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

Glycation and lipid peroxidation are spontaneous reactions that are believed to play a key role in the pathogenesis of many clinical disorders. Glycation of proteins is enhanced by elevated glucose concentrations. However, increased glycated hemoglobin levels have been documented in iron deficiency anemic patients without any history of diabetes. Collective evidences reveal that lipid peroxidation can modulate protein glycation. This study was undertaken to unravel the possible association of malondialdehyde and fructosamine in iron deficient anemic patients and to observe the possible alteration in malondialdehyde and fructosamine levels in these patients after one month supplementation with iron. Twenty non-diabetic anemic patients and 16 age-matched healthy subjects were enrolled for this study. Plasma lipid peroxides, fasting glucose, fructosamine, iron, ferritin and hemoglobin were analyzed in both the groups. Partial correlation analysis was performed to predict the independent association of malondialdehyde and fasting glucose on fructosamine. In anemic patients, while fructosamine and malondialdehyde levels were found to be significantly increased, hemoglobin, iron and ferritin levels decreased significantly when compared to before treatment. Fructosamine was found to have a significant positive correlation with malondialdehyde even after nullifying the effect of glucose. After one month supplementation with iron, both fructosamine and malondialdehyde levels decreased significantly when compared to before treatment. There was a significant increase in iron, ferritin and hemoglobin levels in anemic patients after one month of treatment. In conclusion, an increased level of fructosamine and malondialdehyde was found in anemic patients. These data suggest that fructosamine levels are closely associated with malondialdehyde concentrations in iron deficient anemic patients.
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PMID:Increased plasma malondialdehyde and fructosamine in iron deficiency anemia: effect of treatment. 1769 17

The clinical chemistry of diabetes care is unique in Endocrinology, because many of the commonly performed tests, such as assays for glucose, ketones and hemoglobin A1c, are done by the patient at home or by the nurse at the bedside or clinic. Hence, some may assume that these tests are accurate and precise. However, measurement of these substances is often problematic. While laboratory-based glucose analyzers are generally accurate, pre-analytic variables may introduce confusion. Hand held glucose meters are in widespread use and a number of variables are assumed regarding their use, such as hematocrit, oxygen tension and pH. Urine ketone assays may be confusing during conditions altering the mitochondrial redox potential and they are prone to interference from medications. Many different assays for HbA1c are in use today and the various assay types may each be prone to interference from abnormal hemoglobins, iron deficiency states and medication use. International efforts are underway to standardize HbA1c measurements. Insulin assays are being more commonly used as the prevalence of type 2 diabetes and the metabolic syndrome increases. Unfortunately, insulin assays are not standardized, making comparisons of results from different laboratories difficult. Finally, the assessment of diabetes-associated autoantibodies is becoming clinically useful as our understanding of the immunologic basis of diabetes develops and as protocols for the prediction (and ultimately prevention) of the disease arise. While a physician's clinical sense should always guide the interpretation of laboratory values, an understanding of the basis of commonly ordered clinical tests is critical in the care of patients with diabetes.
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PMID:Understanding and interpreting laboratory test results in the clinical management of diabetes mellitus. 1816 70

Neonatal brain iron deficiency occurs after insufficient maternal dietary iron intake, maternal hypertension, and maternal diabetes mellitus and results in short and long-term neurologic and behavioral deficits. Early iron deficiency affects the genomic profile of the developing hippocampus that persists despite iron repletion. The purpose of the present study was threefold: 1) quantitative PCR confirmation of our previous microarray results, demonstrating upregulation of a network of genes leading to beta-amyloid production and implicated in Alzheimer disease etiology in iron-deficient anemic rat pups at the time of hippocampal differentiation; 2) investigation of the potential contributions of iron deficiency anemia and iron treatment to this differential gene expression in the hippocampus; and 3) investigation of these genes over a developmental time course in a mouse model where iron deficiency is limited to hippocampus, is not accompanied by anemia and is not repletable. Quantitative PCR confirmed altered regulation in 6 of 7 Alzheimer-related genes (Apbb1, C1qa, Clu, App, Cst3, Fn1, Htatip) in iron-deficient rats relative to iron-sufficient controls at P15. Comparison of untreated to treated iron-deficient animals at this age suggested the strong role of iron deficiency, not treatment, in the upregulation of this gene network. The non-anemic hippocampal iron-deficient mouse demonstrated upregulation of all 7 genes in this pathway from P5 to P25. Our results suggest a role for neonatal iron deficiency in dysregulation of genes that may set the stage for long-term neurodegenerative disease and that this may occur through a histone modification mechanism.
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PMID:Iron deficiency alters expression of genes implicated in Alzheimer disease pathogenesis. 1872 4

Iron is a ubiquitous nutrient that is necessary for normal neurodevelopment. Gestational conditions that compromise fetal iron status include maternal iron deficiency, smoking, diabetes mellitus and hypertension. The iron-deficient neonate has altered recognition memory function and temperament while iron-deficient. The memory deficits persist even after iron repletion. Animal models demonstrate that early iron deficiency affects neuronal and glial energy metabolism, monoamine metabolism and myelination, consistent with behavioural findings in human infants. Of particular recent interest are genomic changes in transcripts coding for signal transduction, dendritic structure and energy metabolism induced by early iron deficiency that last well into adulthood in spite of iron treatment. Early iron sufficiency is critical for long-term neurological health.
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PMID:The role of iron in neurodevelopment: fetal iron deficiency and the developing hippocampus. 1902 38

Iron is one of the essential minerals that are required for a variety of molecules to maintain their normal structures and functions and for cells to live, grow, and proliferate. The homeostasis of iron results from a tightly coordinated regulation by different proteins involved in uptake, excretion and intracellular storage/trafficking. Although it is essential, iron can also be toxic once in excess amounts. Through Fenton reaction, iron as a transit mineral can generate various reactive oxygen or nitrogen species; therefore, abnormal metabolism of iron can lead to several chronic pathogenesis. Oxidative stress is one of the major causative factors for diabetes and diabetic complications. Increasing evidence has indicated that iron overload not only increases risks of insulin resistance and diabetes, but also causes cardiovascular diseases in non-diabetic and diabetic subjects. Temporal iron deficiency was found to sensitize insulin action, but chronic iron deficiency with anemia can accelerate the development of cardiovascular diseases in non-diabetic and diabetic patients. In this review, therefore, we will first outline iron homeostasis, function, and toxicity, and then mainly summarize the data regarding the roles of iron deficiency and overload in the pathogenesis of diabetes and diabetic complications, as well as the possible links of iron to diabetes and diabetic complications. In the end, the possible therapy using iron chelators for diabetes and diabetic complications will also be discussed.
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PMID:Role of iron deficiency and overload in the pathogenesis of diabetes and diabetic complications. 1914 65

This communication explores the temporal link between the age-associated increase in body iron stores and the age-related incidence of Alzheimer's disease (AD), the most prevalent cause of senile dementia. Body iron stores that increase with age could be pivotal to AD pathogenesis and progression. Increased stored iron is associated with common medical conditions such as diabetes and vascular disease that increase risk for development of AD. Increased stored iron could also promote oxidative stress/free radical damage in vulnerable neurons, a critical early change in AD. A ferrocentric model of AD described here forms the basis of a rational, easily testable experimental therapeutic approach for AD, which if successful, would be both widely applicable and inexpensive. Clinical studies have shown that calibrated phlebotomy is an effective way to reduce stored iron safely and predictably without causing anemia. We hypothesize that reducing stored iron by calibrated phlebotomy to avoid iron deficiency will improve cerebrovascular function, slow neurodegenerative change, and improve cognitive and behavioral functions in AD. The hypothesis is eminently testable as iron reduction therapy is useful for chronic diseases associated with iron excess such as nonalcoholic steatohepatitis (NASH), atherosclerosis, hereditary hemochromatosis and thalassemia. Testing this hypothesis could provide valuable insight into the causation of AD and suggest novel preventive and treatment strategies.
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PMID:Getting the iron out: phlebotomy for Alzheimer's disease? 1919 95

Evidence is reviewed documenting an intimate relationship among restless legs syndrome (RLS) / periodic limb movements in sleep (PLMS) and hypertension and cardiovascular and cerebrovascular disease. Sympathetic overactivity is associated with RLS/PLMS, as manifested by increased pulse rate and blood pressure coincident with PLMS. Causality is far from definitive. Mechanisms are explored as to how RLS/PLMS may lead to high blood pressure, heart disease, and stroke: (a) the sympathetic hyperactivity associated with RLS/PLMS may lead to daytime hypertension that in turn leads to heart disease and stroke; (b) in the absence of daytime hypertension, this sympathetic hyperactivity may predispose to heart disease and stroke either directly or indirectly via atherosclerotic plaque formation and rupture; and (c) comorbidities associated with RLS/PLMS, such as renal failure, diabetes, iron deficiency, and insomnia, may predispose to heart disease and stroke. One theoretical cause for sympathetic hyperactivity is insufficient All diencephalospinal dopaminergic neuron inhibition of sympathetic preganglionic neurons residing in the intermediolateral cell columns of the spinal cord. We cannot exclude the possibility that peripheral vascular, cardiovascular, and cerebrovascular disease may also contribute to RLS/PLMS, and mechanisms for these possibilities are also discussed.
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PMID:Review of the relationship of restless legs syndrome and periodic limb movements in sleep to hypertension, heart disease, and stroke. 2033 85

Celiac disease is an immune-mediated enteropathy affecting 0.5% to 1% of children and is induced by dietary gluten in susceptible individuals carrying the human leukocyte antigen DQ2 or DQ8 heterodimer. If serological screening is positive or if a patient displays suggestive symptoms, an endoscopic biopsy of the distal duodenum is required to confirm the diagnosis. Symptoms of celiac disease are often mild or absent. Overt malabsorption occurs in only 2% to 10% of children. Individuals with a higher risk of developing celiac disease, including first-degree relatives of affected patients and children with type I diabetes, Turner syndrome, Williams syndrome or Down syndrome, should be offered screening for celiac disease along with a discussion of the implications. If serological testing is negative, a high index of suspicion should remain if malabsorption, iron deficiency or osteopenia is present. Also, immunoglobulin A deficiency should be excluded. At-risk individuals should undergo serial serological screening. Lifelong adherence to a gluten-free diet is the only treatment. If left untreated, symptomatic children with celiac disease carry an increased risk of developing osteoporosis and have a greater lifetime risk of cancer. The long-term outcome of undiagnosed or untreated asymptomatic individuals is less clear.
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PMID:Practical considerations for the identification and follow-up of children with celiac disease. 1968 81

Pernicious anemia (PA) is a macrocytic anemia that is caused by vitamin B(12) deficiency, as a result of intrinsic factor deficiency. PA is associated with atrophic body gastritis (ABG), whose diagnosis is based on histological confirmation of gastric body atrophy. Serological markers that suggest oxyntic mucosa damage are increased fasting gastrin and decreased pepsinogen I. Without performing Schilling's test, intrinsic factor deficiency may not be proven, and intrinsic factor and parietal cell antibodies are useful surrogate markers of PA, with 73% sensitivity and 100% specificity. PA is mainly considered a disease of the elderly, but younger patients represent about 15% of patients. PA patients may seek medical advice due to symptoms related to anemia, such as weakness and asthenia. Less commonly, the disease is suspected to be caused by dyspepsia. PA is frequently associated with autoimmune thyroid disease (40%) and other autoimmune disorders, such as diabetes mellitus (10%), as part of the autoimmune polyendocrine syndrome. PA is the end-stage of ABG. Long-standing Helicobacter pylori infection probably plays a role in many patients with PA, in whom the active infectious process has been gradually replaced by an autoimmune disease that terminates in a burned-out infection and the irreversible destruction of the gastric body mucosa. Human leucocyte antigen-DR genotypes suggest a role for genetic susceptibility in PA. PA patients should be managed by cobalamin replacement treatment and monitoring for onset of iron deficiency. Moreover, they should be advised about possible gastrointestinal long-term consequences, such as gastric cancer and carcinoids.
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PMID:Pernicious anemia: new insights from a gastroenterological point of view. 2127 87

The use of intravenous (IV) iron is now part of the every day management of anaemia in people with Chronic Kidney Disease (CKD). The increase in the number of referrals to renal services since the introduction of estimated glomerular filtration rate (eGFR) reporting in 2006 in England means that people with CKD are being identified earlier and consequently, complications such as anaemia are being highlighted sooner. The prevalence of anaemia of CKD has been estimated in a population study of stage 3-5 CKD as 4.5% (John et al. 2004). People with stage 3 CKD and diabetes have a 22% incidence of anaemia that is much greater than the incidence of 7.9% in those without diabetes (El Achkar et al. 2005). The increase in numbers requiring anaemia management is having an impact on resources and service provision, in particular the treatment of iron deficiency with IV iron. A need to be creative and investigate alternative ways of using resources and providing services in different settings was identified by the multiprofessional members of the Anaemia Nurse Specialist Association (ANSA) and the CKD forum (a project group of the British Renal Society). The outcome has been the production of a practical guide for healthcare professionals to assist with the development of IV iron services in a nonacute hospital setting. The guide was launched at the annual ANSA conference (April 2009) and British Renal Society conference (June 2009).
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PMID:Creative iron management--a practical guide. 1989 84


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