Introduction: Midkine(MDK), found in 1988, a heparin-binding low-molecular protein, is a member of growth factors or cytokines, activated in the process of inflammatory disorders like RA, cancer development, angiogenesis and wound healing etc. It also acts as protecting cell apoptosis, stimulating fibrinolysis on endothelial cells, inhibiting or suppressing the development of regulatory T cells, improving myocardial dysfunction, and promoting the survival of ischemic myocardium. But, little is known in vasculitis syndrome.
Methods: Serum samples, clinical data and laboratory values from17 patients with acute KD patients in before, 1-2 days, and 7-10 days after IVIG. Serum samples were analysed for MDK concentrations by EIA with anti-human MDK antibody.
Results: MDK values were significantly elevated in serum from 1-2d after IVIG; 1-2d after IVIG; mean=1291.6 ± 1119.0, compared with Pre-IVIG; mean=530.9±468.6(p<0.01), and rapidly decreased 7-10d after IVIG; mean=599.4±447.3 pg/ml(p<0.05)(healthy human cut off level; < 300pg/ml). CRP is significantly correlated with MDK (r=0.45, p<0.05). MDK of 2 patient with CAA was higher than that of no CAA.
Discussions and Conclusions: Knockout mice deficient in the MDK gene poorly develop neointima when the artery is damaged by ischemic shock. Clinically, MDK increases in human carcinoma and play a central role in inflammatory pathway. It promotes the migration of inflammatory leucocytes, namely macrophages and neutrophils. Recently, it is becoming a molecular target for the treatment or prevention of inflammatory diseases.
Finally, this preliminary study suggests that MDK is a possible novel effector and may be relevant in the pathogenesis of arteritis in acute KD. IVIG may increase MDK levels and protect from inflammatory vascular damage.