ABSTRACT
AIM: To examine the relationship between iron deficiency (ID) and Helicobacter pylori infection in school-aged children. METHODS: Altogether 363 children from ambulatory admission were consecutively enrolled in the study. Haemoglobin (Hb), soluble transferrin receptor (sTfR), IgG against H. pylori and IgA against tissue transglutaminase were measured. The criteria for ID were sTfR > 5.7 mg/L in children aged 7-12 years and sTfR > 4.5 mg/L in older children, for anaemia Hb < 115 g/L in the younger group and Hb < 130 g/L for older boys and Hb < 120 g/L for girls. RESULTS: Iron deficiency was found in 17% of the children, 5% had also anaemia. H. pylori colonization was detected in 27% and serum markers for coeliac disease in 0.6% of the children. The prevalence of ID and H. pylori seropositivity was higher in older children (23% and 29%, vs 9% and 22%, respectively). Children with H. pylori were significantly shorter [length SDS 1.0 (0.98-1.01) vs 0.98 (0.97-0.99)]. Older children had risk for ID (OR 1.1, 95% CI 1.0-1.3, p = 0.03). Although the prevalence of H. pylori seropositivity was higher in the ID group, it was not significantly associated with ID in multivariate analysis. CONCLUSION: Helicobacter pylori seropositivity was not associated with ID. The associated factor for ID was age.
Subject(s)
Anemia, Iron-Deficiency/epidemiology , Antibodies, Bacterial/blood , Helicobacter Infections/epidemiology , Helicobacter pylori/immunology , Iron Deficiencies , Adolescent , Age Factors , Anemia, Iron-Deficiency/blood , Child , Confidence Intervals , Estonia/epidemiology , Female , Helicobacter Infections/blood , Hemoglobins/analysis , Humans , Immunoglobulin A/blood , Immunoglobulin G/blood , Logistic Models , Male , Odds Ratio , Receptors, Transferrin/blood , Risk Assessment , Seroepidemiologic StudiesABSTRACT
BACKGROUND: In addition to IgA anti-endomysial antibodies, IgA anti-smooth muscle antibodies have been observed in a number of patients with coeliac disease (CoD), but only limited data exist on the frequency and antigen specificity of IgA against cytoskeletal proteins in CoD. METHODS: We evaluated the sera of 42 untreated CoD patients, follow-up sera of 26 CoD patients after treatment, and 116 control sera for IgA reactivity to cytoskeletal proteins from the human umbilical cord (HUC) by immunoblotting, and compared the results with anti-tissue transglutaminase IgA (anti-tTG IgA) ELISA and immunofluorescence results. RESULTS: Serum IgA from CoD patients most frequently recognized a 57-kD antigen in HUC cytoskeletal extract, identified as desmin using mass spectrometry and internal peptide sequencing. Increased IgA reactivity to the human desmin band was detected in 22 children with untreated CoD (52.4%), in 4 treated CoD patients (15.4%), and in 12 control subjects (10.3%) (p < 0.01); similar results were obtained with anti-chicken desmin IgA ELISA. Anti-tTG IgA levels (increased in 71.4% of untreated CoD patients) correlated significantly with anti-desmin IgA levels in untreated CoD, and both autoantibody reactivities decreased in response to a gluten-free diet. Pre-adsorption experiments and affinity purification of anti-desmin IgA antibodies further confirmed that desmin is an IgA autoantigen in CoD and is recognized by antibodies which are not cross-reactive with tTG. CONCLUSIONS: Anti-desmin IgA antibodies are frequently occurring if not the predominant cytoskeletal antibodies in children with untreated CoD and could be related to the disease process in the small intestine.
