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)

The ferritin level in serum was investigated in 9 patients with myocardial infarction, all with a history of chest pain of less than 4 hours before admission. A significant rise in serum ferritin level was found in 8 patients. The rise was generally smaller than that seen in acute infection and not significantly correlated to the size of infarction, as estimated from changes in serum levels of myoglobin, ASAT and LDH. The rise started after a mean of 30 hours, the peak being reached within a week (M 4.3 days). Serum ferritin then fell to 120--300% (M 190) of the initial level, where it remained. An initial rise in serum iron levels was unexpectedly seen within 12 hours in 7 patients.
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PMID:Serum ferritin during inflammation. A study on myocardial infarction. 52 35

Serum ferritin was measured in two groups of alcoholics; one comprised 71 individuals on ambulatory control and with varying current alcohol intake and the other 19 alcoholics followed with serial determinations during two weeks of abstinence Serum ferritin was elevated in 26 subjects in the larger group, and 22 of them had elevated ASAT and ALAT values. Low-grade but significant correlations were found between serum levels of ferritin and serum concentrations of some variables used to detect liver affection (ASAT, ALAT, bilirubin and gamma-GT). Serum ferritin and ASAT declined in a parallel fashion in the 19 patients studied longitudinally, so that the ferritin:ASAT ratio described a straight line. No correlation was found between serum ferritin or the serum ferritin:ASAT ratio and serum iron. Neither was any correlation observed between the magnitude of the changes in serum ferritin and the changes in serum iron, serum transferrin or circulating platelets or reticulocytes observed in the serially followed alcoholics. These data indicate that elevated serum ferritin in alcoholics is associated with the degree of liver affection and not with the degree of erythropoietic activity.
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PMID:Serum ferritin in alcoholics and the relation to liver damage, iron state and erythropoietic activity. 723 11

Histochemical and chemical liver iron and iron status markers (serum (S-) ferritin, transferrin saturation) were determined in 109 patients with various types of liver disease (71 alcoholic, 38 non-alcoholic disease) and 8 normal subjects. In the series as a whole there was a significant correlation between histochemical hepatocyte iron and chemical iron (rho = 0.48, p = 0.0001). Of the iron status markers, only S-ferritin showed clinically significant correlations with histochemical liver iron (rho = 0.54, p = 0.0001) and chemical liver iron (r = 0.45, p = 0.0001) (log vs. log values). The highest correlation was found between S-ferritin and the product of chemical iron x ASAT (r = 0.61, p = 0.0001) (log vs. log values). None of the normal livers had stainable hepatocyte iron; median chemical iron content was 15 mumol/g dry weight (range 8-25). The entire group of alcoholics had a median liver iron content of 21 mumol/g; all patients had a hepatic iron index (hepatic iron/age) of under 1.4. In alcoholic liver disease, median chemical liver iron content was 15 mumol/g (range 3-36) in 35 subjects with grade 0 hepatocyte iron; 24 mumol/g (range 6-90) in 25 subjects with grade 1 + 2 hepatocyte iron; 30 mumol/g (range 14-74) in 11 subjects with grade 3 + 4 hepatocyte iron. Among subjects with alcoholic liver disease and normal liver iron (< 26 mumol/g), 39% had stainable hepatocyte iron vs. 70% in subjects with increased liver iron (> or = 26 mumol/g). The corresponding figures in subjects with non-alcoholic liver disease were 13% and 20%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationships among serum iron status markers, chemical and histochemical liver iron content in 117 patients with alcoholic and non-alcoholic hepatic disease. 817 8

Iron appears to exert self-regulatory control over erythroblast iron uptake, iron storage and its incorporation into haem. It does this via iron regulatory proteins (IRPs) which bind reversibly to the iron responsive elements (IREs) on the mRNA of transferrin receptor (TfR), erythroid 5-aminolaevulinic acid synthase (ALA-S2) and ferritin. Iron deficiency leads to the binding of IRP to IRE. This binding inhibits the translation of mRNA for ALA-S2 and ferritin but stabilizes mRNA for TfR expression. Sideroblastic erythropoiesis is highly ineffective and characterized by mitochondrial iron loading. The study of X-linked sideroblastic anaemia has shown that the entry of iron into the mitochondria is poorly controlled and able to occur when protoporphyrin production is reduced, as is seen with the ALA-S2 mutations, or when it is increased as has been seen with ABC7 transporter mutations. Sideropenia characterises both iron deficiency anaemia (IDA) and the anaemia of chronic disease (ACD). Erythroblasts in ACD seem doubly equipped to protect their iron supply with their ability to increase the efficiency of transferrin-iron uptake as well as to activate the IRP/IRE system to increase surface TfR production. This increase in efficiency restricts the need to increase surface TfR production and maintains serum soluble TfR (sTfR) values within the normal range in iron replete ACD. The coexistence of iron deficiency with chronic disease, however, is associated with an increase in both the efficiency and number and a highly significant rise in sTfR values.
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PMID:Erythroblast iron metabolism in sideroblastic and sideropenic states. 1224 84