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

Eleven anemic children and adolescents with a median age of 14 years (range six months-20 years) on chronic hemodialysis were treated with recombinant human erythropoietin (rHuEPO) intravenously three times a week for an average of 9.2 months. After eight weeks of therapy, hematocrit rose from 20.3 +/- 1.4% to 31.7 +/- 0.7% (0.20 +/- 0.01 to 0.31 +/- 0.007, p less than 0.001, mean +/- SEM). After reaching the target hematocrit of 30% to 33% (0.30 to 0.33), doses were adjusted individually. Blood transfusions were eliminated in all but one patient. All patients experienced an increase in appetite and energy level. Serum ferritin concentrations decreased in all patients who reached target hematocrit and seven required iron supplementation. Hypertension worsened in two patients and developed in two others. One patient's vascular access clotted. Dialysis efficiency and heparin requirements during dialysis did not change significantly. We conclude that rHuEPO is safe, effective, and should be recommended as treatment for anemia in children and adolescents on hemodialysis, but close monitoring for the development of hypertension and/or iron deficiency is necessary.
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PMID:Therapy of renal anemia in children and adolescents with recombinant human erythropoietin (rHuEPO). 154 82

Newborn infants of diabetic mothers have serum biochemical signs of iron deficiency in cord blood directly related to elevations of cord erythropoietin and Hb concentrations. In sheep, chronic fetal hyperinsulinemia results in fetal hypoxemia, expansion of the red cell mass, and decreased iron concentrations, most likely due to increased iron utilization for Hb synthesis. To determine whether fetal insulin exposure also results in reduced tissue iron concentrations, we measured liver, skeletal muscle, small intestine, heart, and brain iron concentrations in newborn rat pups after s.c. fetal injection of insulin or diluent alone on d 19 of gestation. The fetuses of 11 pregnant rats were exteriorized, injected with 2 U neutral protamine Hagedorn insulin or diluent, replaced in utero, and delivered on d 22. To determine dose dependency, the fetuses of six pregnant rats were injected with 3 U of longer-acting protamine zinc insulin and delivered on d 21. At delivery, the insulin-treated groups had higher birth weights than the placebo-treated group, although plasma insulin concentrations were not different. The 2 U neutral protamine Hagedorn insulin-treated fetuses had significantly lower mean +/- SEM liver iron concentrations than the control fetuses (910 +/- 34 versus 1014 +/- 43 micrograms/g dry tissue weight; p less than 0.05), but had similar skeletal muscle iron concentrations. The 3 U protamine zinc insulin-treated fetuses had significantly lower liver and skeletal muscle iron concentrations compared to control and to 2 U neutral protamine Hagedorn insulin-treated fetuses (p less than 0.05). No differences in small intestine, heart, or brain iron concentrations were seen among groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of in utero insulin exposure on tissue iron status in fetal rats. 159 33

Infants of diabetic mothers frequently have polycythemia, elevated serum erythropoietin concentrations, and decreased serum iron and ferritin concentrations, likely representing a redistribution of fetal iron into erythrocytes to support augmented fetal hemoglobin synthesis. We hypothesized that fetal liver, heart, and brain iron concentrations are also reduced in these infants. After obtaining autopsy tissue from infants who had died before 7 days of age, we measured liver, heart, and brain iron concentrations using atomic absorption spectrophotometry. Seven infants of diabetic mothers and seven gestational age-matched control infants were studied. All infants of diabetic mothers had pancreatic islet cell hyperplasia, indicating fetal hyperglycemia and hyperinsulinemia. Liver iron concentrations in the infants of diabetic mothers were 6.6% of control values (489.0 +/- 154.4 vs 7379.7 +/- 1473.8 micrograms/gm dry tissue weight (mean +/- SEM); p less than 0.001), heart iron concentrations were 43.9% of control values (124.7 +/- 20.5 vs 284.1 +/- 34.8 micrograms/gm dry tissue weight; p less than 0.002), and brain iron concentrations were 60.6% of control values (106.1 +/- 13.7 vs 175.2 +/- 10.7 micrograms/gm dry tissue weight; p less than 0.003). Heart and brain iron concentrations were directly correlated with liver iron concentrations (r = 0.80 for both; p less than 0.001) and indicated that hepatic iron was greater than 75% depleted before heart and brain iron reduction. We conclude that severely affected infants of diabetic mothers have reduced liver, heart, and brain iron concentrations. The role of tissue iron deficiency in the genesis of the abnormal clinical findings in these infants deserves further consideration.
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PMID:Iron deficiency of liver, heart, and brain in newborn infants of diabetic mothers. 162 67

Serum erythropoietin (S-EPO) levels were measured in 50 patients with anaemia of chronic disorders (ACD), classified into three groups according to their aetiology: inflammatory (n = 20), infectious (n = 15) and neoplastic (n = 15). The inflammatory group showed a higher mean S-EPO level (mean value +/- SEM, 69 +/- 11 mU ml-1) than the neoplastic (43 +/- 5 mU ml-1; P less than 0.05) and infectious groups (27 +/- 4 mU ml-1; P less than 0.01). The S-EPO level in the inflammatory group also differed from that of 32 healthy controls (36 +/- 3 mU ml-1; P less than 0.05). Fourteen patients with added iron deficiency (12 subjects from the inflammatory group) showed the highest S-EPO concentration (72 +/- 17 mU ml-1). Conversely, S-EPO levels were lower in febrile subjects (12 patients with infection and five with malignancy) than in non-febrile patients (28 +/- 4 mU ml-1 vs. 55 +/- 7 mU ml-1; P less than 0.01). In the infectious group, the logarithm of S-EPO correlated directly with the haemoglobin and haematocrit values. We conclude that differences in S-EPO concentration in ACD may be further related to the patient's iron stores and temperature. A decrease in EPO production may contribute to the pathogenesis of ACD secondary to infection.
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PMID:Serum erythropoietin levels in the anaemia of chronic disorders. 199 63

Iron deficient (ID) and control (C) rats were studied to determine if severe iron deficiency alters insulin-stimulated glucose disposal. Euglycemic hyperinsulinemic glucose clamps were conducted by infusing insulin (2 m mu.kg-1.min-1, constant rate) for 120 min while maintaining euglycemia. In a 12-h fasted state, ID rats were hyperglycemic (109.4 +/- 4.0 mg.dL-1 arterial plasma glucose, x +/- SEM) when compared with C rats (86.9 +/- 3.4 mg.dL-1) (P less than 0.05). Even though insulin was infused identically on a per kilogram body weight basis for both groups, the resulting hyperinsulinemia was higher in ID rats (3.1 +/- 0.27 ng.mL-1) compared with C rats (2.3 +/- 0.4 ng.mL-1) at the end of the clamp. Glucose infusion rates required to maintain euglycemia were twofold higher in ID rats (27.0 +/- 5.4 mg.kg-1.min-1) versus C rats (13.1 +/- 3.3 mg.kg-1.min-1) (P less than 0.05). Circulating lactic acid increased in both groups, and the concentrations in ID rats (3.2 +/- 0.4 mmol.L-1) were significantly higher than those in C rats (1.8 +/- 0.5 mmol.L-1) at the end of the clamp. When the efficiency of insulin to dispose glucose was evaluated by calculating the glucose disposal divided by the prevailing insulinemia, ID rats could dispose of almost twice the glucose per unit of insulin [9.0 +/- 0.6 (mg.kg-1.min-1)/(ng.mL-1)] when compared with C rats [5.6 +/- 0.9 (mg.kg-1.min-1)/(ng.mL-1)] (P less than 0.05). The data indicate that insulin sensitivity is increased in ID rats and that ID rats cannot metabolize exogenous insulin as well as C rats.
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PMID:Increased insulin sensitivity in iron-deficient rats. 304 44

One hundred twenty-four relatives (aged 17-52 years) of 35 children with severe transfusion-dependent beta thalassemia major were investigated for their beta thalassemia carrier status (determined by Hb-A2 level) and iron status (determined by serum ferritin level). Forty-eight males had beta thalassemia trait (BTT) and 18 males did not have BTT (control); 41 females had BTT and 17 females did not have BTT (control). Serum ferritin levels (mean +/- SEM) of male BTT, male control, female BTT, and female control groups were 151.0 +/- 27.4, 59.6 +/- 16.3, 120.6 +/- 36.6, and 17.2 +/- 6.1 mcg/liter respectively; the differences between the two male and the two female groups were statistically significant (p = .05 and p less than .001). Iron deficiency (serum ferritin below 10.0 mcg/liter) was present in 6.3%, 38.9%, 24.4%, and 58.8% of male BTT, male control Female BTT, and female control groups, respectively; the differences between the two male and two female groups were statistically significant (p less than .01 and p less than .01). Serum ferritin was over 1,000 mcg/liter in four individuals with BTT (2 male and 2 female). Thus, the BTT group had better iron nutrition. This may suggest that the BTT group has an advantage in maintaining iron balance.
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PMID:Iron status of beta thalassemia carriers. 381 67

The iron concentration in sweat and serum and related variables (transferrin saturation percentage, hemoglobin concentration) was measured in two groups of distance runners, each consisting of ten persons. In the first group unclear sweat was collected from the back of the athletes during cycling (without previous washing). The iron concentration (means +/- SEM) was 5.2 +/- 1.0 mumol/l of sweat. In the second group the sweat collection was performed similarly, but following elimination of the very first sweat from the site of collection (back) before three consecutive samples were taken. The iron concentration of the three samples was 3.6 +/- 1.1, 2.3 +/- 0.2 and 2.4 +/- 0.3 mumol/1. There was no statistically significant difference between the consecutive samples on the p less than 0.001 level. These results are in accordance with the lowest values found in the literature. There was no correlation between the iron concentration in sweat and in serum of the 20 persons. Seven of the runners had transferrin saturation percentages below 20, suggesting a possible iron deficiency. A daily loss in sweat of more than 18 mumol (1 mg) is possible in these runners training 125-350 km/week all the year round. The dominating iron loss of male endurance athletes is probably through the sweat.
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PMID:Dermal excretion of iron in intensely training athletes. 682 7

Effects of dietary iron deficiency on growth, the distribution of hemoglobin (Hb) at rest and during exercise, the characteristics of muscle fiber types, and glycogen depletion patterns were studied in newly weaned male mice. Forty-eight mice were randomly divided into iron-deficient and control diet groups. Severe iron deficiency impaired general growth, but growth was restored following iron repletion. The mean +/- SEM blood Hb concentrations at rest after 7 weeks were 5.8 +/- 0.7 and 12.5 +/- 0.3 g/dl in iron-deficient and control groups, respectively. The mice fed iron-deficient diet for 7 weeks had an increased Hb level of 10.9 +/- 0.5 g/dl 1 week after an i.p. injection of Imferon (1.25 mg Fe). The Hb contents in brain and gastrocnemius as well as whole body were lowered by iron deficiency. Iron-deficient anemic mice tended to increase the percent distribution of Hb to brain during exercise. This value was significantly greater than in control and iron-treated groups. The iron-deficient group had relatively less glycogen than controls, but no significant tendency in glycogen depletion pattern was observed in any fiber types. It is suggested that decreased Hb content in working muscles due, in part, to greater distribution to brain could be one of the limiting factors for work performance in anemic individuals. It is further suggested that decrease in oxidative muscle fibers as well as the decreased concentration and/or activities of oxidative substances may also be one of the limiting factors.
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PMID:Effects of dietary iron deficiency on muscle fiber characteristics and whole-body distribution of hemoglobin in mice. 688 25

Immunologic studies were performed in ten iron-deficient children, aged 12 to 30 months, before and after iron replacement. Chronic infection, malnutrition, and vitamin deficiency were excluded. Mean hemoglobin levels went from 8.2 +/- 0.2 (SEM) to 12.3 +/- 0.3 g/dL after iron replacement. Mean T-cell percentage increased from 50% +/- 3.0% to 58% +/- 3.7%. Absolute numbers of T cells were unchanged. Three children converted negative in vitro proliferative responses to Candida or tetanus antigen. Mean stimulation indexes increased for Candida (6.8 +/- 1.7 to 17.9 +/- 6.7) and tetanus (19.5 +/- 6.0 to 31.7 +/- 8.5). Nine of 16 delayed hypersensitivity skin tests were positive before and ten of ten were positive after iron therapy. The IgG and IgA levels did not change significantly, but IgM levels decreased from 181 +/- 13 to 128 +/- 5 mg/dL. We conclude that T-cell immunity is slightly impaired in pure iron deficiency and that these subtle defects can be corrected with oral iron replacement.
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PMID:Immune function in pure iron deficiency. 698 45

Urinary and proximal tubular iron are increased after subtotal nephrectomy, and iron depletion has been shown to be beneficial in proteinuric models of chronic renal disease in rats. In this study, iron depletion by low iron pair-fed diet and periodic phlebotomy was induced for 6 months in rats with partial (5/6) nephrectomy, resulting in a reduction in hematocrit and serum iron in all iron-deficiency subgroups. Tubular iron, assessed by energy dispersive analysis and electron microscopy, was reduced in quantity but not number of iron-containing lysosomes only within 1 subgroup of severe iron deficiency (p < 0.05). There was no improvement in serial isotopic glomerular filtration rate measurements, urinary protein and transferrin excretion, tubular damage scores, serum creatinine, or measures of reactive oxygen species (ROS) generation. In a subgroup of rats with no supplementation of sulfhydryl amino acids (cysteine and methionine) which can act as ROS scavengers, iron deficiency increased urinary protein excretion (213.3 +/- 23.0 mg/24 h, mean +/- SEM, vs. 87.4 +/- 16.1, p < 0.001), urinary transferrin excretion (p < 0.05), kidney weight (p < 0.05) and tissue malondialdehyde, a lipid peroxidation product (0.78 +/- 0.16 nmol/mg protein vs. 0.57 +/- 0.19, p < 0.05), consistent with increased ROS generation. Hence, no beneficial effect of iron-deficiency was demonstrated by any measure of structure of function in the remnant kidney, and it may enhance damage if sulfhydryl repletion is not provided.
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PMID:Iron depletion in the remnant kidney. 747 24


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