The results of serum homocysteine (mean S.D.) among the studied groups control ( group I), group II and group III. Mean S.D. of serum homocysteine (umol/L) in group (I) [12.492.02] and in group (II)[14.678.917] and in group (III) [15.523.29], Regarding the p value of this parameter in the studied groups there is very high significant difference in serum homocysteine (p < 0.001) between group (I) and group(III). While there is no significant difference of serum homocysteine (p > 0.05) between group(I) and group(II) and between group(II) and group(III). The results of the diabetic profile (mean S.D.) among the studied groups control ( group I), group II and group III. Mean S.D. of the fasting plasma glucose (mg/dl) in group(I) [90.713.85], and in group (II) [158.9539.99] and in group (III) [191.8556.053] and hemoglobin A1c (%) in group(I) [5.641.66] and in group (II) [9.232.265] and in group (III) [8.861.62]. Regarding the p value of these parameters, there is very high significant difference in fasting plasma glucose (p < 0.001), and in hemoglobin A1c (p< 0.001) when comparing control (group I) with two studied groups in two parameters , while there is no significant difference (p>0.05) between group (II) and group (III) in two parameters. The results of serum total cholesterol (mean S.D.) among the studied groups; control (group I), group II and group III. Mean S.D. of serum total cholesterol (mg/dl) in group (I) [124.6529.16] ,and in group (II) [150.2052.62],and in group (III) [171.247.246]. Regarding the p value of this parameter, there is significant difference in the serum total cholesterol (p < 0.001) between group (I) and group (III), while there is no significance difference of serum total cholesterol (p > 0.05) between group (I) and group (II) and between group (II) and group(III) . CONCLUSIONREFERENCESN.M. Naseb2, J.R. Peela1, S. Shakila1, A.R. Said1, L.T. Peela4, R.N. Yedla3 AM Jarari2

Homocysteine, an early predictor of cardiovascular risk in type2 diabetes mellitus 1Department of Biochemistry, Faculty of Medicine, Quest International University Perak, 30250 Ipoh, Malaysia,2Department of Biochemistry, Faculty of Medicine, University of Bengahzi, Libya,3Department of Medicine, Andhra Medical College, Visakhapatnam, India,4Great Eastern Medical School, Srikakulam, IndiaLogoHereThis study was carried out on sixty male and female subjects. Their age ranged from 30 to 75 years old. They were selected from the outpatients of Diabetes Mellitus Clinic, Seventeenth of February Teaching Hospital, Al- Baida. All laboratory work was carried out at both lab of Biochemistry Department, Omar Al-Mukhtar Faculty of Medicine and Clinical Laboratory at Seventeenth of February Teaching Hospital, Al-Baida. All subjects were divided into three groups: -1- Group I: (Control group) Twenty volunteer controls were selected to be about the same age of the patients. 2- Group II: (Uncomplicated diabetic group): Twenty patients with long history of type 2 diabetes without any accompanying diseases especially coronary heart diseases. All subjects of this group had history of diabetes for at least 5 year. 3- Group III: (Complicated diabetic group): Twenty patients with long history of type 2 diabetes together with coronary heart diseases. All patients in group II ,and group III were selected from Diabetes Mellitus Clinic, Al-Seventeenth of February Teaching Hospital, El-Bieda. Glycosylated hemoglobin was estimated by chromatographic-spetrophotometric ION EXCHANGE method ,(Bisse and Abraham,1985).Homocystine was measured by ARCHITECT Homocysteine Reagent Kit method. Blood glucose was measured glucose oxidase method. Cholesterol was measured by enzymatic method. MATERIALS AND METHODSRESULTS Bagust A, Hopkinson PK, and Currie CJ.,(2001): An economic model of the long term health careburden of Type II diabetes. Diabeologia.; 44 : 2140-55.Bennett, S. and Magnus, P., (1994): Trends in cardiovascular risk factors in Australia. Results from the national heart foundation's risk factor. Med. J. Aust., 161: 519-527.Bisse' E, Abraham EC.,(1985): New less temperature-sensitive micro chromatographic method for the separation and quantization of glycosylated hemoglobin's using a non-cyanide buffer system Chromatog ; 344:81-91.Bores, G., (1998): Moderate hyperhomocysteinemia and vascuolar diseases. Evidence and the effect of treatment. Eur. Eur. J. Pediat., 2: 127-130 J. Bots M.L., Launer, L.J., Lindemans, J., Hoes, A.W., Hofman, A., Witteman, J.C., Koudstaal, P.J. and Grobbee, D.E., (1998): Homocysteine and short term risk of myocardial infarction and stroke in elderly, Int. Med., 159: 38-44. Bradley A. Maron, and Joseph Loscalzo (2009). The Treatment of Hyperhomocysteinemia, Annu Rev Med.; 60: 3954. Brattstrom, L., Lindgren, A., Israelsson, B, Malinow, M.R., Norrving, B., Upson, B., and Hamfelt, A. (1992): Hyperhomocysteinemia in stroke: prevalence, causes and relationship to type of stroke and stroke risk factors. Eur. J. Clin. Invest., 22: 214-221.Bunn, F.H. and Franklin, E. (1990): Elevation of glycated hemoglobin in diabetic patients. Diabetes, 30: 613-619D'Angelo, A., and Selhub, J., (1997): Homocysteine and thrombotic disease. Blood, 90:1-11.David B. Sacks, David E. Bruns, David E., and Marian Parrott. (2002):Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus Clinical Chemistry.;48:436-472.Engbersen AMT., Franken ,D.G, Boers GHJ, Stevens EMB .(1995): Thermolabile 5,10-methylenetetrahydrofolate reductase as a cause of mild hyperhomocysteinemia: Am. J. Hum. Genet., 56: 142-150. Finkelstein ,JD. (1990): Methionine metabolism in mammals: J. Nutr. Biochem., 1: 228-237. Gerhard G.T, Duell P.B (1999): Homocysteine and atherosclerosis. Curr Opin Lipidol, 10(5):417-28.Guthikonda, S, Haynes WG., (2006). Homocysteine: role and implications in atherosclerosis, Curr Atheroscler Rep.8(2):100-6.Heinecke, JW., Rosen, H., Suzuki LA., Chait, A., (1987). The role of sulfur containing amino acids in superoxide production and modification of low density lipoprotein by arterial smooth muscle cells. J. Biol. Chem., 262: 1009810103.Heinz J, Kropf S, Luley C, Dierkes J., (2009). Homocysteine as a risk factor for cardiovascular disease in patients treated by dialysis: a meta-analysis. Am J kidney Dis.2009 Sep:54(3):478-89.Hirano, K., Ogihara, T., Miki M., Yasuda, H., Tamai, H., Kawamura, N., Mino, M., (1994): Homocysteine induces iron-catalyzed lipid peroxidation of low-density lipoprotein that is prevented by alpha-tocopherol. Free Radic Res., 21: 267276. Hoelzel, W., and Miedema, K., (1996): Development of a reference system for the international standardization of HbA1C/ glycohemoglobin determinations. J Int Fed Clin Chem .;9:6267.Hoogeveen , E,K., Kotense, P,J., Mackaay, A.J.C., Jacobs, C., Bouter, L.X., Heine, R.J. and Stehouwer, C.D.A, (1998): Hyperhomocysteinemia is associated with an increased risk of cardiovascular diseases especially in NIDDM, Atherosclerosis,thrombosis and vascular biology,18:133:138. Hultberg, B., Anderson, A., and Lindgren, A.,(1997): Marginal folate deficiency as a possible cause of hyperhomocysteinemia in stroke patients, Eur. J. Clin. Chem., 35: 25-28. Ian, F.W., McDowell, Derek, Lang. (2000): Homocysteine and Endothelial Dysfunction: A Link with Cardiovascular Disease J. Nutri., 130: 369S-372. Lavin, M.A. (2008): Brief: nursing diagnostic applications derived from National Academy of Clinical Biochemistry (NACB) draft guidelines and recommendations for laboratory analysis in the diagnosis management of diabetes mellitus. Int J Nurs Terminol.Lentez, S.R. and Sadler, J.E. (1991): Inhibition of thrombomodulin surface expression and protein C activation by the thrombogenic agent homocysteine. J. Clin.Invest.,88:906-914. Lynn, E.G., Chung, Y.H., Siow, Y.L., Man, R.W., Choy, P.C. (1998): Homocysteine stimulates the production and secretion of cholesterol in hepatic cells. Biochem. Biophys. Acta.,393:317-324. Malinow, M.R. (1995): plasma homocysteine and artelial occlusive diseases. A mini review. Clin Chem 41 (1): 173-6. Mart-Carvajal, A.J, Sol, I., Lathyris D., Salanti, G. (2009):Mart-Carvajal, Arturo J. ed. "Homocystein lowering interventions for preventing Cardiovasculare vents". Cochrane Database Syst Rev(4):CD006612. doi:10.1002/14651858.CD006612.pubPMID19821378 McCully, K. S. (1983): Homocysteine theory of arteriosclerosis: Development and current status. In: Gotto, A. M., Jr, & Paoletti, R. (Eds), Atherosclerosis Reviews (Vol. 11, pp 157246). New York: Raven Press. Refusm, H., Helland, S., Veland, P.M. and Nygard, D. (1998):Homocysteine and cardiovascular diseases. Int. Med., 49: 31-62. Stehouwer, C.D., and Jacobs, G., (1998): abnormalities of vascular function in hyperhomocysteinemia relationship to atherombotic disease. Eur. J. Pediat.,2:107-111.Thomas, G. Guilliams, (2004). Homocysteine A Risk Factor for Vascular Diseases: Guidelines for the Clinical Practice. JANA Vol. 7, No. 1.Yeromenko Y., Lavie L., Levy Y., (2001). Homocysteine and cardiovascular risk in patients with diabetes mellitus. Nutr Metab Cardiovasc Dis . Apr; 11(2):108-16. It could be concluded that serum homocysteine determination could be used as a sensitive, early and more accurate tool for screening and monitoring early detection of atherosclerosis. Table.1 Controls Table.2 Diabetics without complications Table.3 Diabetics with complications In recent years the amino acid homocysteine has achieved the status of a hot topic in vascular disease. Besides arteriosclerosis and heart disease, the significance of this amino acid has also rapidly expanded to areas of biology, physiology, and medicine ranging from endothelial function to aging, oxidative stress, oxidative metabolism, embryology, reproductive physiology, cancer, growth and cell division ,endocrinology ,neural transmission, and neurodegenerative disease, (McCully, 1983). In general population , increased homocysteine concentrations are a risk factor for cardiovascular disease and mortality (Heinz et al, 2009). High homocysteine concentration is prevalent in patients with diabetes mellitus and its relationship with excess cardiovascular morbidity is also studied This study is designed to observe the relationship of homocysteine changes in diabetics with and without coronary artery disease.INTRODUCTION

FBSHbA1cHomocystineTCMean90.75.6412.49124.65STD 13.85 1.66 2.02 29.16

FBSHbA1cHomocystine TCMean 158.959.2314.67150.2STD 39.99 2.265 8.917 52.62t-test-7.298- 6.720- 1.068-1.825p-Value< 0.0001< 0.00010.2930.084significanceH.SN.S.

FbsHbA1cHomocystine TCMean191.858.8615.52171.2STD 56.053 1.62 3.29 47.246t-test-7.657- 5.459-3.056- 3.733p-Value< 0.0001< 0.0001< 0.001< 0.001Significance H.Ssignificant

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