Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine and correlate the liver function profile, hepatitis C virus (HCV) genome, anti-HCV, genotypes, quantitation, and nucleotide sequence variability in polytransfused thalassemic children, 61 such children were studied prospectively for 4 y. Twenty-six had HCV infection. The average age, number of transfusions, and alanine aminotransferase (ALT) levels of the HCV-infected group were higher than those of the 35 children without HCV infection. None was infected after the initiation of anti-HCV screening in donor blood. Liver biopsies were performed in six HCV-infected and eight HCV-noninfected thalassemic children, and portal fibrosis was found more frequently in the HCV-infected group. Quantitation of HCV RNA was done by the competitive polymerase chain reaction method, and the titer was about 1 x 10(6) to 5 x 10(8) copies/mL. The titer did not change significantly over the 4-y follow-up period and did not correlate with ALT levels. Nineteen HCV-infected patients were genotyped; 15 were Okamoto/Simmonds type II/1b, two were type III/2a, and two were type IV/2b. The hypervariable region of the HCV genome (E2/NS1) was cloned and sequenced in two serum samples from one patient collected at a 2-y interval, as the ALT levels decreased. The variation rate was estimated to be 1.2-1.7 x 10(-2)/nucleotide/y. The results showed that, in polytransfused thalassemic children, 43% (26/61) contracted HCV. We conclude that HCV infection may cause elevated ALT levels and portal fibrosis of the liver, whereas the viral titer and genotypes do not parallel ALT levels.
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PMID:Hepatitis C viral infection in thalassemic children: clinical and molecular studies. 882 7

We have conducted a controlled trial in 20 haemophilic patients in which intravenous recombinant interferon alpha-2a, 3 mega units thrice weekly, was used to treat chronic hepatitis C infection. The study endpoints included complete and paritial normalization of serum ALT, and loss of serum HCV RNA as determined by polymerase chain reaction (PCR). Interferon treatment was effective, and resulted in improvement in ALT in nine (45%) and a loss of HCV RNA in five patients (26%), but a sustained normalization of ALT has been seen in only one case. Responses were poor in those with HIV coinfection or with HCV genotype 1 (Simmonds classification). Troublesome side-effects were reported in 80%. The occurrence of a factor VIIIc inhibitor during the study was possibly an autoimmune complication of interferon. In conclusion, we have shown lower response rates than those seen in post-transfusion hepatitis C infection and suspect that current interferon regimes are unlikely to influence the natural history of HCV infection in haemophilia. Consideration should be given to trials of higher dosage interferon, and of long-term maintenance therapy for those who relapse.
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PMID:Alpha interferon for hepatitis C virus infection in haemophilic patients. 2721 22