Thursday, May 12, 2011: 2:00 PM
Elizabeth Ballroom D (Manchester Grand Hyatt)
2:00 PM
A. M. Reynolds1, C. A. Molloy2, S. J. James3, C. Johnson4, T. Clemons5 and S. L. Hyman6, (1)University of Colorado Denver, Aurora, CO, (2)Cincinnati Children's Hospital Medical Center, Cincinnati, OH, (3)University of Arkansas for Medical Sciences, Little Rock, AR, (4)University of Pittsburgh, Pittsburgh, PA, (5)EMMES Corp, Rockville, MD, (6)University of Rochester School of Medicine, Rochester, NY, United States
Background: Children with Autism Spectrum Disorders (ASD) have a high rate of food selectivity and restricted diets which puts them at risk for nutritional deficiencies (Schreck, 2004). Understanding iron status in children with ASD is important because there is mounting evidence that iron deficiency can have a negative impact on development and may be associated with sleep disorders such as restless leg syndrome. Children with ASD have a high rate of sleep disorders (Richdale, 2009). One study (Latif, 2002) found high rates of iron deficiency anemia (11.5%) and low ferritin (52%) in children with ASD. Another study found low ferritin in children with ASD and restless sleep (Dosman, 2007). The diagnosis of iron deficiency is complex, however, major breakthroughs in understanding iron metabolism have occurred over the last several years. Biomarkers such as hepcidin and soluble transferrin receptor (sTfR) have been found to play an important role in iron absorption and transport into red blood cells. Unfortunately, normal values for these markers in children are lacking. The National Health and Nutrition Examination Survey (NHANES) uses the “ferritin model” to define iron deficiency which is defined as low levels on 2 of 3 measures: ferritin, transferrin saturation, and erythrocyte protoporphyrin. The “body iron model” uses ferritin and sTfR (Cogswell, 2009). The World Health Organization (2005) recommends evaluation of iron status for population studies to include CBC, transferrin saturation, ferritin, and sTfR.
Objectives: To determine the rate of iron deficiency in children with ASD.
Methods: Children ages 2-10 years, enrolled in the Autism Treatment Network at 5 sites were eligible. All had a clinical diagnosis of ASD, confirmed by the Autism Diagnostic Observation Schedule. A 3 day diet record, ferritin, CBC, iron, total iron binding capacity (TIBC), and transferrin saturation were collected for each child. Hepcidin, sTfR, and c reactive protein (CRP) were collected from subjects who consented to an ancillary study.
Results: Preliminary data are available for 131 subjects (101 with autism, 8 with PDD, 22 with Asperger) who have had blood drawn for iron studies. Twenty-six (20%) had low ferritin and 41 (33%) had low transferrin saturation, however only 10 (8%) were low for both. There were only 3 subjects with low hematocrit associated with iron deficiency (2%). Iron deficiency defined by low ferritin and transferrin saturation was found in 10 children (8%) with ASD, of those 3 had evidence of mild iron deficiency anemia. This is in contrast to NHANES which found that 3% of 3-5 year olds in the general population have iron deficiency defined by the ferritin model.
Conclusions: While the determination of iron status is complex, children with ASD may be at risk for iron deficiency without anemia at a higher rate than the general population. Once more data are available, iron status will also be evaluated using transferrin receptors, CRP, and hepcidin. Iron status will then be compared to iron intake from both heme and non-heme dietary sources, and to clinical symptoms as measured by the Children’s Sleep Habits Questionnaire and the Child Behavior Checklist.
