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Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology 2014

[Iron deficiency anemia and anemia in chronic celiac disease in children].

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S V Bel'mer
E V Mitina
L M Karpina
N S Smetanina

Palabras clave

Abstracto

Anemia in celiac disease (CD) may be associated with deficiency of iron, vitamins, macro- and micronutrients. It is also possible the development of chronic disease anemia (CDA), associated with activation of proinflammatory cytokines. The aim of this work is to optimize the diagnosis and treatment of celiac disease in children on the basis of study of iron metabolism disorders heterogeneity, including the role of CDA.

METHODS

We observed 34 children with CD aged 1.5 to 17 years, 27 of them children were observed both in the active stage of the disease and in remission. The control group included 25 children aged 1.2 to 17 years who were previously excluded for any chronic (including autoimmune) disease: these children were observed with chronic functional gastrointestinal motility disorders. Special methods of examination were study of iron metabolism, including the determination of the serum hepcidin level, as well as the determination of the serum proinflammatory cytokines (tumor necrosis factor [TNF] -α, interleukin [IL] -2, IL-6, IL-10).

CONCLUSIONS

In active CD in 14.71% of children anemia of varying severity (mild or moderate) were diagnosed. Among these children we observed mild decrease of serum iron in the range 2.2-8.0 g/ml in 15 of 34 children (44%) and a marked reduction in serum ferritin level in 59% of children. In the active celiac disease in the majority of children there is a decrease in the serum hepcidin, but approximately in 20% of children serum hepcidin level was increased. This indicates the development of CDA in these children. During the active stage the average values of IL-2 was significantly increased (p < 0.05). Thus, the iron metabolism disorders in celiac disease is a result of immunopathological process which results in a reduction in iron absorption in the gut due to the intestinal mucosa villous atrophy and to improve the hepcidin production by liver cells and iron depot blocking with the CDA development in 20% of children.

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