Animal and observational studies suggest that the IGF axis is involved in the pathogenesis of ischemic stroke; moreover, endogenous IGF-I could influence the evolution of ischemic stroke in humans and thereby contribute to an improved clinical and functional outcome. To assess and correlate the IGF-I axis with biochemical parameters in young patients experiencing ischemic stroke (32 aged 1545 years,19F, BMI: 25.5±3.4 kg/m2), we evaluated IGF-I, IGFBP-3, ALS, homocysteine, antithrombin, anticardiolipin antibodies (ACA), lupus anticoagulans (LAC), Protein S and C, fibrinogen levels and lipid profile 612 months after stroke. The results were compared with those of 32 age, BMI and sex matched controls. IGF-I levels were lower in patients than in controls (86.3±76.6 vs 262.9±50.5 μg/l; P<0.001) and lower than 2 SD in 24 patients (75%). IGFBP-3 and ALS levels were also significantly reduced in patients than in controls (3394.8±801 vs 3782±762.8 ng/ml, P<0.05; 10.2±3.8 vs 21.2±27.5 μg/ml, P=0.000; respectively. Conversely as expected, homocysteine, total cholesterol and fibrinogen levels were higher in patients than in controls (P<0.001). Significant difference was found between patients and controls in Protein S (P<0.001) and C (P<0.05), while no difference was found in ACA and LAC levels between two groups. In addition in the patients group, IGF-I levels were significantly correlated with homocysteine levels (r=0.411, P<0.05).
In conclusion a significant impairment of IGF-I and ALS secretion was found in young patients 612 months after ischemic stroke. Whether this represents a causal or casual finding remain to be clarified.
03 - 07 May 2008
European Society of Endocrinology