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

The development of hypoproliferative anemia with generally normocytic red blood cells in most patients with chronic renal failure impairs the success of maintenance dialysis therapy, particularly hemodialysis. Anemia can be a complication of the hemodialysis procedure itself, with its associated blood losses and mild effect on oxygen transport functioning. However, the primary cause of anemia in the chronic dialysis patient is decreased erythropoiesis. The most important mechanism leading to decreased erythropoiesis involves the production of subnormal levels of erythropoietin (EPO). Insufficient nephric output of EPO or, possibly, suppression of the effect of EPO by uremic inhibitors may cause this decreased erythropoiesis. Other factors, such as iron deficiency, hyperparathyroidism, systemic infections, and aluminum toxicity may contribute to anemia in some patients. Increased hemolysis, a comparatively mild factor in the anemia of chronic dialysis patients, may be related to retention of protein metabolism products, hypersplenism, hypophosphatemia, drugs, or other conditions in affected patients. There are several traditional treatment options for anemia: transfusions; iron, vitamin B12, or folic acid supplementation when indicated; a change to peritoneal dialysis; parathyroidectomy; and administration of androgens. None of these treatments have proved satisfactory, and some, such as transfusions and androgen therapy, pose risks and have serious side effects. A comparatively new approach, administration of genetically engineered erythropoietin (r-HuEPO; EPOGEN, AMGEN inc, Thousand Oaks, CA), has been found effective in treating anemia in clinical trials. Patients have shown improved cardiac performance as well as enhanced quality of life, and hypertension appears to be the most serious side effect of r-HuEPO therapy.
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PMID:Overview of anemia associated with chronic renal disease: primary and secondary mechanisms. 264 18

Various haematological parameters were followed in a group of 47 Kenyan patients with visceral leishmaniasis during treatment and follow up. The WBC and platelet numbers were normal by the time of cure, the Hb level took longer to become normal. Red cells were microcytic and hypochromic. MCV and MCH increased during follow up but microcytosis persisted up to a year after cure. Low serum iron and transferrin concentration, low total iron binding capacity and normal to high serum ferritin levels were found in 10 patients and are consistent with 'anaemia of chronic inflammation'. Bone marrows of 15 patients before treatment were normo- to hypercellular with increased erythropoietic activity. Low haemosiderin content of the bone marrow was consistent with iron deficiency, but normalization of Hb without iron suppletion would argue against a major role of iron deficiency. Coagulation studies did not indicate diffuse intravascular coagulation. Splenomegaly seems the most important factor in the causation of the pancytopenia. Further studies of contributing factors and of the cause and mechanism of 'hypersplenism' are needed.
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PMID:Haematological investigations in visceral leishmaniasis. 381 Aug 41

Anemia is a frequent clinical feature with adverse prognostic effects in patients with chronic lymphocytic leukemia (CLL). It may complicate CLL at any time during the course of the disease. Different factors concur to the occurrence of anemia in CLL, as in other lymphoproliferative diseases: leukemic bone marrow infiltration, the myelosuppressive effect of chemotherapy and inhibiting cytokines, autoimmune phenomena, hypersplenism, a poor nutritional status that leads to folic acid, vitamin B12 and iron deficiency. In addition, a defective endogenous erythropoietin (EPO) production has also been described in patients with lymphoproliferative diseases. The severity of anemia, which may be worsened by an impaired cardiopulmonary function, may profoundly compromise the patients' quality of life and, indirectly, the outcome of cancer bearing patients. Several Authors have reported the clinical activity of recombinant human (rHu)EPO in anemic patients with lymphoproliferative diseases, including CLL. Low serum EPO levels at baseline and EPO levels inappropriately low for the degree of anemia help to identify patients who are likely to respond to EPO. A clear dose-dependent response to EPO has been reported by different Authors and it has been suggested that 5,000 IU should be considered as an appropriate initial dose for the majority of patients. rHuEPO represents a potentially effective and safe therapy for the management of anemia associated with lymphoproliferative diseases. The reduction of red blood cell transfusion requirement, the improvement of quality of life through the remission of fatigue-related anemia are two important results that should be considered in the management of patients with CLL. In prospect, the availability of new rHuEPO molecules with a more prolonged half-life may open new therapeutic avenues.
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PMID:Erythropoietin and chronic lymphocytic leukemia. 1273 12

Approximately 5-10% of patients with chronic kidney disease demonstrate hyporesponsiveness to erythropoiesis-stimulating agents (ESA), defined as a continued need for greater than 300 IU/kg per week erythropoietin or 1.5 mug/kg per week darbepoetin administered by the subcutaneous route. Such hyporesponsiveness contributes significantly to morbidity, mortality and health-care economic burden in chronic kidney disease and represents an important diagnostic and management challenge. The commonest causes of ESA resistance are non-compliance, absolute or functional iron deficiency and inflammation. It is widely accepted that maintaining adequate iron stores, ideally by administering iron parenterally, is the most important strategy for reducing the requirements for, and enhancing the efficacy of ESA. There have been recent epidemiologic studies linking parenteral iron therapy to an increased risk of infection and atherosclerosis, although other investigations have refuted this. Inflammatory ESA hyporesponsiveness has been reported to be improved by a number of interventions, including the use of biocompatible membranes, ultrapure dialysate, transplant nephrectomy, ascorbic acid therapy, vitamin E supplementation, statins and oxpentifylline administration. Other variably well-established causes of ESA hyporesponsiveness include inadequate dialysis, hyperparathyroidism, nutrient deficiencies (vitamin B12, folate, vitamin C, carnitine), angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aluminium overload, antibody-mediated pure red cell aplasia, primary bone marrow disorders, myelosuppressive agents, haemoglobinopathies, haemolysis and hypersplenism. This paper reviews the causes of ESA hyporesponsiveness and the clinical evidence for proposed therapeutic interventions. A practical algorithm for approaching the investigation and management of patients with ESA hyporesponsiveness is also provided.
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PMID:Erythropoiesis-stimulating agent hyporesponsiveness. 1763 45

Anemia is often observed in digestive diseases such as gastroduodenal ulcers, esophageal varices, atrophic gastritis, malignant neoplasms, inflammatory bowel diseases, gastrectomy, malabsorption syndrome, and liver diseases. Anemia in these digestive diseases is caused by bleeding, iron deficiency, vitamin B12 deficiency including pernicious anemia, chronic inflammation (anemia of chronic disorders), malnutrition, hypersplenism. Especially in case of gastrointestinal bleeding, double balloon enteroscopy has been recently introduced to contribute to the diagnosis and treatment as well as gastroendoscopy and colonoscopy. In the treatment of digestive disease with anemia, it is important to treat digestive diseases appropriately. In treatment of patients with anemia of unknown origin, examinations about digestive diseases should be considered.
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PMID:[Digestive disease with anemia]. 1832 21

Approximately 5-10% of patients with end-stage renal disease (ESRD) exhibit hyporesponsiveness to erythropoiesis-stimulating agents (ESAs), defined as a continued need for higher than 300 IU/kg/week doses of epoetin or a 1.5 mg/kg/week dose of darbepoetin. ESA hyporesponsiveness contributes to the morbidity, mortality and health-care economic burden of ESRD patients. The most common causes of ESA resistance are absolute or functional iron deficiency and inflammation. Maintaining adequate iron stores is clearly accepted as the most important strategy for reducing the ESA requirement and for enhancing ESA efficacy. Recent clinical studies have shown that iron administration to ESRD patients is associated with an increased risk of infection and atherosclerosis. ESA hyporesponsiveness due to chronic inflammation in ESRD patients has been reported to be improved by a number of interventions, including the use of biocompatible hemodialysis membranes, ultrapure dialysate, ascorbic acid therapy, vitamin E supplementation, and statin therapy. Other causes of ESA hyporesponsiveness include inadequate dialysis, hyperparathyroidism, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, primary bone marrow disorders, myelosuppressive agents, hemoglobinopathies, hemolysis, and hypersplenism. This article summarizes the common causes of ESA hyporesponsiveness and the proposed therapeutic interventions.
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PMID:Erythropoiesis-stimulating agent hyporesponsiveness in end-stage renal disease patients. 2602 17