Anthropometric evaluation of children with chronic liver disease
Chronic liver disease (CLD) in children can cause a variety of nutrition disorders, and poor nutrition interferes with growth. Some of the nutrition problems caused by CLD are: reduced appetite; decreased food consumption due to pressure on the stomach from the enlarged liver; and malabsorption of fat. Because fat is inadequately absorbed, deficiencies of the fat-soluble vitamins develop, leading to disorders of the eyes, skeleton, nerves and muscles. Protein metabolism may be disturbed, and the need for energy may be increased, both of which can exacerbate the nutritional deficits caused by inadequate food consumption. Children with CLD need to have their growth monitored carefully to assess whether nutrition support (such as supplemental feedings and intravenous nutrition) is needed. In this study, 56 children with CLD, aged 1 month to 10 years, underwent anthropometric assessment; this refers to obtaining measurements of height, weight, head and arm circumferences, and triceps skinfold thickness (an indicator of body fat stores). The specific liver disease was considered. Children with arteriohepatic dysplasia were shorter and thinner than children with other liver diseases, namely extrahepatic biliary atresia, idiopathic neonatal hepatitis, and other types of CLD. Overall, both chronic malnutrition, which leads to stunting of height growth, and acute malnutrition as reflected by low body weight, were common in children with CLD. Weight for height (an index of thinness) was not dramatically reduced, but this was misleading because some patients' weights were increased by their enlarged livers and other organs. Triceps skinfold was a more accurate indicator of the adequacy of body fat stores than was weight for height. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Normal vitamin E status in sickle hemoglobinopathies in Colorado
Previous research has reported that vitamin E deficiency is fairly common among patients with sickle cell anemia (SCA). In SCA, which is a hereditary chronic condition, red blood cells have an abnormal crescent shape and do not adequately transport oxygen to body tissues. Conflicting results have been reported concerning the possible role of vitamin E in SCA. In two studies, vitamin E appeared to protect the red blood cell membrane (outer covering) from damage that led to sickle-shaped deformities. Another study did not confirm these results. To further investigate vitamin E in SCA, the authors evaluated vitamin E levels in 101 SCA patients who attended a sickle cell clinic in Colorado. The group represented several forms of sickle cell disease, including homozygous SCA, sickle B+ -thalassemia and hemoglobin sickle cell disease. The SCA subjects were compared to normal controls of the same age, sex and race. Subjects were tested for serum (blood) vitamin E levels and the ratio of serum vitamin E to total serum lipids (E:L) (fats). The latter test is considered a more accurate gauge of vitamin E status than the former, because serum lipid levels are linked to serum vitamin E. Using the ratio corrects for individuals who may have low lipid levels, which is common in SCA. The results show that vitamin E deficiency was rare in the group of SCA patients in Colorado. Two of the 101 SCA patients studied were classified as having vitamin E deficiency. Research has not demonstrated that vitamin E supplements help SCA patients who already have normal vitamin E levels, so the authors suggest supplementation only for patients who are vitamin E-deficient according to the E:L test.
Publication Name: American Journal of Clinical Nutrition
Newborn screening for hemoglobinopathies in Colorado: the first 10 years
Newborns are screened for hemoglobinopathies (diseases involving the hemoglobin blood component) primarily to detect sickle-cell anemia, which is a significant cause of infant mortality during the second six months of life. A 10-year study of newborn screening in Colorado indicated that reduced mortality was associated with early diagnosis of the disease when accompanied by treatment with antibiotics and other comprehensive care, and parental education and counseling. Out of 528,711 newborns screened in this study, 47 cases of sickle-cell anemia, and 27 cases of other hemoglobin abnormalities were found. No parents with previously undiagnosed hemoglobin disease were found, and only 40 couples were at risk for having children with sickle-cell disease. These low rates may be a result of many factors including lack of confirmatory testing, incomplete reporting, and refusal of parents to be tested. In formulating mass screening programs, cost effectiveness must be considered. Some have argued that mass testing should be performed only in high-risk populations, such as blacks. However, in this study the sickle-cell trait was not limited to blacks; 12.9 percent of the infants born with the disorder were of non-black parents. Additionally, the reliability of ethnic data on questionnaires is questionable. In many cases it is less costly to perform testing on all newborns rather than to try to determine which population groups should be tested. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Diseases of Children
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