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)

The objectives of this study included: 1) to identify pretreatment variables predictive of absence of response in 107 patients with chronic hepatitis C, genotype 1, treated with interferon-a (IFN-a) at a dose of 3 MU three times weekly for 3-12 months and classified into two groups: group A, nonresponders vs. patients with a complete response, and group B, nonresponding and relapsing patients vs. patients with a sustained response; and 2) to establish a prognostic index using ROC curve analysis. The rate of sustained response was 6. 5% at the 24-month follow-up. The pretreatment characteristics with predictive value using ROC curves were as follows: in group A, age, GGT, serum ferritin, viral load, and grade and stage of the histological lesion; and in group B, known duration of infection, GPT, GGT, serum ferritin, viral load, and grade and stage of the histological lesion. In both group A and group B the positive predictive value (the probability of predicting an absence of response when the variable is present) was greater than the negative predictive value (mean: 84.3% vs. 41.1%, 99% vs. 16.5%, respectively). In group A, based on the prognostic index, the positive predictive value when three variables were present was 96% and the sensitivity was 63.5%, with the test being unequivocal in 6.5%, whereas when four or five variables were present, the positive predictive value was 97% and 100% and the sensitivity was 40.5% and 18%, respectively. In group B, the positive predictive value when two variables were present was 100% and the sensitivity was 87%, whereas when three, four, five and six variables were present the sensitivity was between 73% and 28%. In group A, age, GGT and ferritin were the predictive variables independently associated with an absence of response, with a relative risk of 6.5, 4.8 and 3.1, respectively, whereas in group B we did not find variables independently associated with an absence of response. It was concluded that in patients with genotype 1, it is possible to predict the absence of response to IFN therapy with a high degree of reliability.
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PMID:[ROC curve analysis of factors predictive of non-response to interferon treatment in patients with chronic hepatitis C, genotype 1]. 1085 25

The objectives of this study included: 1) to identify pretreatment variables predictive of absence of response in 107 patients with chronic hepatitis C, genotype 1, treated with interferon-a (IFN-a) at a dose of 3 MU three times weekly for 3-12 months and classified into two groups: group A, nonresponders vs. patients with a complete response, and group B, nonresponding and relapsing patients vs. patients with a sustained response; and 2) to establish a prognostic index using ROC curve analysis. The rate of sustained response was 6.5% at the 24-month follow-up. The pretreatment characteristics with predictive value using ROC curves were as follows: in group A, age, GGT, serum ferritin, viral load, and grade and stage of the histological lesion; and in group B, known duration of infection, GPT, GGT, serum ferritin, viral load, and grade and stage of the histological lesion. In both group A and group B the positive predictive value (the probability of predicting an absence of response when the variable is present) was greater than the negative predictive value (mean: 84.3% vs. 41.1%, 99% vs. 16.5%, respectively). In group A, based on the prognostic index, the positive predictive value when three variables were present was 96% and the sensitivity was 63.5%, with the test being unequivocal in 6.5%, whereas when four or five variables were present, the positive predictive value was 97% and 100% and the sensitivity was 40.5% and 18%, respectively. In group B, the positive predictive value when two variables were present was 100% and the sensitivity was 87%, whereas when three, four, five and six variables were present the sensitivity was between 73% and 28%. In group A, age, GGT and ferritin were the predictive variables independently associated with an absence of response, with a relative risk of 6.5, 4.8 and 3.1, respectively, whereas in group B we did not find variables independently associated with an absence of response. It was concluded that in patients with genotype 1, it is possible to predict the absence of response to IFN therapy with a high degree of reliability.
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PMID:[ROC curve analysis of factors predictive of no response to interferon treatment in patients with chronic hepatitis C, genotype 1] 1087 38

Adult thalassemic patients have reduced bone mass due to disturbances in several different mechanisms affecting bone turnover. To determine if vitamin D deficiency contributes to the low bone mass of adult thalassemic subjects, we studied serum 25-OH-vitamin D levels in 90 patients (age ranging between 21 and 48 years) affected with thalassemia major (TM) and 35 (age 21-56 years) with thalassemia intermedia (TI). TM patients had been receiving regular transfusions from the age of 2 years and had increased serum ferritin, glutamic oxalacetic transaminase, glutamic piruvic transaminase as well as low bone density (L1-L4 Z score -2.07 +/- 0.2). TI patients did not receive transfusions, but their ferritin levels were increased as well (520.3 +/- 138,1). 8 TM patients (10.1%) and 4 TI (11.4%) had serum 25-OH-vitamin D less than 10.4 ng/ml and were considered presenting an absolute deficiency of vitamin D. Mean 25-OH-vitamin D was significantly (P < 0.01) lower in both TM and TI patients (20.3 +/- 0.7 ng/ml and 20.9 +/- 2.3 ng/ml, respectively) than in 100 healthy control subjects of similar age (25.2 +/- 1 ng/ml). 1,25-OH-vitamin D levels were in the normal-lower levels (45.15 +/- 1.5 mg/dl), while 24 H urinary calcium was below the normal range (15.75 mg/dl). In TM patients, the 25-OH-vitamin D levels correlated negatively with age (P < 0.05) and with serum ferritin (P < 0.05). TM and TI patients with low 25-OH-vitamin D levels (<17.8 ng/ml) presented higher serum ferritin levels (P < 0.01) and higher PTH (P < 0.05) compared to those with normal vitamin D. Moreover, TM patients with low 25-OH-vitamin D levels were significantly older (P < 0.05) and had higher GPT (P < 0.05) than patients with normal vitamin D. In conclusion, calcium metabolism is frequently impaired in adult thalassemic patients. An early and effective medical treatment should be taken in consideration by the clinician in order to improve the bone health in these patients.
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PMID:Low serum levels of 25-hydroxy vitamin D in adults affected by thalassemia major or intermedia. 1646 53

To assess the effects of liver iron overload and fibrosis after treatment with a chelating agent in hepatitis C virus (HCV)-infected thalassemia, from April 1999 to July 2004, 45 patients with thalassemia major (age range 9-33 years, mean 19.3) received daily deferiprone (L1) for 23-60 months (75 mg/kg). The patients were divided into two groups on the basis of their hepatitis status (27 with, 18 without). Their serum was analyzed for alanine aminotransferase (GPT), aspartate aminotransferase (GOT), bilirubin (total/direct), r-glutamyl transpeptidase (r-GT), alkaline phosphatase (Alk-P), and ferritin. Liver iron overload and fibrosis were defined by a senior pathologist. No significant differences were demonstrated in serum levels of GPT, GOT, bilirubin, r-GT, Alk-P or ferritin; comparison was made for each group before and after L1 treatment. Iron scores were 2.3 +/- 0.9 and 2.8 +/- 0.9 for the hepatitis C negative and positive groups, respectively (p = 0.07), with liver fibrosis scores of 1.0 +/- 0.5 and 0.4 +/- 0.52 (p = 0.56). The two scores were not higher for the positive group. There was no evidence of: 1) greater iron overload and fibrosis in the HCV-infected thalassemic patients; 2) L1 inducing progressive hepatic fibrosis or worsening iron overload in HCV-infected thalassemic patients after long-term therapy; 3) further damage to liver cells associated with L1 treatment.
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PMID:Effect of deferiprone on liver iron overload and fibrosis in hepatitis-C-virus-infected thalassemia. 1679 45


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