Liver biopsy for haemophilic patients with chronic HCV infection.
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Biopsy↗
Biomedical subjects
P Telfer
Publications and source records attributed to P Telfer.
Ribavirin treatment for patients with chronic hepatitis C: results of a placebo-controlled study.
BACKGROUND/AIMS: Small, uncontrolled studies of ribavirin for patients with chronic hepatitis C have reported efficacy in chronic hepatitis C. We have evaluated the efficacy and safety of a 24-week course of oral ribavirin in patients with chronic hepatitis C, compared to placebo. METHODS: A total of 114 patients were randomised to ribavirin or placebo. Ribavirin was administered in doses of 1000 or 1200 mg/day for 24 weeks. Efficacy was determined in the intention-to-treat population: 76 received ribavirin and 38 placebo. RESULTS: Ribavirin was significantly more effective than placebo in reducing and normalising serum ALT levels: 42/76 (55%) of ribavirin-treated patients vs 2/38 (5%) placebo recipients had either normalisation of the ALT levels or a reduction from baseline of at least 50% (p < 0.001). ALT levels were normal in 22/76 (29%) of ribavirin-treated patients vs 0/38 placebo recipients (p < 0.001). Twenty-four weeks after stopping ribavirin, the majority of patients had abnormal ALT levels. There was no difference between the treatment groups in reduction or disappearance of HCV-RNA levels. HCV RNA disappeared during treatment in 3% of ribavirin-treated patients and 3% of placebo recipients. More ribavirin than placebo patients showed improvement in total Knodell score (45% vs 31%), but these differences were not statistically significant. Analysis of each component of a histology activity index revealed no statistically significant differences between treatment groups. Ribavirin patients had fewer lymphoid aggregates than did placebo recipients at the post-treatment assessment (p = 0.05). Ribavirin was associated with reversible haemolytic anaemia: a fall in haemoglobin occurred in 3% of placebo- and 32% (25/78) of ribavirin-treated patients, respectively (p < 0.001). CONCLUSIONS: These data indicate that ribavirin was no more effective than placebo in reducing or eliminating HCV-RNA levels, and was not significantly more effective than placebo in improving hepatic histology after 6 months of treatment. The role of a 6-month treatment of chronic hepatitis C with ribavirin alone, without a significant effect on HCV RNA, is therefore limited.
Administration, Oral↗
Yersinia enterocolitica transmission from a red cell unit 34 days old.
In 1993 the North London Blood Transfusion Centre received its first report of Yersinia enterocolitica transmission from a unit of red cells supplied to a local hospital. The recipient was a 23-year-old male who was neutropenic following a third cycle of chemotherapy for treatment of acute myeloblastic leukaemia (FAB type M6) and received a 34-day-old red cell unit. During transfusion the patient developed septicaemia and endotoxin-mediated shock. The transfusion was stopped immediately and broad spectrum antibiotics administered immediately on suspicion of bacteraemia from the transfused unit. This prompt action undoubtedly prevented a fatal outcome. Y. enterocolitica was isolated from the blood bag. Antibody was also detected in the bag and in a sample taken from the donor 39 days post-donation. Antibody to serotype 03 was identified, the commonest serotype reported in transfusion-transmitted Y. enterocolitica. The donor reported no gastrointestinal upset or illness prior to donation. This transfusion reaction might not have occurred had the red cells been transfused earlier in their storage period, but would not have been prevented by the exclusion of donors with a history of gastrointestinal illness as the donor was asymptomatic. Nor would it have been prevented by inspecting the blood for a change in colour, as no such change was observed. Y. enterocolitica is a significant problem in transfusion medicine and transmission is generally associated with a high mortality rate. Hospitals should be urged to investigate bacteriologically all appropriate transfusion reactions so that the true extent of the problem in the United Kingdom can be assessed.
Adult↗
Longitudinal genotype analysis and quantification of hepatitis C virus in haemophilic patients receiving interferon-alpha therapy.
Haemophilic patients have a high prevalence of hepatitis C virus (HCV) infection because of the use of unsterilized clotting factor concentrates. Six major genotypes of HCV have been distinguished so far, with epidemiological evidence suggesting that genotypes 1-3 are common in the indigenous UK and US populations. The aim of this study was to analyse the changes in viral load and composition of the HCV quasispecies in haemophilic patients receiving therapy with interferon-alpha (IFN-alpha) using the four major methods currently available for HCV genotyping. The most consistent genotype results were obtained using restriction fragment-length polymorphism (RFLP) analysis when compared with the DNA sequence analysis, and showed that the dominant genotype can change in patients with mixed genotype infections treated with IFN-alpha. This study indicates the difficulties in studying this group of patients with mixed HCV genotype infections, and that frequent sampling is necessary, together with viral load measurement to monitor response to IFN-alpha therapy.
Adult↗
Hepatitis C genotypes in haemophilic patients treated with alpha-interferon.
The effect of alpha-interferon on the hepatitis C genotypes was examined in 25 anti-HCV-positive haemophilic patients. The rate of multiple HCV genotypes in patients who are likely to have mixed infections was also studied. Pretreatment results showed that 3/25 (12%) patients had a change in genotypes, whereas posttreatment this rose to 10/25 (40%). Seven of 10 (70%) patients who showed a change in genotype had a clinical response to alpha-interferon. Six of 25 (24%) patients showed a complete clinical response to alpha-interferon, and the majority of these were either type 2 or 3. This study supports previous evidence that type 1 is less likely to respond to alpha-interferon, and that alpha-interferon may alter the concentrations of the various circulating genotypes present in multiply-infected patients. There are many difficulties in studying hepatitis C in haemophilic patients due to the sequence heterogeneity within each individual, and this study has shown that no ideal method exists as yet for looking at HCV genotypes in multiply-infected individuals.
Alanine Transaminase↗
Isolation and characterization of the first simian immunodeficiency virus from a feral sooty mangabey (Cercocebus atys) in West Africa.
The lineage of HIV-2-like viruses was studied in feral sooty mangabeys (SMs) by serological and genetic methods. Four feral sooty mangabeys were positive for simian immunodeficiency virus (SIV) antibodies and a new isolate, SIVsmSL92a, was obtained. Genetic analysis of gag genes showed that SIVsmSL92a was highly diverse and a distinct sequence subtype within the SIV sm/HIV-2 family. The results showed that SIVsm is the most diverse group of SIVs found thus far in a single monkey species.
Africa, Western↗
The progression of HCV-associated liver disease in a cohort of haemophilic patients.
We have studied morbidity and mortality related to hepatitis C virus infection in haemophilic patients treated at our centre. 11/255 HCV seropositive patients have developed hepatic decompensation. 20 years after first exposure to lyophilized clotting factor concentrate the risk of hepatic decompensation is estimated to be 10.8% (95% CI 3.8-17.8%). There is a significantly increased risk associated with HIV infection, and also with increased age. For HIV seropositive patients the rates of decline in CD4 lymphocyte count and the development of p24 antigenaemia are significant risk factors for hepatic decompensation. Cirrhosis was seen in 9/19 HIV seropositive patients at post mortem. There was an association of cirrhosis with increased age but not with CD4 count, p24 antigenaemia, or AIDS. In conclusion, HCV infection is associated with serious liver disease in haemophilic patients, but so far this has been restricted to a minority of those at risk. HIV co-infection accelerates progression to hepatic decompensation, and we speculate that this is probably due to enhanced HCV replication in the presence of immune deficiency.
Adolescent↗
Hepatitis C antibody profile in adults with haemophilia and their sexual partners.
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Hemophilia A↗