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

(1) Brief introduction to iron metabolism and the biochemistry of ferritin. (2) Early studies of circulating ferritin. (3) Methods for measuring serum ferritin concentrations -- immunoradiometric, radioimmuno- and enzyme-linked immuno assays based on liver or spleen ferritin -- an evaluation of these techniques. (4) Serum ferritin concentrations in normal subjects -- definition of normality -- relationship between storage iron and serum ferritin concentrations -- changes during development from birth to old age -- iron deficiency -- variability of serum ferritin concentration -- evaluation of use of ferritin assay for assessment of storage iron levels. (5) Serum ferritin concentrations in disease -- hemochromatosis -- secondary iron overload -- liver damage -- infection and chronic disease -- cancer. (6) Assay of serum ferritin with antibodies to ferritins other than liver or spleen -- ferritinemia and cancer. (7) Properties of serum ferritin -- molecular weight -- iron content -- isoelectric focusing patterns -- carbohydrate content -- immunological properties. (8) Physiology of circulating ferritin -- release of ferritin from tissues -- origin of circulating ferritin -- clearance from the plasma -- iron and protein turnover. (9) Summary -- factors influencing serum ferritin concentrations and clinical use of ferritin estimations.
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PMID:Serum ferritin. 37 39

Patients with juvenile rheumatoid arthritis may have an anemia attributable to the chronic disease, to iron deficiency, or to a combination of the two. The contribution of iron deficiency is often difficult to determine by routine laboratory studies. We studied 51 patients with pauciarticular and polyarticular juvenile rheumatoid arthritis with red blood cell counts, indices, free erythrocyte protoporphyrin, and serum ferritin. Fifteen of the 18 who were anemic were restudied after a 3 to 6-month period of iron therapy. Thirteen of the 15 responded by these criteria: a rise in hemoglobin of 1.0 gm/dl or more and an increase in mean corpuscular volume of 3 fl or more; in 11 of these 13, hemoglobin values returned to the normal range for age. These findings indicate that iron deficiency can be a major component of the anemia that is commonly found in patients with active juvenile rheumatoid arthritis.
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PMID:Anemia in patients with juvenile rheumatoid arthritis. 66 Mar 58

An accurate determination of the total amount and distribution of body iron stores is essential for prognostic purposes and to evaluate the efficacy of chelation therapy. In the clinical setting, a rough estimate of the total body iron burden may be obtained in patients with transfusion-dependent anemias by calculating the amount of blood administered plus the amount absorbed by the gastrointestinal route, which is influenced by the level of Hb and by bone marrow activity. An increase in serum iron and a decrease in total iron binding capacity are early indicators of iron overload, but their sensitivity and specificity are not very high. In normal individuals, serum ferritin correlates well with iron stores, as measured by phlebotomy, and with directly measured liver iron. However, plasma ferritin, being an acute phase reactant, is increased in cases of chronic disease, disseminated malignancy, or inflammatory disorders. Non-transferrin bound iron, i.e. iron that circulates in plasma unbound to transferrin, is potentially toxic since it is capable of taking part in free radical-mediated reactions that result in irreversible tissue damage. This iron can be measured with a HPLC based assay. At present the most accurate way of estimating the iron burden is by direct measurement of iron concentration in tissues. The liver is the most accessible. The measurement is done by atomic absorption spectrometry on ashed or lyophilized samples obtained by needle biopsy, and correlates well with the total amount of blood transfused and with the extent of hepatic fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methods for evaluating iron stores and efficacy of chelation in transfusional hemosiderosis. 180 47

Dietary, anthropometric, and chronic disease risk factors (CDRF) in vitamin/mineral supplement users (U) and non-users (NU) were measured in a farm population consisting of 162 subjects (46% females and 54% males; 20-79 years of age, mean age: 52 years). Subjects were white, except for two black males. Supplements were used by 62 subjects (38%); 47% of females and 31% of males used supplements; 43% of subjects over 50 years of age and 32% of subjects age 50 or under used supplements. Both dietary intake and energy expenditure were measured using 4-day records. Indices of adiposity included body weight, BMI, and estimated body fat. Total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), serum ferritin, hemoglobin, hematocrit, zinc, copper, and vitamin C were based on 12-hr fasting blood samples. Dietary intake (excluding supplements) for vitamin/mineral U was greater than NU for vitamin C (p = 0.006), thiamin (p = 0.01), riboflavin (p = 0.03), niacin (p = 0.02), folic acid (p = 0.001), vitamin B6 (p = 0.01), and magnesium (p = 0.019). Vitamin C levels were significantly higher and the sum of four skinfolds was significantly lower among U than NU. In this population, 24% of males and 18% of females had TC levels over 240 mg%; 8% of both males and females had blood pressures (BP) greater than 140/90 mm Hg, while 49% of males and 46% of females had BP between 120/80 and 140/90; and 71% of males were more than 25% fat, and 56% of females were more than 35% fat. Despite the high prevalence of CDRF, there were no significant differences between supplement U and NU.
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PMID:Chronic disease risk factors in vitamin/mineral supplement users and nonusers in a farm population. 189 83

In the vast majority of cases, the cause of microcytic hypochromic anemia is clearly suggested by the patient history, physical examination results, red cell indexes, and peripheral blood smear. Thus, further diagnostic testing, if necessary, can be very selective. When the underlying cause of anemia is obscure, the serum ferritin concentration should be measured first. If it is normal or increased, serum iron and free erythrocyte protoporphyrin levels can be determined. The serum iron level is low in anemias caused by iron deficiency and chronic disease but normal or elevated in those resulting from the thalassemias, hemoglobin E disorders, and lead toxicity. The free erythrocyte protoporphyrin level is elevated with iron deficiency, the anemia of chronic disease, and lead toxicity but normal with thalassemias and hemoglobin E disorders. Results of these two test indicate which of the more specific tests is most likely to yield the correct diagnosis.
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PMID:Determining the cause of anemia. General approach, with emphasis on microcytic hypochromic anemias. 202 Jun 45

Out of 104 patients with microcytosis (MCV less than 80 fl), 69% had an iron deficiency, 21% a chronic disease and 10% hemoglobinopathy or thalassemia trait. The absence of bone marrow iron stores or the response to iron supplementation were used to establish the diagnosis iron deficiency. On the basis of sensitivity (90%) and specificity (100%), the serum ferritin concentration is more suitable for assessment of iron deficiency than the serum iron concentration, the total iron-binding capacity or the percentual saturation of transferrin. The red cell distribution width (RDW) is the parameter with the highest sensitivity for iron deficiency (94%). An RDW value within the reference interval can be used to exclude iron deficiency in those cases in which the serum ferritin concentration does not accurately reflect the iron stores owing to severe tissue damage, as in inflammation or malignancy.
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PMID:Evaluation of microcytosis using serum ferritin and red blood cell distribution width. 231 92

The prevalence of iron deficiency anemia has decreased in recent years because of improved dietary habits. Yet, iron deficiency anemia is still the most common anemia. Among mature adults, anemia of chronic disease is probably more common. Mean corpuscular volume and red cell distribution width, along with a peripheral smear examination, can often distinguish iron deficiency anemia from other common microcytic anemias, such as thalassemia minor. A normal serum iron level excludes iron deficiency anemia and indicates other causes for microcytic anemia. Often, a low serum iron level and total iron-binding capacity are due to chronic disease, and measurement of serum ferritin or a bone marrow stain for hemosiderin will be necessary to diagnose iron deficiency. Iron therapy to restore the red cell mass should be continued until iron stores are replenished.
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PMID:Iron deficiency anemia. How to diagnose and correct. 240 79

Moderate anemia was present in 25% and low serum iron levels in 75% of patients with severe nodulocystic acne. These findings, combined with an elevated serum ferritin level and normal transferrin saturation, indicate that the low serum iron levels and anemia are secondary to the chronic disease state of cutaneous inflammation rather than an iron-deficiency state. Successful therapy of the severe cystic acne with isotretinoin (13-cis-retinoic acid) resulted in return of serum iron and hemoglobin values to normal levels and a decrease in serum ferritin level.
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PMID:Low serum iron levels and moderate anemia in severe nodulocystic acne. Reversal with isotretinoin therapy. 315 59

Serum and red cell ferritin were determined in a heterogeneous group of 59 patients with chronic disease undergoing a bone marrow biopsy. There was very little correlation between serum and red cell ferritin (r = 0.53). Although serum ferritin increased in relation to increased bone marrow iron stores, only 1 out of 8 patients with absent marrow iron stores and none of 8 patients with reduced marrow iron stores had a decreased serum ferritin. In contrast, 6 of 8 patients with absent iron stores had a reduced red cell ferritin concentration. There was no significant difference between the mean red cell ferritin of the patients with reduced, normal and mild-moderately increased marrow iron stores (30, 26 and 34 ag/cell). Red cell ferritin was decreased in 78% of a group of 32 patients with a low mean cell volume. In the patients studied, red cell ferritin was a better indicator of absent iron stores than serum ferritin. However, red cell ferritin did not detect a reduction in the iron status until the marrow iron stores were completely depleted. Apparently, during normal erythropoiesis the primitive erythroblasts continue to take up iron irrespective of the amount of iron available in the stores.
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PMID:Red cell ferritin and iron stores in patients with chronic disease. 334 27

Of patients referred to a geriatric service, 66 were identified who were clearly anemic (hemoglobin less than 12 g in men, less than 11 g in women) but whose cause of anemia was not readily identifiable by noninvasive measures. The difficulty in distinguishing iron deficiency from chronic disease as a cause of anemia by noninvasive means (serum iron, total iron binding capacity, transferrin saturation ratio, and serum ferritin), is highlighted by the poor power of these investigations when compared with bone marrow iron stores. A transferrin saturation ratio of less than 11% and a serum ferritin of less than 45 pg/L serve better than currently accepted values to identify iron deficiency in this population.
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PMID:Assessment of iron stores in anemic geriatric patients. 405 71


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