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)

In the bone-marrow, non-haemoglobin iron can predominantly be found in the reticulum. Slight granules containing iron can also be observed in parts of erythroblasts by means of the Berlin blue reaction. These cells are called sideroblasts. In chemical respect, non-haemoglobin iron consists of ferritin soluble in water and haemosiderin insoluble in water. Erythroblasts will only take their iron from plasma transferrin. For the most part, this iron uptake is being regulated by erythropoietin adapting erythropoiesis to the oxygen requirements of the tissue. The iron contained in erythroblasts is predominantly utilized for haemoglobin synthesis in these cells. A slight part is being taken up by ferritin. The bone-marrow reticulum will phagocytise aged erythrocytes and store liberated iron as ferritin and haemosiderin. Part of the iron is being delivered again to plasma transferrin. With constant serum iron level the liberation of iron from the reticulo-endothelial tissue must correspond to the iron uptake by erythropoiesis. The absence of iron capable of being coloured in the bone-marrow reticulum is considered to be a reliable parameter of iron deficiency. It enables the diagnosis of iron deficiency anaemia to be made even in those patients with serum iron level and a total iron binding capacity lying within the normal range and no hypochromia of erythrocytes being present. It enables iron deficiency anaemia to be separated from sideropenic anaemia with reticulo-endothelial siderosis in differential-diagnostic manner. Even in patients with sideroblastic anaemia, iron colouring of bone-marrow smears is required for ensuring the diagnosis. Recently, a separation has also been made for idiopathic anaemia with abnormal sideroblasts. In these patients there is an increased risk for acute leukemia to develop.
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PMID:[Iron in bone marrow]. 618 56

Thyroid function was investigated by a TRH test in 24 clinically prepubertal children, 3-15 years old with beta-thalassaemia major; in 7 of them the test was repeated once and in 2 twice at intervals of at least 12 months. Basal T4, T3, TBG and TSH levels and the TSH levels during a TRH test were determined and correlated with age and serum ferritin levels. Basal serum T4, T3 and TBG levels were lower and serum TSH levels were higher during the test and in the basal state in thalassaemia major children than in control children. These results show a compensated sub-clinical primary hypothyroidism. The transversal study did not show any significant correlation between the hormonal parameters studied and chronological age or serum ferritin levels. In contrast, the longitudinal study showed a significant correlation between pituitary-thyroidal axis function and siderosis (positive correlations between the variations of TSH levels as delta, peak, 30 and 45 min values and the variations of serum ferritin levels). The thyroid impairment seems not to be correlated with serum ferritin levels in the transversal study because of the presence of an individual different sensitivity of the gland to the iron overload. The ferritin dependence of this impairment is shown only by longitudinal studies where individual differences in sensitivity of the gland are absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrine involvement in children with beta-thalassaemia major. Transverse and longitudinal studies. I. Pituitary-thyroidal axis function and its correlation with serum ferritin levels. 643 70

Some parameters of iron metabolism in 26 patients with porphyria cutanea tarda (PCT) which is often associated with mild iron overload and hepatic siderosis, are studied. Serum iron, percent transferrin saturation and ferritin were pathologically increased. Statistical comparisons were performed between PCT patients and healthy controls, liver disease patients (cirrhosis, chronic active hepatitis) and patients with associated liver siderosis (alcoholic cirrhosis, cirrhosis and chronic active hepatitis in thalassemia). Ferritin levels are higher in patients with porphyria than in healthy controls (p less than 0,001) and in patients without liver siderosis (p less than 0,001). No statistical difference is observed between patients with porphyria and patients with siderosis. A significant decrease in ferritin levels is registered after venesection therapy. The conclusion is drawn that serum ferritin increase in PCT is related to hepatic iron store amounts rather than hepatic necrosis. It is assumed that ferritin follow-up during phlebotomy therapy and also during remission is useful to indicate the exhaustion or an early replenishment of hepatic iron stores.
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PMID:[Determination of serum ferritin in porphyria cutanea tarda. A reliable sign of hepatic siderosis]. 670 23

Elevated serum alanine aminotransferase (ALT) for more than one year was found in 36 (28.8%) of 125 patients on maintenance haemodialysis. In 10 the ALT returned to normal spontaneously but in 26 it remained high. Liver tissue from 21 patients with high ALT and seven with normal ALT was examined. Statistically significant correlations were found between the mean ALT during the year prior to the biopsy and assessments of the lymphocytic infiltration (p less than 0.001), fibrosis (p less than 0.001) and amount of silicone particles in the liver (p less than 0.001). Epithelioid cell granulomata, lobular and portal macrophages and perivenular fibrosis were related to silicone particles. Lymphocytes were not spacially related to the particles; nevertheless, there was a significant correlation between amounts of silicone and lymphocytic infiltration (p less than 0.01). No associations were found between high ALT, hepatitis B serology, serum ferritin, parenchymal siderosis, propensity to fluid overload, alcohol abuse and HLA-B8.
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PMID:Chronic liver disease in haemodialysis patients. 687 29

Hepatocellular altered foci were induced in rat liver by cycles of feeding of N-2-fluorenylacetamide and were distinguished by their resistance to iron accumulation following production of hepatic siderosis by dietary administration of 8-hydroxyquinoline and ferrous gluconate. The foci were readily identified by their iron exclusion in plastic-embedded sections stained for iron. Sections from iron-free regions processed for electron microscopy permitted ultrastructural study of cells in foci identified by reduced cytoplasmic ferritin. Altered foci of the eosinophilic type produced by cyclic feeding of carcinogen for 16 weeks were composed of both normal-appearing hepatocytes and others with ultrastructural abnormalities, including increased agranular reticulum with associated glycogen particles, decreased rough endoplasmic reticulum with reduced length of cisternae, degranulated rough vesicles, altered and displaced Golgi complexes, and abnormal bile canaliculi. At 12 and 24 weeks after cessation of carcinogen exposure, cells in persistent eosinophilic foci continued to display ultrastructural abnormalities. They possessed increased rough endoplasmic reticulum with rather regular cisternal arrangement and relatively increased smooth endoplasmic reticulum. Golgi complexes were abnormal. Bile canaliculi were abnormal and occasionally increased in number. Nuclei displayed prominent nucleoli. Cells in a basophilic focus were characterized by the presence of numerous free polyribosomes diffusely scattered throughout the cytoplasm, distended rough endoplasmic reticulum with loss of parallel-stack and hypertrophic dilated Golgi complexes, and prominent marginated nucleoli. The finding that persistent foci continued to display ultrastructural abnormalities, some of which changed or progressed in the absence of further carcinogen exposure, suggests that the persistent iron-excluding foci are a permanently altered population.
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PMID:Ultrastructural abnormalities in carcinogen-induced hepatocellular altered foci identified by resistance to iron accumulation. 707 12

Personal experience confirms the diagnostic value of serum ferritin estimation in the iron deficient microcytic anemia, where there are low levels. The clinical significance of the test is restricted by the not negligible incidence of levels like that of iron overload in the hepatic and neoplastic diseases. In hepatic diseases the test resulted to be related to the changes of serum transaminases. In malignant neoplasms the high serum ferritin levels had been only sometimes associated with transfusional siderosis.
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PMID:[Clinical aspects of the radioimmunological determination of serum ferritin]. 710 8

Liver iron concentrations were determined in 60 alcoholics with liver disease of varying severity, 15 patients with untreated idiopathic hemochromatosis, and 16 control subjects with biliary tract disease. Mean liver iron concentrations (microgram/100 mg dry weight) were significantly greater in the alcoholics (156.4 +/- 7.8 (SEM); P less than 0.05) and in patients with idiopathic hemochromatosis (2094.5 +/- 230.7; P less than 0.01) than in control subjects (53.0 +/- 7.0). Liver iron concentrations of greater than 140 micrograms/100 were found in 17 alcoholics (29%) and in all 15 patients with idiopathic hemochromatosis. Liver iron concentrations greater than 1000 micrograms/100 mg were found in all patients with idiopathic hemochromatosis but in none of the alcoholics. In the alcoholics no relationship existed between liver iron concentrations and the amount of alcohol consumed daily, the length of the drinking history, the amount of beverage iron consumed daily, or the severity of the liver disease. Serum ferritin concentrations reflected iron stores in patients with hemochromatosis and in alcoholics with minimal liver disease. However, in alcoholics with significant liver disease serum ferritin concentrations did not reflect iron stores accurately, although with normal values iron overload is unlikely. Serum iron concentration and percentage saturation of total iron-binding capacity were of little value in assessing iron status in either alcoholics or patients with hemochromatosis. Measurement of the liver iron concentration clearly differentiates between alcoholics with significant siderosis and patients with idiopathic hemochromatosis.
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PMID:Hepatic iron stores and markers of iron overload in alcoholics and patients with idiopathic hemochromatosis. 711 74

In the acute phase of acute viral hepatitis high serum iron and serum ferritin levels were found in all patients. The normalisation of the serum ferritin concentration parallelled that of the serum glutamic pyruvic transaminase activity. However serum iron levels remained elevated for a long period of time. Chemical analysis of liver tissue showed a low total liver depot iron concentration during the first two weeks of the disease, indicating that the high serum iron levels are caused by iron liberation from disintegrated hepatocytes. Patients studied after two weeks showed higher liver iron concentrations, in particular the non-ferritin iron fraction, reflecting iron accumulation in the reticulo-endothelial system. Indeed, histological examination in the patients studied after two weeks showed sinusoidal lining cell siderosis in addition to "diffuse iron" in clusters lining cells which in electron microscopical studies proved to be macrophages. These cells showed a positive immunohistological reaction for ferritin protein. It is suggested that during acute viral hepatitis two mechanisms act together, i.e. changes in iron metabolism caused by damage of the main iron depot organ (specific liver pathology) and changes in iron metabolism common to all infectious processes.
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PMID:Some aspects of iron metabolism during acute viral hepatitis. 712 35

Iron in the tissues of the digestive tract of the common vampire bat (Desmodus rotundus) has been studied using histochemical, electron microscopic, and autoradiographic methods. This animal is an obligate sanguivore and has a daily intake of dietary iron 800 times that of man. The amount and distribution of tissue iron is not affected by either a single blood meal or starvation but does reflect the degree of siderosis of each animal's liver and spleen. By 7 days after the injection of a trace amount of 55Fe into the peritoneal cavity, labelled siderotic macrophages are present both on the serosa and within the walls of the stomach and intestine. In the lower intestine, such cells can be derived from the germinal centers of Peyer's patches. Siderotic macrophages are often situated in the lamina propria under areas of siderotic epithelium. Label is also present in the apical cytoplasm of mucosal epithelial cells, a region of abundant siderosomes. The ultrastructure of these organelles is extremely variable. Accumulations of membranous whorls and stacks, "stippled bodies," ferritin molecules, and larger "ferruginous" complexes are bounded by one or a number of membranes. Iron is excreted when these epithelial cells are desquamated into the gut lumen. Similar Prussian blue-positive granules are present in the feces. Unlike other glandular cells, the parietal cells of the fundic caecum are siderotic. Their cytoplasm contains abundant siderosomes and ferritin with accumulations of amembranous ferritin bodies in the intracellular canalicular spaces. Prussian blue-positive granules are present in the lumens of fundic glands.
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PMID:Distribution of iron in the gastrointestinal tract of the common vampire bat: evidence for macrophage-linked iron clearance. 721 3

A non-specific iron fraction, not bound to transferrin, has been looked for in the sera of 42 never-transfused patients with beta-thalassaemia trait, 17 of whom had chronic active hepatitis, negative for HBV infection or alcohol abuse. Non-specific iron was found only in the sera of those patients with beta-thalassaemia trait plus chronic active hepatitis who had complete transferrin saturation, high serum ferritin levels and urinary iron excretion and a high degree of hepatic siderosis. In view of the known toxicity of non-transferrin iron, we suggest that this non-transferrin iron fraction may be responsible for the liver damage in these patients. Furthermore, the positive correlation between the presence and the amount of non-transferrin iron and the levels of serum ferritin suggests that this fraction is a sensitive indicator of iron-induced toxicity when severe iron overload slowly develops in patients with beta-thalassaemia trait even in the absence of any iron administration.
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PMID:Non-specific iron in patients with beta-thalassaemia trait and chronic active hepatitis. 725 13


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