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

There is increasing evidence that both iron overload and iron deficiency are associated with significant abnormalities of immune function. In diseases associated with iron overload there is increased susceptibility to both infection and neoplasia. The precise mechanisms are still being unravelled but iron overload has been shown to impair antigen-specific immune responses and to reduce the number of functional helper precursor cells. Similarly, iron in vitro in concentrations reported to be present in the serum of patients with iron overload impairs the generation of cytotoxic T-cells, enhances suppressor T-cell activity and reduces the proliferative capacity of helper T-cells. The predominant tumor seen in iron overload is primary hepatocellular carcinoma; however other aetiological factors appear to be involved in addition to iron overload, especially hepatic cirrhosis. Nevertheless, primary liver cancer occurs much more frequently in hemochromatosis than in other forms of cirrhosis. Iron deficiency is associated with an altered response to infection but the relationship is again a complex one. The cellular mechanisms involved have yet to be clearly defined, although impaired T and B cell function have been demonstrated.
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PMID:Iron status and cellular immune competence. 328 53

Plasma ferritin is a secretory component of intracellular ferritin synthesis. In normal persons its amount reflects the size of iron stores. A decrease to less than 12 mug per liter indicates iron deficiency. Increased iron stores are associated with an increased plasma ferritin level. Various other conditions, however, can increase the plasma ferritin concentration including increased metabolism, inflammation, tissue damage and neoplastic disease. The use of the plasma ferritin determination in diagnosing iron overload depends on excluding these other causes, leaving storage iron as the only explanation for the increased plasma ferritin. It is then necessary to establish the parenchymal nature of the iron overload by showing an elevated transferrin saturation and, if elevated, the more definitive liver biopsy should be done.
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PMID:Plasma ferritin determination as a diagnostic tool. 354 87

The hematologic status of 265 patients with rheumatoid arthritis was assessed. In the group as a whole, a mild depression in the hemoglobin concentration and mean cell volume (MCV) was associated with an increase in the red blood cell distribution width (RDW), erythrocyte sedimentation rate (ESR), and platelet count. Bone marrow trephine biopsies and further measurements of iron status and disease activity were done in [a further] 38 more anemic patients, and the findings in those with absent marrow iron (iron deficiency) were compared with those having stainable stores (anemia of chronic disorders). The RDW was raised in both, and there was no significant difference between the two groups. The concentrations of nonheme iron in the marrow and of serum ferritin were significantly lower in the iron-deficient group, but the geometric mean serum ferritin of 34 micrograms/L was still a good deal higher than that associated with uncomplicated iron deficiency. This was presumably because of the fact that the serum ferritin, which was significantly correlated with the ESR (r 0.55; P less than 0.0004) and C-reactive protein (CRP) r 0.41; P less than 0.01), was also functioning as an acute phase protein. While there was a weak correlation (r 0.37; P less than 0.04) between the marrow nonheme iron and the serum ferritin concentrations, it disappeared when nonactive patients with normal CRP concentrations were excluded. The absence of a correlation is unlike the findings that have previously been noted in other chronic inflammatory conditions and in neoplasia. This raises the possibility that serum ferritin concentrations in rheumatoid arthritis may reflect, in part at least, another store of iron located in affected joints.
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PMID:Hematologic and iron-related measurements in rheumatoid arthritis. 381 50

Normal and neoplastic cells have similar needs for iron, but the latter may exhibit altered mechanisms of iron acquisition that permit continued multiplication in host iron-restricted tissues. For example, neoplastic cells may form low molecular weight siderophores as well as increase the number of transferrin binding glycoproteins on their cell surfaces. The hosts attempt to withhold iron from neoplastic cells by preventing the return of the metal to plasma and diverting it to storage, by increasing the synthesis of ferritin to accommodate the added stores, and by surrounding tumor cells with macrophages that can ingest lactoferrin-bound iron, but these mechanisms are often not effective against the iron-accumulating mechanisms of the tumor. Persons or animals with iron overload (via ingestion, inhalation, injection, or pathophysiologic process) tend to be at greater risk than normal hosts in the development of neoplasms. The tumors are often associated with the site(s) of deposition of the metal. In addition to its neoplastic cell nutrient function, excess iron might suppress tumorcidal action of macrophages and interfere with lymphocyte traffic. Severe iron deficiency can interfere with the ability of the host to detoxify potential carcinogens as well as with its ability to activate antitumor lymphocytes.
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PMID:Iron in neoplastic disease. 630 39

The introduction of a WHO Standard for serumferritin effected a standardisation of different methods, improving quality and security for clinical routine diagnostic purposes. Therefore the clinical evaluation of serumferritin gained even more importance. For Evaluation of iron stores of children, pregnant women, population studies, patients on hemodialysis or patients with rheumatoid arthritis low serumferritin values give safe results. In addition serumferritin is of clinical usefulness in monitoring therapy of both iron deficiency and iron overload. Evaluating a single serumferritin value one should consider the total clinical situation of the patient. As some tumors can produce and secrete serumferritin, e. g. acute myeloblastic leukemia, germ cell tumors, malignant melanoma, serumferritin might be helpful in monitoring the malignant disease. The ongoing characterization of tissue isoferritin, especially acidic isoferritin, may eventually lead to a clinically significant diagnostic marker of neoplasia.
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PMID:[Serum ferritin--its diagnostic relevance and clinical significance]. 638 4

An 11-year-old boy was noted to have microcytic anemia, growth retardation, polyclonal hypergammaglobulinemia, and abnormal platelet function. An angiomatous lymphoid hamartoma was removed from the retroperitoneal space. Postoperatively the child exhibited a dramatic growth spurt and complete resolution of the abnormal laboratory measurements. Studies were performed before and after tumor removal to investigate the nature of the associated anemia, growth retardation, and altered hemostasis. There was no evidence of iron deficiency, thalassemia, or an antierythropoietin factor. Prolonged bleeding time and impaired ristocetin-induced platelet aggregation normalized following tumor resection. Serum obtained before surgery inhibited lymphocyte proliferation in mixed lymphocyte culture as well as fibroblast growth in vitro. Detailed study of growth regulatory hormones failed to reveal significant alterations except for significantly reduced somatomedin which normalized after surgery. The factor(s) which inhibit in vitro cellular growth and lower in vivo plasma somatomedin concentration remain unknown.
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PMID:Angiomatous lymphoid hamartoma: inhibitory effects on erythropoiesis, growth, and primary hemostasis. 726 91

The effect of iron deficiency on tumour growth and on host survival was studied in BALB/c mice with transplanted Merwin Plasma Cell-II tumors. Iron deficiency was induced by maintaining the animals on an iron-free diet consisting of milk-cornflour supplemented with CuCl2 and vitamins A and D. Iron deficiency resulted in retardation of both body and tumor growth in weanling BALB/c mice. Their survival, however, was not significantly different from that of iron supplemented controls. The inhibitory effect of iron deficiency on host and tumour growth could not be reproduced in adult BALB/c mice. The survival of tumor-bearing hosts maintained on a milk-cornflour diet (whether supplemented with iron or not) was significantly longer than that of animals maintained on a purina diet.
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PMID:Effect of iron deficiency on transplantable murine plasmacytoma. 734 86

The relationship between iron deficiency and carcinogenesis was studied using the carcinogen dimethylhydrazine to induce gastrointestinal tumors in Fischer 344 control and iron-deficient rats. Dimethylhydrazine (30 mg/body wt) was administered by gastric intubation 10 times over nine weeks. After 32 weeks, rats were sacrificed, and tumor incidence was assessed. The overall incidence of gastrointestinal tract tumors (colonic and duodenal) was higher in the iron-deficient (66%) than in the control group (46%). Whereas the incidence of colonic tumors was identical in control and iron-deficient groups, the duodenal tumor incidence was significantly elevated in iron deficiency. Five of 15 rats, i.e., 33.3%, in the iron-deficient group developed duodenal tumors; in the control group, only 1 of 15 rats developed a tumor (i.e., 6.6%). Also, iron-deficient rats had multiple tumors. Histological examination of the colon and duodenum revealed that the tumors were adenocarcinomatous in nature. Another notable feature in the iron-deficient group was the presence of atypical cells in the livers of carcinogen-treated iron-deficient rats. This study thus suggests that there is a greater incidence of tumors in iron deficiency and that the proximal part of the intestines seems to be the preferred site. The presence of atypical cells in the liver suggests that in iron deficiency, besides gastrointestinal tract tumors, the liver may also be a favored site for abnormalities.
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PMID:Effect of iron deficiency on DMH-induced gastrointestinal tract tumors and occurrence of hepatocyte abnormalities in Fischer rats. 787 98

Occult gastrointestinal bleeding is loss of blood into the digestive tract that is not apparent to the patient or physician by physical examination. It is detected by examination of the stool for chemical evidence of blood by laboratory techniques or by the observation of iron deficiency. The presence of occult blood is important because it may indicate otherwise asymptomatic gastrointestinal neoplasia, assist with the evaluation of gastrointestinal symptoms in the absence of visible bleeding, and point toward a digestive tract source of blood loss in the patient with iron-deficiency anemia.
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PMID:Occult gastrointestinal bleeding. 813

Transferrin receptors are present on almost all mammalian cells. The receptor participates in the cellular acquisition of iron from transferrin by receptor-mediated endocytosis. Receptor abundancy is generally regulated by two factors: i) cellular iron status and ii) cell growth. These two factors form the basis for the utilization of transferrin receptor determination as a diagnostic tool. In the assessment of body iron status and erythropoietic activity the measurement of circulating transferrin receptor has proved to be of value as a measure of mild tissue iron deficiency, to distinguish iron deficiency anemia from the anemias of chronic disease, and as a sensitive index of iron deficiency during pregnancy. Histochemical analysis of the presence and abundancy of the transferrin receptor will continue to serve as an additional tool in special cases to distinguish between malignant and normal cell growth, and to provide additional information about the biological behaviour of tumor cells. Finally, the transferrin receptor holds a potential as a target for direct and indirect drug delivery in the therapy of malignant cell growth.
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PMID:The transferrin receptor: its diagnostic value and its potential as therapeutic target. 832 47


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