OBJECTIVES: METHODS: Molecular - genetic examination of Gilbert\'s syndrome using fragment analysis method was carried out in collaboration with the Centre for Medical Genetics, University Hospital in Bratislava. Total cholesterol and triglycerides in plasma were analyzed from lipid parameters by means of enzymatic CHOD-PAP method, Roche Diagnostics, Germany. Biochemical parameters - bilirubin (total, conjugated and unconjugated), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transpeptidase (GMT), (Roche Diagnostics, Germany), TSH, FT3, fT4 (Siemens) were also examined. Serum lipoproteins and their subfractions were examined using Lipoprint LDL System Quantimetrix, CA, USA (12). RESULTS: CONCLUSION: The presence of atherogenic lipoprotein spectrum is determined by the particular representation of small dense LDL. Atherogenic spectrum was presented significantly less in patients with Gilbert\'s syndrome compared with the control group (5% vs. 18%). In our study, we have not followed the risk of coronary heart disease or other manifestations of atherosclerotic arteries disability. However, we found the inverse relationship of serum bilirubin levels and atherogenic small dense LDL. We found out that the protective antiatherogenic effect of hyperbilirubinemia is potentiated by low occurence of strongly atherogenic small dense LDL and persons with byperbilirubionemia (in our case represented Gilbert's syndrome), could be protected against the development of atheroscleosis.
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