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) .

CONCLUSION
REFERENCES
N.M. Naseb
2
, J.R. Peela
1
, S. Shakila
1
, A.R. Said
1
, L.T. Peela
4
, R.N. Yedla
3
AM Jarari
2


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, India
Logo
Here
This 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 METHODS
RESULTS

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: 613-619
D'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
FBS HbA1c Homocysti
ne
TC
Mean
90.7 5.64 12.49 124.65
STD
13.85 1.66 2.02 29.16
FBS HbA1c Homocysti
ne
TC
Mean
158.95 9.23 14.67 150.2
STD
39.99 2.265 8.917 52.62
t-test
-7.298 - 6.720 - 1.068 -1.825
p-Value
< 0.0001 < 0.0001 0.293 0.084
significanc
e
H.S

N.S.

Fbs HbA1c Homocysti
ne
TC
Mean
191.85 8.86 15.52 171.2
STD
56.053 1.62 3.29 47.246
t-test
-7.657 - 5.459 -3.056 - 3.733
p-Value
< 0.0001 < 0.0001 < 0.001 < 0.001
Significanc
e
H.S

significant

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