Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with characteristic features of iron deficiency was unexpectedly found to have circulating siderocytes. Bone marrow iron stain at this time showed absence of both hemosiderin and ringed sideroblasts; electron microscopy revealed absence of mitochondrial iron loading but presence of cytoplasmic ferritin in normoblasts. Replenishment of iron stores led to development of typical sideroblastic anemia. These observations suggest that increased percentage of siderocytes in otherwise typical iron deficiency anemia may signify the presence of a sideroblastic process masked by iron deficiency due to bleeding.
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PMID:Primary sideroblastic anemia masked by bleeding. 7 31

The serum ferritin concentration was measured in 1417 Indians and 310 Inuit aged 1 to 89 years. The subjects were initially selected to produce a representative sample of the entire native population, but the rate of nonresponse was high, and the results reported in this paper are representative only of the people studied.In males the median serum ferritin values increased during early life and tended to plateau after the age of 30 years. In females the median values rose during childhood, tended to plateau during adolescence, increased slightly during the reproductive period, then gradually rose thereafter. Ranges of values were wide in all age groups, reflecting the variations in body iron stores. When compared with the Inuit, the Indians had a significantly higher prevalence of abnormal serum ferritin values.From an analysis of the serum ferritin values in Indians it is probable that iron stores were reduced in approximately 30% of children, 40% of adolescents, 34% of nonpregnant women of reproductive age, 11% of older women and 5% of adult males. The corresponding figures for the Inuit were 15%, 23%, 22%, 6% and 1%. In contrast, iron deficiency anemia was found in only 3% to 4% of native peoples. If "normality" requires more than small amounts of iron stores to meet physiologic needs, the results suggest a high probability of iron deficiency in 20% to 40% of native children, adolescents and nonpregnant women of reproductive age, and in 0% to 10% of other subjects; but if "normality" is defined as adequate iron stores for erythropoiesis the prevalence of iron deficiency was approximately 1% to 2% in children and adolescents, 3% to 5% in women and less than 1% in adult males.
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PMID:Evaluation of the body iron status of native Canadians. 42 65

Serum ferritin estimation was used to determine the iron stores in 55 patients with severe iron deficiency anaemia in pregnancy. The response to oral or intravenous iron therapy was monitored in 18 of these patients. The results in all cases indicated deficient iron stores. Replenishment of iron stores was significantly greater in those patients treated with parenteral iron. This may be the treatment of choice for severe iron deficiency anaemia during pregnancy.
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PMID:Serum ferritin estimation in the assessment of iron stores in severe iron deficiency anaemia in pregnancy and the response to treatment. 44 79

A controlled, prospective study compared the effectiveness of oral ferrous sulfate to intravenous iron dextran, each with and without concurrent intramuscular androgen for therapy of iron deficiency anemia in patients with chronic renal failure treated with maintenance hemodialysis. During the 12-week period of therapy, the patients who received oral ferrous sulfate and androgens showed an increment in their mean hematocrit of 16.3% and those who received oral ferrous sulfate alone had an increase of 8.3%. Patients treated with intravenous iron dextran androgens showed an increment in their mean hematocrit of 9.4% and those given iron dextran alone showed an increase of 3.5%. Serum ferritin levels increased with iron repletion but correlated inversely with the erythropoietic response. The serum ferritin assay provides a simple and reliable method to demonstrate iron repletion, and oral ferrous sulfate is the preferred method of iron repletion in compliant patients.
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PMID:Therapy of iron deficiency anemia in patients on maintenance dialysis. 47 Nov 41

A direct radioimmunoassay for ferritin in serum is described in which Bolton and Hunter reagent is used to label ferritin. The detection limit of the assay is 150 pg; 95% reference ranges were found to be 12-200 microgram/l for men and 5-76 microgram/l for women. Ferritin concentrations in patients with iron deficiency anaemia were found to be uniformly low in subjects with uncomplicated iron deficiency but were normal or even raised in subjects with iron deficiency anaemia associated with malignant or inflammatory conditions.
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PMID:Measurement of serum ferritin by radioimmunoassay. 63 7

Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r = -0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 microgram/l. In a group of apparently hematologically normal children between the age of 10--14 years (hemoglobin greater than 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 mumole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.
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PMID:The diagnosis of iron deficiency by erythrocyte protoporphyrin and serum ferritin analyses. 65 13

Nonheme iron and ferritin in the bone marrow and serum ferritin was investigated in patients with iron deficiency anaemia or iron overload. As controls served patients without any disturbance of the iron metabolism. There is a precise correlation between the nonheme iron and ferritin in the bone marrow of patients with and without disturbance of iron metabolism. A correlation was also found between the ferritin in the bone marrow and the serum. Nonheme iron and ferritin in the bone marrow and serum ferritin was decreased in patients with iron deficiency anaemia. Conversely, the same parameters were increased in patients with iron overload.
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PMID:Ferritin in bone marrow and serum in iron deficiency and iron overload. 68 38

Knowledge of disturbancies of iron utilization has been considerably extended by histochemical-ultrastructural findings and the results of immunoradiometric assays for serum ferritin. -- In chronic anaemia due to infections or neoplastic diseases hyposideraemia and normal unsaturated iron binding capacity were associated with increased iron retention in macrophages and slightly to highly increased serum ferritin (500--4000 ng/ml). -- 117 patients with sideroblastic anaemia formed a heterogenous group of diverse aetiology. The iron granules of ringed sideroblasts contained nonferritin iron in mitochondria. At diagnosis, a normal iron status was found in single cases. More frequently, praelatent and latent iron overload with ferritin levels up to more than 2000 ng/ml were observed. Manifest iron overload with tissue damage was mostly the result of numerous transfusions (ferritin 4700 bis 9500 ng/ml). -- After i.v. application of colloidal iron endothelial siderosis was a regular finding. The typical uniform granules representing nonferritin-iron in lysosomes disappeared in the course of 1--3 years completely. In contrast, the colloidal iron taken up simultaneously by the macrophages was rapidly transformed into ferritin and easily used up for haemoglobin synthesis when required. The corresponding increase of serum ferritin up to maximal 4000 mg/ml was dose related. Continued blood losses lead to residual endothelial siderosis after exhaustion of macrophageal iron and recurrence of iron deficiency anaemia. The serum ferritin fell to low levels (0--12 ng/ml) as observed in untreated cases.
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PMID:[Disturbancies of iron utilization: chronic anaemia, sideroblastic anaemia, and residual endothelial siderosis (author's transl)]. 73 33

Red cell indices, plasma iron, total iron-binding capacity and serum ferritin levels were measured in 73 patients with iron deficiency anaemia. There was decreased plasma iron and MCHC with an increased total iron-binding capacity in 38 patients (type I iron deficiency anaemia). There was no hypochromia in 18 patients with decreased plasma iron and normal total iron-binding capacity; haemoglobin concentration was higher than 90 g/l (type II). Normal MCHC, plasma iron and total iron-binding capacity were found in 17 patients with haemoglobin values higher than 105 g/l (type III). Serum ferritin measurements were made by the immunoradiometric assay. The ferritin concentration was less than 40 micron/l in 66 patients with iron deficiency anaemia. The test proved reliable in diagnosing mild iron deficiency anaemia (types II and III) without bone marrow aspiration.
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PMID:[Serum ferritin in iron deficiency anaemia (author's transl)]. 89 8

Ferrritin can be measured in blood serum radioimmunometrically. Serum ferritin is directly correlated to body iron stores. In comparison to other parameters of storage iron (bone marrow iron, intestinal iron absorption) this quantitative diagnostic parameter is easily available. Thus it can be used to judge body iron status. In 20 patients with chronic haemorrhagic and 7 patients with posthaemorrhagic iron deficiency anaemia as well as nine blood donors with latent iron deficiency serum ferritin was used to control oral iron therapy. The continuous determination of serum ferritin during therapy gives a quantitative value of the relevant level of body iron stores. This value shows whether therapy was effective and when iron stores are replenished. The results demonstrate that oral iron therapy should be continued for at least 3 months from the time of normalisation of haemoglobin to obtain a sufficient restoration of iron depots.
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PMID:[Serum ferritin as a control parameter for oral iron therapy (author's transl)]. 89 9


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