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

Two infants, a sister with motor retardation and brother with slight microcephaly and an undescended testis, died of hepatoblastoma. Only another documented familial occurrence of this tumor, affecting siblings of the same sex, can be found in the literature. The two patients described in this paper exhibited high platelet counts prior to liver resection. Although iron deficiency may have contributed to the thrombocytosis, the finding of many megakariocytes within the hepatoblastomas suggests an intra-tumoral production of platelets. An epidemiological investigation of the family under study failed to yield conclusive data. Hepatoblastoma is a rare tumor, but it may affect more than one sibling. Therefore, periodic clinical and laboratory evaluations of the siblings at risk appear to be justified.
Cancer 1977 Jun
PMID:Hepatoblastoma in infant sister and brother. 19 74

The authors report a personal chronological series of 100 cancer patients submitted to an analytical study, and noted thrombocytosis in 18% of cases. They attempt to draw up a correlation between the presence of increased platelets, and the site of the primary tumour, its spread, the state of anemia or iron deficiency in these patients. During a general review of the literature, they compare their results with those of various american and german series and report the various pathogenic hypotheses suggested upto date. They emphasise the fact that routine platelet counts may be of great interest in the detection of certain early carcinomas in spite of the generally moderate levels of thrombocytosis observed. They therefore have a place in routine health checks.
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PMID:[Thrombocytosis and cancer. Apropos of a chronological series of 100 patients]. 20 58

Secondary anemias due to infections, malignancies, endocrinopathies, hepatic and renal disorders, are discussed in terms of pathogenesis, diagnosis and treatment. Typical features for each type of secondary anemia are presented to enable a diagnosis by means of simple laboratory methods. Differential diagnosis is rather difficult due to complex mechanisms of pathogenesis. The differentiation of iron deficiency, lack of growth factors, and hemolysis is of utmost importance. Frequently too little diagnostic work up is contrasted by too much mostly unnecessary treatment. The significance of neuraminidases in infections needs further research.
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PMID:[Anemias in infection, inflammation, tumors and liver, kidney and endocrine diseases]. 29 13

A prospective study was performed over 15 months to determine the cause of iron deficiency in adult males and postmenopausal females attending a general hospital. The laboratory computer identified all subjects with a haemoglobin less than 10.6 g/dl and a mean corpuscular volume less than 86 fl. Patients becoming anaemic after trauma or recent surgery were excluded. The iron status of each patient was assessed by serum iron studies, serum ferritin or sternal marrow aspiration. Reduced red cell indices and blood film morphology were not diagnostic of iron deficiency. Of 215 patients assessed, about half (103) were found to be iron replete. This group had a variety of disorders--malignancy, chronic inflammation, chronic renal and non-malignant haematological diseases. The other group of 104 patients satisfied criteria for iron deficiency, and 100 of these were investigated further. The cause of iron deficiency was found in all but three subjects. Inadequate dietary intake was a contributing factor in over half of the patients and 40 regularly took salicylates. Investigation defined a source of chronic gastrointestinal blood loss in most instances.
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PMID:Iron deficiency anaemia--a prospective study. 31 71

(1) Brief introduction to iron metabolism and the biochemistry of ferritin. (2) Early studies of circulating ferritin. (3) Methods for measuring serum ferritin concentrations -- immunoradiometric, radioimmuno- and enzyme-linked immuno assays based on liver or spleen ferritin -- an evaluation of these techniques. (4) Serum ferritin concentrations in normal subjects -- definition of normality -- relationship between storage iron and serum ferritin concentrations -- changes during development from birth to old age -- iron deficiency -- variability of serum ferritin concentration -- evaluation of use of ferritin assay for assessment of storage iron levels. (5) Serum ferritin concentrations in disease -- hemochromatosis -- secondary iron overload -- liver damage -- infection and chronic disease -- cancer. (6) Assay of serum ferritin with antibodies to ferritins other than liver or spleen -- ferritinemia and cancer. (7) Properties of serum ferritin -- molecular weight -- iron content -- isoelectric focusing patterns -- carbohydrate content -- immunological properties. (8) Physiology of circulating ferritin -- release of ferritin from tissues -- origin of circulating ferritin -- clearance from the plasma -- iron and protein turnover. (9) Summary -- factors influencing serum ferritin concentrations and clinical use of ferritin estimations.
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PMID:Serum ferritin. 37 39

We examined the relationship of serum ferritin to bone marrow iron stores in 73 anemic male medical inpatients with liver disease, alcoholism, chronic inflammatory disease, and malignancies. A correlation of r = 0.75 (P less than .00005) was found between serum ferritin and bone marrow iron stores (BMIS) for the entire group. Liver disease as manifested clinically or by increased levels of serum glutamic-oxaloacetic transaminase did not appear to significantly affect this relationship. Patients with folic acid deficiency did tend to have a disproportionate increase in ferritin in relation to BMIS, but this did not seem to destroy the usefulness of ferritin levels. A useful clinical rule seems to be that serum ferritin of greater than 100 ng/ml tends to exclude iron deficiency, and a level of less than 30 ng/ml tends to confirm decreased iron stores.
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PMID:Ferritin as an index of bone marrow iron stores. 72 24

A brief survey of the literature on the side effects of oral contraceptives is given. Of the many influences on laboratory results those related to (reversible) cholestasis or to a change in protein synthesis are the most important ones. A decrease of the tolerance for glucose is sometimes observed. Few of the clinical side effects attributed to oral contraceptives can be directly correlated with the pharmaceutical action of these drugs. Many so-called side effects of the pill are due to other factors such as altered psychosociological or sexual behavior, etc. However, among users of oral contraceptives there is a significant decrease in the number of benign tumors, particularly of the breast, the uterus and the ovaries. It is still an open question if this also signifies protection against cancer. Anemias due to iron deficiency are less frequent among users of the pill. According to recent studies arterial hypertension and cholecystopathies are probably directly related to oral contraceptives, but a causal relation has not been proven for migraine, headaches, depression etc. An elevated risk for vascular complications seems to be well established: there is a 4-6-fold increase of the estimated risk for venous thrombo-embolism and a 4-9-fold increase for cerebrovascular accidents among users of oral contraceptives when compared with nonpregnant women of the same age not using the pill. Oral contraceptives act as a supplementary factor of risk which may cumulate with other similar factors, such as arterial hypertension, hyperlipidemia, overweight, smoking etc. Mortality due to oral contraceptives is very much 10-50 x) inferior to the one caused by delivery and the post partum state. Since the number of failures in prevention of pregnancies is less for oral contraceptives than for any other method of contraception, the overall risk of death under oral contraceptives in this age group of women is least.
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PMID:[Real and seeming side-effects of oral contraceptives with an emphasis on medical and haematological problems. Review of literature (author's transl)]. 79 Mar 74

A preliminary study of iron absorption by whole body counting was carried on a group of 16 women. The cases included 8 patients suffering from iron deficiency anaemia and various infections as well as 8 healthy controls. High iron absorption is associated with iron deficiency, these changes being more marked in iron deficient controls than in those with infection or malignancy. In iron deficient controls results of whole body counting correlate very well with other haematological investigations.
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PMID:A preliminary study of iron absorption by whole body counting and correlation with DFO excretion. 80 99

Iron deficiency, by far the most common cause of microcytic anemia, may be traced to abnormal bleeding, rapid growth, or rarely, inadequate diet. A search for the source of abnormal bleeding is particularly important because it may lead to detection of an ulcer or cancer. Orally administered iron supplements usually are effective; parenteral therapy is rarely needed.
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PMID:Microcytic hypochromic anemias. 86 82

The kinetics of erythroblast proliferation were studied by means of quantitative 14C-autoradiography in 5 patients showing anemia due to infection or malignancy, in 7 patients suffering from iron deficiency anemia, and in two individuals with bleeding enemia. Compared with a group of 5 healthy persons a markedly reduced turnover of erythroblasts was found in the anemia due to infection, malignancy, and iron deficiency, whereas this turnover was normal or increased in the case of bleeding anemia. The reduction is caused by a progressively decreasing rate of erythroblast proliferation and maturation with advancing development into mature cells. No indications of a change in the number of cell divisions were found in the anemia of infection, malignancy, and of iron deficiency, nor was there evidence of an intramedullary death of nucleated red cell percursors. The imbalance between production and loss of red cells causing anemia shows a different pattern in the 3 groups of disease: In bleeding anemia the insufficiency of supply is not yet apparent from the rate of erythroblast turnover giving weight to the factor of blood loss. In anemia due to infection, malignancy, and iron deficiency the but moderately increased rate of red cell destruction cannot be compensated because of several impairments: The rate of erythroblast turnover is reduced, and, in addition, a moderate portion of maturing cells is destroyed, probably at the reticulocyte stage. As the most significant factor, the bone marrow is unable to compensate the anemia by an effective erythroblast hyperplasia. In iron deficiency this hyperplasia is inadequately low, in infection and malignancies, however, it is more or less missing.
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PMID:[Erythropoiesis in iron deficiency]. 88 Mar 76


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