Low Plasma Prealbumln and Carotenoid Levels in Sickle Cell Disease Patients

Jain, Sushil K.; Ross, Jean D.; Duett, John; Herbst, John J.

doi:10.1097/00000441-199001000-00004

Cited by 8 publications

(7 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TTR also proved useful for monitoring the dietetic management of anorexia nervosa ( 59 ) and weight-reduction programs ( 60 ). Likewise, the use of TTR is recommended for the nutritional follow-up of a variety of genetic and metabolic disorders such as uncontrolled diabetes ( 61 ), cystic fibrosis ( 62 ), drepanocytosis ( 63 ), Reye syndrome ( 64 ), inborn errors of AA metabolism ( 65 ), and defects of the urea cycle ( 66 ).…”

Section: Importance Of Ttr In Protein-depleted Statesmentioning

confidence: 99%

Plasma Transthyretin as a Biomarker of Lean Body Mass and Catabolic States

Ingenbleek¹,

Bernstein

2015

Advances in Nutrition

View full text Add to dashboard Cite

Plasma transthyretin (TTR) is a plasma protein secreted by the liver that circulates bound to retinol-binding protein 4 (RBP4) and its retinol ligand. TTR is the sole plasma protein that reveals from birth to old age evolutionary patterns that are closely superimposable to those of lean body mass (LBM) and thus works as the best surrogate analyte of LBM. Any alteration in energy-to-protein balance impairs the accretion of LBM reserves and causes early depression of TTR production. In acute inflammatory states, cytokines induce urinary leakage of nitrogenous catabolites, deplete LBM stores, and cause an abrupt decrease in TTR and RBP4 concentrations. As a result, thyroxine and retinol ligands are released in free form, creating a second frontline that strengthens that primarily initiated by cytokines. Malnutrition and inflammation thus keep in check TTR and RBP4 secretion by using distinct and unrelated physiologic pathways, but they operate in concert to downregulate LBM stores. The biomarker complex integrates these opposite mechanisms at any time and thereby constitutes an ideally suited tool to determine residual LBM resources still available for metabolic responses, hence predicting outcomes of the most interwoven disease conditions.

show abstract

Section: Importance Of Ttr In Protein-depleted Statesmentioning

confidence: 99%

Plasma Transthyretin as a Biomarker of Lean Body Mass and Catabolic States

Ingenbleek¹,

Bernstein

2015

Advances in Nutrition

View full text Add to dashboard Cite

show abstract

“…68,69 Pre-albumin, used to assess nutritional status, has been reported to be low in SCD. 70 Urinary loss of amino acids might also contribute to slow growth. One study reported no differences in the concentration of serum total proteins between SCD children and controls, but serum levels of pre-albumin, all essential and most nonessential amino acids were significantly lower with higher urinary concentration of amino acids.…”

Section: Body Composition and Energy Metabolismmentioning

confidence: 99%

Growth and nutritional status of children with homozygous sickle cell disease

Al-Saqladi

Cipolotti

Fijnvandraat

et al. 2008

Annals of Tropical Paediatrics

View full text Add to dashboard Cite

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.

show abstract

“…In such cases, the amount of vitamin E that is present and availability of redox‐active metal centers determines its prooxidant or antioxidant effect 35,36. There is ∼40% reduction in plasma carotene levels and ∼30% reduction in plasma vitamin E levels in sickle cell disease 37,38. Red blood cell membrane vitamin E levels were also depleted in these patients 38…”

Section: Altered Defense Mechanisms Against Oxidative Stress In Sicklmentioning

confidence: 99%

Reactive Species in Sickle Cell Disease

Aslan

Thornley‐Brown

Freeman

2000

Annals of the New York Academy of Sciences

118

View full text Add to dashboard Cite

A BSTRACT : The red cell is a relatively abundant locus of both free radical generation and reaction. Erythrocytes have a high content of unsaturated membrane lipids, a rich oxygen supply and are densely packed with redox-active hemoglobin residues. In response, red cells have a highly evolved and well-integrated network of oxidant defense mechanisms that lend an ability to withstand oxidative stress. In the case of congenital hemoglobin mutations that underlie sickle cell disease, they become very susceptible to free radical-mediated injury by virtue of enhanced endogenous rates of production of reactive species and impairment of tissue free radical defense mechanisms. In sickle cell disease, a combination of these susceptibility factors are hypothesized to lead to an overall impairment of vascular function, in large part due to loss of "bioactive" nitric oxide via the free radical-mediated consumption of this vasoactive molecule.

show abstract

Low Plasma Prealbumln and Carotenoid Levels in Sickle Cell Disease Patients

Cited by 8 publications

References 14 publications

Plasma Transthyretin as a Biomarker of Lean Body Mass and Catabolic States

Plasma Transthyretin as a Biomarker of Lean Body Mass and Catabolic States

Growth and nutritional status of children with homozygous sickle cell disease

Reactive Species in Sickle Cell Disease

Contact Info

Product

Resources

About