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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fanconi anaemia (FA) is a recessively inherited disorder associated with a typical physical appearance and a spectrum of clinical and laboratory characteristics. Parental heterozygotes of FA patients are superficially normal in appearance and lack overt laboratory abnormalities. Furthermore, they are indistinguishable from normal subjects on chromosome analysis. In order to determine if any of the clinical or laboratory abnormalities seen in FA patients were detectable to a lesser degree in heterozygotes, we carried out detailed skeletal measurement and laboratory investigation on 16 obligate FA heterozygotes and compared the results with 40 normal control subjects. Skeletal proportions in FA heterozygotes showed significant differences from normal subjects in the ratio of the height to the inter-acromial distance (p less than 0.001), and in having significantly shorter forearms (p less than 0.05). Apart from two patients with presumed iron deficiency, haemoglobin levels were normal, but three patients showed neutropenia (less than 1.5 X 10(9)/l). Foetal haemoglobin measurements were significantly higher (p less than 0.01) and natural killer cell subsets lower (p less than 0.05) in heterozygotes. Significantly reduced mitogenetic responses to phytohaemagglutinin and interleukin-2 of peripheral blood lymphocytes in heterozygotes was also demonstrated. These results suggest that heterozygotes show minor physical and haematological abnormalities consistent with partial expression of the Fanconi gene in the heterozygote.
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PMID:Physical and laboratory characteristics of heterozygote carriers of the Fanconi aplasia gene. 226 25

The effects of iron deficiency on immunity remain controversial. This study was designed to assess the impact of iron supplementation on the immune status, in 81 children aged 6 months-3 years, at high risk for iron deficiency, using a longitudinal double blind randomised and placebo-controlled study. Lymphocytes of iron-deficient children produced less interleukin-2 in vitro. Iron supplementation for 2 months increased mean corpuscular volume, serum ferritin and serum transferrin, but had no effect on the parameters of T-cell mediated immunity. The lower interleukin-2 levels in iron-deficient suggest that cell-mediated immunity may be impaired in iron deficiency.
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PMID:The immune response in iron-deficient young children: effect of iron supplementation on cell-mediated immunity. 844 18

Ulcerative colitis (UC) patients frequently require iron supplementation to remedy anemia. The impact of systemic iron supplementation (intraperitoneal injection) on UC-associated carcinogenesis was assessed in mice subjected to cyclic dextran sulfate sodium (DSS) treatment and compared with dietary iron enrichment. Systemic iron supplementation, but not a twofold iron diet, remedied iron deficiency as indicated by the histochemical detection of splenic iron stores. A twofold iron diet, but not systemic iron, increased iron accumulation in colonic luminal contents, at the colonic mucosal surface, and in superficial epithelial cells. Colitis-associated colorectal tumor incidence after 15 DSS cycles was not affected by systemic iron (2/28; 7.1%) compared to nonsupplemented controls (4/28; 14.1%) but was significantly increased by the twofold iron diet (24/33; 72.7%) (P < 0.001). Mechanistic study revealed that systemic iron had no effect on DSS-induced inflammation, or colonic iNOS and COX-2 protein levels, compared to controls. Systemic iron supplementation for 16 weeks replenished splenic iron in a spontaneous colitis model (interleukin-2-deficient mice) and significantly reduced colonic inflammation compared to interleukin-2 (-/-) controls without increasing hyperplastic lesions. These results suggest that iron supplemented systemically could be used to remedy anemia in UC patients without exacerbating inflammation or enhancing colon cancer risk. These findings need to be verified in clinical studies.
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PMID:Systemic iron supplementation replenishes iron stores without enhancing colon carcinogenesis in murine models of ulcerative colitis: comparison with iron-enriched diet. 1584 5