Enoxaparin versus unfractionated heparin in acute ischemic stroke [in-evolution type] differential effects of enoxaparin on von Willebrand factor release and a possible relation to improved clinical outcomes

The significance of low-molecular-weight heparins [LMWHs] in the management of acute stroke remains controversial. One hundred patients with acute ischemic stroke in evolution were enrolled [with symptoms of stroke within eight hours of randomization]. Patients were randomized to receive Unfractionated Heparin [UFH] at a dose 5000 IU by IV bolus, followed by a continuous IV infusion; or to Enoxaparin [ENOX] at a dose of 0.5 mg per kilogram body weight. Therapy was continued for 10 days. National Institutes of Health Stroke Scale [NIHSS] and Computed Tomography [CT] scan were performed in all patients at the time of admission, and after 48 hours of randomization. It was found that, the mean baseline National Institutes of Health Stroke Score [NIHSS] was 9.14 +/- 0.62 among patients randomized to UFH, vs. 7.86 +/- 0.54 among patients randomized to ENOX [p = 0.2]. At discharge, the mean NIHSS showed a statistically significant difference in favor of the ENOX group [7.9 +/- 0.82 for the UFH arm versus 4.96 +/- 0.54 for the ENOX arm; p = 0.002]. The mean NIHSS after therapy in patients who demonstrated neurological improvement was 5.6 +/- 0.46 in the UFH arm, as opposed to 3.65 +/- 0.39 in the ENOX arm [p = 0.001]. A deterioration in the clinical neurological condition [progressive stroke symptoms] inspite of treatment with anticoagulant therapy was seen in 20% [n = 10] of the patients in the UFH treatment arm and no patients in the ENOX treatment arm showed this condition [p = 0.005]. No statistically significant differences were observed for pulmonary embolism, deep venous thrombosis, recurrent strokes, or death. It was concluded that, Enoxaparin [+ aspirin] was superior to UFH [+ aspirin] in reducing adverse neurological disability after acute ischemic stroke in evolution. This superiority was not associated with reductions in mortality, and could be explained by blunting of von Willebrand factor release by Enoxaparin

Cystatin C as marker of glomerular filtration rate in children with nepthrotic syndrome

Nephrotic syndrome [NS] is the most common chronic renal disease of childhood. The rapid and accurate evaluation of renal function is important to detect the extent and progress of renal affection. Glomerular filtration rate [GFR] is the best marker for renal function. Serum cystatin C; a cysteine proteinase inhibitor; has been proposed as a sensitive marker for GFR. Our study was conducted on 50 patients with NS [23 with minimal change disease 'MCD', 12 with focal segmental glomerulosclerosis 'FSGS' and 15 with mesangioproliferative glomerulonephritis 'MP'], as well as 20 age and sex matched normal controls. In addition to routine assessment, creatinine clearance and serum cystatin C were measured in a trial to evaluate the importance of serum cystatin C versus serum creatinine in the detection of early impairment of renal function. Our results showed a significant 'positive' correlation between the creatinine clearance and the 'reciprocals' of both serum cystatin C and serum creatinine in all the 70 studied cases [P<0.0005]. The correlation was significantly better for serum cystatin C [r = 0.879] than the serum creatinine [r = 0.776]. Also serum cystatin C was significantly higher in nephrotic patients than in controls [P < 0.0005] while the serum creatinine was less significantly elevated [P < 0.05]. Mean while, serum cystatin C showed higher negative and positive predictive values [95% and 92% respectively] as compared to serum creatinine [88% and 76% respectively] in the detection of impairment of GFR, denoting the ability of serum cystatin C to detect the early changes in renal function. The reference interval of serum cystatin C as measured in our controls was independent on age or sex, and ranged between 0.6-1.32 mg/L. The highest diagnostic accuracy [95.7%] was obtained when the upper limit of 1.43 mg/L was used. So we could conclude that serum cystatin C is more sensitive and specific than serum creatinine in the detection of early impairment of GFR