Iron Deficiency Anemia in Alaska Native Children -- Hooper Bay, Alaska, 1999

During fall 1998, health-care providers in Hooper Bay, Alaska, reported that hemoglobin data from a local Head Start program indicated that 14 (31%) of the 45 children aged 2-4 years had anemia (hemoglobin less than 11.0 g/dL), with an overall mean hemoglobin of 11.2 g/dL (standard deviation [SD] plus or minus 1.3 g/dL) (CDC, unpublished data, 1996-1997). This proportion was substantially higher than the estimated prevalence in the United States of 8% among children aged 1-5 years (1). Because the region's economy is heavily dependent on fishing and the region experienced a poor salmon run in 1998, the Alaska State Health Department was concerned that economic hardships could exacerbate the anemia problem. In January 1999, CDC and the Yukon-Kuskokwim Health Corporation assessed the prevalence of anemia among Hooper Bay children aged 1-5.9 years to determine factors contributing to anemia in this population, and to identify recommendations for potential interventions. The findings indicated that the estimated prevalence of anemia among these children was more than twice the U.S. average.

Of the 128 children aged 1-5.9 years living in Hooper Bay, 86 (67%) participated in a cross-sectional survey. All the children were Alaska Natives, 44 (51%) were girls, and 73 (85%) were aged 2-5.9 years. Height, weight, general health, and nutrition variables were assessed, including parent reports of food frequency data for the previous month, household information (e.g., family composition and number of rooms in the house), and medical record review of infection (e.g., otitis media and pneumonia). Venous blood samples were collected to assess hemoglobin, blood lead, iron status (serum ferritin and transferrin receptor), C-reactive protein (CRP) (a nonspecific marker of inflammation or infection), and Helicobacter pylori infection (serum IgG antibody testing by enzyme-linked immunosorbent assay, which indicates current or past infection). Stool samples were collected from 53 children for fecal blood analysis. Informed consent for the children's participation was obtained from parents or guardians.

Using age-appropriate hemoglobin cutoffs (2), the prevalence of anemia was 17% (n=15), and the mean hemoglobin value was 11.9 g/dL (SD plus or minus 0.94 g/dL). None of the children had elevated blood lead levels ( greater than 10.0 µg/dL). Iron deficiency was associated strongly with anemia; 67% of the anemic children had low ferritin concentrations compared with 32% of the nonanemic children (p=0.01), and 60% of the anemic children had high transferrin receptor concentrations compared with 6% of the nonanemic children (p=0.001). After adjusting for age, sex, and inflammation using logistic regression, associations between iron deficiency and anemia became stronger.

Evaluation of a 1-month food history indicated that 54 children (63%) were not consuming the recommended dietary allowance of 10 mg of iron per day, but the mean amount of iron consumed each day (9.7 mg [SD plus or minus 6.7 mg]) was close to this allowance. Dietary iron intake was not significantly associated with anemia or iron deficiency in either crude or adjusted analyses. However, anemia was associated with lower intake of foods that enhance iron absorption such as citrus juices (p=0.04); these results were confirmed after adjusting for age, sex, dietary iron intake, and iron inhibitors.

Overall, 11 (14%)* of the children had elevated CRP levels; four (27%) of the anemic children had elevated CRP levels compared with seven (11%) of the nonanemic children, but this difference was not statistically significant (p=0.10). Analyses with medical records of infections, such as otitis media and pneumonia, during the month preceding the investigation and during the previous 2 years did not show any association with anemia.

H. pylori-specific IgG antibodies were present in 34 (41%) of the children (optical density values: greater than or equal to 1.30), absent in 30 (36%) (optical density values: less than 0.80), and indeterminate in 19 (23%) (optical density values: 0.80-1.29). Twelve (80%) of the anemic children and 22 (32%) of the nonanemic children were seropositive for H. pylori infection. H. pylori seropositivity was significantly associated with anemia (p=0.02) and with low ferritin (p=0.04) in this population. Children with indeterminate values were eliminated from these analyses. Of the 53 children for whom stool samples were available, three (6%) had an elevated stool heme content; testing positive for fecal heme was not associated with anemia.

Reported by: BD Gold, MD, M Owens, Dept of Pediatrics, Emory Univ School of Medicine, Atlanta, Georgia. DA Ahlquist, MD, J McConnell, MD, Mayo Clinic, Rochester, Minnesota. E Provost, DO, D Kruse, MD, J Klejka, MD, Yukon-Kuskokwim Health Corporation, Bethel; B Olson, Hooper Bay Traditional Council, Hooper Bay; E Jarin, Special Supplemental Nutrition Program for Women, Infants, and Children Office, Providence Alaska Medical Center, Anchorage; J Middaugh, MD, State Epidemiologist, Alaska State Health Dept; V Johnson, J Jordon, Alaska Native Medical Center Laboratory, Anchorage. P Klein, PhD, K Bush, MBA, Meretek Diagnostics, Inc., Houston, Texas, and Nashville, Tennessee. S Hooper, Summers & Hooper, Inc., Cincinnati, Ohio. Maternal and Child Nutrition Br, Div of Nutrition and Physical Activity, National Center for Chronic Disease Prevention and Health Promotion; Arctic Investigations Program, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases; Nutritional Biochemistry Br, Clinical Biochemistry Br, Div of Environmental Health and Laboratory Sciences, and Health Studies Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health; and an EIS Officer, CDC.

Editorial Note:

The estimated prevalence of anemia among Alaska Native children in this study was more than twice the average in the United States (1). Results supported data from previous studies in this region, which indicated that anemia primarily was related to iron deficiency (3). Iron deficiency anemia in early childhood is associated with potentially permanent cognitive and developmental deficits (2).

Children with anemia in this population had a significantly lower intake of foods that enhance iron absorption than nonanemic children, which indicates that dietary iron absorption may be a problem. In addition, H. pylori seropositivity emerged as a risk factor for anemia. Studies of the association between H. pylori infection and anemia in children have produced conflicting results (4,5); in a study in Bangladesh of children aged 0.5-2 years, a positive association was found between H. pylori infection and anemia (6). Studies have suggested several possible mechanisms for the association between anemia and H. pylori infection, including H. pylori-induced gastric hypoacidity, or achlorhydria, which may contribute to poor iron absorption, and an increase in iron demand because of bacterial competition for iron (7). Gastrointestinal loss of blood and iron, as estimated by fecal heme, did not explain the association between H. pylori and anemia in this group of children, as has been suggested in earlier studies with adults (8); however, results were based on one stool sample, and the normal levels for fecal heme have not been validated in young children.

The prevalence of anemia found in this investigation was lower than previously reported by health-care providers in the region (CDC, unpublished data, 1996-1997). Lower prevalence may be related to the different methods used to determine hemoglobin levels. Venous blood, a more reliable specimen for hemoglobin analysis (9), was used in this investigation, whereas most anemia screening programs collect capillary blood by finger stick, often the most feasible method for small clinics. Capillary sampling generally results in higher hemoglobin values (9), but if performed improperly, this technique might lower the hemoglobin estimates (10). In areas where capillary sampling is relied on to assess hemoglobin levels, appropriate training and periodic follow-up may increase data reliability.

The findings in this report are subject to at least three limitations. First, small sample size may make it difficult to detect differences, and reliance on a cross-sectional design limits inferences about the directionality of associations and causality. Second, children who participated may not be representative of all of the children in the village. Third, although the food frequency questionnaire was piloted in Alaska, it was not specifically validated against 24-hour recalls with children in this village.

Given the potential association between H. pylori and anemia, and the role of H. pylori in the development of peptic ulcer disease, chronic gastritis, and gastric cancer, more research is needed to identify modes of transmission and appropriate interventions for H. pylori infection. Efforts are under way to ensure that anemic children are followed closely and to address issues related to anemia screening and surveillance. Prevention and control strategies for iron deficiency anemia should be implemented in this population of children in accordance with CDC recommendations (2).

References

1. CDC. Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III Examination Data File [CD-ROM]. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1996. (Public use data file documentation No. 76200.)
2. CDC. Recommendations to prevent and control iron deficiency in the United States. MMWR 1998;47(no. RR-3).
3. CDC. High prevalence of iron deficiency anemia among Alaskan Native children. MMWR 1988;37:200-2.
4. Friedman CR, Quick R, Khanna B, et al. Epidemiology of Helicobacter pylori infection in rural Bolivian children. J Pediatr Gastroenterol Nutr 1997;25:466.
5. Dufour C, Brisigotti M, Fabretti G, Luxardo P, Mori PG, Barabino A. Helicobacter pylori gastric infection and sideropenic refractory anemia. J Pediatr Gastroenterol Nutr 1993;17:225-7.
6. Bardhan PK, Hildebrand P, Sarker SA, et al. Helicobactor pylori infection in children: is there an association with anemia? Gastroenterology 1997;112:A65.
7. Milman N, Rosenstock S, Andersen L, Jorgensen T, Bonnevie O. Serum ferritin, hemoglobin, and Helicobacter pylori infection: a seroepidemiologic survey comprising 2794 Danish adults. Gastroenterology 1998;115:268-74.
8. Yip R, Limburg PJ, Ahlquist DA, et al. Pervasive occult gastrointestinal bleeding in an Alaska Native population with prevalent iron deficiency: role of Helicobacter pylori gastritis. JAMA 1997;277:1135-9.
9. Thomas WJ, Collins TM. Comparison of venipuncture blood counts with microcapillary measurements in screening for anemia in one-year-old infants. J Pediatr 1982;101:32-5.
10. CDC. Final report on USDA funded pilot project to improve hemoglobin screening in Alabama and Georgia WIC clinics. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, CDC, 1996.

* Denominators may vary because of missing data on some of the variables.

Disclaimer   All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

Page converted: 8/19/1999

HOME  |  ABOUT MMWR  |  MMWR SEARCH  |  DOWNLOADS  |  RSS |  CONTACT POLICY  |  DISCLAIMER  |  ACCESSIBILITY

Morbidity and Mortality Weekly Report Centers for Disease Control and Prevention 1600 Clifton Rd, MailStop E-90, Atlanta, GA 30333, U.S.A Department of Health and Human Services

This page last reviewed 5/2/01