Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We report an 18-year-old male patient who developed chronic hepatitis C after blood transfusion and had testicular dysfunction after irradiation for a testicular relapse of childhood acute lymphocytic leukemia after cessation of maintenance therapy, and the initiation of testosterone replacement therapy at puberty. Concomitant administration of estradiol resulted in a reduction in serum alanine aminotransferase and ferritin levels and hepatic iron concentration and staining after 2 years of estrogen therapy, although interferon therapy was withdrawn because of adverse effects. This observation suggests that endogenous estradiol may play a beneficial role in male patients with chronic hepatitis C.
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PMID:Estrogen therapy in a male patient with chronic hepatitis C and irradiation-induced testicular dysfunction. 1130 Jan 39

In patients with chronic hepatitis C, prior studies have suggested that increased hepatic iron concentration (HIC) is predictive of a poor response to interferon (IFN) monotherapy. The aim of this study was to assess the importance of HIC on the virologic response to therapy with IFN alone or when combined with ribavirin. Records of 91 patients were reviewed for inclusion in this study. Fifty-one received IFN alone, and 40 received IFN plus ribavirin. HIC and serum iron studies, alanine aminotransferase (ALT) values, hepatitis C virus (HCV) genotype, and HCV RNA were determined prior to therapy. Sustained response was defined as the absence of HCV RNA 6 months after the end of therapy. In the IFN monotherapy group, mean HIC was higher for nonresponders (803 + 89 microg/g, range 130-2808 microg/g) compared with sustained responders (241 + 54 micro g/g, range 187-295 microg/g) (p < 0.01). In contrast, in the combination therapy group, the mean HIC was similar for both groups (533 + 86 microg/g, range 79-1338 microg/g in the nonresponders, and 662 + 95 microg/g, range 94-2031 microg/g, in the sustained responders). No difference between transferrin saturation and serum ferritin level was observed in sustained responder or nonresponder patients treated with IFN plus ribavirin. IFN monotherapy nonresponder patients tended to have a higher HIC. With IFN plus ribavirin, the sustained virologic response rate was not affected by the HIC.
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PMID:Hepatic iron concentration does not influence response to therapy with interferon plus ribavirin in chronic HCV infection. 1203 31

Elevations in serum transferrin-iron saturation and ferritin are common in patients with chronic hepatitis C infection, especially if they have concomitant elevations in serum aminotransferases. However, serum markers of iron stores do not accurately reflect hepatic iron content, or predict clinically important endpoints such as response to interferon and disease progression. In contrast, hepatic iron concentration, which is usually normal or only mildly elevated in chronic hepatitis C infection in the absence of cirrhosis, is one of the strongest predictors of response to interferon monotherapy. Iron depletion by phlebotomy consistently reduces serum aminotransferases and in combination with interferon may have improved antiviral efficacy compared to interferon alone. Unfortunately, no data are available on the role, if any, of iron depletion therapy, as an adjunct to interferon and ribavirin combination treatment. Future studies should focus on the efficacy of combining iron depletion with pegylated interferon and ribavirin and on the effect of long-term iron depletion on histologic progression of chronic hepatitis C infection.
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PMID:Iron in hepatitis C: villain or innocent bystander? 1206 65

In our studies on the biological function of the mengovirus leader protein, we identified a casein kinase II (CK-2) phosphorylation site in the protein. Here we report that the mengovirus leader protein can be phosphorylated by CK-2 in vitro. Expression of a recombinant leader protein in which the consensus CK-2 sequence around threonine 47 was disturbed resulted in a mutant protein that could no longer be phosphorylated. The CK-2 consensus sequence was modified by site-directed mutagenesis and subsequently introduced into a mengovirus cDNA clone to investigate the effect of the phosphorylation of the leader protein on virus replication and on the host cell response. Modifications by which the CK-2 consensus sequence was disturbed resulted in mutant viruses with reduced growth kinetics. We demonstrated that the integrity of the CK-2 phosphorylation site of the mengovirus leader protein was specifically related to the suppression of NF-kappa B activation and subsequent suppression of alpha/beta interferon production in infected cells. We also found that the integrity of the CK-2 phosphorylation site of the leader protein coincided with an increase of ferritin expression in the infected cell. These data indicate that the leader protein suppresses the iron-mediated activation of NF-kappa B and thereby inhibits alpha/beta interferon expression in the infected cell.
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PMID:The mengovirus leader protein suppresses alpha/beta interferon production by inhibition of the iron/ferritin-mediated activation of NF-kappa B. 1220 45

We describe two cases of transfusion dependent thalassaemics with chronic hepatitis C virus infection whom were treated successfully with interferon and ribavirin, following failure of response or relapse after an initial response to interferon monotherapy. They had sustained virological response for more than twelve months after completing therapy. Transfusion requirements were significantly increased during the combination therapy, probably due to ribavirin-induced haemolysis. Serum ferritin level decreased significantly during the treatment. Combination therapy with interferon alfa and ribavirin may be a feasible treatment option for some nonresponders to prior interferon monotherapy.
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PMID:Treatment of chronic hepatitis C virus infection with interferon alfa and ribavirin: sustained response in two patients with transfusion dependent thalassaemia. 1244 Feb 76

Black race and increased hepatic iron stores predict poor response to interferon treatment for chronic hepatitis C virus (HCV) infection. We tested the hypothesis that these 2 observations are linked by investigating whether HCV-infected African-Americans have increased iron stores relative to uninfected persons. Using data from the third National Health and Nutrition Examination Survey (NHANES III), we determined the risk of having increased iron stores, defined as elevation of both serum ferritin and transferrin-iron saturation (TS), in HCV-RNA-positive blacks (n = 100) and nonblacks (n = 126) relative to HCV-RNA-negative blacks (n = 4,002) and nonblacks (n = 10,943). HCV-positive blacks were 5.4 times (95% CI, 1.2 to 24) more likely to have increased iron stores than HCV-positive nonblacks. The proportion of HCV-positive blacks who had increased iron stores was 16.4% among those with abnormal liver enzymes and 2.8% among those with normal liver enzymes, compared with only 0.6% among HCV-negative blacks. After adjustment for age, alcohol intake, gender, menopausal status, education, body mass index, and poverty index, HCV-positive blacks with abnormal liver enzymes had an elevated risk of having increased iron stores (odds ratio, 17.8; 95% CI, 5.1 to 63). In contrast, among persons of other races, there was a much smaller difference in the proportion of persons with increased iron stores between HCV-positive persons with (3.4%) or without (1.4%) abnormal liver enzymes and HCV-negative persons (0.9%). In conclusion, a greater proportion of blacks than persons of other races respond to HCV infection with an increase in iron stores. This finding may partly explain the reduced response of HCV-positive African-Americans to antiviral treatment.
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PMID:Racial differences in the relationship between hepatitis C infection and iron stores. 1266 72

Mild iron overload in chronic hepatitis C is associated with liver fibrosis, hepatitis C virus (HCV) genotype 1b infection, and an impaired response to interferon therapy. In this study we evaluated whether polymorphisms in the hemochromatosis gene HFE and the transferrin receptor gene TFR1 are associated with these typical findings. The study considered 246 HCV-infected patients and 200 blood donors as controls, in which C282Y, H63D, and S65C mutations ( HFE) and the S142G polymorphism ( TFR1) were detected. HCV genotype, serum ferritin levels, stainable intrahepatic iron, and grade of fibrosis according to the METAVIR score (F0-F4) were determined. In HCV-infected patients, heterozygosity for the C282Y mutation in HFE was significantly associated with elevated serum ferritin levels, stainable liver iron, and advanced fibrosis or cirrhosis (F2-F4). By multivariate logistic regression analysis the odds ratio for the development of advanced fibrosis or cirrhosis (F2-F4) was 2.5 for HCV-infected patients carrying a heterozygous C282Y mutation and 4.8 for HCV-infected patients with C282Y/H63D and C282Y/S65C compound heterozygosity. Heterozygosity for the C282Y mutation in HFE contributes to iron accumulation and fibrosis progression in chronic hepatitis C.
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PMID:Hemochromatosis and transferrin receptor gene polymorphisms in chronic hepatitis C: impact on iron status, liver injury and HCV genotype. 1476 Aug 28

Interferon has been shown to be an effective treatment of congenital dyserythropoiesis type I (CDA-I), but the optimal dose and the feasibility of this treatment remains to be determined. Here, in a 9-yr follow-up of a single patient, we show that interferon remains active during such a long period. The optimal dose of conventional alpha interferon could be evaluated at 2 million units twice a week. Pegylated interferon could be used as well at a dose of 30 microg/wk. During interferon treatment, serum and erythrocyte ferritin levels decreased progressively, and remained inversely correlated with haemoglobin levels. On repeated liver biopsies, iron overload could be normalized. Low dose interferon is a long-term treatment of CDA-I, and allows a significant decrease in iron overload, that could be interesting even in patients who are only moderately anaemic.
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PMID:Long-term alpha interferon treatment is effective on anaemia and significantly reduces iron overload in congenital dyserythropoiesis type I. 1545 19

The role of hepatocyte steatosis in interferon (IFN) resistance is still unclear, especially in patients infected with hepatitis C virus (HCV) genotype 2a. The present study was conducted in 364 consecutive non-cirrhotic naive patients infected with genotype 2a, who were evaluated for the severity of steatosis and response to IFN monotherapy after a 24-week median duration of therapy. The patients were examined for factors associated with steatosis and treatment efficacy according to the grade of steatosis. Early viral kinetics was also evaluated in 64 patients for predictors of response to therapy. Nine IFN-resistant patients were assessed for the relationship between amino acid sequence of HCV core region/NS5A and severity of steatosis. Multivariate analysis identified two independent factors associated with steatosis; serum ferritin > or =200 microg/l and body mass index > or =25.0 kg/m(2). The sustained virological response rate in patients with high-grade steatosis was significantly lower than in the low-grade group. Study of early viral kinetics showed a significantly lower cumulative HCV-RNA negative rate for the high-grade than low-grade steatosis group. Sequence analysis of HCV core region/NS5A in IFN-resistant patients with or without steatosis failed to identify steatosis-specific amino acid substitutions associated with resistance. This study of HCV genotype 2a suggested that steatosis is associated with excess iron storage, and that it is an important predictor of efficacy of IFN monotherapy. Further large-scale studies are warranted to examine the role of amino acid substitutions on IFN resistance specific for steatosis.
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PMID:Hepatocyte steatosis is an important predictor of response to interferon (IFN) monotherapy in Japanese patients infected with HCV genotype 2a: Virological features of IFN-resistant cases with hepatocyte steatosis. 1571 92

In untreated hepatitis virus (HCV)-positive renal transplant patients, the rate of liver fibrosis progression is low. In contrast, in those treated by ribavirin monotherapy, liver fibrosis score increased significantly after only 1 year of ribavirin monotherapy. The aim of this study was to identify the factors that might contribute to accelerate liver fibrosis progression in this population. Eleven patients were included in the study. Intrahepatic transforming growth factor (TGF)-beta, interferon (IFN)-gamma, and interleukin (IL)-10 mRNA quantification determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) were similar before and after ribavirin therapy. The number of amino acid substitutions observed in the hypervariable region (HVR)-1 of the HCV genome between baseline and 1 year after ribavirin monotherapy was low, i.e., 3 (1-11) amino acid substitutions, suggesting the absence of a high selection pressure induced by ribavirin. In contrast, due to ribavirin-induced hemolysis, there was a significant increase in serum ferritin levels (P = 0.02) and in intrahepatic iron deposition (P = 0.04). Transferrin level and total iron-binding capacity decreased significantly during ribavirin monotherapy (P = 0.004). The increased liver fibrosis observed in renal transplant patients receiving ribavirin monotherapy could be related to ribavirin-induced anemia. Severe chronic hemolysis is responsible for iron overload, liver iron deposition, and an acceleration in the progression of liver fibrosis.
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PMID:Factors accelerating liver fibrosis progression in renal transplant patients receiving ribavirin monotherapy for chronic hepatitis C. 1577 76


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