Apolipoprotein(a) size polymorphism in young adults with ischemic stroke |
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| Institution: | 1. Service de Biochimie et de Biologie Moléculaire, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris cedex 10, France;2. Service de Neurologie, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris cedex 10, France;3. Service de Biophysique, Hôpital Feranad Widal, 200 rue du Faubourg Saint-Denis, 75010 Paris, France;1. Nightingale Hospital, Kolkata, India;2. Fortis CDOC Hospital for Diabetes and Allied Specialties, Chirag Enclave, New Delhi, India;3. AMRI Hospitals, Kolkata, India;4. National Diabetes, Obesity and Cholesterol Foundation, New Delhi, India;5. Diabetes Foundation (India), New Delhi, India;1. Inborn Error of Metabolism Reference Centre, La Timone Teaching Hospital, 264, rue Saint-Pierre, 13385 Marseille, France;2. Inborn Error of Metabolism Reference Centre, Necker Teaching Hospital, 149–161, rue de Sèvres, 75743 Paris cedex 15, France;1. Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou, 550025, China;2. Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou, 550025, China;3. Department of Nephrology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 550002, China |
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| Abstract: | High serum lipoprotein(a) (Lp(a)) concentration which is largely determined by genetic factors, mainly the apolipoprotein(a) (apo(a)) polymorphism, is associated with ischemic cerebrovascular disease. The aim of this study was to investigate whether apo(a) size was associated with acute ischemic stroke in young adults for which causal factors often remain undetermined. Lipid parameters, Lp(a) concentration and apo(a) isoform size distribution were determined in 90 young patients (37.4±8.7 years) with acute cerebral ischemia, and compared to those of control subjects with similar age and sex ratio. Apo(a) size was expressed as its apparent number of kringle 4 (Kr 4) repeats. Serum Lp(a) concentrations were significantly higher in patients than in controls (median values: 0.18 vs. 0.07 g/l, P=0.009) and were as expected inversely related to the number of kringle 4 repeats in both controls (r2=?0.61, P<0.001) and patients (r2=?0.56, P<0.001). However there was no difference in the apo(a) isoform size distributions between the two groups (median isoform size: 27 vs. 27 Kr 4, P=0.25). Lp(a) levels were increased as well in patients with size apo(a) isoform≤22 Kr 4 as in those with isoforms>25 Kr 4. Multivariate analysis showed that apo(a) phenotype did not appear as a risk factor for cerebrovascular infarction. Thus, our results indicate that serum Lp(a) was significantly increased in young people with ischemic stroke but fail to reveal a role of small-sized apo(a) isoforms in the occurrence of this event. They suggest that other factors, genetic or environmental in nature, than the apo(a) size contribute to increase the serum Lp(a) concentrations in these young patients. |
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