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

Hemodialysis patients treated with recombinant human erythropoietin (rhEPO) need adequate iron supplementation to avoid rhEPO hyporesponsiveness due to iron deficiency. Low serum ferritin reflects absolute iron deficiency, whereas normal or high ferritin values in combination with low transferrin saturation (< 20%) indicate functional iron deficiency. In this study, healthy subjects (group I) were compared with intravenous (i.v.) rhEPO-treated and i.v. iron-saccharate-treated regular hemodialysis patients that were subdivided into three groups as follows: patients with serum ferritin > 100 and < 350 micrograms/L (group II), patients with ferritin < 60 micrograms/L (group III), and patients with ferritin > 650 micrograms/L but transferrin saturation < 20% (group IV). Polymorphonuclear leukocyte (PMNL) parameters (phagocytosis, intracellular killing of bacteria, oxidative metabolism, glucose uptake, intracellular calcium) for each group were compared with those of multitransfused, iron-overloaded primary hematologic patients (group V) and those of patients suffering from hereditary hemochromatosis (group VI). Compared with PMNL obtained from healthy subjects (group I), group II hemodialysis patients showed mild inhibition of phagocytosis but significant inhibition of intracellular killing of bacteria. Oxidative burst of PMNL from group II patients was also significantly reduced after stimulation in vitro. These dysfunctions were not affected by absolute iron deficiency (comparable data in group III patients). However, impairment of PMNL was markedly aggravated in group IV patients. Intracellular calcium concentration under basal conditions and after stimulation was not different. These data suggest that iron is responsible for the PMNL dysfunctions observed in group IV patients. The PMNL defect of group IV patients was comparable to group V and group VI patients with normal renal function, suggesting again a direct inhibitory effect of iron. It is concluded that hemodialysis patients with high ferritin but low serum iron and low transferrin saturation ("functional iron deficiency") display a significant impairment of fundamental PMNL functions during i.v. iron and rhEPO therapy. This may result in increased risk of infectious complications. Therefore, overtreatment of hemodialysis patients with i.v. iron should be avoided.
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PMID:Neutrophil impairment associated with iron therapy in hemodialysis patients with functional iron deficiency. 955 68

The digestive utilization of Fe and its nutritive interaction with Ca, P, and Mg were studied in rats with nutritional ferropenic anemia. The diet contained 80% ferric citrate and 20% heme iron (80/20 diet). The weight gain, digestive utilization of Fe, and regeneration efficiency of hemoglobin and seric Fe were higher in iron-deficient rats (ID) fed the 80/20 diet than in iron-deficient rats fed the 50/50 diet (Campos et al., 1996). The phospho-calcic metabolism, which is adversely affected in ferropenic anemia, returned to normal values when iron was added to the diet. The digestive utilization of Mg, which fell with the 50/50 diet (Campos et al., 1996), returned to normal values when the ferropenic anemia was reversed with the 80/20 diet. In a state of iron deficiency, certain parameters related to the glucose and lipid metabolism are affected; the glucose and triglycerides values return to a normal range with the 80/20 diet.
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PMID:The importance of the proportion of heme/nonheme iron in the diet to minimize the interference with calcium, phosphorus, and magnesium metabolism on recovery from nutritional ferropenic anemia. 1055 90

Every once in a while, female athletes hear the rumor that oral contraceptives (OCs) keep them from performing their best. Yet, studies that have tried to evaluate the effects of OCs on physically active women have not been conclusive. This rumor probably started with the initial, higher-dose formulations instead of with the current biphasic or triphasic OCs. Side effects of the higher-dose OCs included weight gain, nausea, fatigue, headaches, and increased risks of hypertension, thromboembolism, and changes in glucose and lipid metabolism. Current OCs minimize these side effects and the risk of complications. In fact, the aerobic exercise female athletes undergo most likely neutralizes the negative effects of OCs on coagulation and lipid metabolism. Further, OCs may even improve athletic performance because they can decrease bleeding, the risk of iron deficiency, and frequency of cramps. Moreover, athletes can use OCs to orchestrate their menstrual cycles around competitive meets. Some studies with small sample sizes show that athletes on OCs experience a slight reduction in functional aerobic capacity and endurance capability. A Swedish study of female soccer players reported that OC users suffer fewer traumatic injuries than nonusers. It is difficult to attribute this to OCs, because there is considerable psychological control over sports performance. A sports physician in Hawaii is aware of rumors that OCs induce sluggishness or fatigue during certain days of the month, but he does not know a female athlete who believes this. The head trainer of the US Olympic Committee says that many female Olympic athletes use OCs. Strenuous exercise, considerable weight loss, and possibly other stress factors induce athletic amenorrhea, especially in adolescent females. In many cases, OCs can treat it. They are especially needed to minimize the risk of reduced bone density and musculoskeletal injury.
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PMID:Exercise and "the pill": putting a rumor to rest. 1228 95

Probiotic bacteria are used for production of fermented dairy products. The use of probiotic bacteria has the potential to replenish the natural intestinal flora of the body. These bacteria competitively inhibit the growth and colonization of pathogenic bacteria. Breastmilk is the best food for babies, also from a probiotic point of view. Human milk, in fact, contains many substances that stimulate the growth of bifidobacteria in vitro and in the small intestine of infants. Improvement of lactose digestion and avoidance of symptoms of intolerance in lactose malabsorbers are the most profoundly studied health-relevant effects of fermented milk. In fact fermented milks are nutritionally similar to unfermented milk, except that some of lactose is broken down to glucose and galactose. The role of fermented milk in complementary feeding and in particular for the prevention of anaemia is an innovative theme, recently focused. Iron deficiency in infants and young children is widespread and has serious consequences for child health. Prevention of iron deficiency should therefore be given high priority. The too-early introduction of unmodified cow's milk and milk products is an important nutritional risk factors for the development of iron-deficiency anaemia. Fermented milks represent an excellent source of nutrients such as calcium, protein, phosphorus and riboflavin. During the fermentation of milk, lactic acid and other organic acids are produced and these increase the absorption of iron. If fermented milk is consumed at mealtimes, these acids are likely to have a positive effect on the absorption of iron from other foods.
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PMID:The role of fermented milk in complementary feeding of young children: lessons from transition countries. 1255 42

There is growing evidence that increases in both hematocrit and body iron stores are components of the insulin resistance syndrome. The ability of insulin and of IGF-I - whose effective activity is increased in the context of insulin resistance - to boost activity of the transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha), may be at least partially responsible for this association. HIF-1alpha, which functions physiologically as a detector of both hypoxia and iron-deficiency, promotes synthesis of erythropoietin, and may also mediate the up-regulatory impact of hypoxia on intestinal iron absorption. Insulin/IGF-I may also influence erythropoiesis more directly, as they are growth factors for developing reticulocytes. Conversely, the activation of HIF-1alpha associated with iron deficiency may be responsible for the increased glucose tolerance noted in iron-deficient animals; HIF-1alpha promotes efficient glucose uptake and glycolysis - a sensible adaptation to hypoxia - by inducing increased synthesis of glucose transporters and glycolytic enzymes. Recent reports that phlebotomy can increase the efficiency of muscle glucose uptake in lean healthy omnivores are intriguing and require further confirmation. Whether increased iron stores contribute to the elevated vascular risk associated with insulin resistance is doubtful, inasmuch as most prospective studies fail to correlate serum ferritin or transferrin saturation with subsequent vascular events. However, current data are reasonably consistent with the possibility that moderately elevated iron stores are associated with increased overall risk for cancer - and for colorectal cancer in particular; free iron may play a catalytic role in 'spontaneous' mutagenesis. Thus, iron excess may mediate at least some of the increased cancer risk associated with insulin resistance and heme-rich diets. People who are insulin resistant can minimize any health risk associated with iron overload by avoiding heme-rich flesh foods and donating blood regularly.
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PMID:Hyperinsulinemia may boost both hematocrit and iron absorption by up-regulating activity of hypoxia-inducible factor-1alpha. 1459 87

The major form of glycohemoglobin is hemoglobin A1c (HbA1c). The HbA1c fraction is abnormally elevated in chronic hyperglycemic diabetic patients and correlates positively with glycemic control. Previous studies suggest that iron deficiency anemia (IDA) affects the levels of HbA1c. The aim of this study was to determine the effect of IDA on HbA1c levels in nondiabetic patients. The population studied consisted of 50 patients (30 women, 20 men, mean age 35.7 +/- 11.9 years) with IDA and 50 healthy subjects that were matched for age and sex. Patients who had glucose tolerance abnormalities (impaired glucose tolerance or diabetes mellitus), hemoglobinopathies, hemolytic anemia, chronic alcohol ingestion and chronic renal failure were excluded from the study. Hematologic investigations, fasting and postprandial glucose and HbA1c levels were measured in all subjects before iron therapy. All patients with IDA were treated with iron 100 mg/day for 3 months. We repeated the laboratory investigation after iron therapy. Before iron treatment, the mean HbA1c (7.4 +/- 0.8%) level in patients with IDA was higher than in a healthy group (5.9% +/- 0.5) (p < 0.001). In patients with IDA, HbA1c decreased significantly after iron treatment from a mean of 7.4% +/- 0.8 to 6.2% +/- 0.6 (p < 0.001). Iron deficiency must be corrected before any diagnostic or therapeutic decision is made based on HbA1c.
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PMID:Effect of iron deficiency anemia on the levels of hemoglobin A1c in nondiabetic patients. 1534 93

As many as 10% of pregnancies are complicated by maternal glucose intolerance. With the risk of diabetes and gestational diabetes rising because of the obesity epidemic, that figure is likely to rise. Many obese individuals suffer from the metabolic syndrome, which makes them more prone to glucose intolerance when they are pregnant. Among the potential risks posed by poor maternal glucose control are those to the developing fetal brain. The goal of this article is to acquaint physicians with the results and clinical implications of studies conducted at the University of Minnesota on outcomes of infants of diabetic mothers and, in particular, on the role of iron deficiency in differential brain processing.
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PMID:The effect of maternal diabetes during pregnancy on the neurodevelopment of offspring. 1666 33

The hippocampus is injured in both hypoxia-ischemia (HI) and perinatal iron deficiency that are co-morbidities in infants of diabetic mothers and intrauterine growth restricted infants. We hypothesized that preexisting perinatal iron deficiency predisposes the hippocampus to greater injury when exposed to a relatively mild HI injury. Iron-sufficient and iron-deficient rats (hematocrit 40% lower and brain iron concentration 55% lower) were subjected to unilateral HI injury of 15, 30, or 45 mins (n=12 to 13/HI duration) on postnatal day 14. Sixteen metabolite concentrations were measured from an 11 microL volume on the ipsilateral (HI) and contralateral (control) hippocampi 1 week later using in vivo 1H NMR spectroscopy. The concentrations of creatine, glutamate, myo-inositol, and N-acetylaspartate were lower on the control side in the iron-deficient group (P<0.02, each). Magnetic resonance imaging showed hippocampal injury in the majority of the iron-deficient rats (58% versus 11%, P<0.0001) with worsening severity with increasing durations of HI (P=0.0001). Glucose, glutamate, N-acetylaspartate, and taurine concentrations were decreased and glutamine, lactate and myo-inositol concentrations, and glutamine/glutamate ratio were increased on the HI side in the iron-deficient group (P<0.01, each), mainly in the 30 and 45 mins HI subgroups (P<0.02, each). These neurochemical changes likely reflect the histochemically detected neuronal injury and reactive astrocytosis in the iron-deficient group and suggest that perinatal iron deficiency predisposes the hippocampus to greater injury from exposure to a relatively mild HI insult.
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PMID:Perinatal iron deficiency predisposes the developing rat hippocampus to greater injury from mild to moderate hypoxia-ischemia. 1686 55

Statistical data indicate a chronic shortage of work-force due to overwork, ill health state and increased risk of chronic noninfectious diseases in Hungarian health care personnel, which needs investigations in order to decrease the risk. Nurses of oncology units, often exposed to carcinogens when preparing and handling cytostatic drugs, are especially at high risk. In the present publication we report a complex clinical, geno- and immunotoxicology risk assessment of altogether 500 nurses, performed during the last 10 years at various oncology units in Hungary. The obtained results indicate that the health status of nurses at oncology units is better than the Hungarian average, especially of hypertonia and type II diabetes. However, the prevalence of iron deficiency anemia and different thyroid gland diseases is significantly higher than those of the controls matched for sex and age. The results suggest that iron deficiency can potentiate the resistance to insulin, i.e. the persistence of iron deficiency may increase the serum glucose levels and thus the risk of diabetes. Among the studied geno- and immunotoxicology biomarkers, the frequency of chromosome aberrations, sister chromatid exchange and B lymphocytes was significantly increased compared to the matched controls. The obtained alterations demonstrate the occupational exposure of the nurses to cytostatic drugs, thus the introduction of more strict hygienic controls and compliance with the European Union chemical safety regulations is necessary.
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PMID:[The state of health of oncology nurses characterized by genetic and immunotoxicologic biomarkers]. 1688 79

Suicidal death of erythrocytes (eryptosis) is characterized by cell shrinkage, membrane blebbing, activation of proteases, and phosphatidylserine exposure at the outer membrane leaflet. Exposed phosphatidylserine is recognized by macrophages that engulf and degrade the affected cells. Eryptosis is triggered by erythrocyte injury after several stressors, including oxidative stress. Besides caspase activation after oxidative stress, two signaling pathways converge to trigger eryptosis: (a) formation of prostaglandin E(2) leads to activation of Ca(2+)-permeable cation channels, and (b) the phospholipase A(2)-mediated release of platelet-activating factor activates a sphingomyelinase, leading to formation of ceramide. Increased cytosolic Ca(2+) activity and enhanced ceramide levels lead to membrane scrambling with subsequent phosphatidylserine exposure. Moreover, Ca(2+) activates Ca(2+)-sensitive K(2+) channels, leading to cellular KCl loss and cell shrinkage. In addition, Ca(2+) stimulates the protease calpain, resulting in degradation of the cytoskeleton. Eryptosis is inhibited by erythropoietin, which thus extends the life span of circulating erythrocytes. Eryptosis may be a mechanism of defective erythrocytes to escape hemolysis. Conversely, excessive eryptosis favors the development of anemia. Conditions with excessive eryptosis include iron deficiency, lead or mercury intoxication, sickle cell anemia, thalassemia, glucose 6- phosphate dehydrogenase deficiency, malaria, and infection with hemolysin-forming pathogens.
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PMID:Mechanisms and significance of eryptosis. 1691 Jul 66


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