There are few data on the prevalence and clinical outcome of hepatitis C infection in children. We studied 458 children who underwent cardiac surgery in Munich, Germany, before 1991, when blood-donor screening for hepatitis C was introduced in Germany. Their mean age at first operation was 2.8 years; none of the children had received blood transfusions before or 'after cardiac surgery, and none of their mothers had antibodies to the hepatitis C virus (anti-HCV). We compared these patients with 458 control subjects matched for age and sex.
Sixty-seven (14.6 percent) of the 458 patients who had undergone cardiac surgery had anti-HCV, as compared with 3 (0.7 percent) of the control subjects (P<0.001). At a mean interval of 19.8 years after the first operation, 37 (55 percent) of the 67 patients who were positive for anti-HCV had detectable HCV RNA in their blood. The infection had cleared in the other 30 patients, as evidenced by negative results on three polymerase-chain-reaction analyses performed at six-month intervals. Only 1 of the 37 patients who were positive for HCV RNA had elevated levels of liver enzymes; that patient had severe right-sided congestive heart failure. Of the 17 patients who underwent liver biopsies, only 3 had histologic signs of progressive liver damage. These three patients had additional risk factors: two had congestive heart failure, and the third had also been infected with hepatitis B virus.
Children who had undergone cardiac surgery in Germany before the implementation of blood-donor screening for hepatitis C had a substantial risk of acquiring the infection. However, after about 20 years, the virus had spontaneously cleared in many patients. The clinical course in those still infected seems more benign than would be expected in people infected as adults.
"Given the high uncertainty associated with this approach, a range of 4–54% was used for all regions. An average viraemic rate of 50% (uncertainty interval of 50–75%) was applied to the infected population aged <15 years    . "
[Show abstract][Hide abstract] ABSTRACT: The treatment of chronic hepatitis C virus (HCV) infection has the potential to change significantly over the next few years as therapeutic regimens are rapidly evolving. However, the burden of chronic infection has not been quantified at the global level using the most recent data. Updated estimates of HCV prevalence, viremia and genotypes are critical for developing strategies to manage or eliminate HCV infection. To achieve this, a comprehensive literature search was conducted for anti-HCV prevalence, viraemic prevalence and genotypes for all countries. Studies were included based on how well they could be extrapolated to the general population, sample size and the age of the study. Available country estimates were used to develop regional and global estimates. Eighty-seven countries reported anti-HCV prevalence, while HCV viraemic rates were available for fifty-four countries. Total global viraemic HCV infections were estimated at 80 (64-103) million infections. Genotype distribution was available for ninety-eight countries. Globally, genotype 1 (G1) was the most common (46%), followed by G3 (22%), G2 (13%), and G4 (13%). In conclusion, the total number of HCV infections reported here are lower than previous estimates. The exclusion of data from earlier studies conducted at the peak of the HCV epidemic, along with adjustments for reduced prevalence among children, are likely contributors. The results highlight the need for more robust surveillance studies to quantify the HCV disease burden more accurately.
Journal of Hepatology 07/2014; 61(1). DOI:10.1016/j.jhep.2014.07.027 · 11.34 Impact Factor
"Studies indicate that the effectiveness of IFN and/or RBV is incomplete, because if the treatment was 100% effective it would lead to rapid and complete eradication of the virus in the blood rather than just diminishing it in the binary phase. It is interesting that the effectiveness of IFNα-inhibition on HCV replication can be measured by the viral decline during the first 24 hours of treatment (Takahashi et al, 1993; Kobayashi et al, 1996; Vogt et al, 1999). The addition of RBV leads to increased rates of decline of the virus in the blood and thus the rate of the patient's response to treatment. "
[Show abstract][Hide abstract] ABSTRACT: Since the discovery of the hepatitis C virus, the goal of all treatment is to clear the virus and normalise the liver function, stopping the progression of the disease and thus reducing long-term complications of cirrhosis and hepatocellular carcinoma. The therapy for CHC used to consists of pegylated interferon alpha in combination with ribavirin and others new approved protease inhibitors, but still few of those treated can not achieved a compleat SVR. The reasons for failure are unknown, but may result from viral and host factors combined. The review here is to highlights and compare of what has been published previously. Interferon alpha (IFN-α) Interferon alpha is a member of the Interferon family, comprising a large group of multifunctional secreted proteins which have anti-viral, immunomodulatory and anti-proliferative activities. The Interferons can be classified into three types: Type I IFNs consist of IFN-alpha (IFN-α), IFN-beta (IFN-β) and IFN-omega (IFN-ω). They are produced in direct response to the virus infection and induce intracellular signalling pathways to activate transcription factors, such as the Interferon regulatory factors (IRF)-3, IRF-5, IRF-7 and NF-κB, which in turn initiates the transcription of interferon sensitive genes. IFN-α is a multi-gene family comprising more than 20 types which are synthesised by leukocytes, whereas IFN-β synthesis is seen in most cell types, in particular fibroblasts. The type II IFNs consist of INF-gamma (IFN-γ), which is synthesised by activated T lymphocytes and NK cells, in response to cytokines such as IL-12 and IL-18 or via the stimulation of T-cell or NK cell antigen receptors (Lemon et al, 2010). The third type is IFN–lamda (IFN-λ) or interleukin 28/29 -a class of cytokine with IFN-like activity.
"A liver biopsy is recommended before beginning the treatment. Some serious studies performed in children with chronic hepatitis C in most of cases have shown few histological lesions and the evaluation by biopsy has been controversy, but still today remains the only method to evaluate the severe cases [15-17] Only 1.3% (one in 80 children) can achieve to cirrhosis [18,19]. Theoretically cirrhosis could be developed after a mean time of 28 years [20,21]. "
[Show abstract][Hide abstract] ABSTRACT: Treatment of Hepatitis C in children has a better outcome than in adults, and for this reason the treatment had different views. However, in pediatric age hepatitis C is seen to have an evolution towards chronicity. Today is a normal option to treat chronic hepatitis C as early as possible according to certain criteria. The aim of this study is to show the results of treatment with interferon and ribavirin and the follow-up of children diagnosed with chronic hepatitis C in our service.
This is a prospective study which has included children 3 up to 15 years old (13 boys and 4 girls) diagnosed with chronic hepatitis C. All patients underwent a certain protocol, including liver biopsy prior to treatment. Treatment consisted in use for 48 weeks of INF α-2b, 3 MIU/m2 three times a week s/c and ribavirin 15 mg/kg orally divided bid. Two patients were treated with PEGINF α-2b with dose 1.5 mcg/kg once a week s/c and ribavirin 15 mg/kg. After the treatment all patients have stayed under our control for an average period of 24 weeks.
At the end of the treatment we detected a patient with HCV-RNA positive. End Treatment Viral Response was 94%. Six months later we found three patients who showed relapse of disease. Sustained Viral Response was approximately 83%
The combination therapy of interferon with Ribavirin in treatment of children with chronic hepatitis C provides a higher SVR when treatment is initiated at the earliest stages of hepatic changes. Side effects of therapy are insignificant in comparison with results obtained.
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