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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 characterised by a complaint of an almost irresistible urge to move the legs. RLS is diagnosed clinically by means of the four essential criteria of the International Restless Legs Syndrome Study Group. In doubtful cases, neurophysiological examinations, such as polysomnography and/or a suggested immobilisation test, can be performed to confirm a clinical suspicion of RLS. Several other conditions may present sensorimotor complaints with features similar to RLS; a careful sleep history is required to avoid a misdiagnosis. Three different scales have been validated to assess the severity of RLS. In the general population, RLS prevalence ranges from 0.1% to 11.5%, with a high number of patients affected by a primary form of the sleep disturbance (70%-80%). However, several clinical conditions have been associated with RLS, such as iron deficiency, uraemia, pregnancy and polyneuropathy. Furthermore, recent studies show that RLS may be associated also to type 2 diabetes mellitus and to multiple sclerosis. RLS has a negative impact on sleep, cognitive functions, quality of life and mental status. Higher awareness of RLS among physicians is required; it remains an underdiagnosed clinical condition.
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PMID:Restless legs syndrome: diagnosis, epidemiology, classification and consequences. 1723 30

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

Iron overload can cause insulin deficiency, but in some cases this may be insufficient to result in diabetes. We hypothesized that the protective effects of decreased iron would be more significant with increased beta-cell demand and stress. Therefore, we treated the ob/ob mouse model of type 2 diabetes with an iron-restricted diet (35 mg/kg iron) or with an oral iron chelator. Control mice were fed normal chow containing 500 mg/kg iron. Neither treatment resulted in iron deficiency or anemia. The low-iron diet significantly ameliorated diabetes in the mice. The effect was long lasting and reversible. Ob/ob mice on the low-iron diet exhibited significant increases in insulin sensitivity and beta-cell function, consistent with the phenotype in mouse models of hereditary iron overload. The effects were not accounted for by changes in weight or feeding behavior. Treatment with iron chelation had a more dramatic effect, allowing the ob/ob mice to maintain normal glucose tolerance for at least 10.5 wk despite no effect on weight. Although dietary iron restriction preserved beta-cell function in ob/ob mice fed a high-fat diet, the effects on overall glucose levels were less apparent due to a loss of the beneficial effects of iron on insulin sensitivity. Beneficial effects of iron restriction were minimal in wild-type mice on normal chow but were apparent in mice on high-fat diets. We conclude that, even at "normal" levels, iron exerts detrimental effects on beta-cell function that are reversible with dietary restriction or pharmacotherapy.
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PMID:Dietary iron restriction or iron chelation protects from diabetes and loss of beta-cell function in the obese (ob/ob lep-/-) mouse. 2035 57

Blood bankers have focused their energy to secure blood transfusion, and only recently have studies been published on the effect of blood donation on iron metabolism. In many facilities, hemoglobin measurement is only performed just before or even during blood donation, but the determination of iron stores is largely ignored. The 2013 paradox of transfusion medicine is due to the fact that blood donation may be harmful and leads to iron deficiency with or without anemia, but for other individuals, it may be a healthy measure preventing type 2 diabetes. The purpose of this review is to discuss iron metabolism in the perspective of blood donation, notably regarding their possible genetic profiles that eventually will discriminate "good" iron absorbers from "bad" iron responders.
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PMID:Iron and transfusion medicine. 2414 56

Dysregulation of iron homeostasis is a potential risk factor for type 2 diabetes mellitus (T2DM) and insulin resistance. Iron transported into mitochondria by mitoferrins is mainly utilized for the biosynthesis of iron-sulfur clusters, heme, and other cofactors. Recent studies revealed that mitochondrial dysfunction leads to impaired adipogenesis and insulin insensitivity in adipocytes. However, it is unknown whether mitochondrial iron import and iron status affect the biogenesis and function of mitochondria during adipogenic differentiation. In this study, we used double knockdown of mitoferrin 1 and mitoferrin 2 (Mfrn1/2) to investigate the role of mitochondrial iron homeostasis in mitochondrial bioenergetic function and adipogenic differentiation. The results showed that depletion of Mfrn1/2 in 3T3-L1 preadipocytes impaired the biosynthesis of iron-sulfur proteins in mitochondria due to a decrease in mitochondrial iron content. This was associated with a decrease in mitochondrial oxygen consumption rate and intracellular ATP level in adipocytes with Mfrn1/2 knockdown. Remarkably, Mfrn1/2 deficiency reduced the expression of adipogenic genes and lipid production during adipogenic differentiation. Moreover, insulin-induced glucose uptake and Akt phosphorylation at the Ser473 residue were decreased concurrently in adipocytes differentiated from 3T3-L1 preadipocytes after knockdown of Mfrn1/2. These findings suggest that dysregulation of mitochondrial iron metabolism elicited by knockdown of Mfrn1/2 results in mitochondrial dysfunction, which culminates in the compromise of differentiation and insulin insensitivity of adipocytes. This scenario may explain the recent findings that iron deficiency or alterations in iron metabolism are associated with the pathogenesis of T2DM.
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PMID:Depletion of mitoferrins leads to mitochondrial dysfunction and impairment of adipogenic differentiation in 3T3-L1 preadipocytes. 2611 15

We report the case of a 73-year-old man with massive swelling of the lower extremities, with a chronic and rather uncommon form of stasis dermatitis - stasis papillomatosis. The patient was also diagnosed with severe heart failure, including dilated cardiomyopathy, hypothyroidism that required a substantial dose of exogenous tyrosine, microcytic and megaloblastic anemia, iron deficiency, and type 2 diabetes. The cause of stasis dermatitis lesions is not completely understood. It may be caused by the allergic reaction to some epidermal protein antigen formation or chronic damage to the dermal-epidermal barrier that makes the skin more sensitive to irritants or trauma. It has, however, been suggested that the term stasis dermatitis should be used to refer only to cases caused by chronic venous insufficiency, which belongs to a group of lifestyle diseases and affects both women and men more and more frequently.
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PMID:Stasis papillomatosis with cardiac complications and vein insufficiency. 2622 26

Intravenous iron products are essential for the treatment of anemia in end-stage renal disease patients maintained on hemodialysis. Although proper use of these compounds is necessary for the prevention of iron deficiency, their indiscriminate use could potentially cause insidious adverse consequences. Iron overload can intensify the chronic kidney disease-associated oxidative stress, inflammation, and cardiovascular disease; increase the risk of infections; worsen the severity of type 2 diabetes; and exacerbate neurologic and cognitive dysfunction. These and other adverse effects largely are mediated by iron-catalyzed generation of reactive oxygen species. Unlike conventional oral iron products, the newly released iron-containing phosphate binder ferric citrate has been shown to increase iron stores in end-stage renal disease patients. Therefore, iron indices should be monitored in patients receiving this product. Two published studies have shown a high prevalence of hepatic iron loading among hemodialysis patients treated with erythropoiesis-stimulating agents and intravenous iron compounds. Given the potential risks related to iron treatment in this vulnerable population, studies to better understand safety are needed.
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PMID:Safety Issues in Iron Treatment in CKD. 2723 32

Diabetes mellitus is frequently associated with iron overload conditions, such as primary and secondary hemochromatosis. Conversely, patients affected by type 2 diabetes mellitus (T2DM) show elevated ferritin levels, a biomarker for increased body iron stores. Despite these documented associations between dysregulated iron metabolism and T2DM, the underlying mechanisms are poorly understood. Here, we show that T2DM patients have reduced serum levels of hepcidin, the iron-regulated hormone that maintains systemic iron homeostasis. Consistent with this finding, we also observed an increase in circulating iron and ferritin levels. Our analysis of db/db mice demonstrates that this model recapitulates the systemic alterations observed in patients. Interestingly, db/db mice show an overall hepatic iron deficiency despite unaltered expression of ferritin and the iron importer TfR1. In addition, the liver correctly senses increased circulating iron levels by activating the BMP/SMAD signaling pathway even though hepcidin expression is decreased. We show that increased AKT phosphorylation may override active BMP/SMAD signaling and decrease hepcidin expression in 10-week old db/db mice. We conclude that the metabolic alterations occurring in T2DM impact on the regulation of iron homeostasis on multiple levels. As a result, metabolic perturbations induce an "iron resistance" phenotype, whereby signals that translate increased circulating iron levels into hepcidin production, are dysregulated.
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PMID:Uncoupled iron homeostasis in type 2 diabetes mellitus. 2897 Dec 21

Pregnant women are particularly vulnerable to iron deficiency and related adverse pregnancy outcomes and, as such, are routinely recommended for iron supplementation. Emerging evidence from both animal and population-based studies, however, has raised potential concerns because significant associations have been observed between greater iron stores and disturbances in glucose metabolism, including increased risk of type 2 diabetes among nonpregnant individuals. Yet, the evidence is uncertain regarding the role of iron in the development of gestational diabetes mellitus (GDM), a common pregnancy complication which has short-term and long-term adverse health ramifications for both women and their children. In this review, we critically and systematically evaluate available data examining the risk of GDM associated with dietary iron, iron supplementation, and iron status as measured by blood concentrations of several indicators. We also discuss major methodologic concerns regarding the available epidemiologic studies on iron and GDM.
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PMID:Dietary iron intake, iron status, and gestational diabetes. 2907 May 54

Specific skeletal myopathy constitutes a common feature of heart failure, chronic obstructive pulmonary disease, and type 2 diabetes mellitus, where it can be characterized by the loss of skeletal muscle oxidative capacity. There is evidence from in vitro and animal studies that iron deficiency affects skeletal muscle functioning mainly in the context of its energetics by limiting oxidative metabolism in favour of glycolysis and by alterations in both carbohydrate and fat catabolic processing. In this review, we depict the possible molecular pathomechanisms of skeletal muscle energetic impairment and postulate iron deficiency as an important factor causally linked to loss of muscle oxidative capacity that contributes to skeletal myopathy seen in patients with heart failure, chronic obstructive pulmonary disease, and type 2 diabetes mellitus.
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PMID:Iron deficiency as energetic insult to skeletal muscle in chronic diseases. 3017 22


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