Hepatitis C Support Group

Hepatitis C is a blood-borne viral disease which can cause liver inflammation, fibrosis, cirrhosis and liver cancer. The hepatitis C virus (HCV) is spread by blood-to-blood contact with an infected person's blood. Many people with HCV infection have no symptoms and are unaware of the need to seek treatment. Hepatitis C infects an estimated 150-200 million people worldwide. It is the leading cause of liver transplant.

Hepatitis C is an inflammation of the liver caused by infection with the hepatitis C virus (HCV). The hepatitis C virus is one of five known hepatitis viruses: A, B, C, D, E. Hepatitis C was previously known as non-A, non-B hepatitis prior to isolation of the virus in 1989.

Acute hepatitis C refers to the first 6 months after infection with HCV. Remarkably, 60% to 70% of people infected develop no symptoms during the acute phase. In the minority of patients who experience acute phase symptoms, they are generally mild and nonspecific, and rarely lead to a specific diagnosis of hepatitis C. Symptoms of acute hepatitis C infection include decreased appetite, fatigue, abdominal pain, jaundice, itching, and flu-like symptoms.

Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months. The course of chronic hepatitis C varies considerably from one person to another. Virtually all people infected with HCV have evidence of inflammation on liver biopsy, however, the rate of progression of liver scarring (fibrosis) shows significant inter-individual variability. Recent data suggests that among untreated patients, roughly 1/3 progress to liver cirrhosis in less than 20 years. Another 1/3 progress to cirrhosis within 30 years. The remainder of patients appear to progress so slowly that they are unlikely to develop cirrhosis within their lifetime. Factors that have been reported to influence the rate of HCV disease progression include age (increasing age associated with more rapid progression), gender (males have more rapid disease progression than females), alcohol consumption (associated with an increased rate of disease progression), HIV coinfection (associated with a markedly increased rate of disease progression), and fatty liver (the presence of fat in liver cells has been associated with an increased rate of disease progression).

Symptoms specifically suggestive of liver disease are typically absent until substantial scarring of the liver has occurred. However, hepatitis C is a systemic disease and patients may experience a wide spectrum of clinical manifestations ranging from an absence of symptoms to debilitating illness prior to the development of advanced liver disease. Generalized signs and symptoms associated with chronic hepatitis C include fatigue, flu-like symptoms, muscle pain, joint pain, intermittent low-grade fevers, itching, sleep disturbances, abdominal pain (especially in the right upper quadrant), appetite changes, nausea, dyspepsia, cognitive changes, depression, headaches, and mood swings.

Once chronic hepatitis C has progressed to cirrhosis, signs and symptoms may appear that are generally caused by either decreased liver function or increased pressure in the liver circulation, a condition known as portal hypertension. Possible signs and symptoms of liver cirrhosis include ascites (accumulation of fluid in the abdomen), bruising and bleeding tendency, bone pain, varices (enlarged veins, especially in the stomach and esophagus), fatty stools (steatorrhea), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy.

Current standard of care treatment is a combination of (pegylated) interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on genotype.

Should treatment with pegylated ribivirin-interferon not return a 2-log viral reduction after 12 weeks, the chance of treatment success is less than 1%.

Current indication for treatment include patients with proven hepatitis C virus infection and persistent abnormal liver function tests. Sustained cure rates (sustained viral response) of 75% or better occur in people with genotypes HCV 2 and 3 in 24 weeks of treatment, about 50% in those with genotype 1 with 48 weeks of treatment and 65% for those with genotype 4 in 48 weeks of treatment. About 80% of hepatitis C patients in the United State have genotype 1. Genotype 4 is more common in the Middle East and Africa.

Treatment during the acute infection phase has much higher success rates (90%+) with a shorter duration of treatment.

Those with low initial viral loads respond much better to treatment than those with higher viral loads (>2 million virons/ml). Current combination therapy can only be supervised by physicians in the fields of gastroenterology, hepatology and infectious disease.

The treatment is physically demanding for some, particularly those with a prior history of drug or alcohol abuse. It can qualify for temporary disability in some cases. A substantial percentage of patients will experience a panoply of side effects ranging from a 'flu'-like syndrome (the most common, experienced for a few days after the weekly injection of interferon) to severe adverse events including anemia, cardiovascular events and psychiatric problems such as suicide ideation and attempts. The latter are complemented and escalated by the general physiological stress experienced by the patient.

In addition to the standard treatment with interferon and ribavirin, several studies have shown higher success rates when the antiviral drug amantadine (Symmetrel®) is added to the regimen. Sometimes called "triple therapy", it involves the addition of 100mg of amantadine twice a day, for a total of 200mg per day. Studies indicate that this may be especially helpful to "nonresponders" - patients who have not been successful in previous treatments using interferon/ribavirin only.[12] Currently, amantadine is not approved for treatment of Hepatitis C, and studies are ongoing to determine when it is most likely to benefit the patient.

Current guidelines strongly recommend that hepatitis C patients be vaccinated for hepatitis A and B if they have not yet been exposed to these viruses, as this would radically worsen their liver disease.

Alcoholic beverage consumption accelerates HCV associated fibrosis and cirrhosis, and makes liver cancer more likely; insulin resistance and metabolic syndrome may similarly worsen the hepatic prognosis.