Abstrak AIP didefi nisikan sebagai log (TG/HDL-C).Hasil AIP dan rasio (Ox-LDL/HDL) lebih tinggi secara signifi kan pada subjek DM tipe 2 tidak terkontrol dibanding DM terkontrol (0,72 ± 0,13 vs 0,47 ± 0,22 , p < 0,001) dan (1738,8 ± 625,5 vs 1418 ± 535,3, p = 0,02), sedangkan rasio (Lp-PLA2/HDL) tidak berbeda secara bermakna (5,09 ± 2,17 vs 5,95 ± 3,11, p = 0,16). Kesimpulan Nilai AIP dan rasio (Ox-LDL/HDL) lebih tinggi secara bermakna pada DM tipe 2 tidak terkontrol dibandingkan dengan DM tipe 2 terkontrol. Parameter ini dapat dimanfaatkan dalam memprediksi risiko aterosklerosis pada penderita diabetes. (Med J Indones 2010; 19: 103-8) Abstract Aim to assess the differences between Atherogenic Index of Plasma (AIP), ratio of oxidized-Low Density Lipoprotein (Ox-LDL)/High Density Lipoprotein (HDL) and ratio of Lipoprotein-associated Phospholipase A2 (Lp-PLA2)/HDL in predicting the risk of coronary heart disease (CHD) in patients with controlled and uncontrolled type 2 Diabetes Mellitus (T2DM).Methods The study was done observationally with cross sectional design. A total of 80 patients, consisted of 40 controlled and 40 uncontrolled T2DM. The serum triglyceride (TG), HDL-C, Ox-LDL, Lp-PLA2 were examined in their relationship with T2DM risk. AIP is a ratio calculated as log (TG/HDL-C).Results AIP and ratio of Ox-LDL/HDL were signifi cantly higher in uncontrolled than controlled T2DM (0.72 + 0.13 vs 0.47 ± 0.22 , p < 0.001) and (1738.8 ± 625.5 vs 1418 ± 535.3, p = 0.02), but no signifi cant difference was found in ratio of Lp-PLA2/HDL (5.09 ± 2.17 vs 5.95 ± 3.11, p = 0.16).Conclusion AIP and ratio of Ox-LDL/HDL value were signifi cantly higher in uncontrolled than in controlled T2DM. These parameters may be benefi cial in predicting the risk of atherosclerosis in diabetic patients. (Med J Indones 2010; 19:103-8)

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BACKGROUND: Vascular remodeling was an adaptive process of the vascular wall that occured in response to long-term changes in hemodynamic conditions that contribute to the changes of the vascular structure and the pathophysiology of vascular disease. On the other hand, Endothelial Progenitor Cells (EPC) derived from bone marrow had the capacity to migrate to the peripheral circulation and to differentiate into mature endothelial cells. Therefore, EPC could contribute in the endothelial repairing after endothelial injury.METHODS: This study was a cross sectional design. Analysis was done among 30 subjects with normoalbuminuria normotension, 55 subjects with normoalbuminuria hypertension and 30 subjects with with microalbuminuria hypertension. TGF-β1, MMP-9 and VEGFR-2 testing were performed by ELISA method. All statistical calculations were performed using the SPSS 11.5 statistical software package. We used the Independent sample T test, Mann-Whitney, One Way Annova and Kruskal Wallis to establish the difference among various biochemical measures.RESULTS: TGF-β1 concentration was increased from normoalbuminuria normotension to normoalbuminuria hypertension and to microalbuminuria hypertension (27.63178±12.97246 vs. 38.61193±17.09546 vs. 38.73939±12.63911 ng/mL). TGF-β1 concentration was higher significantly in normotension as compared to hypertension (27.63178±12.97246 vs. 38.65692±15.58950, p<0.001) and to microalbuminuria hypertension (38.73939±12.63911, p<0.001). MMP-9 concentration was increased in normotension to normoalbuminuria hypertension but was decreased in microalbuminuria hypertension (438.1967±156.4268 vs. 564.5873±291.2876 vs. 418.6900±188.3801 ng/mL). MMP-9 concentration was higher significantly in normoalbuminuria hypertension as compared to microalbuminuria hypertension (p=0.028). VEGFR-2 concentration was decreased from normotension to normoalbuminuria hypertension to microalbuminuria hypertension (9.90552±1.85185 vs. 9.39561±1.75413 vs. 9.00506±1.47173 ng/mL). VEGFR-2 concentration was higher significantly in normotension as compared to microalbuminuria hypertension (p=0.042). CONCLUSIONS: The increasing concentration level of TGF-β1 and decreasing concentration level of MMP-9 in microalbuminuria hypertension showed that the remodeling process was getting increased. The decreasing concentration level of VEGFR-2 in microalbuminuria hypertension showed that the repairing process was getting decreased.KEYWORDS: vascular remodelling, vascular repairing, TGF-β1, MMP-9, VEGFR-2

BACKGROUNDS: Heart failure, a new epidemic of cardiovascular disease, has become an important issue and its prognosis is poor. Heart failure is the condition where the impaired heart cannot pump enough blood to provide the needs of metabolic tissues and organs. Early diagnosis of heart failure is really crucial to determine the success of treatment and to prevent further myocardial dysfunction and worsening clinical symptoms. This condition can be worsened by ET-1, which triggers the secretion of IL-6 and TNF-α as pro inflammation factors. In Systolic Heart Failure, systolic function changes are accompanied by changes in diastolic function. Thus, the condition of systolic heart failure is worse than Diastolic Heart Failure. The purpose of this study is to assess the relationship of ET-1 with diastolic and systolic heart failure groups and the relationship of ET-1 with TNF-α and IL-6 as pro inflammation factors.METHODS: The design of this study was cross-sectional analysis on 62 patients with heart failure, grouped according to the classification of diastolic and systolic heart failure.RESULTS: A significant positive correlation of ET-1 with diastolic and systolic heart failure was found (p=0.008; r=0.324). A significant positive correlation was also found between ET-1 and IL-6 (p=0.001; r=0.393), but a less significant correlation was noted between ET-1 and TNF-α (p=0.201; r=-0.158).CONCLUSIONS: ET-1 has the strongest correlation (p=0.033) with prevalence ratio 3.930 and can differentiate between Diastolic and Systolic Heart Failure.KEYWORDS: Endothelin-1 (ET-1), Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α), heart failure

BACKGROUND: Central obesity is the accumulation of visceral (intra-abdominal) fat and is strongly known to be associated with insulin resistance and type 2 diabetes mellitus (T2DM). Obesity can cause adipocyte hypertrophy that results in dysregulation of adipokine expression. The abnormal function of adipocytes may play an important role in the development of a chronic low-grade proinflammatory state associated with obesity. Adiponectin, retinol binding protein (RBP)-4 and fetuin-A play a role in the pathophysiology of insulin resistance. Expression of fetuin-A is increased due to fat accumulation in the liver. Elevated concentration of fetuin-A in the circulation can impair insulin signaling in muscle and liver as well as suppress adiponectin secretion, although its molecular mechanism is still unclear. The aim of this study was to identify the relationship of fetuin-A, adiponectin, RBP-4 and hsCRP with insulin resistance in obese non diabetic men.METHODS: This was an observational study with a cross-sectional design. The study subjects were 64 men with non diabetic abdominal obesity, characterized by waist circumference of 98.47 ± 5.88 cm and fasting blood glucose of 85.75±8.36 mg/dL.RESULTS: This study showed that fetuin-A was positively correlated with HOMA-IR in obese non diabetic men with insulin resistance (r = 0.128; p = 0.570), although not significant. Fetuin-A was found to be correlated with adiponectin, RBP-4 and hsCRP (r=0.150; p=0.233; r=0.050; p=0.711; r=-0.04; p=0.445), although not significant.CONCLUSIONS: The concentration of fetuin-A showed a tendency to be positively correlated with HOMA-IR and with RBP-4 in obese non diabetic men, although statistically not significant. The concentration of fetuin-A showed a tendency to be negatively correlated with adiponectin and hsCRP although statistically not significant. There was no interrelationship between fetuin-A, adiponectin, RBP-4, hsCRP and HOMA-IR. Elevated concentrations of fetuin-A were noted in obese subjects, which in turn might impair insulin signaling. This finding might suggest that fetuin-A may represent a new target for the prevention of insulin resistance. Further studies might be needed on obese population with fatty liver.KEYWORDS: fetuin-A, adiponectin, RBP-4, hsCRP, insulin resistance

Cerebrovascular disease are the third most common cause of death in Western countries. The most frequent manifestation of disease is a sudden episode of neurological deficit termed stroke which is the result of cerebral haemorrhage or cerebral infaction in the mayority of cases. Stroke secondary to atherosclerosis is most common in people over 50 years old.The incidence of stroke rises dramatically with ages, with the risk doubling with each decade after 35 years old. About 5 % of people over 65 years old have at least one stroke. Atherosclerosis is condition where fatty acid deposits occur in the inner lining of arteries and the forming of atherosclerotic plaque,a mass consisting of fatty deposit, and blood platelets.The plaque may obstruct or my trigger clot,a trombus,at that location causing cerebral trombosis.It is called ischemmic stroke. The basis of the response to injury hypothesis introduced by Russel Ross is that the earliest cellular events that occur during atherosclerosis is a specialized type of chronic inflammatory response to cell injury. What may begin as a protective inflammatory reponse can become excessive and deleterious to the cell of the artery wall. The adhesion of leucocytes on endothelial cells and their trans –endothelial migration into intima are mediated by adhesion molecules on the endothelial cell membrane that mainly belong to two protein families:the selectin and the addhesion molecules.