The World Health Organization classifies hepatitis as one of more than 100 diseases transmitted by blood-sucking insects, such as mosquitoes and phlebotomine sandflies, collectively known as the'vector diseases'.\n
Hepatitis is a contagious disease and infections occurring before the development of the chronic form can result in remission, whereas those occurring later are likely to be chronic in nature. Hepatitis B virus may be especially associated with chronic infections. Risk factors for progression to chronicity include the degree and severity of viral antigenicity, the presence of antigens in the blood, and the presence of antigens in the gut.
Hepatitis is not a curable disease. The cure rate of standard management is low. It depends the cause of chronic hepatitis, the severity and the age of the patient. However, patients with hepatitis A can be cured, while hepatitis B, hepatitis C, and HBV hepatitis are mostly incurable.
Most people with hepatitis feel tired. Others feel weak, fatigued and have headaches. Complications, including inflammation of the brain, include loss of appetite and shortness of breath. Hepatitis can cause fatty liver, which is associated with jaundice (abnormal yellowing of the skin and the whites of the eyes). Other complications can include cirrhosis or cancer of the liver. The liver normally clears the products of liver illness, but after long-term heavy liver infections, a scar may be formed. This scar, known as fibrosis, may eventually lead to liver cancer or liver failure.
The estimated number of new U.S. hepatitis infections in 2006 was 15 million with an estimated incidence rate of 6.4/10,000/year for hepatitis A; 4.9/10,000/year for hepatitis B; and 3.9/10,000/year for hepatitis C. The estimates for hepatitis E and hepatitis G were 4.3/10,000/year and 4.1/10,000/year, respectively.
Most treatment strategies are directed towards the patient's symptoms. If an underlying cause is discovered, various treatment options may be considered. These include vaccination, medications to treat or prevent viral hepatitis, liver function tests for screening in case a hepatitis is a contributing factor, or transplantation if the condition proves fatal or is refractory.
We identified a strong risk of HCC development in familial cases. This indicates a high level of familial risk for HCC, and therefore of familial risk for other diseases predisposing to HCC. Further research is warranted for other cancers in these families.
A new drug, telbivudine, has been approved by the US Food & Drug Authority for treating hepatitis B virus-related liver diseases. A more recent development is peginterferon and ribavirin which are effective in treating chronic hepatitis C, but are still more efficacious when used together with other medications in treating hepatitis C and C virus-related liver diseases.
A single prior NS5A assay result is unlikely to influence subsequent decisions on treatment, but if a patient receives two sofosbuvir/velpatasvir doses from 4 weeks apart, both viral assays should be required to determine the effectiveness of sofosbuvir/velpatasvir. Further clinical and virologic testing should be considered in patients with cirrhosis or a serum creatinine >2 mg/dL.
This was a randomized clinical trial assessing the relative effectiveness and safety of sofosbuvir/velpatasvir and a comparison to placebo in HCV treatment-naïve patients in 24 weeks to treatment end for a variety of adverse covariates including liver fibrosis. Relative to placebo there was no evidence of increased risk of SAE, including worsening of cirrhosis which were both significantly lower in patients treated with sofosbuvir/velpatasvir.
Sofosbuvir/velpatasvir was shown to be safe and effective in treatment-naive and previously treated patients with HCV genotype 1. More patients in both groups (80%) had a sustained response compared with the placebo group (65%). There are limited long-term data on safety and efficacy in patients with cirrhosis and/or compensated cirrhosis.
This evidence suggests that people treated with sofosbuvir/velpatasvir might benefit from some or all of the same considerations that may be applied to other DAAs such as glecapreant and daclatasvir. The use of NS3/4A protease inhibitors prior to the adoption of sofosbuvir/velpatasvir may have shielded it from the emergence of sofosbuvir-resistant variants. However, the use of the same NS3/4A inhibitors post-sofosbuvir does not preclude the development of resistance to sofosbuvir/velpatasvir.