Defibrase

Atherosclerosis is a complex disease process in which genetic, lipid, cellular and immunological factors combine to determine the location, severity and timing of lesion development and clinical events. It has been demonstrated, however, that inflammation governs atherosclerosis during the course of development of atherosclerosis. It has also been demonstrated that regulation of the inflammatory reaction (e.g. statins) is effective in decreasing the cardiovascular events and improving the prognosis of atherosclerotic diseases. Other anti-atherosclerosis agents introduced in this study are adiponectin, testosterone, defibrase, angiotensin-converting enzyme inhibitors, dextromethorphan, paeonol, 15-lipoxygenase inhibitors, curcumin, interferon-beta, quercetin, AGI-1067, peroxisome proliferator-activated receptor gamma ligands and garlic. Some antiplatelet drugs described here are aspirin, clopidogrel and glycoprotein IIb/IIIa receptor antagonist. The mechanism of action of these agents is depicted. A new way of targeting anti-atherosclerosis and antiplatelet drugs to atherosclerosis areas is introduced. The author uses an antioxidized low-density lipoprotein antibody that is also conjugated to a mixture of anti-atherosclerosis agents or antiplatelet drugs to target these agents specifically to the atherosclerosis area. With this kind of targeting, we can use a much higher dose of anti-atherosclerosis agents or antiplatelet drugs and have much fewer side effects.

To evaluate the therapeutic effect of individualized defibrase therapy according to the level of plasma fibrinogen (FIB) in patients with acute cerebral infarction (ACI).

Sixty patients with ACI (within 72 h after onset) were randomly divided into defibrase group (n=30) and control group (n=30). The patients in defibrase group received intravenous defibrase infusion at different first doses (15, 10, and 5 U) according to plasma FIB level (>4 g/L, 2-4 g/L, and 1.3-2 g/L) before treatment. Plasma FIB was measured every 12 h after the first dose of defibrase, and when plasma FIB was over 1.3 g/L, intravenous infusion of 5 U defibrase was given to maintain plasma FIB within the range of 0.70-1.13 g/L over a period of 7 days. The plasma prothrombin time (PT), activated partial thromboplastin time (APTT) and FIB before and after the 7-day treatment were measured, and the scores of Chinese stroke scale (CSS) after 14 days of treatment and Activity of Daily Living (ADL) after 3 months were recorded.

After 7 days of treatment, plasma PT and APTT were significantly prolonged lengthened and plasma FIB was lowered in defibrase group. The scores of CSS improved in defibrase group after 14 days of treatment, showing significant difference from those of the control group. The clinical effective rate was 80% in defibrase group, significantly higher than that in the control group (50%). The scores of ADL after 3 months were similar between the 2 groups, but the percentage of independent living and mild dependency was significantly higher in defibrase group (93.3% vs 70.0%). No intracerebral and extracerebral hemorrhage occurred in defibrase group the during treatment, no did death occur after 3 months of treatment.

Defibrase therapy based on plasma FIB level can rapidly and effectively lower plasma FIB, reduce neurological impairment and improve the quality of life in patients with ACI.