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1547 Lipoprotein Cholesterol and Triglyceride in Children with Steady-State Sickle Cell Disease

Oral and Poster Abstracts
Poster Session: Hemoglobinopathies, excluding Thalassemia Poster I
Saturday, December 5, 2009, 5:30 PM-7:30 PM
Hall E (Ernest N. Morial Convention Center)
Poster Board I-569

Magda Oliveira Seixas II1*, Larissa Rocha Jr.2*, Mauricio Carvalho Sr.3*, Joelma Menezes Jr.1*, Isa Lyra Jr.2*, Valma Nascimento Jr.2*, Ricardo Couto3*, Ajax Atta Sr.3*, Mitermayer Galvão Reis1* and Marilda Souza Goncalves, Dr4*

1Centro de Pesquisas Gonçalo Moniz - FIOCRUZ, Salvador, Brazil
2Outpatient Unit, Fundacao HEMOBA, Salvador, Brazil
3Faculdade de Farmacia, Universidade Federal da Bahia, Salvador, Brazil
4Molecular Biology, Centro de Pesquisa Gonçalo Muniz-Fiocruz, Salvador, Brazil

Introduction: Levels of high-density lipoprotein cholesterol have been correlated with anti-inflammatory, anti-oxidative, anti-aggregation, anti-coagulant and pro-fibrinolytic activities. We hypothesized that lipoprotein cholesterol and triglycerides have important roles in sickle cell disease pathogenesis. Patients and Methods: A prospective study of biochemical and hematological analyses of 152 steady-state children with sickle cell disease and 132 healthy subjects using immunochemistry, immunoassay and electronic cell counter respectively. Clinical data were collected from patient medical records. Data analyses were performed using Prism 5.01 (Graphpad Software, San Diego, CA), EPIinfo 6.04 (CDC, Atlanta, Georgia) and STATA SE 10 software (StataCorp, Texas, USA).Results: There was a significant positive association of high-density lipoprotein cholesterol with hemoglobin (p<0.001), hematocrit (p<0.001) and total cholesterol (p<0.001) and a negative association with reticulocytes (p=0.046), leukocytes (p=0.015), monocytes (p=0.004) and platelets (p=0.005), bilirubins [total bilirubin (p<0.001), direct bilirubin (p<0.001) and indirect bilirubin (p<0.001], iron (p<0.001), aminotransferases [aspartate aminotransferase (p=0.004), alanine aminotransferase (p=0.035)], lactate dehydrogenase (p<0.001), urea (p=0.030), alpha 1-antitrypsin (p<0.001), very low-density lipoprotein cholesterol (p=0.003), triglycerides (p=0.005) and hemoglobin S (p=0.002). Low high-density lipoprotein cholesterol concentration was associated with cardiac abnormalities (p<0.025), pneumonia history (p=0.033) and blood transfusion use (p=0.025). Triglycerides (p=0.047), very low-density lipoprotein cholesterol (p=0.044), low-density lipoprotein cholesterol (p=0.033), total cholesterol (p=0.007), alpha 1-antitrypsin (p=0.040) and ferritin (p=0.008) levels were associated with cholelithiasis. Conclusion: We hypothesize that some SCD patients can have a specific dyslipidemic subphenotype characterized by hypertriglyceridemia, high VLDL-C and low plasma LDL-C and HDL-C in association with other biomarkers, including those related to inflammation. This represents an important step toward a more reliable clinical prognosis. We suggest further studies and continued research into new mechanisms involving this complex network of markers in order to establish their role in SCD pathogenesis.

Disclosures: No relevant conflicts of interest to declare.

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