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Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia.

Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Research Abstract Details 

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  • Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Abstract Text:

    jacqueline m hibbertJacqueline M Hibbert,melissa s crearyMelissa S Creary,beatrice e geeBeatrice E Gee,iris d buchananIris D Buchanan,alexander quarshieAlexander Quarshie,lewis l hsuLewis L Hsu,

    OBJECTIVES: We hypothesized that an elevated hemoglobin synthesis rate (SynHb) and myocardial oxygen consumption (MVO2) contribute to the excess protein and energy metabolism reported in children with sickle cell anemia. PATIENTS AND METHODS: Twelve children (6-12 years old) with asymptomatic sickle cell and 9 healthy children matched for age and sex were studied. Measurements were whole-body protein turnover by [1-C]leucine, SynHb by [N]glycine, resting energy expenditure by indirect calorimetry and the systolic blood pressure-heart rate product used as an index of MVO2. Protein energy cost was calculated from protein turnover. Statistical analysis included Spearman correlations and partial correlation analyses. RESULTS: Although body mass index was significantly lower for sickle cell versus controls (P < 0.02), children with asymptomatic sickle cell had 52% higher protein turnover (P < 0.0005). Proportional reticulocyte count, SynHb, MVO2 and resting energy expenditure were also significantly higher in children with sickle cell (P < 0.01). Protein turnover correlated significantly with both SynHb (r = 0.63, P < 0.01) and reticulocyte percentage (r = 0.83, P < 0.0001). Partial correlation of these 3 variables showed reticulocyte percentage as the only variable to be significantly associated with protein turnover, even after adjusting for sickle cell anemia (P = 0.03). Partial correlation of log resting energy expenditure on MVO2 was significant, controlling for protein energy cost, sex and age (P = 0.03). CONCLUSION: These results indicate that metabolic demands of increased erythropoiesis and cardiac energy consumption account for much of the excess protein and energy metabolism in children with sickle cell anemia.

    Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Publishing Authors By Initials

    jm hibbertJM Hibbert,ms crearyMS Creary,be geeBE Gee,id buchananID Buchanan,a quarshieA Quarshie,ll hsuLL Hsu,

    For similar diagnosis: laboratory techniques and procedures: hematologic tests: blood cell count: erythrocyte count: reticulocyte count research abstracts see: diagnosis: laboratory techniques and procedures: hematologic tests: blood cell count: erythrocyte count: reticulocyte count research

    PUBMED ID PMID:

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    Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of pediatric gastroenterology and nutritio

    VOLUME: 43

    Page Numbers: 680-7

    Journal Abbreviation: J. Pediatr. Gastroenterol. Nut

    ISSN: 1536-4801

    DAY: 3

    MONTH: Nov

    YEAR: 2006

    Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8211545

    Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Keywords Mesh Terms:

    KEYWORDS: Reticulocyte Count

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. Information

    Substance Name: Hemoglobins

    Registry Number: 0

    Grant and Affiliation Information for Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia.

    AFFILIATION: Department of Biochemistry, Morehouse School of Medicine, Atlanta, GA, USA. jhibbert@msm.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIGMS

    GRANT: S06 GM-008248

    ACRONYM: GM

    MEDLINETA: J Pediatr Gastroenterol Nutr

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