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

Anemia due to decreased erythropoietin production is one of the major complications in uremic patients. The aim of the study is to evaluate the clinical efficiency and safety of rHuEPO in the treatment of anemia in uremic children receiving regular hemodialysis. Three uremic children, age 8, 12, and 14 year-old, under maintenance hemodialysis with hematocrit (Hct) value lower than 20% were observed for 6 months. rHuEPO 50 u/kg were given intravenously three times a week initially. Hct value of 30% was the target of therapy. All 3 children responded to the therapy and reached the target Hct value within 11 to 18 weeks. They received no further transfusion after the therapy. The maintenance dose to keep Hct value around 30% is 75 to 120 u/kg/wk. The serum biochemistry examination showed no difference before and after the therapy. The physical endurance, body weight and height increased in all children. The left ventricular end-diastolic dimension in echocardiography decreased and the ejection fraction increased after 6 months of the treatment. Serum ferritin concentrations decreased in all children. Mild hypertension developed in one child. Heparin dose was increased when the target Hct value was around 30% in 2 children. We suggested that low dose rHuEPO therapy was safe and effective in uremic children, but close monitoring for the development of hypertension and iron deficiency was mandatory.
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PMID:Clinical experience of recombinant human erythropoietin in uremic children: report of three cases. 893 79

The discovery of recombinant human erythropoietin has enabled treatment of anaemia in patients whose anaemia was primarily caused by the lack of erythropoietin. This agent was most widely used in the treatment of anaemia in chronic renal failure patients. Non-regulated hypertension is considered to be the only absolute contraindication for recombinant human erythropoietin application, but thrombocytosis, predisposition to thromboses of arterio-venous fistulae, and convulsions are regarded as relative contraindications. Recombinant human erythropoietin may be administered intravenously, but the subcutaneous route is considered more rational. The treatment is initiated by low doses with gradual dose increase, what enables gradual anaemia correction and prevents the appearance of adverse effects. Haemoglobin level of around 100 g/l is considered the target haemoglobin level. The majority of patients respond well to treatment by human recombinant erythropoietin and the absence of anaemia improvement may be the result of iron deficiency, occult haemorrhages, chronic infection, inadequate dialysis, secondary hyperparathyroidism, aluminium intoxication. Anaemia improvement during the treatment with recombinant erythropoietin leads to the improvement of function of most organs and the quality of life in general as well as avoidance of blood transfusions and their adverse effects. The most frequent adverse effect of recombinant erythropoietin is the development of iron deficiency or hypertension aggravation.
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PMID:[Treatment of anemia in patients with chronic renal insufficiency with recombinant human erythropoietin]. 910 27

The target organ failures associated with uremia are most often considered to be caused by processes other than uremia per se. Heart disease, for example, is considered the product of hypertension, lipid abnormalities, and so forth, rather then the uremic state. Erythropoietin deficiency, blood loss, and iron deficiency are believed to cause anemia, rather than the uremic state. Malnutrition is believed to be the product of poor nutrient intake and perhaps nutrient losses, rather than uremia per se. This article reviews evidence suggesting that anemia and malnutrition share a common cause; the acute-phase inflammatory process that is a normal host-defense mechanism. Given the high prevalence of heart disease among patients with end-stage renal disease (ESRD), data indicating activation of the acute-phase process in patients with kidney failure, and emerging evidence that the process has a significant role in the risk for cardiovascular disease among patients without kidney failure, there is a strong likelihood that heart disease will share with anemia and malnutrition the acute-phase state as a contributing cause. Thus, instead of disconnected target organ failures, each with different antecedent causes, we see emerging the likelihood of a unifying pathobiology for uremia. The antecedents of morbidity and mortality appear as a web of organ failures connected by a common pathobiology. Whereas each failure likely has contributing causes other than the acute-phase state, they probably share the state as a causative, contributing, or exacerbating factor.
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PMID:Acute-phase inflammatory process contributes to malnutrition, anemia, and possibly other abnormalities in dialysis patients. 989 76

This article, based on our own studies and those of others, presents evidence to show that the anemia of chronic renal failure in the predialysis period is, to a significant extent, caused by iron deficiency and can be improved in most cases by the administration of intravenous (i.v.) but not oral iron. We estimate that in approximately 30% of all predialysis patients with anemia, a target hematocrit (Hct) of 35% can be reached and maintained by giving i.v. iron alone without exceeding currently acceptable limits of serum ferritin (500 microg/liter) or the percentage of iron saturation (40%). If, in addition, subcutaneous erythropoietin (EPO-usually in only low doses-is added, the combination has an additive effect on the Hct response, and almost all anemic predialysis patients can reach and maintain the target Hct of 35% over a one-year period. Therefore, the advantage of maintaining adequate iron stores with i.v. iron is that if EPO is needed, lower doses will be required to achieve the target Hct than if EPO were used alone. This not only avoids the high cost of EPO therapy but also its associated side-effects, especially hypertension. Using Venofer, a ferric hydroxide sucrose complex, as our i.v. iron supplement, we have seen no anaphylactic reactions in over 20,000 infusions over a four-year period in 360 hemodialysis, 123 predialysis, and 58 peritoneal dialysis patients.
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PMID:Intravenous iron for the treatment of predialysis anemia. 1008 91

A prospective randomized study of the use of recombinant human erythropoietin (rHuEPO) in children with chronic renal disease was conducted to assess dosing requirements and side effects. Forty-four children with chronic renal failure, aged 4 months to 21 years, were studied. Twenty-five patients were pre dialysis, 10 on peritoneal dialysis, and 9 on hemodialysis. Patients received either 150 U/kg per week or 450 U/kg per week divided thrice weekly of rHuEPO for 12 weeks or until target hemoglobin (Hb) was attained. Dose was then adjusted to maintain a normal Hb. Eighty-two percent of patients reached target Hb by 7.9+/-5.6 weeks (mean+/-SD); 95% of patients in the high-dose group and 66% in the low-dose group reached target Hb within 12 weeks. The overall median rHuEPO dose at target Hb was 150 U/kg per week. Hemodialysis patients tended to require more rHuEPO to maintain a normal Hb (median 250 U/kg per week). Transfusion requirements and panel-reactive antibody levels decreased during the 12 weeks. Iron deficiency and/or hypertension occurred in 30% of children. In conclusion, rHuEPO at 150 U/kg per week is safe and effective in treating anemia in children with chronic renal disease.
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PMID:Safety and efficacy of erythropoietin in children with chronic renal failure. 1065 38

Erythropoietin (EPO) treatment dramatically changes the life of a child with end-stage renal disease. The administration of recombinant human (rHu)EPO is beneficial and safe in the predialysis period, during hemodialysis or peritoneal dialysis, and after renal transplantation. The goal of hemoglobin correction should be the level at which normal quality of life is possible without adverse events: in children this is usually 10-11 g/dl. rHuEPO is administered once to twice a week subcutaneously to children before dialysis, during peritoneal dialysis, and after transplantation. There is no real benefit of intraperitoneal administration. In children on hemodialysis two to three times a week IV administration is preferred. Among the many reasons for non-response to rHuEPO, iron deficiency (absolute or functional), infections, and hyperparathyroidism are the most common in the pediatric renal patient. Hypertension is the most-frequent side effect of rHuEPO treatment and needs careful monitoring. Iron should be supplemented orally or IV. No significant beneficial effect of rHuEPO on growth has been demonstrated. However, the association with recombinant human growth hormone therapy is not detrimental in children.
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PMID:Erythropoietin treatment in children with renal failure. 1065 38

A negative association between anemia and duration of gestation and low birth weight has been reported in the majority of studies, although a causal link remains to be proven. This paper explores potential biological mechanisms that might explain how anemia, iron deficiency or both could cause low birth weight and preterm delivery. The risk factors for preterm delivery and intrauterine growth retardation are quite similar, although relatively little is understood about the influence of maternal nutritional status on risk of preterm delivery. Several potential biological mechanisms were identified through which anemia or iron deficiency could affect pregnancy outcome. Anemia (by causing hypoxia) and iron deficiency (by increasing serum norepinephrine concentrations) can induce maternal and fetal stress, which stimulates the synthesis of corticotropin-releasing hormone (CRH). Elevated CRH concentrations are a major risk factor for preterm labor, pregnancy-induced hypertension and eclampsia, and premature rupture of the membranes. CRH also increases fetal cortisol production, and cortisol may inhibit longitudinal growth of the fetus. An alternative mechanism could be that iron deficiency increases oxidative damage to erythrocytes and the fetoplacental unit. Iron deficiency may also increase the risk of maternal infections, which can stimulate the production of CRH and are a major risk factor for preterm delivery. It would be useful to explore these potential biological mechanisms in randomized, controlled iron supplementation trials in anemic and iron-deficient pregnant women.
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PMID:Biological mechanisms that might underlie iron's effects on fetal growth and preterm birth. 1116 May 91

This report encourages clinicians to consider a diagnosis of Carney's triad in patients with multifocal gastric stromal sarcoma, extraadrenal paraganglioma (predominantly mediastinal), or pulmonary chondroma. The authors conducted a retrospective 20-year survey at the Hospital for Sick Children and identified two children with Carney's triad. One child, presenting atypically with papilledema and fundal hemorrhages from malignant hypertension and benign intracranial hypertension from chronic iron-deficiency anemia, is the second patient ever to date be described with the complete Carney's triad of neoplasms at diagnosis. Another child presented more typically with gastric stromal sarcoma and pulmonary chondroma without paraganglioma. Carney's triad is a rare differential diagnosis for "idiopathic" hypertension or iron-deficiency anemia from chronic gastrointestinal bleeding. If missed, patients with Carney's triad may have the debilitating physical and mental consequences of chronic iron deficiency and may die of untreated prolonged hypertension and metastatic leiomyosarcoma.
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PMID:Typical and atypical Carney's triad presenting with malignant hypertension and papilledema. 1187 80

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

An increased level of soluble transferrin receptor (sTfR) has been recognized as a useful indicator of iron deficiency, especially in tumour anaemia and in chronic diseases. In cases of erythropoietin substitution, however, it indicates a successful stimulation of erythropoiesis. We report an "unusual" increase in sTfR in a 60-year-old man who suffered from end-stage hypernephroma with extended lung metastases. He showed pulmonal hypertension, polycythaemia and a high serum level of erythropoietin. We assume that, in this case, the increased sTfR originates not only from bone marrow but could be partly contributed also by the malignant tissue of the hypernephroma.
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PMID:Increased soluble transferrin receptor in a case of hypernephroma accompanied by polycythaemia and elevated erythropoietin. 1238 76


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