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)

Thirty-seven children with beta-thalassaemia major, eight children with liver cirrhosis, and 20 matched controls were enrolled in this study. Serum ferritin was determined in each subject by radio-immunoassay and liver enzymes by standard methods. The liver, spleen, kidney and pancreas densities were obtained by computed tomography using a Siemens Somatom 2 Scanner with 8-mm slice thickness. The iron content of liver biopsies from 10 patients was graded by staining. The mean serum ferritin of the thalassaemic patients was significantly higher than that of the control group (p = 0.0001). The ferritin of patients with cirrhosis and Wilson's disease was similar to that of the control group. The liver density of the thalassaemic patients was significantly higher than that of the control group (p less than 0.0001) while that of patients with liver cirrhosis and Wilson's disease was similar to the control group. The liver iron content of patients with liver cirrhosis was within the normal range. The spleen and kidney densities of patients with thalassaemia were higher than that of the control group with p values of 0.02 and 0.056, respectively. The density of the pancreas in patients with thalassaemia was not significantly different from that of the control group, (p = 0.52). There was correlation between the liver density and serum ferritin in patients with thalassaemia (r = 0.432, p less than 0.01) while there was no correlation between spleen, pancreas and kidney densities with serum ferritin.
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PMID:Comparison between serum ferritin and computed tomographic densities of liver, spleen, kidney and pancreas in beta-thalassaemia major. 368 72

Twenty-five patients with overt clinical and biochemical findings of porphyria cutanea tarda took part in a study comparing intensive phlebotomy with slow subcutaneous desferrioxamine treatment. Fifteen male patients (Group A) had intensive venesection therapy. Ten patients (Group B) with associated diseases (minor thalassemia, cardiovascular impairment, pulmonary tuberculosis or severe liver cirrhosis) received 1.5 g of desferrioxamine by slow subcutaneous infusion using an automatic syringe pump 5 days a week. No patient complained of appreciable side effects. Serum iron, ferritin and uroporphyrins were normalized in all subjects by the end of treatment. The mean time necessary for complete recovery was 13.8 months (range 9-19) and 11.2 months (range 6-14) in Groups A and B, respectively. Liver function significantly improved during and after the treatments in both groups. We conclude that recovery from porphyria cutanea tarda can be achieved equally well using phlebotomy or desferrioxamine subcutaneous infusion. Phlebotomy is easily performed and remains the treatment of choice; slow subcutaneous desferrioxamine treatment, although expensive, is recommended when severe associated diseases contra-indicate venesection.
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PMID:Iron removal therapy in porphyria cutanea tarda: phlebotomy versus slow subcutaneous desferrioxamine infusion. 371 53

Malotilate, a sulphur-containing compound with antifibrotic and hepatoprotective properties in several animal models, has been investigated in cirrhotic patients. Nine patients with cirrhosis of various aetiologies and severity, and 4 healthy volunteers, participated in a pharmacokinetic study. After a single dose of 500 mg malotilate p.o. peak malotilate plasma concentration measured by GC-MS was 35 times higher in patients (median 0.70 micrograms/ml) than in controls (median 0.019 micrograms/ml). The median apparent oral clearance was approximately 50 times lower in cirrhotics (median 2.21/min) than in healthy volunteers (1181/min). The apparent oral clearance was significantly correlated with indicators of portal-systemic shunting, such as the 2-h postprandial serum bile acids and the bioavailability of oral nitroglycerine. Urinary output of the glucuronidated metabolite-(M3), measured by HPLC, was normal in patients, whereas recovery of metabolite-M6 (resulting from ring opening and loss of sulphur) was reduced. Six patients in an open 6-month trial received malotilate 200 mg t.i.d. for 2 months and 400 mg t.i.d. for 4 months. The thrombocyte count increased and serum ferritin level fell in all patients, and serum cholinesterase rose and IgA decreased in 5 of 6. The other indicators of liver function did not show a significant change. Dry skin was the only possible adverse effect. It is concluded that first-pass elimination of malotilate is dramatically reduced in cirrhotics, and that a smaller amount of the drug reaches the liver in such patients. Malotilate was well tolerated, even in patients with advanced disease.
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PMID:Treatment of liver disease with malotilate. A pharmacokinetic and pharmacodynamic phase II study in cirrhosis. 374 16

Under normal conditions, vitamin D absorbed from the diet or synthesized in the skin is transported to the liver where it undergoes hydroxylation. The purpose of this study was to determine whether excess hepatic iron affects this process and the subsequent production of 1,25-dihydroxyvitamin D (1,25-[OH]2D) in the kidney. Mean serum 25-hydroxyvitamin D (25-OHD) concentrations in untreated hereditary hemochromatosis were 13 +/- 6 (SD) in 9 patients with cirrhosis, 13 +/- 6 in 5 patients with hepatic fibrosis, and 22 +/- 6 in 10 patients with normal hepatic architecture aside from siderosis and were significantly lower than the levels found in 24 controls matched for age, sex, and season, p less than 0.05. The mean serum 25-OHD levels in the two groups with hemochromatosis and hepatic damage were significantly lower than the value in the group with normal hepatic architecture, p less than 0.05. Serum 25-OHD levels in individual patients were inversely related to the size of body iron stores as measured by exchangeable body iron, r = -0.64, or serum ferritin, r = -0.47, p less than 0.05. In 15 patients removal of excess body iron by venesection therapy produced a significant increase in the mean serum 25-OHD from 20 ng/ml to 30 ng/ml, p less than 0.05. In contrast, mean serum 1,25-[OH]2D levels were similar in iron-loaded and control subjects, indicating that the regulation of this metabolite was intact in patients with hemochromatosis. The results reveal that the low serum 25-OHD concentration in patients with hemochromatosis is directly related to the extent of iron loading and it is improved by venesection therapy.
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PMID:Low serum 25-hydroxyvitamin D in hereditary hemochromatosis: relation to iron status. 383 88

We analyzed the clinical data and liver histology for iron overload in 74 renal allograft recipients. Twenty of the 74 patients had histological evidence of hemosiderosis. Four patients had hemochromatosis. Of the 2 noninvasive diagnostic tests the serum ferritin level was more reliable than percent saturation of transferrin in predicting the histological diagnosis of hemosiderosis. Of the 20 patients with hemosiderosis 14 died either from liver failure or concomitant sepsis. Female patients and those who received long-term dialysis had higher susceptibility for developing hemosiderosis. Of the 6 patients treated with phlebotomies, the response was good in 4 and incomplete in 2. Hemosiderosis and hemochromatosis should be considered in the differential diagnosis of posttransplant liver disease. Intermittent phlebotomies if carried out early may prevent the progression of hemosiderosis to micronodular cirrhosis.
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PMID:Hemosiderosis and hemochromatosis in renal transplant recipients. Clinical and pathological features, diagnostic correlations, predisposing factors, and treatment. 390 17

Serum ferritin, an index of iron stores, was studied in 60 patients with porphyria cutanea tarda (PCT), in 21 patients who had other liver diseases without siderosis (cirrhosis [LC] and chronic active hepatitis [CAH]), and in 32 patients with associated liver siderosis (alcoholic LC, LC and CAH in minor thalassemia). Ferritin levels were higher in patients with porphyria than in healthy controls and patients without liver siderosis (P less than 0.001), whereas no statistical difference was observed between patients with porphyria and those with liver siderosis. Because iron removal is considered the treatment of choice for PCT, some patients with PCT underwent phlebotomy and others received chelating therapy with subcutaneous infusion of deferoxamine. Follow-up of the patients showed a correlation between serum ferritin level and urinary porphyrin excretion; when the clinical and biochemical syndrome became normal, serum iron and ferritin had fallen to normal values (t test pair data analysis before and after: P less than 0.001 in each group). No appreciable difference was found between controls and patients with PCT whose conditions had been normalized, irrespective of the chronic liver damage always present in PCT. Our results suggest that serum ferritin increase in PCT is related more to liver iron overload than to liver damage, and ferritin follow-up is recommended to indicate the exhaustion of hepatic iron stores during iron depletion therapy, as well as to detect an early replenishment after remission.
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PMID:Serum ferritin in the assessment of liver iron overload and iron removal therapy in porphyria cutanea tarda. 394 Dec 93

The accidental finding of raised levels of serum aminotransferase levels may lead to extensive investigations of the liver in apparently healthy people. To identify diagnostic groups and their need for investigations, we have evaluated the results of all investigative procedures carried out in 149 asymptomatic patients with persistently raised serum levels of aminotransferases. Fatty liver was found in 64%. These patients often had a high body weight. A high alcohol intake and diabetes mellitus were also noted. Chronic active or persistent hepatitis was found in 20% of the patients. Six per cent had cirrhosis, 4% had alpha 1-antitrypsin deficiency, and 3.5% had hemochromatosis. Apart from ferritin, alpha 1-antitrypsin, and markers for hepatitis B, blood tests were of little value for distinguishing among different diagnostic groups. This was the case also for the imaging procedures, and neither liver scintigraphy nor ultrasonography was a reliable source of diagnostic information. The results of our study indicate that diagnosis in this group of patients cannot be made without liver biopsy.
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PMID:Liver investigation in 149 asymptomatic patients with moderately elevated activities of serum aminotransferases. 395 45

In our study alcoholic patients with and without cirrhosis have a decreased serum zinc. They also have increased serum copper and iron with an increase in the serum ferritin. There is no evidence of selenium deficiency in either alcoholic group. Alcohol when given with zinc in a single dose to normal volunteers increases the serum zinc and therefore appears to increase the absorption of zinc.
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PMID:Trace elements and alcohol. 401 73

A liver antigen, LA-1, was detected by immunoelectrophoresis in the sera of 79 percent of patients with viral hepatitis A, 77 percent of patients with viral hepatitis B, and 62 percent of patients with alcoholic hepatitis. The occurrence of LA-1 was lower in liver cirrhosis (28 percent) and primary extra-hepatic disorders (18 percent) and absent in the sera of healthy subjects. Liver antigen, LA-1, is detectable in human kidney, lung, spleen, heart and skeletal muscle, and rhesus monkey liver; however, it is not found in the livers from dog, rat, cat, or pig. This antigen is characterized as a protein with beta-globulin electrophoretic mobility and a molecular weight in the range 67,000 to 80,000, which distinguishes it from liver ferritin and previously defined bile antigens and liver-specific antigens detected in sera from patients with liver diseases. The presence of LA-1 in serum appears to denote non-specific liver injury.
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PMID:The occurrence and properties of a serum hepatic antigen in various liver diseases. 403 2

Liver biopsies from 4 baboons taken during 15 months of iron-polymaltose injections, were compared with specimens from 2 controls. A morphometric method was used to assess ferritin concentration in various cells. Initially, ferritin and siderosomes were conspicuous in reticuloendothelial cells but rare in hepatocytes. Unusual findings included intranuclear ferritin and coalesced ferritin within bile canaliculi. With advancing overload, ferritin and hemosiderin increased not only in sinusoidal cells, but also in hepatocytes, with concomitant elevation of transaminases. The hepatocytes now showed evidence of damage and excessive collagen was present mainly around portal spaces. A year after cessation of iron injections, hepatocyte ultrastructure was near normal while sinusoidal cells were still heavily overloaded. The baboon appeared to be a useful model for the study of iron overload. Although in this study most of the damage was reversible, it is suspected that more prolonged overload, a different route of administration or other, more toxic iron compounds, may lead to cirrhosis similar to that of the iron-loading anemias.
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PMID:Iron overload of the liver in the baboon. An ultrastructural study. 406 58


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