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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the relationship of serum ferritin to bone marrow iron stores in 73 anemic male medical inpatients with liver disease, alcoholism, chronic inflammatory disease, and malignancies. A correlation of r = 0.75 (P less than .00005) was found between serum ferritin and bone marrow iron stores (BMIS) for the entire group. Liver disease as manifested clinically or by increased levels of serum glutamic-oxaloacetic transaminase did not appear to significantly affect this relationship. Patients with folic acid deficiency did tend to have a disproportionate increase in ferritin in relation to BMIS, but this did not seem to destroy the usefulness of ferritin levels. A useful clinical rule seems to be that serum ferritin of greater than 100 ng/ml tends to exclude iron deficiency, and a level of less than 30 ng/ml tends to confirm decreased iron stores.
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PMID:Ferritin as an index of bone marrow iron stores. 72 24

Increase in serum ferritin, which occurs in 40 to 70% of chronic alcoholics, remains poorly understood. We tested the hypothesis which links hyperferritinemia in chronic alcoholism not only to ferritin release from damaged liver cells, but also to increased ferritin secretion. Fifty-eight chronic alcoholic patients hospitalized for alcohol withdrawal were subdivided into three groups according to liver damage. Their serum levels of ferritin and ferritin bound to concanavalin A (ferritin Con A, which represents glycosylated, i.e., secreted ferritin) were measured serially on days 1, 7, and 11 of withdrawal and compared with a control group. The results were: (1) Total serum ferritin increased in alcoholics. Both free and Con A ferritins increased in equal proportions, the ferritin Con A to total ferritin ratio remaining unchanged. The increase was dependent on liver disease, as both free and Con A ferritins increased significantly with the severity of liver illness. Serum ferritin levels were related to iron status: it correlated with hepatic iron concentration (obtained in 19 patients); however, high ferritin values were not related to the degree of iron overload, which remained low. Finally, there was no correlation between serum ferritin and the average of alcohol consumption. (2) Both free and Con A ferritin decreased by about 40% during alcohol withdrawal. In conclusion, we have demonstrated that (1) total serum ferritin is increased in chronic alcoholism and (2) that this ferritin increase is due in part to an increase in ferritin Con A, proof of the induction of ferritin secretion by alcohol in humans.
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PMID:Increase in glycosylated and nonglycosylated serum ferritin in chronic alcoholism and their evolution during alcohol withdrawal. 168 73

We assessed the prevalence of previously unrecognized hemochromatosis among patients in whom diabetes mellitus was diagnosed after the age of 30 yr, and we evaluated the positive predictive value of biochemical screening tests for hemochromatosis in diabetic subjects. Thirty-eight of 572 patients screened (6.6%) had a serum ferritin level greater than 324 micrograms/L; 16 patients had normal levels on repeat testing. Four patients' serum ferritin levels fell to less than 400 micrograms/L. Seven of 18 patients with a persistently elevated serum ferritin level did not undergo a liver biopsy because of a recognized cause of hyperferritenemia (carcinoma, alcoholism, or systemic lupus erythematosus). The diagnosis of hemochromatosis seemed certain in 1 of 3 patients who were not biopsied for technical reasons. Of 8 patients biopsied, 2 had hemochromatosis, 4 had fatty liver, 1 had hemosiderosis, and 1 had a chronic inflammatory cell infiltrate with no iron deposition. Of 4 patients with a raised transferrin saturation level, 2 had raised serum ferritin levels and hemochromatosis, 1 had raised serum ferritin and hemosiderosis on liver biopsy, and 1 had a normal transferrin saturation level on repeat testing. Two of 3 cases of hemochromatosis had other clinical markers of the condition. Therefore, routine screening of diabetic patients for hemochromatosis is not necessary, because patients with hemochromatosis will often have other clinical features of the disease. When screening diabetic patients for hemochromatosis, it should be remembered that a persistently raised serum ferritin level has a low positive predictive value (16.6%) and that a normal transferrin saturation level does not exclude the diagnosis.
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PMID:Usefulness of biochemical screening of diabetic patients for hemochromatosis. 235 Oct 33

The known relationship between ethanol and the two main proteins of iron metabolism, transferrin and ferritin, are reviewed. Transferrin synthesis decreases in alcoholic cirrhosis, and increases in alcoholic fatty liver. In the latter case, its turnover is accelerated. Serum desialylated transferrin increases in chronic alcoholism and could be the best marker of heavy drinking. The increased uptake of desialylated transferrin by the liver could explain the development of hepatic siderosis in some alcoholics. Serum ferritin increases in chronic alcoholism, much more because of liver damage than in relation to iron stores. It is clear in this review that few experimental studies have been interested in the investigation of these relationships.
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PMID:[Interactions of alcohol and iron proteins]. 265 33

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of iron preparations. 267 7

In order to develop a diagnostic approach to the common problem of anemia associated with alcoholism, 121 chronic alcoholics admitted to a general medical service with a low hematocrit were evaluated. Multiple contributing causes of anemia were present in most patients. Megaloblastic marrow change was found in 33.9% of patients, sideroblastic change in 23.1%, absent iron stores in 13.2%, aggregated macrophage iron in 81.0%, and acute blood loss in 24.8%. The MCV was of little value in predicting the presence of megaloblastic change unless markedly elevated (greater than 110 fl). In 15 of 41 patients with megaloblastic marrow morphology (36.6%) the MCV was normal or low. Among 40 patients with MCV values between 100 and 110 fl, megaloblastic change was not present in the bone marrow smears of 24 (60.0%). Neutrophil hypersegmentation was 95% specific but only 78% sensitive for megaloblastic change; in contrast, the presence of macroovalocytosis was 90% sensitive but only 68% specific. Serum lactic dehydrogenase, plasma folate, and erythrocyte folate levels had such low sensitivities and specificities for megaloblastic change as to be of little predictive value. Hematologic responses to folic acid were often inadequate in patients with megaloblastic morphologic changes, apparently because of associated acute and chronic illness. Our findings are consistent with the hypothesis that 2 mechanisms account for the development of megaloblastic hematopoiesis in alcoholics: induction of folate deficiency and a direct toxic effect of alcohol on erythroid precursors independent of folate depletion, as reflected by the presence of normal plasma and erythrocyte folate levels in several patients with megaloblastic change. In no patient was sideroblastic change the sole apparent cause of anemia. Megaloblastic hematopoiesis and aggregated macrophage iron frequently accompanied sideroblastic change. Examination of the blood smear revealed siderocytes in one-third of patients with sideroblastic marrows and dimorphic erythrocyte morphology in the majority. Dimorphic blood smears, however, were neither sensitive nor specific for sideroblastic change. Serum iron concentrations were usually not elevated in the group with sideroblastic abnormalities. In predicting marrow iron stores, serum iron and iron-binding capacity concentrations were often non-diagnostic or misleading. Serum ferritin levels less than 100 ng/ml, however, showed 100% sensitivity and 95% specificity for absent marrow iron stores despite the frequent presence of abnormal liver function. On the basis of our findings, practical guidelines have been formulated for the evaluation and therapy of anemia in alcohol
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PMID:Anemia in alcoholics. 374 28

The effects of biological (age, sex, weight) and pathological factors on plasma ferritin concentrations were documented in 776 unselected elderly patients aged 80.9 +/- 9.7 yr. A marked shift towards high values (159 +/- 142 micrograms/l) was observed in this elderly population together with the persistence of the well-known sex-related difference in ferritin levels (higher levels in men). Twenty-five percent of the population had high levels of ferritin (greater than or equal to 220 micrograms/l) but 75% of these high values (i.e. 18.5% of the population) could be readily explained by their known association with a particular pathology (inflammatory syndrome, renal failure, cardiovascular diseases, alcoholism). Only 6% of the population had unexplained high ferritin concentrations. Therefore, our data strongly suggest that the repeatedly reported increase of ferritin in the aged population is merely related to an age-associated pathology and may not be a normal physiological event occurring during the process of aging.
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PMID:Plasma ferritin in old age. Influence of biological and pathological factors in a large elderly population. 402 33

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
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PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3

A survey is given of methods involving decalcification and paraffin embedding of iliac crest biopsy for osteological and haematological diagnostic procedures. In order to avoid shrinkage, loss of antigens, and fading of ferritin iron and enzymes, a fixative has been designed that is composed of an aqueous solution of calcium acetate (10(-1) M), glutaraldehyde (0.5%), and formaldehyde (1%; CGF). CGF-fixated specimens are decalcified in an aqueous solution of 10% di-sodium ethylene-diaminotetraacetate (EDTA) neutralized by tris[hydroxy]methylaminomethane and embedded in paraffin. Tissue prepared in this manner allows histochemical detection of naphthol AS-D chloroacetate esterase in the neutrophilic cell line and in tissue mast cells, tartrate-resistant acid phosphatase in hairy cells and certain other low malignant B-cell lymphomas, in Gaucher cells, and in osteoclasts, and a specific platelet esterase in megakaryocytes and leukaemic megakaryoblasts. A broad panel of antigens is well preserved. Beside haemosiderin, cytosolic ferritin can be detected by Perls' reaction in acute phase-stimulated macrophages. Emphasis is placed on the diagnostic impact of plasma cell siderosis and lysosomal sideroblastocytosis in haemochromatosis and in alcoholism respectively. A technique is presented to discriminate mineralized and non-mineralized bone even after decalcification.
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PMID:[Histological processing of iliac crest biopsies based on decalcification and paraffin embedding with reference to osteolytic and hematologic diagnosis]. 788 10

Serum ferritin increases in chronic alcoholism, without clear explanation. We have previously shown that alcohol increases ferritin levels in a human hepatoblastoma cell line (HepG2). The aims of the present work were: 1) To extend our results in normal rat hepatocyte cultures, and 2) To determine the mechanism by which alcohol enhances ferritin levels. In HepG2 cells, high alcohol concentrations (300 mM) during long exposure (4 days) increased the synthesis of H and L ferritin subunits, in association with increased levels of ferritin mRNAs. In rat hepatocyte cultures, the synthesis of L ferritin increased after 24 h of exposure to lower alcohol concentrations (10 mM); alcohol had no effect on ferritin mRNAs levels. In both cell types, the alcohol effect was not related to an increase in iron intracellular incorporation. In HepG2 cells, desferrioxamine (Df), a potent iron chelator, abolished ferritin synthesis in the presence or absence of alcohol, and abolished the alcohol induction of ferritin mRNAs. In rat hepatocytes, Df decreased ferritin synthesis to a similar level in the presence or absence of alcohol. Alcohol increased ferritin synthesis differently in HepG2 cells and in normal rat hepatocyte cultures. In the latter case, the alcohol effect was observed at low concentration. Despite a striking inhibiting effect of Df on ferritin synthesis, in both cellular models a mechanism accounting for increased ferritin synthesis independently of iron is suggested. Globally, these data strongly suggest that hyperferritinemia in chronic alcoholism could be related to the induction of ferritin by alcohol.
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PMID:Regulation of ferritin expression by alcohol in a human hepatoblastoma cell line and in rat hepatocyte cultures. 865 61


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