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

Machine autotransfusion using cell-saver is a well-established method of saving homologous blood during extensive surgical procedures. The processing of blood may induce the initiation of lipid peroxidation (LPO) with the release of hepatotoxic products. A series of 42 patients undergoing primary (n = 20) or revision (n = 22) hip arthroplasty comprised the study group. Patients received an average of 1,260 ml of autologous blood and 2.2 units of homologous packed cells. The concentration of thiobarbituric acid reactive substances (TBARS) as LPO metabolites was measured in the patients' plasma, in the autologous packed cells as well as in the supernatants of the cell-saver-processed blood. Additionally, parameters of iron metabolism, haemoglobin levels, haematocrit as well as the activities of so-called liver enzymes aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltranspeptidase and cholinesterase were determined. An initiation of LPO was detectable during the process of machine autotransfusion, but this took place mainly ex vivo. High concentrations of TBARS were detectable in the supernatants after cell-separation processing. We observed a decline in haemoglobin concentration and haematocrit during the perioperative period. Postoperatively, we found a significant iron deficiency as a consequence of the perioperative blood loss. There was not sufficient evidence of a postoperative liver disorder induced by toxic metabolites of LPO. To sum up, there is only a low contamination of the organism with LPO products during the process of machine autotransfusion. Therefore, an induction of liver damage seems to be improbable.
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PMID:[Initiation of lipid peroxidation (LPO) in blood during intraoperative mechanical autotransfusion--is hepatotoxicity of lipid peroxidation products of clinical significance?]. 1081 96

The content of body iron is regulated primarily by absorption since humans have no physiological mechanism by which excess iron is excreted. This regulation, however, is not absolute. Many factors such as the content of diets, iron doses, life styles, etc. influence iron absorption. In the past, nutrition programs for iron fortification and the ingestion of iron preparations have been widely practiced because of the seriousness of worldwide iron deficiency. Also, we now know that a significant number of asymptomatic people carry the hemochromatosis gene, HFE, indicating that these people have the potential to accumulate excess body iron in their lifetime. Excess body iron can be highly toxic. This toxicity involves many organs leading to a variety of serious diseases such as liver disease, heart disease, diabetes mellitus, hormonal abnormalities, dysfunctional immune system, etc. The tissue damage associated with iron overload is believed to result primarily from free radical reactions mediated by iron. Iron is an effective catalyst in free radical reactions. The diseases associated with iron overload can be managed effectively or prevented. Therefore, early diagnosis of iron overload and appropriate therapy are critical. By providing the necessary laboratory data, clinical chemistry laboratories can play the pivotal role in the management of these health problems.
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PMID:Chronic iron overload and toxicity: clinical chemistry perspective. 1151 32

Anemia in children is commonly encountered by the family physician. Multiple causes exist, but with a thorough history, a physical examination and limited laboratory evaluation a specific diagnosis can usually be established. The use of the mean corpuscular volume to classify the anemia as microcytic, normocytic or macrocytic is a standard diagnostic approach. The most common form of microcytic anemia is iron deficiency caused by reduced dietary intake. It is easily treatable with supplemental iron and early intervention may prevent later loss of cognitive function. Less common causes of microcytosis are thalassemia and lead poisoning. Normocytic anemia has many causes, making the diagnosis more difficult. The reticulocyte count will help narrow the differential diagnosis; however, additional testing may be necessary to rule out hemolysis, hemoglobinopathies, membrane defects and enzymopathies. Macrocytic anemia may be caused by a deficiency of folic acid and/or vitamin B12, hypothyroidism and liver disease. This form of anemia is uncommon in children.
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PMID:Anemia in children. 1168 80

Reference values for Ferritin Flex on the Dimension RxL analyzer calibrated against the 3rd International Standard for Ferritin (recombinant) and N-Latex Ferritin on the BNA II nephelometer calibrated against the 2nd International Standard for Ferritin (spleen) both from Dade Behring (Marburg, Germany) were established (77 men and 182 women). Exclusion criteria were iron deficiency or iron deficiency anemia, inflammation, liver disease, malignancy, and other hematological or chronic disorders. The reference values (5.0th-95th percentiles) were as follow: for N-Latex Ferritin - men, 12-399 microg/l; women <50 years, 11-102 microg/l and women > or =50 years, 17-219 microg/l; for Ferritin Flex - men, 14-415 microg/l; women <50 years, 11-111 microg/l and women > or =50 years, 22-224 microg/l. Both assays correlated very closely with each other (r=0.993). The linearity was acceptable down to 2 microg/l for the Ferritin Flex method, but only down to 15 microg/l for the N-Latex Ferritin assay. The mean recovery of the 3rd International Standard by N-Latex Ferritin and Ferritin Flex was comparable (approximately 80%). We conclude that the new Ferritin Flex assay, which is based on the new 3rd International Standard, should be used for ferritin measurement in the routine medical laboratories in the future.
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PMID:Reference values for a heterogeneous ferritin assay and traceability to the 3rd International Recombinant Standard for Ferritin (NIBSC code 94/572). 1205 77

Haemochromatosis may be inherited or acquired. The commonest inherited form is HFE-related genetic haemochromatosis (GH). This is associated with homozygosity for the C282Y mutation in the HFE gene. Individuals with GH present in several ways depending upon the severity of iron overload. However, only a small proportion of genetically susceptible individuals develop disease. Diagnosis of GH is based on measurement of transferrin saturation, serum ferritin levels and mutation analysis of HFE. Liver biopsy is not necessary for diagnosis. It is used to establish the severity of liver disease in selected patients. Other complications of iron overload are identified by specific tests. Initial management of GH is by weekly venesection until borderline iron deficiency is achieved. The serum ferritin is then maintained at 50 microg/l by 3-6 monthly venesection. Specific organ damage is managed appropriately. Early diagnosis and treatment before irreversible damage has occurred gives a normal life expectancy. Non-HFE related inherited iron overload may be due to mutations in other iron related genes. Management is along the same lines as for GH, although if venesection is not tolerated, other approaches may be necessary.
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PMID:Diagnosis and management of genetic haemochromatosis. 1240 8

Iron deficiency is the most common disorder of iron metabolism worldwide, but there is concern that iron accumulation resulting from enhanced iron absorption may also be a cause of morbidity. In patients with genetic haemochromatosis the clinical manifestations of iron overload are well-known. In northern Europe 90% of such patients are homozygous for the C282Y mutation of the HFE gene and this genotype is found in 1 in 200 of the population. Heterozygosity for C282Y occurs in 15% of the population and 25% carry another mutation, H63D. Population studies have revealed (i) the serum transferrin saturation is strongly influenced by HFE genotype, being lowest in subjects lacking mutations and highest in those homozygous for C282Y; (ii) most subjects homozygous for C282Y accumulate iron but do not present with the clinical manifestations of iron overload. Testing for HFE mutations in clinics for diabetes, liver disease and cardiovascular disease has shown that homozygosity for C282Y is not commonly found. Heterozygosity for either C282Y or H63D does not appear to be a risk factor for these common conditions.
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PMID:HFE Mutations as risk factors in disease. 1240 9

The clinical presentation of adult coeliac disease is often uncharacteristic, with extraintestinal symptoms being the main findings. We report a 48-year-old woman who presented with type II, hepatitis-C-negative cryoglobulinaemia, elevated liver enzymes, and iron deficiency. Antinuclear antibodies were positive, and immunoglobulin G (IgG) levels were elevated. On liver biopsy, a diagnosis of type I autoimmune hepatitis with a possible autoimmune cholangitis overlap syndrome was made. Immunosuppressive treatment led to a normalization of transaminase levels and resolved the cryoglobulinaemic vasculitis. In addition, the patient exhibited low ferritin and iron levels, which led to the diagnosis of coeliac disease. Long-standing, untreated coeliac disease is recognized to be a trigger for autoimmune disorders and is known to be associated with other autoimmune diseases, but the association with autoimmune hepatitis or autoimmune cholangitis is reported rarely. We conclude that in patients with autoimmune liver disease and unspecific clinical signs, such as iron deficiency, coeliac disease must be ruled out.
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PMID:Autoimmune hepatitis, cryoglobulinaemia and untreated coeliac disease: a case report. 1265 65

Manganese (Mn), an element found in many foods, is an important and essential nutrient for proper health and maintenance. It is toxic in high doses, however, and exposure to excessive levels can result in the onset of a neurological disorder similar to, but distinct from, Parkinson's disease. Historically, Mn neurotoxicity was most commonly associated with various occupations, such as Mn mining, welding and steel production. More recently, increases in both blood and brain Mn levels have been observed in persons with liver disease or those receiving prolonged parenteral nutrition. Additionally, rodent data suggest that iron deficiency and anemia may be risk factors for Mn neurotoxicity. Clinically, brain Mn accumulation can be monitored in vivo using non-invasive magnetic resonance imaging (MRI) due to the paramagnetic nature of this element. Indeed, MRI has been used in a variety of settings to evaluate the brain Mn deposition in various populations. This review focuses on the use of MRI technology in studies related specifically to Mn neurotoxicity. Thus, we will examine reports using MRI to confirm brain Mn accumulation in human populations, and conclude with data from non-human primate and rodent models of Mn neurotoxicity.
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PMID:The use of magnetic resonance imaging (MRI) in the study of manganese neurotoxicity. 1662 Sep 89

Bivariate mixture modeling was used to analyze joint population distributions of transferrin saturation (TS) and serum ferritin concentration (SF) measured in the Hemochromatosis and Iron Overload Screening (HEIRS) Study. Four components (C1, C2, C3, and C4) with successively age-adjusted increasing means for TS and SF were identified in data from 26,832 African Americans, 12,620 Asians, 12,264 Hispanics, and 43,254 whites. The largest component, C2, had normal mean TS (21% to 26% for women, 29% to 30% for men) and SF (43-82 microg/L for women, 165-242 microg/L for men), which consisted of component proportions greater than 0.59 for women and greater than 0.68 for men. C3 and C4 had progressively greater mean values for TS and SF with progressively lesser component proportions. C1 had mean TS values less than 16% for women (<20% for men) and SF values less than 28 microg/L for women (<47 microg/L for men). Compared with C2, adjusted odds of iron deficiency were significantly greater in C1 (14.9-47.5 for women, 60.6-3530 for men), adjusted odds of liver disease were significantly greater in C3 and C4 for African-American women and all men, and adjusted odds of any HFE mutation were increased in C3 (1.4-1.8 for women, 1.2-1.9 for men) and in C4 for Hispanic and white women (1.5 and 5.2, respectively) and men (2.8 and 4.7, respectively). Joint mixture modeling identifies a component with lesser SF and TS at risk for iron deficiency and 2 components with greater SF and TS at risk for liver disease or HFE mutations. This approach can identify populations in which hereditary or acquired factors influence metabolism measurement.
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PMID:Bivariate mixture modeling of transferrin saturation and serum ferritin concentration in Asians, African Americans, Hispanics, and whites in the Hemochromatosis and Iron Overload Screening (HEIRS) Study. 1820 77

Patients with chronic kidney disease (CKD), especially those requiring maintenance hemodialysis treatments, may lose up to 3 g of iron each year because of frequent blood losses. Higher doses of erythropoiesis-stimulating agents (ESAs) may worsen iron depletion and lead to an increased platelet count (thrombocytosis), ESA hyporesponsiveness, and hemoglobin variability. Hence, ESA therapy requires concurrent iron supplementation. Traditional iron markers such as serum ferritin and transferrin saturation ratio (TSAT) (ie, serum iron divided by total iron-binding capacity [TIBC]), may be confounded by non-iron-related conditions. Whereas serum ferritin <200 ng/mL suggests iron deficiency in CKD patients, ferritin levels between 200 and 1,200 ng/mL may be related to inflammation, latent infections, malignancies, or liver disease. Protein-energy wasting may lower TIBC, leading to a TSAT within the normal range, even when iron deficiency is present. Iron and anemia indices have different mortality predictabilities, in that high serum ferritin but low iron, TIBC, and TSAT levels are associated with increased mortality, whereas hemoglobin exhibits a U-shaped risk for death. The increased mortality associated with targeting hemoglobin above 13 g/dL may result from iron depletion-associated thrombocytosis. Intravenous (IV) iron administration may not only decrease hemoglobin variability and ESA hyporesponsiveness, it may also reduce the greater mortality associated with the much higher ESA doses that have been used in some patients when targeting higher hemoglobin levels.
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PMID:Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia? 1923 73


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