title: Influence of anti-VEGF about cardiovascular biomarkers in age related macular degeneration.
abstract: Systemic VEGF inhibition disrupts endothelial homeostasis and accelerates the atherogenesis, suggesting that these events contribute to the clinical cardiovascular adverse events of VEGF-inhibiting therapies. The objective of the current study was to analyze the effect of anti-VEGF therapy on cardiovascular risk factors in patients with exudative age related macular degeneration. A total of 73 patients with exudative age related macular degeneration (without previous anti-VEGF therapy) were treated with two anti-VEGF: Ranibizumab and Pegaptanib sodium. The follow up was 6 months. The following parameters were determined before and after treatment: homocysteine, lipids (total cholesterol, triglycerides, HDL-c, LDL-c), C-Reactive Protein and fibrinogen. There were not statistically significant differences in parameters studied before and after treatment with both Pegaptanib sodium and Ranibizumab, except C-Reactive Protein. Of all patients analyzed, only 3 of them have initially C-Reactive Protein levels above normal levels and after antiangiogenic therapy, there was a significant increase in C-Reactive Protein. We have not found results in our study who to suspect that treatment with anti-VEGF in the patients with exudative age related macular degeneration increases cardiovascular risk predictors. However, after therapy was increased the CRP and fibrinogen may mean that anti-VEGF contribute an alteration of endothelial homeostasis in exudative AMD.
authors: N. Manresa, Department of Food Technology and Nutrition, Catholic University of San Antonio, Murcia 30107, Spain. Email: noemi-mr@hotmail.com, Phone: +34968278705, Fax: +34968278622.
authors: N
authors: N
authors: Manresa
authors: J
authors: J
authors: Mulero
authors: M
authors: M
authors: Losada
authors: P
authors: P
authors: Zafrilla
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects* / Q000627:therapeutic use; D052157:Aptamers, Nucleotide / Q000009:adverse effects* / Q000627:therapeutic use; D050197:Atherosclerosis / Q000139:chemically induced; D015415:Biomarkers / Q000032:analysis*; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000097:blood* / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006710:Homocysteine / Q000032:analysis / Q000378:metabolism; D006801:Humans; D008055:Lipids / Q000097:blood; D008268:Macular Degeneration / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D000069579:Ranibizumab; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors*; D057135:Wet Macular Degeneration / Q000097:blood / Q000188:drug therapy
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D052157:Aptamers, Nucleotide; D015415:Biomarkers; D008055:Lipids; D042461:Vascular Endothelial Growth Factor A; D006710:Homocysteine; C495058:pegaptanib; D005340:Fibrinogen; D002097:C-Reactive Protein; D000069579:Ranibizumab
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