Homocysteine a risk factor for cardiovascular disease in patients with type 2 diabetes mellitus

Diabetes mellitus has been widely recognized as major risk factor for coronary artery disease and, at the present time, diabetics are considered at high risk for coronary events independently of prior evidence of atherosclerotic disease [1]. Hyperhomocysteinemia has emerged as a novel risk factor for myocardial infarction. Diabetes shares many common mechanisms of plaque development with hyperhomocysteinemia, such as those related to endothelial dysfunction, thrombosis and oxidative stress [2]. To study the importance of serum homocysteine [Hcy] level as a predictor of myocardial infarction in patients with type 2 diabetes mellitus and to detect that this level is of an equal importance as other cardiovascular risk factors such as hypertension, hypercholesterolemia and smoking. Forty individuals were divided into three groups: group I [acute myocardial infarction with type 2 diabetes group, n=15], group II [uncomplicated type 2 diabetes group, n=15] and group III [normal control, n=10]. Diagnosis of myocardial infarction was confirmed from ECG criteria together with significant elevations in serum creatine kinase activity and echocardiographic examination. Higher homocysteine levels was found in AMI patients with type 2 diabetes and in uncomplicated type 2 diabetic patients [P< 0.01] than the normal control. Homocysteine was positively associated with total cholesterol, LDL-c, P.PB.S, and negatively associated HDL-c. Higher homocysteinemia was predominantly observed in type 2 diabetic patients with myocardial infarction especially those presenting low HDL-c, high LDL-c. Serum homocysteine is considered to be one of the strong and important predictor of myocardial infarction in type 2 diabetes

Interleukin - 8 in chronic renal failure and patients on peritoneal dialysis

The present study included 35 subjects classified into four groups. Group 1 included 20 chronic uremic patients with ages ranged from 19 to 61 years, group 2 included 9 patients with chronic peritoneal dialysis with ages ranged from 35 to 61 years] and group 3 included 6 patients on chronic peritoneal dialysis without peritonitis aged between 45 and 57 years. They were compared with group 4 including 10 age and gender matched individuals with ages between 25 and 60 years. Complete history, clinical examination, complete urine analysis, serum urea, creatinine and creatinine clearance assessment and measurement of interleukin-8 assessment were done. It could be concluded that patients with renal failure had an increased serum IL-8 level. IL-8 concentration was higher in cases with peritonitis than those without. These results could be important in the subsequent disturbed immune status of these patients

Serum soluble fas in children with idiopathic dilated cardiomyopathy

The present study aimed to evaluate the role of serum soluble Fas [sFas] "APO-l receptor", as an inhibitor of apoptosis [programmed cell death] in children patients suffering from idiopathic dilated cardiomyopathy [IDCM] and its association to New York Heart Association [NYHA] Functional class. The study included 20 children patients aged 5-13 years, suffering from IDCM and 20 age and sex matched control subjects. Serum level of sFas was measured by enzyme linked immunosorbent assay [ELIZA] which showed that sFas is increased significantly with increased NYHA functional class. However, serum levels of sFas were similar in normal subjects and patients with functional class I, but there were significant differences between functional classes II, III and IV. Serum levels of sFas were significantly higher in patients with an elevated Pulmonary Capillary Wedge Pressure [PCWP] > 18 mm Hg than in those with values <18 mm Hg. Six months later, all patients were re-evaluated for their functional class and serum sFas levels. Serum levels of sFas decreased in four patients with clinical improvement but were similar in patients with no change in functional class. The increase in sFas may play an important role in the pathophysiologic mechanisms of IDCM in children