Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of coeliac disease (CD) in the adult population is unknown because silent and latent stages do exist. Type 1 diabetes mellitus may be associated with CD because of common genetic background and/or shared pathogenetic mechanisms. We investigated 74 adults with type 1 diabetes (32+/-11 yr, disease duration 13+/-9 yr), 69 parents of diabetic probands (56+/-10 yr), 59 siblings (30+/-11 yr) and 50 healthy controls (35+/-10 yr) for the presence of circulating islet cell antibodies (ICA), anti-glutamic acid decarboxylase antibodies (GADA65), anti-gliadin immunoglobulins A and G (IgA- and IgG-AGA). All patients with raised AGA, performed also IgA anti-endomysium antibody (EmA) indirect immunofluorescence assay. Samples were positive for ICA in 19 diabetics (26%), 4 parents (6%), 4 siblings (7%), 0 controls (p<0.001); for GADA in 34 diabetics (46%), 4 parents (6%), 1 sibling (2%), 0 controls (p<0.001). Twenty-five diabetic patients (34%), 10 parents (14%), 5 siblings (8%), 3 controls (6%) (p<0.001) had raised IgA-AGA (>4.4 mg/l). Four diabetic patients (5%), 5 parents (7%), 0 siblings (0%), 4 controls (8%) had raised IgG-AGA (>18 mg/l). Both IgA- and IgG-AGA were detected in 1 diabetic and 2 parents. The prevalence of ICA, GADA, and IgA-AGA positivity in Type 1 diabetes patients was significantly higher than in controls (p<0.001). Finally, 50 AGA-positive subjects performed EmA test: only 2 of them resulted EmA-positive, a diabetic patient and a sibling. The patient with Type 1 diabetes had a small-bowel biopsy specimen consistent with CD and, as sole evidence of malabsorption, sideropenic anaemia. EmA-positive sibling also showed severe iron deficiency, yet refused endoscopy. We conclude that: 1) CD cannot be diagnosed on the basis of associated IgA- and IgG-AGA alone. Nevertheless, detection of such antibodies is useful, in combination with EmA, in screening for endoscopic biopsy; 2) too high rate of detection of IgA-AGA in Type 1 diabetic patients in comparison with other groups excludes a false positivity of the test itself, while suggests a pathogenetic association of both immunological disorders, perhaps related to abnormal gammadelta TCR-bearing intraepithelial lymphocytes.
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PMID:Screening for coeliac disease in families of adults with Type 1 diabetes based on serological markers. 1134 64

The interaction of CD28 and its ligands (CD80, CD86) on antigen presenting cells and that of TCR/CD3-MHC are required for T lymphocyte activation. To determine whether impaired lymphocyte proliferation associated with iron deficiency is due to reduced expression of these ligands, spleen cells obtained from eight to nine C57BL/6 mice/group of iron deficient (ID), iron replete (R), control (C), pair-fed (PF), and high iron (HI) mice were labeled with anti-CD80-fluorescein isothiocyante (FITC) and anti-CD86-FITC. Diets differed only in iron concentration: 5, 50, and 125 mg/kg for the ID, C, and HI, respectively. Mean levels of hemoglobin and liver iron stores of ID and R mice were less than 50% those of C mice (P < 0.005). In non-activated and concanavalin A-treated cultures, significant differences were observed among groups in the percentage of CD80 + cells: ID>R > C = PF = HI (P < 0.05). The same trend was observed for CD86 + cells (P > 0.05). Fluorescence intensity (FI) of either marker did not significantly change by iron status. In vitro iron chelation by deferoxamine (20, 200 microg/ml) for 1, 2, and 24 h increased FI of both markers on unactivated B and T cells (P < 0.05). However, it had no effect on FI of either marker of mitogen-treated cells presumably because the maximum levels are achieved by the mitogen. Lymphocyte proliferative responses to mitogens positively and significantly correlated with CD80 and CD86 FI (r = 0.41-0.59) but negatively correlated with the percentages of CD80 + cells (r = -0.48) (P < 0.05). Data suggest that impaired lymphocyte proliferation associated with iron deficiency is not due to reduced CD80 and CD86 expression.
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PMID:Differential effects of iron deficiency on the expression of CD80 and CD86 co-stimulatory receptors in mitogen-treated and untreated murine spleen cells. 1221 Jul 63