15:S1–S5, 2004
    [12] Nosadini R, Velussi M, Brocco E, Bruseghin M, Abaterusso C,Saller A, Dalla Vestra M, Carraro A, Bortoloso E, Sambataro M,Barzon I, Frigato F, Muollo B, Chiesura-Corona M, Pacini G,Baggio B, Piarulli F, Sfriso A, Fioretto P: Course of renal function in type 2 diabetic patients with abnormalities of albumin excretion rate. [J]Diabetes 49: 476–484, 2000
    [13]贾晓炜,李德强,张雅萍,张南雁,李小苗,马彦,姬秋和:2型糖尿病患者肾小球滤过率相关因素分析. [J]第四军医大学学报,2008,29(13),1223-1225.
    [14] ADA : Standars of medical care in diabetes-2006. [J]Diabete Care 29(Suppl.1): S4-42,2006
    [15] Little RR,Rohlfing CL,Wiedmeyer H-M,Myers GL,Sacks DB,Goldstein DE:The National Glycohemoglobin Standardization Program (NGSP):a five year progress report. [J]Clin Chem 47:1985-1992,2001
    [16] Michael J.Fowler,MD:Microvascular and macrovascular complications of diabetes. [J]Clinical diabetes 26(2):77-82,2008
    [17] 9Gross JL, de Azevedo MJ, Silveiro SP, Canani LH, Caramori ML, Zelmanovitz T: Diabetic nephropathy: diagnosis, prevention, and treatment. [J]Diabetes Care 28:164–176, 2005
    [18] Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA, Holman RR: Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int 63:225–232, 2003
    [19] The DCCT Research Group: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. [J] N Engl J Med 329:977–986, 1993
    [20] Vandana Menon, Tom Greene,Arema A. Pereira,Xuelei Wang,Gerald J. Beck,John W. Kusek,Allan J. Collins,Andrew S. Levey, and Mark J. Sarnak: Glycosylated Hemoglobin and Mortality in Patients with Nondiabetic Chronic Kidney Disease. [J]J Am Soc Nephrol 16: 3411–3417, 2005
    [21] UKPDS: Intensified blood glucose control with sulphonilureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. [J]Lancet 352:837– 852,1998
    [22] Lewis E, Huinsiker L, Bain R, Rohde R: The effects of angiotensin converting enzyme inhibition on diabetic nephropathy. [J] N Engl J Med 329:1456–1462, 1993
    [23] Brenner BM, Cooper M, De Zeeuw D, Keane W, Mitch WE, Parving HH,Remuzzi G,Snapinn SM, Zhang Z, Shahinfar S, the RENAAL Study Investigators: Effects of Losartan on renal and cardiovascular outcomes in patients with type 2 diabetes mellitus and nephropathy. [J] N Engl J Med 345:861– 869, 2001
    [24] Lewis E, Hunsicker L, Clarke W, Berl T, Pohl MA, Lewis JB, Ritz E, Atkins RC, Rohde R, Raz I, the Collaborative Study Group: Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to diabetes mellitus. [J]N Engl J Med 345:851– 860, 2001
    [25] Barnett A, Bain S, Bouter P, Karlberg B, Madsbad S, Jervell J, Mustonen J:Diabetics Exposed to Telmisartan and Enalapril Study Group:angiotensinreceptor blockade versus converting-enzyme inhibition in type 2 diabetes and nephropathy. [J]N Engl J Med 351:1952–1961, 2004
    [26] Nosadini R, Velussi M, Brocco E, Abaterusso C, Piarulli F, Morgia G, Satta A, Faedda R, Abhyankar A, Luthman H, Tonolo GC: Altered transcapillary escape of albumin and microalbuminuria reflects two different pathogenetic mechanisms. [J]Diabetes 54:228–233, 2005
    [27] Adler SG, Kang SW, Feld S, Cha DR, Barba L, Striker L, Striker G, Riser BL,LaPage J, Nast CC: Glomerular mRNAs in human type 1 diabetes biochemical evidence for microalbuminuria as a manifestation of diabetic nephropathy. [J]Kidney Int 60:2330–2336, 2001.
    [28] Ki-Ho Song, MD, Department of Internal Medicine, St.Vincent Hospital, Catholic University of Korea, 93 Chi-Dong, Paldal-Ku, Suwon, Korea: Prospective Study of Lipoprotein(a) as a Risk Factor for Deteriorating Renal Function in Type 2 Diabetic Patients With Overt Proteinuria. [J] Diabetes Care 28:1718–1723, 2005.
    [29] Greiber S, Kreusel M, Pavenstadt H ,Schollmeyer P, Wanner C:Lipoprotein(a)induces glomerular superoxide anion production. [J] Nephrol Dial Transplant 12:1330–1335, 1997.
    [1] Hotamisligil GS, Shargill NS, Spiegelman BM.(1993) Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance.Science 259:87–91.
    [2] Uysal KT, Wiesbrock SM, Marino MW, HotamisligilGS. (1997) Protection from obesity-induced insulin resistance in mice lacking TNF-alpha function. Nature 389:610–4.
    [3] PA, Sa Kern ghizadeh M, Ong JM, Bosch RJ,Deem R, Simsolo RB. (1995) The expression of tumor necrosis factor in human adipose tissue:regulation by obesity, weight loss, and relationship to lipoprotein lipase. J. Clin. Invest.95:2111–9.
    [4] Dandona P, Weinstock R, Thusu K, Abdel-Rahman E, Aljada A, Wadden T. (1998) Tumor necrosis factor-alpha in sera of obese patients: fall with weight loss. J. Clin. Endocrinol. Metab. 83:2907–10.
    [5] Herbert Tilg and Alexander R Moschen:Inflammatory Mechanisms in theRegulation of Insulin Resistance.[J]Mol Med 2008, 14(3-4)222-231.
    [6]赖战峰,沈寒蕾,谭晓丹,黄媛:2型糖尿病患者IL-6和TNF-α的变化.[J]广西医科大学学报,2007.24(3)395-396.
    [7] Carantono M,Zuliani G,VolpatoS,et al.Relaytionships between fasting plasma insulin,Annthr Opometrics,and metabolic parameters in a very old healthy population[J].metabolism,1998,47(5):535-540.
    [8] Hamsten A,Wiman B,de Faire U,et al .Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction[J].N Engl Med,1985,313(25):1557-1563.
    [9] JoséRoberto Matos Souza, Romulo Tadeu Oliveira:Serum Levels of Interleukin-6 (IL-6), Interleukin-18 (IL-18) and C-Reactive Protein (CRP) in Patients with Type-2 Diabetes and Acute Coronary Syndrome without ST-Segment Elevation.[J] Arq Bras Cardiol 2008;90(2):86-90.
    [10] The role of interleukin-6 in insulin resistance, body fat distribution and energy balance Hoene M. and Weigert C.Obesity Reviews 2008 9:1 (20-29) .
    [11] Kishi.moto T, Akira S, Narazaki M, Taga T. (1995) Interleukin-6 family of cytokines and gp130. Blood 86:1243–54.
    [12] Kopp HP, et al. (2003) Impact of weight loss on inflammatory proteins and theirassociation with the insulin resistance syndrome in morbidly obese patients. Arterioscler. Thromb. Vasc. Biol.23:1042–7.
    [13] Flier JS. (2004) Obesity wars: molecular progress confronts an expanding epidemic. Cell 116:337–50.
    [14] Febbraio MA. (2007) gp130 receptor ligands as potential therapeutic targets for obesity. J. Clin.Invest. 117:841–9.
    [15] Kanemaki T et al, Interleukin 1beta and interleukin 6, but not tumor necrosisfactor alpha, inhibit insulin-stimulated glycogen synthesis in rat hepatocytes.Hepatology. 1998 May;27(5):1296-303
    [16] Tedgui, Alain, and Ziad Mallat. Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways. Physiol Rev86: 515–581, 2006; doi:10.1152/ physrev. 00024.2005.
    [17] Dinarello CA. (2005) Blocking IL-1 in systemic inflammation. J. Exp. Med. 201:1355–9.
    [18] Matsuki T, Horai R, Sudo K, Iwakura Y. (2003) IL-1 plays an important role in lipid metabolism by regulating insulin levels under physiological conditions. J. Exp. Med. 198:877–88.
    [19] Spranger J, et al. (2003) Inflammatory cytokines and the risk to develop type 2 diabetes: results of the prospective population-based European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study. Diabetes 52:812–7
    [20] Jager J, Gremeaux T, Cormont M, Marchand-Brustel Y, Tanti JF. (2007) Interleukin-1beta-induced insulin resistance in adipocytes through down-regulation of insulin receptor substrate-1expression. Endocrinology 148:241–51.22. Wernstedt I, Edgley A, Berndtsson A, Faldt J,Bergstrom G, Wallenius V, Jansson JO. (2006) Reduced stress- and cold-induced increase in energy expenditure in interleukin- 6-deficient mice. Am. J.Physiol. Regul. Integr. Comp. Physiol. 291:R551–7.
    [21] Zirlik A, et al. (2007) Interleukin-18, the metabolic syndrome, and subclinical atherosclerosis:results from the Dallas Heart Study. Arterioscler.Thromb. Vasc. Biol. 27:2043–9.
    [22] Kim HJ, et al. (2007) Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin-18 is an independent factor for the improvement of homeostasis model assessment-beta in type 2 diabetes mellitus. Clin. Endocrinol. (Oxf.) 66:282–9.
    [23] Netea MG, et al. (2006) Deficiency of interleukin-18 in mice leads to hyperphagia,obesity and insulin resistance. Nat. Med. 12:650–6.30. Kanda H, et al. (2006) MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity.J. Clin. Invest. 116:1494–505.31. Weisberg SP, et al. (2006) CCR2 modulates inflammatory and metabolic effects of high-fat feeding. J. Clin. Invest. 116:115–24.32. Inouye KE, Shi H, Howard JK, Daly CH, Lord GM,Rollins BJ, Flier JS. (2007) Absence of CC chemokine ligand 2 does not limit obesity-associated infiltration of macrophages into adipose tissue. Diabetes 56:2242–50.
    [24] Rotter V, Nagaev I, Smith U. Interleukin-6 ( IL-6 ) induces insulin resistance in 3T32L1 adipocytes and Is, like IL28 and tumor necrosis factor2alpha, overexp ressed in human fat cells from insulin2resistant subjects. J Biol Chem, 2003, 278: 45777245784.
    [25] Senn JJ, Klover PJ, Nowak IA, et al. Interleukin-6 induces cellular insulin resistance in hepatocytes. Diabetes, 2002, 51: 339123399.
    [26]洪天配.白细胞介素18与1型糖尿病.中国糖尿病杂志, 2001, 9:177-179.
    [27] Esposito K, Pontillo A, Di Palo C, et al. Effect of weight loss and lifestyle changes on vascular inflammatory markers in obese women: a randomized trial. JAMA, 2003, 289: 179921804.
    [28] Esposito K, Pontillo A, Ciotola M, et al. Weight loss reduces interleukin218 levels in obese women. J Clin EndocrinolMetab, 2002,87: 386423866
    [29] Yang YS, Song HD, ShiWJ, et al. Chromosome localization analysis of genes strongly exp ressed in human visceral adipose tissue. Endocrine,2002, 18: 57266.23 Olee T, Hashimoto S, Quach J, et al. IL218 is p roduced by articular chondrocytes and induces p roinflammatory and catabolic responses. JImmunol, 1999, 162: 109621100.
    [30]宁光,脂肪炎症因子在2型糖尿病发病中的重要性中华内分泌代谢杂志, 2006,22:2S-1—2S-3.
    [31] Netea MG, et al. (2006) Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance. Nat. Med. 12:650–6.
    [32] Yang YS, Song HD, Li RY, et al. The gene exp ression p rofiling of human visceral adipose tissue and its secretory functions. Biochem Biophys Res Commun, 2003, 300: 8392846.
    [33] Festa AD ,Agostion R Jr ,Howard G. Chronic subclinical inflammationas part of the insulinResistance syndrome :the Insulin Restance Athero2sclerosis Study( IRSA) [J ] . Circulation ,2000 ,120(1) :42247.
    [34] Zhiguo Zhang, Xiaoying Li, Wenshan Lv, Yisheng Yang, Hong Gao, Jun Yang, Yun Shen, and Guang Ning : Ginsenoside Re Reduces Insulin Resistance through Inhibition of c-Jun NH2-Terminal Kinase and Nuclear Factor-_B. [j]Molecular Endocrinology 22: 186–195,2008.
    [35]肖新华:胰岛素抵抗的病理生理机制和治疗选择.[J]国外医学内分泌学分册2005,5(25)179-181.
    [36] Yin MJ, Yamamoto Y, Gaynor RB. (1998) The anti-inflammatory agents aspirin and salicylate inhibit the activity of I(kappa)B kinase-beta. Nature 396:77–80.
    [37] Yuan M, Konstantopoulos N, Lee J, Hansen L, LiZW, Karin M, Shoelson SE. (2001) Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta. Science 293:1673–7.
    [38] Hajra L, Evans AI, Chen M, Hyduk SJ, Collins T, and Cybulsky MI. The NF-_B signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation. Proc Natl Acad Sci USA 97: 9052–9057,2000.
    [39] Alain Tedgui , Ziad Mallat:Cytokines in Atherosclerosis:Pathogenic and Regulatory Pathways.[J] Physiol Rev 86: 515–581, 2006
    [40] Kanters E, Pasparakis M, Gijbels MJ, Vergouwe MN, Partouns-Hendriks I, Fijneman RJ, Clausen BE, Forster I, Kockx MM, Rajewsky K, Kraal G, Hofker MH, and de Winther MP.Inhibition of NF-kappaB activation in macrophages increases atherosclerosis in LDL receptor-deficient mice. J Clin Invest 112:1176–1185, 2003.
    [41] M. Hassinen, T. A. Lakka, P. Komulainen, H. Gylling, A. Nissinen,and R.Rauramaa,“C-reactive protein andmetabolic syndromein elderly women: a 12-year follow-up study,”DiabetesCare, vol. 29, no. 4, pp. 931–932, 2006.
    [42] Axel Franke, Wolfgang Lante, Volker Fackeldey, Horst P. Becker, Edmond Kurig:Pro-inflammatory cytokines after different kinds of cardio-thoracic surgical procedures: is what we see what we know? [J]Eur J Cardiothorac Surg 2005; 28:569-575.
    [43] Ruan H,Lodish HF.Insulin resistance in adipose tissue:direct and indirect effects of tumor necrosis factor-alpha Cytokine Growth Factor Rev,2003,14:447-445.
    [44] Festa A, et al. Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects: The Insulin Resistance Atherosclerosis Study. Kidney Int. 2000 Oct;58(4):1703-10.
    [45] Rodolfo Le?o Borges, Fernando Flexa Ribeiro-Filho, Kenia Mara Baiocchi Carvalho,and Maria Teresa Zanella et al. Impact of Weight Loss on Adipocytokines, C-Reactive Protein and Insulin Sensitivity in Hypertensive Women with Central Obesity. Arq Bras Cardiol 2007;89(6):371-375.
    [46] Alan Chait,Chang Yeop Han, John F. Oram, and Jay W. Heinecke : Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease? [J] Journal of Lipid Research 2005(46) 389-403.
    [47] Ballou SP,Lozanski G. Induction of inflammatory cytokine release from cultured human monocytes by C-reactive protein [J].Cytokine,1992;4:361-8.
    [48] Claudia Langenberg, Jaclyn Bergstrom, Christa Scheidt-Nave: Cardiovascular Death and the Metabolic Syndrome.[J] Diabetes Care 29:1363–1369, 2006.
    [49] Bharadwaj D, Stein MP,Volzer M,et al.The major receptor for C-reactive protein on leukocytes is fc receprorⅡ[J]. J Exp Med,1999;190:585-90.
    [50] JoséRoberto Matos Souza, Romulo Tadeu Oliveira, Maria Heloisa S. L. Blotta, Otávio Rizzi Coelho et al. Serum Levels of Interleukin-6 (IL-6), Interleukin-18 (IL-18) andC-Reactive Protein (CRP) in Patients with Type-2 Diabetes and AcuteCoronary Syndrome without ST-Segment Elevation. Arq Bras Cardiol 2008;90(2):86-90.
    [51] G.Novo,E.Corrado,I.Muratori, R.Tantillo A.Bellia,A.Galluzzo,G.Vitale,S.Novo,”Makers of inflammation and prevalence of vascular disease in patients with metabolic syndrome”Int angiol 2007;26:312-7.

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