ANTIOXIDANT STATUS IN CORONARY HEART DISEASE (CHD) PATIENTS WITH TYPE 2 DIABETES MELLITUS
Abstract
Background: The present study was carried out to see the levels of vitamin C, vitamin E and totalantioxidant (AO) in Coronary Heart Disease (CHD) patients with and without Type-2 DiabetesMellitus (T2DM). In various previous studies it has been reported that, diabetes, hypertension andsmoking are risk factors for CHD and all risk factors were common in these patients. Methods:Serum was tested from 80 CHD patients and 21 healthy controls, matched for age, height, andweight. Results: No significant difference was seen between the age, height and weight of thesubjects and controls. CHD patients were mostly male, smokers, over 40 year of age and belongingupper class families. The mean plasma glucose was significantly higher (p<0.05) in CHD patientshaving T2DM as compare to CHD patient with out T2DM. Risk factors for CHD, like diabetes,hypertension and smoking were common in these patients. No significant difference was seen invitamin C level of patients of CHD. Vitamin E level was significantly (p<0.05) low among the CHDpatients as compared to controls and a significant (p<0.05) decrease in mean vitamin E level wasobserved among smoker CHD patients as compared to non-smoker CHD patients. But no significantdifference in vitamin C and vitamin E levels of CHD patients with diabetes and hypertension wereobserved when compared with CHD patients having no such complaints. The CHD patients’ totalantioxidant level was significantly (p<0.05) decreased as compared to controls. Conclusion: Thetotal AO (Vit. C and E) were not significantly higher in CHD patients with hypertension and diabetesas compared to those patients of CHD having no hypertension and diabetes.Keywords: Coronary Heart Disease (CHD), Ischemic Heart Disease (IHD). Type 2 DiabetesMellitus (T2DM), Fasting Plasma Glucose (FPG), Antioxidant (AO)References
Paffenbarger RS Jr, Hyde RT, Wing AL, Lee IM, Jung DL,
Kampert JB. The association of changes in physical-activity
level and other lifestyle characteristics with mortality among
men. N Engl J Med 1993;328:538–45.
Buja LM. The heart. In: Robbin and Kumar (eds). Basic
Pathology. 4th Ed. WB Saunders Company, 1988: pp 312–50.
Kannel WB, Castelli WP, Gordon T. Chole sterol in the
prediction of atherosclerotic disease. New perspectives based
on the Framingham study. Ann Intern Med 1979;90:85–91.
Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum
JL. Beyond cholesterol. Modificati ons of low -density
lipoprotein that increase its atherogenicity. N Engl J Med
;320:915–24.
Smith C, Mitchinson MJ, Aruoma OI, Halliwell B .
Stimulation of lipid peroxid ation and hydroxyl -radical
generation by the contents of Human atherosclerotic lesions.
Biochem J 1992;286:901–5.
Hoff HF, O'Neil J. Extracts of human atherosclerotic lesions
can modify LDL leading to enhanced uptake by macrophages.
Atherosclerosis 1988;70:29–41.
Halliwell B. Oxidation of low density liporproteins: Questions
of Initiation, propagation and the effect of antioxidants. Am J
Clin Nutr 1995;61:670S–677S.
Gutteridge JM. Lipid peroxidat ion and antioxidants as
biomarkers of tissue damage. Clin Chem 1995;41:1819–28.
Byer T, Bowman B. Vitamin E supplements and coronary heart
disease. Nutr Rev. 1993;51:333–6.
Meigs JB, D'Agostin o RB Sr, Wilson PW, Cupples LA ,
Nathan DM, Singer DE. Risk variable clustering in the insulin
resistance syndrome. The Frami ngham offspring study.
Diabetes 1997;46:1594–600.
Stewart MW, Humphriss DB, Mitc heson J, Webster J,
Walker M, Laker MF . Lipoprotein composition and serum
apolipoproteins in normoglycaemic first degree relations of non
insulin dependent diabetic patients. Atherosclerosis
;139(1):115–21.
Peter A. Mayes. Lipids of phys iological significance. In:
Harper’s Biochemistry. Murray RK, Granner DK, Mayes PA,
Rodwell VW eds. 24th edition. United States. Appleton and
Lange,1996. p 147-57.
Stampfer MJ, Hennekens CH, Man son JE, Colditz GA,
Rosner B, Willett WC. Vitamin E Consumption and the risk of
coronary disease in women. N Engl J Med 1993;328:1444–9.
Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz
GA, Willett WC. Vitamin E consumption and th e risk of
coronary artery disease in men. N Engl J Med 1993;328:1450–6.
Baker H, Frank O. In: Verley’sPractical Clinical Biochemistry 6th
ed. Gowenlock AH, McMurrary JR, McLamchlam DM, editors.
Trowbridge Wiltshire:Redwood Burn Ltd;1988. p 894-930.
Brewster MA, Turley CP. Vitamin C. In: Method in clinical
Chemistry. Pesce AJ, Kaplan LA , editors. Toronto: CV
Mosbyy Company; 1987:p 574–81.
Meilling GE. Clin Chem 1979;22;1581. In: Varley’s Practical
Clinical Biochemistry, 6 th edition. Trowbridge Wiltshire:
Redwood Burn Ltd;1988;pp326-32
Massie BM, Heart. In: Current Medical Diagnosis and
Treatment. 44th ed Lawrence M, Tiemey, Jr. Steph en J.
McPhee, Maxime A, Papadakis, editors. McGraw-Hill
Companies, 2005:p 308-403.
Hultqvist M, Hegbrant J, Nilss on-Thorell C, Lindholm T,
Nilsson P, Lindén T, et al. Plasma concentrations of vitamin
C, vitamin E and/or malondialdehyde as markers of oxygen
free radical production during hemodialysis. Clin Nephrol
;47:37–46.
Jackson P, Loughrey CM, Lightb ody JH, McNamee PT,
Young IS. Effect of hemodialysis on tota l antioxidant
capacity and serum antioxidants in patients with chronic renal
failure. Clin Chem 1995;41:1135–8.
Riemersma RA, Wood DA, Macinty re CC, Elton RA, Gey
KF, Oliver MF. Risk of angina pectoris and p lasma
concentrations of vitamins A, C, and E and carotene. Lancet
;337:1–5.
Asayama K, Uchida N, Nakane T, Hayashibe H, Dobashi K,
Amemiya S, et al. Antioxidant in the serum of children with
insulin dependent diabetes mellitus. Free Radic Biol Med.
;15:597–602.
Benzie IF, Strain JJ. The ferr ic reducing ability of plasma
(FRAP) as a measure of “antioxidant power”. The FRAP assay.
Anal Biochem 1996;239:70–6.
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