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

Restless-legs syndrome (RLS) is a sensorimotor disorder, characterized by an irresistible urge to move the legs usually accompanied or caused by uncomfortable and unpleasant sensations. It begins or worsens during periods of rest or inactivity, is partially or totally relieved by movements and is exacerbated or occurs at night and in the evening. RLS sufferers represent 2 to 3% of the general population in Western countries. Supportive criteria include a family history, the presence of periodic-leg movements (PLM) when awake or asleep and a positive response to dopaminergic treatment. The RLS phenotypes include an early onset form, usually idiopathic with a familial history and a late onset form, usually secondary to peripheral neuropathy. Recently, an atypical RLS phenotype without PLM and l-DOPA resistant has been characterized. RLS can occur in childhood and should be distinguished from attention deficit/hyperactivity disorder, growing pains and sleep complaints in childhood. RLS should be included in the diagnosis of all patients consulting for sleep complaints or discomfort in the lower limbs. It should be differentiated from akathisia, that is, an urge to move the whole body without uncomfortable sensations. Polysomnographic studies and the suggested immobilization test can detect PLM. Furthermore, an l-DOPA challenge has recently been validated to support the diagnosis of RLS. RLS may cause severe-sleep disturbances, poor quality of life, depressive and anxious symptoms and may be a risk factor for cardiovascular disease. In most cases, RLS is idiopathic. It may also be secondary to iron deficiency, end-stage renal disease, pregnancy, peripheral neuropathy and drugs, such as antipsychotics and antidepressants. The small-fiber neuropathy can mimic RLS or even trigger it. RLS is associated with many neurological and sleep disorders including Parkinson's disease, but does not predispose to these diseases. The pathophysiology of RLS includes an altered brain-iron metabolism, a dopaminergic dysfunction, a probable role of pain control systems and a genetic susceptibility with nine loci and three polymorphisms in genes serving developmental functions. RLS treatment begins with the elimination of triggering factors and iron supplementation when deficient. Mild or intermittent RLS is usually treated with low doses of l-DOPA or codeine; the first-line treatment for moderate to severe RLS is dopaminergic agonists (pramipexole, ropinirole, rotigotine). In severe, refractory or neuropathy-associated RLS, antiepileptic (gabapentin, pregabalin) or opioid (oxycodone, tramadol) drugs can be used.
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PMID:[Restless-legs syndrome]. 1865 14

Restless legs syndrome (RLS) is a sensorimotor disorder, characterized by an irresistible urge to move the legs and usually accompanied or caused by uncomfortable and unpleasant sensations. It begins or worsens during periods of rest or inactivity, is partially or totally relieved by movement and is exacerbated or occurs mainly in the evening or night. People suffering from RLS are estimated to represent 2-3% of the general Japanese population, which is relatively lower than the estimated prevalence in western countries. Supportive diagnostic critevia include family history, the presence of periodic-leg movements (PLM) when awake or asleep, and a positive response to dopaminergic treatment. RLS phenotypes include an early onset form that is usually idiopathic with frequent familial history and a late onset form that is usually secondary to other somatic conditions that are causative factors in RLS occurrence. In all patients presenting with complaints of insomnia or discomfort in the lower limbs, diagnosis of RLS should be considered. RLS should be differentiated from akathisia, which is an urge to move the whole body in the absence of uncomfortable sensations. Polysomnographic studies and the suggested immobilization test (SIT) can detect PLM in patients that are asleep or awake. RLS may cause severe sleep disturbances, poor quality of life, depressive and anxious symptoms, and may be a risk factor for cardiovascular disease. Secondary RLS may occur due to iron deficiency, end-stage renal disease, pregnancy, peripheral neuropathy and drug use including antipsychotics and antidepressants. Small fiber neuropathy can trigger RLS or mimic its symptoms. RLS is associated with many neurological disorders, including Parkinson disease and multiple system atrophy; althoughit does not predispose to these diseases. A symptom rating scale for RLS authorized by the International RLS Study Group (IRLS) would facilitate accurate diagnosis of this condition.
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PMID:[Diagnosis and symptom rating scale of restless legs syndrome]. 1951 13

Chronic kidney disease (CKD) is a widespread health problem in the world and anemia is a common complication. Anemia conveys significant risk for cardiovascular disease, faster progression of renal failure and decreased quality of life. Patients with CKD can have anemia for many reasons, including but not invariably their renal insufficiency. These patients require a thorough evaluation to identify and correct causes of anemia other than erythropoietin deficiency. The mainstay of treatment of anemia secondary to CKD has become erythropoiesis-stimulating agents (ESAs). The use of ESAs does carry risks and these agents need to be used judiciously. Iron deficiency often co-exists in this population and must be evaluated and treated. Correction of iron deficiency can improve anemia and reduce ESA requirements. Partial, but not complete, correction of anemia is associated with improved outcomes in patients with CKD.
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PMID:Anemia in renal disease: diagnosis and management. 1983 21

Chronic kidney disease (CKD) is a widespread health problem in the world and anaemia of renal origin is a common problem. Anaemia associated with CKD covers significant risk for faster progression of chronic renal failure, decreased quality of life, and clinical manifestation of cardiovascular disease. The mainstay of anaemia treatment secondary to end-stage renal disease (ESRD) has become erythropoiesis stimulating agents (ESAs). More than 90 % of ESRD patients maintained on dialysis respond to traditional recombinant human erythropoietin (rHU EPO) or to EPO analogues, also called "biosimilars". Iron deficiency often co-exists in dialysis patients and must be evaluated and treated to reduce ESA requirements. Partial, but not complete correction of renal anaemia is associated with improved outcomes in patients with CKD. The use of ESAs does carry risks such as hypertension, pure red cell aplasia, or cancer, and these agents need to be used judiciously.
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PMID:Erythropoiesis stimulating agents and anaemia of end-stage renal disease. 2044 66

Although iron is an essential mineral for maintaining good health, excessive amounts are toxic. Nowadays, much interest is focused on the mechanisms and regulation of iron metabolism by down-regulation of the hormone hepcidin. The HAMP gene encodes for hepcidin appears to be exceptionally preserved. Disorders of iron metabolism could lead to iron overload, mainly causing the rare disease hereditary hemochromatosis, or on the other hand, iron deficiency and iron deficiency anaemia. Currently, these alterations constitute an important problem of public health. The genetic variation implicated in iron overload and iron deficiency anaemia, involves mutations in several genes such as HFE, TFR2,HAMP, HJV, Tf and TMPRSS6. Iron has the capacity to accept and donate electrons easily and can catalyze reactions of free radicals production. Therefore, iron overload causes lipid peroxidation and increases cardiovascular risk. Recently, a relationship between iron metabolism and insulin resistance and obesity has been described. In contrast, regarding a possible relationship between iron deficiency anaemia and cardiovascular disease, many aspects remain controversial. This review presents an overview of the most recent information concerning iron metabolism, iron bioavailability and iron overload/deficiency related diseases. The relation between iron and cardiovascular risk, in iron overload and in iron deficiency situations, is also examined. Finally, strategies to modify dietary iron bioavailability in order to prevent iron deficiency or alleviate iron overload are suggested.
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PMID:[Iron deficiency and overload. Implications in oxidative stress and cardiovascular health]. 2059 15

Iron deficiency is frequently seen in patients with end-stage renal disease, particularly in those treated by dialysis, this is because of an impairment in gastrointestinal absorption and ongoing blood losses or alternatively, due to an impaired capacity to mobilize iron from its stores, called functional iron deficiency. Therefore, these patients may require intravenous iron to sustain adequate treatment with erythropoietin-stimulating agents. Aside from this, they are also prone to vascular calcification, which has been reported a major contributing factor in the development of cardiovascular disease and the increased mortality associated herewith. Several factors and mechanisms underlying the development of vascular calcification in chronic kidney diseased patients have been put forward during recent years. In view of the ability of iron to exert direct toxic effects and to induce oxidative stress on the one hand versus its essential role in various cellular processes on the other hand, the possible role of iron in the development of vascular calcification should be considered.
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PMID:Iron and vascular calcification. Is there a link? 2132 49

Anemia is a common comorbidity in children with chronic kidney disease (CKD). This condition is associated with multiple adverse clinical consequences and its management is a core component of nephrology care. Increased morbidity and mortality, increased risk of cardiovascular disease and decreased quality of life have been associated with anemia of CKD in children. Although numerous complex factors interact in the development of this anemia, erythropoietin deficiency and iron dysregulation (including iron deficiency and iron-restricted erythropoiesis) are the primary causes. In addition to iron supplementation, erythropoietin-stimulating agents (ESAs) can effectively treat this anemia, but there are important differences in ESA dose requirements between children and adults. Also, hyporesponsiveness to ESA therapy is a common problem in children with CKD. Although escalating ESA doses to target increased hemoglobin values in adults has been associated with adverse outcomes, no studies have demonstrated this association in children. The question of appropriate target hemoglobin levels in children, and the approach by which to achieve these levels, remains under debate. Randomized, controlled studies are needed to evaluate whether normalization of hemoglobin concentrations is beneficial to children, and whether this practice is associated with increased risks.
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PMID:Anemia in children with chronic kidney disease. 2189 83

Iron deficiency is a common cause of anemia in patients with end stage renal disease (ESRD). Intravenous iron administration, especially in those requiring treatment with erythropoiesis stimulating agents (ESA) is an essential component of the management of anemia in ESRD patients. Iron improves hemoglobin, reduces ESA dose requirement and also has nonerythropoietic effects including improvement in physical performance, cognition and amelioration of restless leg syndrome. However, iron can promote oxidative stress, cause endothelial dysfunction, inflammation and tissue injury, and has a potential to cause progression of both CKD and cardiovascular disease. In this review, we discuss the benefits and risks associated with i.v. iron and the practical aspects of iron administration that can minimize the complications related to iron therapy in ESRD.
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PMID:Pumping iron: revisiting risks, benefits and strategies in treatment of iron deficiency in end-stage renal disease. 2237 49

Body iron status has been suggested to be related to the development of cardiovascular disease (CVD). Biologically plausible mechanisms for this association have been described, however epidemiological studies on iron status and CVD risk have provided conflicting results. The lack of consistency is likely explained by differences in the study design, the measures used for the assessment of iron status, the definition of outcomes, and adjustment for confounders. To help clarify the available evidence, we report a systematic review of published cross-sectional, longitudinal, and intervention studies evaluating the relationship between different measures of iron status and CVD risk. The most likely scenario that emerges from the available studies is that, in the reference range, iron status has a neutral effect. Extreme conditions of iron deficiency, as well as of iron overload, are associated with modestly increased CVD risk, although with different proposed mechanisms.
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PMID:Iron deficiency and cardiovascular disease: an updated review of the evidence. 2405 93

Loss of blood associated with hemodialysis procedures and laboratory testing, together with impaired iron absorption due to elevation of hepcidin, invariably cause iron deficiency in end-stage renal disease patients. For this reason, nearly all ESRD patients require intravenous iron to replete iron stores. Unfortunately, intravenously administered iron is often used routinely with inadequate attention to the body iron stores or severity of systemic inflammation. This has led to an epidemic of iron overload in the ESRD population. Only a minute amount (3-4 mg) of the total body iron (3-4 g in an adult man) resides in the plasma bound to transferrin, which serves as a safe vehicle for iron transport in the circulation. IV iron products are generally administered as bolus injections of 100 to 1000 mg, which far exceeds the available pool of free transferrin and represents a huge quantity compared to the intestinal iron absorption of 1 to 2 mg/day in the course of 3 to 4 meals. Administration of these products results in an increased plasma level of catalytically active non-transferrin bound iron and the rise in the biomarkers of oxidative stress and inflammation. IV iron bypasses the biological safeguards for the transport and handling of iron and helps to intensify chronic kidney disease-associated oxidative stress and inflammation. As briefly described in this review, indiscriminate use of IV iron can accelerate cardiovascular disease, promote microbial infections, aggravate viral hepatitis, and worsen diabetes and diabetic complications in such patients. For these reasons IV iron should be used judiciously in this vulnerable population.
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PMID:Toxic effects of IV iron preparations in CKD patients. 2464 44


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