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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.
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PMID:Hepatoblastoma in infant sister and brother. 19 74

A retrorectal tumor-simulating mass of extramedullary hematopoiesis was discovered during work-up for uterine bleeding in a 40-year-old woman. It was excised in toto. The only hematologic abnormality at the time was iron deficiency, which was corrected. Six years later the patient is free of recurrence or any hematologic abnormality. It is suggested that this case represents heterotopic marrow arising either as a remnant of embryonic hematopoiesis or from activated primitive cells retaining the embryonic potentiality of hematopoiesis. The difficult diagnostic problems, pathogenesis and treatment are discussed, and the importance of recognizing the trilineage of hematopoiesis using Wright's-stained imprints of the mass is emphasized.
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PMID:Tumor-simulating retrorectal heterotopia of bone marrow. 47 29

The bromodeoxyuridine (BRDU) labelling of bone marrow cells was studied in 46 subjects. The labelling in 14 patients, mostly untreated, with the myelodysplastic syndrome (MDS) and four lymphoma patients was significantly (p = 0.043) higher (11.38 +/- SE 2.3% S-phase cells) than that of marrow cells (7.18 +/- SE 1.04%) from 14 apparently healthy normal controls and from nine patients with non hematologic disease. Six iron deficiency had numerically but not significantly increased values. Bone marrow samples from MDS-patients showing the highest numbers of cells in the DNA-synthesis phase had the lowest numbers of colonies and clusters in the CFU-C assay (p < 0.03). The data suggest that the DNA-synthesis period is longer in MDS than in controls.
Med Oncol Tumor Pharmacother 1992
PMID:Bone marrow cells in the DNA-synthesis-phase in the myelodysplastic syndrome and lymphome. 134 21

Cytogenetic studies of bone marrow fibroblasts and blood cells from peripheral blood or bone marrow were performed in 19 patients with myelofibrosis with myeloid metaplasia (group 1), nine patients with other myeloproliferative syndromes without myelofibrosis (group 2), and 12 patients with anaemia secondary to iron deficiency or chronic inflammatory disease (group 3). Clonal cell populations with abnormal karyotypes were seen in the bone marrow or blood in five of 14 (36%) group 1 patients, one of nine (11%) group 2 patients and none (0%) of the group 3 patients. Abnormal karyotypes of bone marrow fibroblasts were found in three of 16 (19%) of patients of group 1, and in two of nine (22%) and two of 12 (17%) patients each of groups 2 and 3, respectively. Since abnormal karyotypes can be found in bone marrow fibroblasts cultured from normal subjects, and since the abnormalities seen in the bone marrow fibroblasts differed from those found in bone marrow or blood cells, it is suggested that abnormal karyotypes found in bone marrow fibroblasts cultured from patients with primary myelofibrosis do not necessarily reflect neoplasia. The results of this study are compatible with the widely accepted hypothesis that in patients presenting with 'primary' myelofibrosis, the fibrosis is a secondary reactive process.
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PMID:Cytogenetic studies of bone marrow fibroblasts cultured from patients with myelofibrosis and myeloid metaplasia. 155 Jul 74

ACD is probably the most common anemia among hospitalized medical patients. It is variably defined by its clinical and, particularly, its laboratory manifestations. The most consistent features are low serum iron and normal or increased serum ferritin levels, reflecting normal or increased iron stores and distinguishing ACD from iron deficiency anemia. ACD often coexists with iron deficiency and the anemia of renal insufficiency. Most patients have an underlying infectious, inflammatory, or neoplastic disease, but as many as one quarter of patients do not. Several mechanisms have been proposed, the most significant of which are a block in reutilization of hemoglobin iron for red cell production and relative deficiency of erythropoietin, but the pathogenesis and mediators involved remain uncertain. The anemia itself seldom requires treatment and is ameliorated by successful treatment of the underlying disease.
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PMID:Anemia of chronic disease. 157 57

Natural killer (NK) cell activity is impaired in iron-deficient rats. Natural killer cells destroy tumor cells; therefore, iron-deficient rats may be less able to combat cancer growth. Natural killer cell cytotoxicity, both basal and interferon gamma (IFN gamma)-stimulated, was studied in moderately and severely iron-deficient rats challenged with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed ad libitum semipurified diets containing 8, 13 or 42 mg Fe/kg. A pair-fed group was fed the 42 mg Fe/kg diet at the level consumed by the 8 mg Fe/kg group. Following 6 wk of dietary treatment, DMBA-treated rats received a single intragastric dose of DMBA. Dietary treatment was continued. Rats were killed at 1, 4, 8, 14 and 20 wk post-DMBA treatment. Natural killer cell cytotoxicity (both basal and IFN gamma-stimulated) was analyzed. Feeding the 13 mg Fe/kg diet resulted in lower NK cell activity (P = 0.006) and greater tumor burden (P = 0.045) and tumor incidence. Interferon gamma treatment relieved the lower NK cell cytotoxicity observed in moderate iron deficiency. Feeding the 8 mg Fe/kg diet impaired NK cell activity (P = 0.006), but tumor burden and incidence were less than in moderate iron deficiency. In this model, iron deficiency, particularly moderate iron deficiency, contributed to cancer development and compromised NK cell cytotoxicity.
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PMID:Iron deficiency alters DMBA-induced tumor burden and natural killer cell cytotoxicity in rats. 172 72

The hypothesis that low body iron stores are protective against cancer whereas high body stores promote tumor occurrence was examined in the 1-methyl-1-nitrosourea (MNU)-induced experimental model for breast cancer. Twenty-one-day-old female Sprague-Dawley rats were randomized into one of three experimental groups and fed a formulation of AIN-76A diet modified to be low in iron (2 p.p.m.), or the same diet supplemented with an adequate (120 p.p.m.) or excess (1200 p.p.m.) amount of iron provided as FeSO4.7H2O. Rats were maintained on their respective diets throughout the experiment which was terminated 32 weeks post carcinogen administration. Rats were injected i.p. with either 25 mg MNU/kg body wt or the saline-solvent in which MNU was dissolved at 50 days of age. In the first 14 weeks, dietary iron deficiency resulted in a low hematocrit and a decrease in weight gain. The appearance of mammary tumors was markedly suppressed in this group compared to those given an adequate or excess level of iron. It has been reported in the literature that reduction in weight gain due to food restriction at a period immediately after carcinogen administration severely inhibits the subsequent development of tumors. Thus the low tumor incidence in the iron-deficient rats during this time frame could be attributed to the combined effects of low hematocrit and depressed weight gain. For the period between week 14 and week 32, the hematocrit in the iron-deficient animals was maintained at a normal level, and the body wt of these rats was comparable to that of the controls given an adequate level of iron. The rate of tumor appearance in the iron-deficient group during the second half of the experiment was similar to that of the iron-adequate group in the first half of the experiment. In other words, it appeared that once hematocrit and body wt gain were restored to normal in the iron-deficient animals, tumor incidence was only minimally affected by low dietary iron. In the second half of the experiment, the tumor incidence in the adequate iron group seemed to have plateaued, whereas it continued to rise in the excess iron group. Thus excess iron appears to be more prominent than iron deficiency in modification of mammary carcinogenesis, especially when the confounding effects of low hematocrit and reduced weight gain are taken into consideration in the latter case.
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PMID:Effect of dietary iron deficiency or excess on the induction of mammary carcinogenesis by 1-methyl-1-nitrosourea. 198 69

Most anemias can be classified using the reticulocyte count, PCV, MCV, and MCHC. Regenerative anemias are characterized by reticulocytosis. Polychromasia and increased MCV usually are present. Hemolytic mechanisms and hemorrhage should be considered in a systemic evaluation of the blood and the patient. In animals with chronic external blood loss, a microcytic, hypochromic anemia develops secondary to iron deficiency. Nonregenerative anemias generally are characterized by normocytic, normochromic erythrocytes and the lack of reticulocytosis. Patients with nonregenerative anemia should be evaluated for chronic inflammation or neoplasia, renal disease, endocrine insufficiency, or hypoplasia of the bone marrow.
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PMID:Erythrocytes. 267 33

In order to further investigate the known influence of iron deficiency on 4NQO oral carcinogenesis in the rat, groups of iron-deficient and iron-sufficient Charles River white rats were painted with carcinogen for 8 weeks or 14 weeks and then left untreated for 32 weeks or 26 weeks respectively. Tumour development and epithelial dysplasia were assessed at the time of killing. Animals painted for 14 weeks showed more severe dysplasia than those painted for 8 weeks, but no significant differences were noted between corresponding iron-deficient and iron-sufficient groups.
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PMID:The effect of iron deficiency on early oral carcinogenesis in the rat. 309 92

In healthy subjects normal plasmalactoferrin (PLf) concentrations were found to be 0.206 +/- 0.06 mg/l in 49 men and 0.148 +/- 0.06 mg/l in 62 women. A highly significant correlation of PLf with the number of circulating neutrophils (PMN) and a PLf/PMN relationship suggesting proportionality was demonstrated. Among 73 patients absolute PLf concentrations were significantly increased in septicemia, cirrhosis of the liver and tumors with liver metastases, decreased in localized infection, tumors without liver involvement, iron deficiency and acute hepatitis B, and normal in acute myocardial infarction. The PLf/PMN ratio, on the other hand, was normal in liver cirrhosis, hepatitis B and in a part of the patients with septicemia and tumor disease with liver involvement. The ratio was increased in a part of the septicemic patients, and decreased in the remaining disease types. Positive PLf/PMN correlations were found in myocardial infarction, septicemia and liver cirrhosis, whereas a very close, negative correlation existed in acute hepatitis B. These findings are discussed on the basis of existing knowledge on lactoferrin physiology, the intravascular fate of PMN and the RES function.
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PMID:Plasmalactoferrin and the plasmalactoferrin/neutrophil ratio. A reassessment of normal values and of the clinical relevance. 313 91


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