An association between Helicobacter pylori infection and iron deficiency anemia has been reported in children, and it has been proposed that H. pylori infection needs to be eradicated to treat absolutely iron deficiency anemia (IDA). We investigated whether there was any correlation between H. pylori infection and iron deficiency (ID) and IDA in children, and whether the eradication of H. pylori infection without iron treatment would lead to the resolution of ID. Hemoglobin and ferritin levels, H. pylori stool antigen test and (14)C urea breath test were measured in 140 children aged 6--16 years (median 9.5 years). Children with H. pylori infection were divided into three groups on the basis of hemoglobin, mean corpuscular volume (MCV), and serum ferritin levels: groups of IDA, ID, and control. All the children received anti-H. pylori combination therapy consisting of amoxicillin, clarithromycin, and lansoprazole. Hemoglobin and MCV values rose significantly compared with baseline values after H. pylori eradication without iron supplementation in children with IDA (p=0.002 and p=0.003, respectively). Ferritin values increased significantly after H. pylori eradication in children with ID (p<0.001). We conclude that complete recovery of ID and IDA can be achieved with H. pylori eradication without iron supplementation in children with H. pylori infection.

The aim of this study was to investigate the changes in the peripheral blood of newborns of hypertensive mothers. The umbilical cord blood from newborns of 31 hypertensive mothers and 32 healthy mothers were examined. In all subjects, complete blood count, peripheral blood smear, reticulocyte count, vitamin B12, folate, ferritin levels and hemoglobin electrophoresis were performed. The subjects were followed up on for 1 year in terms of infections. RBC, hemoglobin, reticulocyte count and normoblast count were higher in the newborns of hypertensive mothers compared to the control group, and total leukocytes, neutrophil, lymphocyte, monocyte, eosinophil, and thrombocyte counts were lower. The number of neutropenic and thrombocytopenic subjects in newborns of hypertensive mothers was higher compared to the control group. On peripheral smears, dysplastic changes in neutrophils and erythrocytes were observed with a higher rate in newborns of hypertensive mothers compared to the control group. HbF levels were found to be higher in newborns of hypertensive mothers compared to the control group. During the follow-up period of 1 year, the number of infections in newborns of hypertensive mothers was found to be higher than the control group. Conclusion: Newborns of hypertensive mothers should be carefully evaluated and monitored in terms of hematologic abnormalities. Complete blood counts and peripheral blood smears can be used as significant parameters for early diagnosis of possible complications.

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On the contrary of children with beta-thalassemia major, renal tubular dysfunction has not been determined in children with beta-thalassemia minor in the present study.

This study was performed to investigate the platelet aggregation alterations in platelet-rich plasma (PRP) samples of children with Helicobacter pylori (H pylori) infection. Platelet aggregation induced by adenosine diphosphate (ADP), collagen, ristocetin, or epinephrine was studied with photometric aggregometry in 30 patients before and after eradication therapy and in a control group including 15 children. The pretreatment mean maximum aggregation values and slope were significantly lower (P < .0001) in the study group at 10 μmol/L concentrations of ADP (ADP-like defect). The maximum aggregation values and slope revealed no significant differences (P > 0.05) between the study group after therapy and the control group. We concluded that H pylori infection may cause dysfunction of platelets in children and can be reversed by H pylori eradication therapy. Further studies should be carried out to determine the mechanisms of platelet dysfunction in children with H pylori infection.