Anemia and Iron Deficiency in Children With Potential Celiac Disease.
Active screening for celiac disease frequently detects seropositive children with normal villous morphology (potential celiac disease). It remains unclear whether these subjects should be treated. We here investigated the prevalence of anemia and iron deficiency in children with potential and mucosal atrophy celiac disease.



The prospective study involved 19 children with potential disease, 67 with partial or subtotal villous atrophy (P/SVA), and 16 with total villous atrophy (TVA). Twenty-three healthy children comprised the control group. The groups were compared for various clinical, histological, and laboratory parameters and hepcidin.



The prevalence of abnormal parameters was as follows (controls, potential celiac disease, P/SVA, and TVA, respectively): anemia 0%, 15%, 22%, and 63%; low iron 5%, 0%, 14%, and 50%; increased transferrin receptor 1 5%, 16%, 20%, and 47%; low ferritin 0%, 21%, 35%, and 87%; and low transferrin saturation 10%, 11%, 41%, and 71%. One subject had low folate and none had low vitamin B12. The median values for hemoglobin, total iron, ferritin, and transferrin saturation were significantly lower and transferrin receptor 1 values higher in TVA group compared with other groups. After a median of 7 months on a gluten-free diet hemoglobin, total iron, ferritin, and albumin in children with P/SVA exceeded the baseline values in the potential celiac disease group.



The development of anemia and iron deficiency in celiac disease is a continuum and may already be present in children with normal villous morphology, advocating an early diagnosis and possible dietary treatment of these patients.
*Tampere Centre for Child Health Research, University of Tampere and Tampere University Hospital †Tampere School of Health Sciences, University of Tampere, Tampere ‡Molecular Genetics of Immunological Diseases Group, University of Helsinki, Helsinki §Department of Internal Medicine, Tampere University Hospital ||School of Medicine, University of Tampere, Tampere, Finland.
Marleena
M
Repo
Katri
K
Lindfors
Markku
M
Mäki
Heini
H
Huhtala
Kaija
K
Laurila
Marja-Leena
ML
Lähdeaho
Päivi
P
Saavalainen
Katri
K
Kaukinen
Kalle
K
Kurppa
D000293:Adolescent; D000740:Anemia / Q000097:blood / Q000209:etiology*; D018798:Anemia, Iron-Deficiency / Q000097:blood / Q000209:etiology*; D001284:Atrophy; D002446:Celiac Disease / Q000097:blood / Q000175:diagnosis / Q000178:diet therapy / Q000473:pathology*; D002648:Child; D002675:Child, Preschool; D055050:Diet, Gluten-Free; D018450:Disease Progression; D005260:Female; D005293:Ferritins / Q000097:blood; D005494:Folic Acid Deficiency / Q000097:blood / Q000209:etiology; D006454:Hemoglobins / Q000378:metabolism; D064451:Hepcidins / Q000097:blood; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology*; D007501:Iron / Q000097:blood; D000090463:Iron Deficiencies; D008297:Male; D011446:Prospective Studies; D011990:Receptors, Transferrin / Q000097:blood; D012709:Serum Albumin / Q000378:metabolism; D014168:Transferrin / Q000378:metabolism
D006454:Hemoglobins; D064451:Hepcidins; D011990:Receptors, Transferrin; D012709:Serum Albumin; D014168:Transferrin; D005293:Ferritins; D007501:Iron