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Nutrition and sickle cell disease.

J D Reed, R Redding-Lallinger, E P Orringer

    American Journal of Hematology
    |April 1, 1987
    PubMed
    Summary

    Protein and calorie deficiency in sickle cell disease (SCD) are not well understood. While some nutritional markers are abnormal in SCD patients, results are mixed, requiring further research into nutrient supplementation benefits.

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    Area of Science:

    • Hematology
    • Nutritional Science
    • Genetics

    Background:

    • The relationship between protein-calorie malnutrition and sickle cell disease (SCD) is unclear.
    • Clinical features like growth retardation suggest undernutrition, but direct nutritional parameter measurements in SCD patients yield inconsistent results.
    • Previous studies show mixed findings for anthropometric measurements, serum proteins, and lipids in SCD.

    Purpose of the Study:

    • To investigate the role of protein and calorie deficiency in sickle cell disease.
    • To evaluate the impact of various micronutrient deficiencies, including folate, vitamin B6, vitamin E, zinc, and iron, on SCD.
    • To determine the effectiveness of nutritional supplementation in managing SCD complications.

    Main Methods:

    • Review of existing literature on nutritional status in sickle cell disease.
    • Analysis of studies on anthropometric measurements, serum protein, and lipid levels.
    • Examination of clinical trial data on the effects of folate, vitamin B6, vitamin E, zinc, and iron supplementation.

    Main Results:

    • Mixed results for anthropometric measurements; normal serum protein but low lipids reported.
    • Folic acid deficiency is significant only in a minority; routine supplementation benefits unclear.
    • Vitamin E deficiency linked to red blood cell oxidative stress and hemolysis; clinical trials show no clear hematologic response.
    • Zinc deficiency is suggested to correlate with SCD complications like poor healing and growth delays.
    • Iron deficiency is common in SCD, particularly in children and pregnant women; benefits of iron supplementation require clinical trials.

    Conclusions:

    • The precise role of protein and calorie deficiency in sickle cell disease requires further investigation.
    • Clinically significant folate deficiency is rare; routine supplementation needs cost-benefit analysis.
    • While deficiencies in zinc and iron are common and linked to complications, their supplementation benefits in SCD need more robust clinical evidence.
    • Current evidence does not support routine supplementation of vitamin B6 or E for hematologic improvement in SCD.

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