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

Serum ferritin, aspartate aminotransferase (AST), alkaline phosphatase and hydroxybutyrate dehydrogenase (HBD) were studied during 21 vaso-occlusive crises in 12 adults with sickle cell disease (11 SS, 1 S beta degrees). The patients comprised three groups: those who had been untransfused (4), those who had received occasional exchange transfusion in crisis (3), and those who had been multiply transfused (5). Serum ferritin concentrations in crisis were compared with those of the steady state value. Rises in serum ferritin concentrations occurred in all crises in all groups. Although AST, alkaline phosphatase, and HBD rose, there was no correlation between these and log ferritin concentrations. The clinical impression was that the degree of rise in ferritin related to the severity of the particular crisis, and the above results showed that haemolysis and liver damage were not causally related to this rise. An estimate of serum ferritin cannot be used to assess the state of iron balance in sickle cell disease unless the patient is in the steady state. The considerable rise in serum ferritin concentration found in crisis, however, may be a useful marker of the extent of vaso-occlusion and tissue damage.
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PMID:Serum ferritin concentration in sickle cell crisis. 395 15

The effects of minimal acute liver injury on circulating ferritin levels have been examined in the rat both in vivo and in the isolated perfused liver. Liver damage produced by 6 mmol/kg of D-galactosamine (GalN) in vivo resulted in a marked rise in plasma ferritin levels 4 h after administration, 2 h before any significant increase in plasma aspartate transaminase. In the isolated perfused liver, damage produced by 5mM GalN introduced into the perfusate also produced an early increase in circulating ferritin before any evidence of release of intracellular enzymes, or alteration in liver histology as assessed by light microscopy was apparent. It is concluded that minimal acute liver damage results in a pronounced increase in circulating ferritin levels before other evidence of liver dysfunction. This is unlikely to be due solely to increased release from damaged cells but may rather result from an alteration in the mechanism responsible for ferritin homeostasis.
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PMID:The effect of acute liver damage on circulating ferritin levels in vivo and in the isolated perfused rat liver. 398 31

We examined the efficacy of long-term subcutaneous deferoxamine therapy in the prevention of iron-related cardiac disease in patients with thalassemia major who began treatment after the age of 10 years. Of 36 such patients without preexisting cardiac disease, 19 did not comply with the program of chelation therapy. Over the course of treatment (1977 to 1983) serum ferritin and aspartate aminotransferase levels fell in the compliant group, from mean values (+/- S.D.) of 4765 +/- 2610 to 2950 +/- 1850 ng per milliliter and 58.1 +/- 22 IU to 30 +/- 20 IU per liter, respectively (P less than 0.05), but rose in the noncompliant group, from 5000 +/- 2316 to 6040 +/- 2550 ng per milliliter and 56.6 +/- 20 to 90 +/- 35 IU per liter, respectively. Only one patient in the compliant group acquired cardiac disease and died of fulminant congestive heart failure. In contrast, 12 noncompliant patients acquired cardiac disease, and 7 died. In addition, the mean age of the compliant population (18.9 +/- 4.5 years) now approaches the mean age of acquisition of cardiac disease in the noncompliant group (19 +/- 4.3). These data demonstrate that compliance with treatment with deferoxamine may protect patients from cardiac disease induced by iron overload.
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PMID:Prevention of cardiac disease by subcutaneous deferoxamine in patients with thalassemia major. 400 Jan 98

Serum ferritin and hepatic enzyme concentrations were measured in 30 alcoholic subjects. Both the serum ferritin and gamma-glutamyltranspeptidase (GGT) values were raised in 23 subjects and a significant correlation was noted between the two measurements (r = 0,51; P less than 0,01). There was, however, no correlation between the initial serum ferritin concentration and the serum alanine transaminase and serum aspartate transaminase concentrations. The serum ferritin and GGT levels were followed serially during a period of abstinence in 9 subjects; values fell in parallel in all of them. The data indicate that a serum ferritin level above 300 micrograms/l is very unlikely to be the result of alcohol-induced liver damage if the serum GGT value is less than 50 U/l. The combined measurement of serum ferritin and GGT values should therefore prove useful in epidemiological studies concerned with defining the prevalence in different population groups of the HLA-linked iron-loading gene that leads to the clinical disorder of idiopathic haemochromatosis.
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PMID:Effects of heavy alcohol consumption on serum ferritin concentrations. 614 24

The deliberate ingestion of carbon tetrachloride by a 48-year-old woman provided an opportunity to study the sequential biochemical changes of a severe but self-limited event of hepatocellular damage. The initial phase of cellular injury characterised by high levels of serum aspartate aminotransferase, ferritin and bile acids was followed by a period of partial cholestasis. This was indicated by a marked decrease in secondary bile acids and small rises in alkaline phosphatase and 5' nucleotidase. Improving liver function and regeneration became evident during this period and was associated with abnormal levels of gamma glutamyl transpeptidase. A late rise in serum ferritin and alphafetoprotein may represent a non-specific inflammatory reaction.
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PMID:Serum bile acids and other liver function tests in hepatocellular damage from carbon tetrachloride ingestion. 615 37

Serum ferritin and biochemical liver tests (serum bilirubin, serum aspartate transaminase, serum gamma-glutamyl transpeptidase (gamma-GT), and serum alkaline phosphatase) were recorded at regular intervals from admission to recovery in six patients with acute viral hepatitis. There was a proportional, significant decrease in ferritin bilirubin, and transaminase were reached simultaneously, whereas gamma-GT and alkaline phosphatase remained elevated for a slightly longer time. The correlations between corresponding measurements of ferritin and biochemical liver tests were as follows: ferritin and alkaline phosphatase, r = 0.72, P less than 0.001; ferritin and bilirubin, r = 0.68, P less than 0.001; ferritin and transaminase, r = 0.53, P less than 0.001; ferritin and gamma-GT. r = 0.50, P less than 0.001. In viral hepatitis serum ferritin offers no diagnostic advantage compared with already established tests for hepatocellular damage.
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PMID:Serum ferritin in acute viral hepatitis. 671 75

In this study maximum urinary iron elimination with continuous desferrioxamine subcutaneous infusion was obtained in thalassemia major patients with chronic persistent or active hepatitis with lower doses (60 mg/kg) than those necessary in patients without hepatitis (80 mg/kg). Since dose-response curves were highly variable the treatment schedule should be tailored to the individual needs of each patient. Both groups may achieve iron balance but chronic hepatitis patients have more frequently a net urinary iron excretion. In patients with chronic hepatitis no correlation was found between serum ferritin levels or serum ferritin/aspartate aminotransferase ratios and transfusional iron overload while serum ferritin/aspartate aminotransferase ratios were seen to be correlated with liver iron stores.
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PMID:Iron chelation in transfusion-dependent thalassemia with chronic hepatitis. 680 Feb 2

Thirty-four of 99 multiply transfused Chinese (49 females, 50 males) with thalassaemia major were positive for antibody to hepatitis C virus. There was no sex predominance in seropositivity with 18 females and 16 males positive. The mean (+/- SD) age and units of blood transfused were significantly higher in the seropositive patients (167 +/- 48 months, 206 +/- 82 units respectively) than the seronegative patients (113 +/- 56 months, 124 +/- 80 units respectively). The seropositive patients had higher mean (+/- SD) serum alanine aminotransferase, aspartate aminotransferase and ferritin concentrations (91 +/- 82 IU/L, 67 +/- 38 IU/L, 4797 +/- 2522 ng/ml respectively) than the seronegative patients (38 +/- 29 IU/L, 48 +/- 28 IU/L, 3620 +/- 2140 ng/ml respectively). Serum ferritin had an independent and significant effect on serum alanine aminotransferase in addition to that of seropositivity to hepatitis C virus.
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PMID:Hepatitis C virus antibody in multiply transfused Chinese with thalassaemia major. 769 Jun 34

Between 1990-1992, 18 patients with beta-thalassemia/Hb E age between 2-13 years (mean 7.4 +/- 3 years) were examined. Three patients were splenectomized and the rest were nonsplenectomized. They were divided into 3 groups. Group A:5 nonsplenectomized and 3 splenectomized patients had high transfusion rates with subcutaneous desferrioxamine injections. Five patients in group B received only high transfusion whereas in 5 patients in group C the levels pretransfusion Hb were maintained between 6-7 g/dl. The mean blood consumption in the nonsplenectomized groups were 220 +/- 25.3, 221 +/- 59 and 175.4 +/- 45.4 ml/kg/year in groups A, B and C, respectively. In group A, the mean blood requirement was 40% higher in the nonsplenectomized group. In the high transfusion regimen the spleen size did not increase and serum aspartate aminotransferase showed a striking fall in the majority of cases. The absolute increases in serum ferritin were 843.2 +/- 395, 861 +/- 252 and 1,262 +/- 440 ng/ml in groups A, B and C, respectively. These data demonstrated that high transfusion with desferrioxamine injection could improve the clinical well being of the patients.
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PMID:High transfusion in children with beta-thalassemia/Hb E: clinical and laboratory assessment of 18 cases. 788 17

Tissue iron loading in hypotransferrinaemic (hpx/hpx) mice was investigated as a model for genetic (primary) haemochromatosis. Iron loading of liver preceded that in the pancreas and heart. One-year-old hpx/hpx mice showed iron staining in exocrine pancreas, liver parenchymal cells, and cardiac and intestinal smooth muscle cells. Iron-loaded macrophages were observed in all these tissues. Islets of Langerhans, biliary epithelial cells, and spleen were iron-free. The pancreas was fibrotic with massive macrophage infiltration and loss of secretory epithelium. Liver showed evidence of chronic inflammatory infiltration with increased collagen fibres in the parenchymal region but no cirrhosis. Serum aspartate aminotransferase activity and plasma glucose were increased in hpx/hpx compared with wild-type mice. Heavy iron loading with haemosiderin deposition in the liver could be demonstrated in hpx/hpx mice from 6 weeks of age. Heterozygous hypotransferrinaemic mice showed minor increases in liver iron stores at 6-12 weeks, but not at 1 year of age. Serum ferritin levels in heterozygous mice were also increased at 6-8 weeks of age. It was concluded that 1-year-old hpx/hpx mice showed evidence of liver and pancreatic damage secondary to tissue iron overload. The iron loading pattern and tissue damage showed some features which were distinct from those observed in haemochromatosis.
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PMID:Tissue iron loading and histopathological changes in hypotransferrinaemic mice. 827 72


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