PURPOSE: To study the levels of lipids in serum, in patients with age-related macular degeneration (AMD), and to establish its pathogenic relevance in the disease. METHODS: The serums of a total of 40 patients, distributed in a AMD group (25 patients) and a control group (15 patients, with similar ages and without ocular affectation) were studied, correlating the biochemical findings with the clinical examination of these patients. RESULTS: We have observed a mean level of serum total cholesterol statistically superior in AMD patients (control= 200.18+/-18.89 mg/dL; AMD= 227.28+/-5.46 mg/dL; p<0.01). These significant differences are repeated for different lipoproteins (triglycerides, LDL, VLDL and apolipoprotein B), not appearing for the HDL and apolipoprotein A-1. We have not found correlations of these concentrations with the clinical or functional stage of the AMD. CONCLUSIONS: Serum lipids could take part in the pathogenic mechanism of AMD, either by their relation with arteriosclerosis, which would diminish the choroidal flow, or by direct deposit in the Bruch's membrane. However, more longitudinal studies are needed to understand the relation of serum lipids and AMD, and to establish therapeutic approaches on the matter.
PURPOSE: To study the levels of lipids in serum, in patients with age-related macular degeneration (AMD), and to establish its pathogenic relevance in the disease. METHODS: The serums of a total of 40 patients, distributed in a AMD group (25 patients) and a control group (15 patients, with similar ages and without ocular affectation) were studied, correlating the biochemical findings with the clinical examination of these patients. RESULTS: We have observed a mean level of serum total cholesterol statistically superior in AMDpatients (control= 200.18+/-18.89 mg/dL; AMD= 227.28+/-5.46 mg/dL; p<0.01). These significant differences are repeated for different lipoproteins (triglycerides, LDL, VLDL and apolipoprotein B), not appearing for the HDL and apolipoprotein A-1. We have not found correlations of these concentrations with the clinical or functional stage of the AMD. CONCLUSIONS: Serum lipids could take part in the pathogenic mechanism of AMD, either by their relation with arteriosclerosis, which would diminish the choroidal flow, or by direct deposit in the Bruch's membrane. However, more longitudinal studies are needed to understand the relation of serum lipids and AMD, and to establish therapeutic approaches on the matter.