Growth Status of Children with Sickle-Cell Anemia

Whitten, Charles F.

doi:10.1001/archpedi.1961.02080010357009

Cited by 27 publications

(15 citation statements)

References 14 publications

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“…As children with sickle cell anaemia have been found to be smaller than normal in other studies (Sharpe and Vonder Heide, 1944;Whitten, 1961), and as the average height of a series of Jamaican adult patients was as great as that of controls (Ashcroft and Serjeant, 1972), it seems probable that in sickle cell anaemia the increase of stature during adolescence is, on average, greater than normal-a feature that may be associated with delay in skeletal maturation. Longitudinal studies now in progress will reveal with greater accuracy the growth patterns of sickle cell anaemia.…”

Section: Discusionmentioning

confidence: 80%

“…Little has been recorded about growth changes in sickle cell anaemia, particularly during adolescence, though the body habitus of a few patients has been briefly described by Burch (1944, 1945), Sharpe and Vonder Heide (1944), Whitten (1961), and Jimenez et al (1966). These studies suggested that adolescents with sickle cell anaemia were shorter than normal and it is therefore surprising that Serjeant et al (1968) found that the mean stature of 60 Jamaican adults with sickle cell anaemia was as great as that of healthy Jamaicans, a finding that has been confirmed by Ashcroft and Serjeant (1972) in a further series of 121 adult patients.…”

mentioning

confidence: 99%

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Heights, Weights, and Skeletal Age of Jamaican Adolescents with Sickle Cell Anaemia

Ashcroft¹,

Serjeant²,

Desai³

1972

Archives of Disease in Childhood

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Section: Discusionmentioning

confidence: 80%

mentioning

confidence: 99%

Heights, Weights, and Skeletal Age of Jamaican Adolescents with Sickle Cell Anaemia

Ashcroft¹,

Serjeant²,

Desai³

1972

Archives of Disease in Childhood

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“…The abnormalities documented in children and adolescents include: delay in skeletal maturation [15][16][17][18][19][20], delay in pubertal growth spurt [15][16][17][18][19][20][21][22], eunuchoid habitus [ 15,23- These manifestations tend to be more pronounced in male subjects [16,19,21,31]. Endocrinologic studies fail to show a consistent relationship between growth retardation and abnormalities in growth hormone [20,29,35], somatomedin C [29,36] or thyroid hormone [ 13,291.…”

Section: Indirect Evidence For Macronutrient Deficiencies In Sickle Cmentioning

confidence: 99%

Nutrition and sickle cell disease

1987

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The role of protein and calorie deficiency in sickle cell disease remains poorly defined. While such features as growth retardation, impaired immune function, and delayed menarche do suggest a relationship between sickle cell disease and undernutrition, measurement of more direct nutritional parameters in these patients have yielded mixed results. Anthropometric measurements such as skinfold thickness are subnormal in many but not all reports. Serum protein levels are normal, but low values for serum lipids have been reported. Finally, one small study shows an improvement in both growth parameters and clinical course following caloric supplementation. A variety of micronutrient deficiencies have been suggested in sickle cell disease. Numerous case reports describing an exacerbation of the chronic anemia that was reversed by folic acid therapy led to routine folate supplementation. More recent studies have shown, however, that clinically significant folic acid deficiency occurs only in a small minority of sickle cell patients. Clearly, more work is necessary to define the cost/benefit ratio of routine folic acid supplementation. Pharmacological amounts of vitamin B6 and certain of its derivatives possess in vitro antisickling activities. Nevertheless, a small clinical trial failed to demonstrate any consistent hematologic effects of B6 supplementation. Several reports indicate that vitamin E levels are low in sickle erythrocytes. Since these abnormal red cells both generate excessive oxidation products and are more sensitive to oxidant stress, and because oxidants appear to play a role in ISC formation, vitamin E deficiency could well be linked to ISC formation and hemolysis. Small clinical trials, however, have again failed to produce a clear hematological response in sickle cell anemia. The role of zinc in sickle cell disease has received considerable attention. Though studies are generally small, most do support a relationship between sickle cell disease and zinc deficiency. Etiologic associations between zinc deficiency and such complications of sickle cell disease as poor ulcer healing, growth retardation, delays in sexual development, immune deficiencies, and high ISC counts have all been suggested. Most of these studies need further corroboration. Iron deficiency is now known to be a relatively common occurrence in sickle cell anemia, especially in children and pregnant women. The theoretical benefits of concomitant iron deficiency and sickle cell anemia remain to be proven in a controlled clinical trial.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…S tudies of children with SCD from the 1960s to 1990s described poor growth and delayed skeletal and sexual maturation (1)(2)(3)(4)(5), demonstrating low growth percentiles in height and weight among children older than 2 to 5 y of age, especially for children with type SCD-SS. Among studies conducted in the United States, only one was longitudinal (1), documenting short stature, poor weight gain, and delayed adolescent growth, particularly among males with SCD.…”

mentioning

confidence: 99%