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Vol. 29. Núm. 2.
Páginas 72-80 (Febrero 2002)
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Vol. 29. Núm. 2.
Páginas 72-80 (Febrero 2002)
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Commentary:Iron needs in adolescents
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JM. Andrés del Llanoa
a Rio Carrión Hospital, Palencia, Spain.
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Iron is an essential nutrient in the human species. It is found in all cells and is involved in a variety of vital functions such as oxygen transport to tissues from the lungs via hemoglobin (bound to the prosthetic heme group of hemoglobin. In addition, it facilitates oxygen supply to the muscles (bound to the heme prosthetic group of myoglobin), forms part of respiratory enzymatic systems within cells via cytochromes of the mitochondrial respiratory chain, and participates in enzymatic reactions in many tissues. A low level of iron can interfere with these vital functions and increase morbidity and mortality. Certain periods of life, such as adolescence, are characterized by rapid growth, which involves in increase in iron requirements.

Iron is obtained by the body from meat, eggs, cereals, vegetables, fruits and juices. It is absorbed best as heme. In contrast, the absorption of nonheme iron is limited, although it is facilitated by consuming meat and ascorbic acid, whereas the intake of large amounts of calcium delays iron absorption.1 The recommended iron intake for persons aged 11 to 18 years is about 12 milligrams per day for males and about 15 milligrams per day for females.2

Classically, iron deficiency is considered to develop in three consecutive phases. In the first stage, latent iron deficiency results from the depletion of iron stores in the reticulo-endothelial system, liver, spleen and bone marrow. The laboratory finding that identifies latent iron deficiency is a decrease in serum ferritin. As the disorder progresses, iron deficiency without anemia appears, and is characterized by a reduction in sideremia, an increase in total transferrin saturation capacity (above 480 mg/dL) and a decrease in transferrin saturation index (below 15%). The final stage, if the disorder progresses further, is iron-deficiency anemia, with its characteristic hypochromia and microcytosis.

Iron deficiency is the most frequent nutritional deficiency in our setting. In children, iron deficiency can lead to delayed development and behavioral alterations. Its prevalence is high in school-aged children and adolescents, although the figures vary widely between different studies. The prevalence can range from 4% in Scandinavian countries or 8-12% in adolescents from the province of Navarra in northern Spain3 to as high as 25% in some studies of teenage girls in the USA.1 Such studies are rare in Spain.

Cross-sectional or prevalence studies still represent the Cinderella of epidemiological study designs. Although such studies are at the lower end of the quality scale in terms of scientific evidence, it should be recalled that prevalence studies have a number of advantages, among which are their straightforward methods, relatively low cost, the fact that they make it possible to describe the distribution of a given disease, the fact that they suggest hypotheses and analytical studies, and their usefulness in planning health care.

For these reasons the study by Durá Travé and colleagues is to be applauded. This study, carried out in the Estella Basic Health Zone in the province of Navarra, places the prevalence of iron deficiency at 8.6% among adolescent men and 12.6% in adolescent women.3 Their findings allow them to draw conclusions that suggest the need to extend and modify adolescent health care programs.

Serum ferritin is considered a valid diagnostic marker that reflects the status of iron deposits. The appropriate cut-off value for a diagnosis of iron deficiency in adolescents is controversial, and this makes it difficult to compare results across different studies; nonetheless the most widely accepted value is 12 ng/dL. It should be recalled that serum ferritin behaves as an acute phase reactant, and is elevated in infectious and inflammatory processes and in hepatic and neoplasic diseases.

The amount of hemoglobin is related with blood volume and increased fat-free mass. Initially, young men require more iron as a result of their more rapid growth spurt at puberty. It is only after menarche, and as a result of menstrual losses, that the risk of iron deficiency increases in young women and their requirements surpass those of young men.

There is no consensus among the recommendations offered by different groups of experts. Screening for iron deficiency in (non-pregnant) adolescents is not recommended by most organizations included in the Bright Futures report, the American Academy of Family Physicians, and the United States Preventive Services Task Force.4,5 The Bright Futures group recommends selective screening in adolescents at high risk for iron deficiency. This groups includes in its list of risk factors physical activity (especially in male athletes), vegetarian diets, malnutrition and low body weight, chronic diseases, and a history of large blood losses during menstruation (greater than 80 mL/month).5 The American Academy of Pediatrics recommends at least one set of laboratory tests of hemoglobin and hematocrit for all adolescents who have reached menarche, preferably at the age of 15 years. If dietary problems exits or if the clinical situation so requires, these tests should be more frequent.6

Bibliography
[1]
Nutrición en la adolescencia. En: Ballabriga A, Carrascosa A, directores. Nutrición en la infancia y adolescencia. 2.a edición. Madrid: Ergón, 2001; p. 449-91.
[2]
Recommended dietary allowances. 10th edition. Washington DC: National Academy Press, 1989;24:38.
[3]
Carencia de hierro en adolescentes (10-14 años). Aten Primaria 2002; 29(2):72-8.
[4]
S. Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd edition. Baltimore: Williams & Wilkins, 1996; p. 231.
[5]
Bright futures: National Guidelines for Health Supervision of Infants, Children, and Adolescents. Arlington: National Center for Education in Maternal and Child Health, 1994.
[6]
Committee on Practice and Ambulatory Medicine. Recommendations for preventive pediatric health care. Policy statement (RE9535), 2000.
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