Project Details

Early Career

Status: Funded - Open

Contribution of inherited hemoglobin disorders to anemia among children in urban Cameroon

Reina Engle-Stone, Ph.D.


BACKGROUND: Causes of child anemia include nutritional deficiencies, malaria and helminth infections, and inherited hemoglobin disorders, such as sickle cell disease and thalassemias. Presumptive treatment of anemia with iron supplements is ineffective and possibly harmful if anemia is not due to iron deficiency.

GAP: Inherited hemoglobin disorders (IHD) are assumed to be common in sub-Saharan Africa, but only limited data are available on the prevalence of these conditions in representative, population samples and the extent to which they contribute to anemia. Such data are necessary to construct public health programs that permit appropriate treatment of the affected individuals and avoid unnecessary supplementation with iron.

HYPOTHESIS: We hypothesized that the selected hemoglobin (Hb) disorders (Hb S and C, and alpha-thalassemia) would be present among young children in urban Cameroon, and that each disorder will be associated with reduced Hb concentration and greater prevalence of anemia, after controlling for malaria and markers of inflammation and nutritional status.

METHODS: Among 291 children selected during a representative survey in Yaoundé and Douala, Cameroon, we assessed malaria infection and measured Hb, plasma indicators of iron, folate, and vitamin A and B-12 status, and markers of inflammation. Blood samples were analyzed for Hb variants (S, A, and C) and alpha-thalassemia (3.7-kb alpha-globin deletions).

RESULTS: Mean ± SE Hb concentration among children was 110 ± 1 g/L, and 46% of children were anemic (hemoglobin < 110 g/L). Malaria was diagnosed in 8% of children, and 46% of children had evidence of subclinical inflammation (elevated C-reactive protein and/or α1-acid glycoprotein). The prevalence of HbAS and HbSS was 13.7% and 1.6%, and 30.6% and 3.1% of children had heterozygous and homozygous α+thalassemia, respectively. Compared with HbAA children, HbAS children were more likely to be anemic (60.3 vs 42.0%, P=0.038; although mean Hb did not differ, P=0.38) and had higher inflammation-adjusted ferritin (36.8 vs 30.3 µg/L, P=0.040). Among children with and without heterozygous α+thalassemia, Hb, anemia, and micronutrient status did not differ. In multi-variable models, anemia was independently predicted by HbAS, HbSS, malaria, iron deficiency (inflammation-adjusted ferritin <12 µg/L), higher CRP, lower plasma folate, and younger age.

IMPACT:  IHD are prevalent but contribute modestly to anemia among children in urban Cameroon. Anemia control programs should address both nutritional status and infectious disease.

Anemia, Malaria, Micronutrients, Retrospective Cohort, Diagnosis, Human

Supervising Institution:
University of California, Davis

Kenneth Brown, Ralph Green

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