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)

Eleven patients with porphyria cutanea tarda were studied. Biochemical confirmation of the clinical diagnosis required only determination of the total urine porphyrin concentration in a sample of urine voided on rising in the morning. The patients were divided for convenience of discussion into four groups differing in age, sex and etiologic factors. Of the six patients in whom a liver biopsy was done one was shown to have micronodular cirrhosis. Except for a modest elevation in the serum glutamic oxaloacetic transaminase values when the patients were first seen, no evidence was found for liver disease apart from the presence of porphyria cutanea tarda. One patient recovered solely by abstaining from alcohol consumption. Five patients underwent phlebotomy; their iron stores had been found to be between 2 and 3 g. Decreasing urine porphyrin values correlated well with decreasing serum ferritin values during the course of phlebotomy. Porphyria cutanea tarda, which is due to a deficiency of uroporphyrinogen decarboxylase, is manifested in association with alcohol abuse, estrogen therapy, exposure to chlorinated hydrocarbons or increased tissue iron stores, or a combination of these factors. Although relatively uncommon, this condition raises important and unresolved issues regarding the hepatotoxicity of alcohol, estrogens, chlorinated hydrocarbons and iron.
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PMID:Porphyria cutanea tarda: clinical and laboratory features. 42 87

278 azathioprine and methylprednisolone (AZA)-treated and 406 ciclosporin (CS) treated patients with a kidney graft functioning for more than 1 year were investigated for the presence of chronic liver disease (CLD), defined as an increase in transaminases of 1.5 times the upper normal limits for a period of at least 12 months. The prevalence of CLD was 36 and 27% in the two groups, respectively. The univariate analysis showed that male sex, alcohol abuse and HBsAg positivity correlated with CLD onset in the AZA group while blood transfusions, length of dialysis treatment, pretransplantation CLD, HBsAg positivity and ferritin levels over 800 ng/ml correlated with CLD onset in CS. The multivariate analysis identified male sex and HBsAg positivity in the AZA group and age over 18 years, high ferritin levels and HBsAg positivity in the CS group as risk factors predictive of CLD onset. Liver failure represented the 4th cause of death in the AZA group but 1 of the 2 most important causes of death in CS in the long term. However, these drawbacks were overcome by the overall low mortality rate in CS. Therefore, renal transplantation should not be refused to patients positive for HBsAg and/or with preexisting liver disease.
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PMID:Renal transplant recipients and chronic liver disease: statistical evaluation of predisposing factors. 150 27

Alcohol abuse is associated with disturbances to iron metabolism in man, ranging from anemia to siderosis. Also seen in these patients are increased serum ferritin levels. Since the liver not only stores iron in cytosolic ferritin, but has also been shown to take up this molecule from the plasma by an active transport mechanism, it has been suggested that the iron in this circulating ferritin may contribute to the increased incidence of siderosis seen in alcoholics. As part of an ongoing study of these disturbances, using a rat model, we have examined the uptake of ferritin by freshly isolated hepatocyte suspension to test the hypothesis that increased hepatocyte uptake of ferritin iron contributes to the siderosis seen in some alcoholics. Incubation of hepatocytes in the presence of ethanol resulted in a progressive reduction in uptake with increasing alcohol concentration, from 1.23 +/- 0.05 ng of ferritin/10(6) cells/min to 0.65 +/- 0.02 ng/10(6) cells/min (mean +/- SD) at an ethanol concentration of 100 mM. 4-Methylpyrazole (0.1 mM) restored 70% of this activity, but higher concentrations also decreased ferritin uptake in the absence of ethanol. The addition of 5 microM cyanamide decreased ferritin uptake slightly in the presence of ethanol (0.82 +/- 0.04 ng of ferritin/10(6) hepatocytes/min vs. 0.86 +/- 0.03 ng/10(6) cells/min for ethanol alone), while having no effect in the absence of ethanol (1.01 +/- 0.04 vs. 1.12 +/- 0.05 ng/10(6) cells/min). Preincubation of the hepatocytes with acetaldehyde resulted in a dose-dependent reduction to a maximum reduction of approximately 25% at 300 microM acetaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of ethanol metabolism on ferritin uptake by freshly isolated rat hepatocytes: is acetaldehyde responsible for this alteration? 159 May 51

The frequency of the HLA linked iron-loading gene was assessed in 1783 Afrikaner men over the age of 40 years living in the South Western Cape. Measurements, made on three occasions over a 4.5 year period, included the serum ferritin concentration, a screening test for reduced unsaturated iron-binding capacity and the percentage transferrin saturation. The serum gamma-glutamyl transferase concentration was used as a marker of alcohol abuse. The diagnosis of homozygosity was based on a serum ferritin concentration that was persistently greater than 400 micrograms l-1 and a percentage transferrin saturation greater than 55%. Using these criteria, 17 subjects were diagnosed as homozygous, corresponding to a disease frequency of 0.0095, a gene frequency of 0.0976 and a heterozygote frequency of 0.176 (95% confidence limits: 0.135-0.213). None of the subjects had overt clinical haemochromatosis. Typing for the HLA-A, -B, -C and -DR loci showed that the HLA-A3 allele (frequency 0.6471 and relative risk 4.4) was the only independent marker for the iron-loading gene in this asymptomatic population. Using the present approach it was not possible to distinguish between heterozygotes, alcohol abusers and normal subjects with serum ferritin concentrations at the upper end of the normal range.
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PMID:Phenotypic expression of the HLA linked iron-loading gene in males over the age of 40 years: a population study using serial serum ferritin estimations. 197 75

It was hypothesized that maternal blood lead level at delivery and cord blood lead level of the neonate would be affected by maternal use of alcohol, history of alcohol abuse, and smoking. The possibility that iron status, as reflected in maternal serum ferritin, would be related to lead level was also explored. The maternal history of alcohol abuse was unrelated to lead level in 208 samples of maternal blood and 178 samples of cord blood. However, alcohol use during pregnancy was related in a dose-response fashion to maternal and to cord blood lead level. This effect was significant with and without control of maternal smoking. The effect of maternal smoking and serum thiocyanate on maternal and cord blood lead level were also highly significant with and without control of the maternal drinking variable. Serum ferritin was marginally related to lead level for white women and for black infants, but tests of the dichotomized maternal ferritin variable did not yield a significant linkage with maternal or cord blood lead level. The results further support recommendations that women abstain from alcohol consumption and cigarette smoking in pregnancy.
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PMID:Fetal lead exposure: antenatal factors. 407 12

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

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

A proposed rate-nephelometric inhibition immunoassay of phenytoin and phenobarbital in human serum involves the sequential addition to buffer of 42-microL aliquots of sample containing the hapten (drug) of interest, a hapten conjugate (drug-equine apoferritin), and specific antibody to the hapten. The drug and the drug conjugate compete for the binding sites on the antibody. The free hapten-antibody complex is soluble and so does not scatter light, whereas the complex of antibody and drug conjugate is insoluble and thus scatters light. The latter immunoprecipitation is competitively inhibited by free hapten. Thus the higher the concentration of free hapten present, the fewer immunoprecipitin complexes are formed, and the less light scatter. Precision, accuracy, linearity, analytical recovery, and comparison with patients' samples assayed with the DuPont aca were excellent. There was no significant interference from hemolysis, icterus, or lipemia. Many potentially interfering drugs and metabolites were checked for cross reactivity, with negative results. Reaction times range from 30 to 50 s.
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PMID:Rate-nephelometric inhibition immunoassay of phenytoin and phenobarbital. 747 88

Alcohol abuse is known to cause disturbances to iron homeostasis in man and is associated with elevated serum ferritin levels. We have previously shown that ethanol metabolism in the rat hepatocyte is associated with an immediate reduction in ferritin uptake by this cell. In this study we have examined the effect of pair-feeding the Lieber-DeCarli liquid alcohol diet on ferritin uptake by rat hepatocytes. Rat liver ferritin was radiolabeled with 59Fe in vivo and isolated by conventional techniques. Rats were pair-fed the Lieber-DeCarli liquid alcoholic diet for 4-6 weeks. Hepatocytes, isolated from their livers by collagenase perfusion, were incubated with [59Fe]ferritin in L-15 medium at 37 degrees C and 4 degrees to measure ferritin uptake and binding. The in vitro effect of ethanol on these hepatocytes was also studied. Ferritin and iron parameters were measured in the sera and hepatocytes of these animals and a comparable group of normal chow-fed rats. The rate of ferritin uptake by hepatocytes from alcohol-fed rats was significantly faster than that of their pair-fed controls (0.743 +/- 0.061 vs. 0.540 +/- 0.042 ng/min/10(6) cells, p < 0.05). However, the rats on Lieber-DeCarli control diet exhibited a lower hepatocyte ferritin uptake rate than chow-fed animals (79.3 +/- 8.1% of the control values, p < 0.01). In vitro incubation of cells in 100 mM ethanol resulted in less inhibition of ferritin uptake by hepatocytes from alcoholic rats than from their pair-fed controls (11 +/- 7.1% inhibition vs. 43.6 +/- 10.7% for controls, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic alcohol feeding on hepatic iron status and ferritin uptake by rat hepatocytes. 848 84

The consumption of excessive amounts of alcohol affects human iron homeostasis and an association of iron overload and heavy alcohol consumption has been recognized for many years. Both major proteins of iron metabolism, ferritin and transferrin, are affected by alcohol. Increased hepatic iron levels are seen in a high proportion of alcoholic subjects, sometimes causing confusion in diagnosis between alcoholic liver disease and iron-overload disease. The pattern of deposition of this iron in alcoholics, however, differs from that seen in the iron-overload disease haemochromatosis. Excessive alcohol consumption causes transferrin to become carbohydrate deficient, which allows it to be used as an efficient biochemical marker of alcohol abuse. It is concluded that alcohol consumption in moderation is unlikely to have deleterious health consequences.
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PMID:Alcohol and iron: one glass of red or more? 898 26


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