Nutritional Status and Dietary Intake of Children with Sickle Cell Anemia

Gray, Nancy Thomas; Bartlett, Jonathan; Kolasa, Kathryn M.; Marcuard, Stefan P.; Holbrook, C. Tate; Horner, Ronnie D.

doi:10.1097/00043426-199221000-00008

Cited by 62 publications

(45 citation statements)

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“…Specifically, we found that rates of resting energy expenditure were accelerated, due, in part, to a dramatic increase in the energy consuming processes of basal whole-body protein breakdown and synthesis. These results support previous findings in children, adolescents, and adults with homozygous SCD (4)(5)(6)(7)(8). Because SCD patients have greater rates of resting energy expenditure and basal whole-body protein breakdown and synthesis than do healthy African Americans, the dietary energy and protein requirements of individuals with SCD may be greater.…”

Section: Introductionsupporting

confidence: 89%

“…Previously, we (3) and others (4)(5)(6)(7)(8) showed clearly that basal rates of whole-body protein breakdown and synthesis as well as resting energy expenditure are higher in African American children, adolescents, and adults with SCD than in healthy African Americans. The present study extends these findings by showing that the rates of these processes are also significantly increased during exogenous nutrient availability in SCD patients.…”

Section: Figurementioning

confidence: 82%

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Protein turnover and energy expenditure increase during exogenous nutrient availability in sickle cell disease

Borel

Buchowski

Turner

et al. 1998

The American Journal of Clinical Nutrition

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In the present study, energy expenditure (EE) and rates of whole-body protein, glucose, and lipid metabolism were assessed in 8 African American sickle cell disease (SCD) patients and in 6 healthy African American control subjects during the infusion of amino acids, glucose, and lipid. Wholebody protein, glucose, and lipid kinetics were estimated by using L-[1-13 C]leucine, D-[6,6-2 H 2 ]glucose, and [ 2 H 5 ]glycerol, respectively. After a 2-h tracer equilibration period and a 0.5-h basal period, nutrients were administered intravenously for 3 h with 16% of the energy as protein, 52% as carbohydrate, and 32% as fat. Breath and blood were collected during the last 30 min of nutrient infusion and EE was measured by indirect calorimetry. EE was 14% greater (P ≤ 0.05) in SCD patients [145.0 ± 3.5 kJ · kg fat-free mass (FFM). Whole-body protein breakdown (4.4 ± 0.4 compared with 3.1 ± 0.1 mg · kg FFM Ϫ1 · min Ϫ1 , P ≤ 0.05) and protein synthesis (4.6 ± 0.4 compared with 3.2 ± 0.1 g · kg FFM Ϫ1 · min Ϫ1 , P ≤ 0.05) were 42% and 44% greater, respectively, in the SCD patients than in control subjects, but whole-body amino acid oxidation (0.90 ± 0.05 compared with 1.03 ± 0.09 mg · kg FFM Ϫ1 · min Ϫ1 ) was not significantly different between the 2 groups. Wholebody glucose and lipid kinetics did not differ significantly between the groups. EE increased in SCD patients during exogenous nutrient availability, and the additional energy required for the accelerated rates of whole-body protein breakdown and synthesis made a significant contribution to the increase in EE. These metabolic aberrations may increase the dietary energy and protein requirements of SCD patients.

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Section: Introductionsupporting

confidence: 89%

Section: Figurementioning

confidence: 82%

Protein turnover and energy expenditure increase during exogenous nutrient availability in sickle cell disease

Borel

Buchowski

Turner

et al. 1998

The American Journal of Clinical Nutrition

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“…Despite an adequate dietary intake of energy, protein, zinc and vitamin A, these children with SCD were leaner and lighter with lower red blood-cell zinc and serum vitamin A concentrations, and higher resting energy expenditure than controls. 97 These findings were reflected in a survey of 61 American SS patients and their families on nutrition knowledge and practice. Overall, 90% of participants were familiar with the different food groups but most failed to consume an appropriate amount of different food groups, and 59% had incomes below the poverty level.…”

Section: Micronutrient Deficiencymentioning

confidence: 93%

Growth and nutritional status of children with homozygous sickle cell disease

Al-Saqladi

Cipolotti

Fijnvandraat

et al. 2008

Annals of Tropical Paediatrics

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Background: Poor growth and under-nutrition are common in children with sickle cell disease (SCD). This review summarises evidence of nutritional status in children with SCD in relation to anthropometric status, disease severity, body composition, energy metabolism, micronutrient deficiency and endocrine dysfunction. Methods: A literature search was conducted on the Medline/PUBMED, SCOPUS, SciELO and LILACS databases to July 2007 using the keywords sickle cell combined with nutrition, anthropometry, growth, height and weight, body mass index, and specific named micronutrients. Results: Forty-six studies (26 cross-sectional and 20 longitudinal) were included in the final anthropometric analysis. Fourteen of the longitudinal studies were conducted in North America, the Caribbean or Europe, representing 78.8% (2086/2645) of patients. Most studies were observational with wide variations in sample size and selection of reference growth data, which limited comparability. There was a paucity of studies from Africa and the Arabian Peninsula, highlighting a large knowledge gap for low-resource settings. There was a consistent pattern of growth failure among affected children from all geographic areas, with good evidence linking growth failure to endocrine dysfunction, metabolic derangement and specific nutrient deficiencies. Conclusions: The monitoring of growth and nutritional status in children with SCD is an essential requirement for comprehensive care, facilitating early diagnosis of growth failure and nutritional intervention. Randomised controlled trials are necessary to assess the potential benefits of nutritional interventions in relation to growth, nutritional status and the pathophysiology of the disease.

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Section: Vitamin Amentioning

confidence: 99%

“…27 ), there is some evidence that children affected may have lower micronutrient levels [ 50 ]. Despite similar dietary intake, children with SCD had lower red blood cell zinc levels, lower serum vitamin A levels, and lower urine nitrogen levels versus controls [ 50 ]. However, a 12-month vitamin A supplementation program in US children with SCD did not improve serum retinal values in a randomized, double-blind, placebo controlled trial, suggesting that (1) further research is needed and (2) higher doses than the recommended dietary allowance of vitamin A may be required to achieve adequate Vitamin A status [ 51 ].…”

Section: Vitamin Amentioning

confidence: 99%