Estimated 150-200 million people world wide including 4 million in
the US are infected with hepatitis C, which is spread
by blood to blood contact with the infected person. 10-20,000 deaths year in
the US. The
virus (non A-B) was confirmed in 1988, and named in April of 89. Reliable screening
of blood transfusion was not available until 1992.
Acute Hepatitis C refers to the first 6 months after infection with HCV. Between 60-70% of the people infected develop at most mild nonspecific symptoms during
this phase. Symptoms during acute hepatitis C infection include decreased appetite,
fatigue, abdominal pain, jaundice, itching, and flu-like symptoms. . Antibodies are generally detectable within 3-12 weeks of infection.
Approximately 20-30 of the persons infected clear the virus from their bodies during the acute phase as shown by normalization
in liver function tests as well as plasma clearance of HCV-RNA. The remaining
70-80% of patients develop chronic hepatitis C; i.e., infection lasting more than 6 months. Recent
studies have shown that treatment during the acute phase of genotype 1 infections has a greater than 90% success rate with
half the treatment time required for chronic infections. The natural course of chronic C varies considerably. The rate of progression
to liver scarring (fibrosis), with approximately 1/3rd progress to liver cirrhosis in less than 20 years; another
1/3rd within 30 years. HIV co-infection is associated with a markedly
increased rate. Age and alcohol consumption are other factors. Symptoms specifically suggestive of liver disease are typically absent until substantial scarring of the
liver has occurred. With cirrhosis there is generally decreased liver function
and increased pressure in the liver circulation (portal hypertension). The level of elevation of liver tests do not correlate well with the amount of liver injury uncovered through biopsy. Viral genotype and viral load also do not
correlate well. Liver biopsy is the best test; radiographic studies such as ultrasound
or CT scan do not show liver injury until it is fairly advanced.
Chronic hepatitis C, more than other forms of hepatitis,
is diagnosed because of extrahepatic manifestations associated with the presence of HCV such as thyroiditis (inflammation of the thyroid) with hyperthyreosis or hypothyreosis, porphyria cutanea tarda, cryoglobulinemia (a form of vasculitis)[8] and glomerulonephritis (inflammation of the kidney), specifically membranoproliferative glomerulonephritis (MPGN)[9]. Hepatitis C is also associated with sicca syndrome, thrombocytopenia, lichen planus, diabetes mellitus and with B-cell lymphoproliferative disorders.
The Hepatitis C virus (HCV) is
a small (50 nm in size), enveloped, single-stranded, positive sense RNA virus in the families Flaviviridae.
Anti-HCV antibodies indicate exposure to the
virus, but cannot determine if ongoing infection is present. All persons
with positive anti-HCV antibody tests must undergo additional testing for the presence of the hepatitis C virus itself to
determine whether current infection is present. The presence of the virus is tested for using molecular nucleic acid testing
methods such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), or branched DNA (b-DNA). All
HCV nucleic acid molecular tests have the capacity to detect not only whether the virus is present, but also to measure the
amount of virus present in the blood (the HCV viral load). The HCV viral load is an important factor in determining the probability
of response to interferon-based therapy, but does not indicate disease severity nor the likelihood of disease progression. There are 6 major genotypes of C which are numberically indicated. HCV genotype testing is used to determine the required length and potential response to interferon-base
therapy.
Approximately 6 out of 100 births result in the trnasmission,
when the mother is HCV RNA positive. There is a small chance (~ 0.65/year)
will clear of HCV without treatment. (Tramission runs 19% for HIV). Current treatment is a combination of pegylated interferon alpha (brand names Pegasys and PEG-Intron) and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on genotype. Indications 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,[20]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 States have genotype 1. Genotype 4 is more common
in the Middle East and Africa. Should treatment with pegylated
ribivirin-interferon not return a 2-log viral reduction or complete clearance of RNA (termed early virological response)
after 12 weeks for genotype 1, the chance of treatment success is less than 1%.
Treatment during the acute infection phase has
much higher success rates (greater than 90%) with a shorter duration of treatment (but balance this against the 80% chance
of spontaneous clearance without treatment. Treatment during the acute infection
phase has much higher success rates (greater than 90%) with a shorter duration of treatment (but balance this against the
80% chance of spontaneous clearance without treatment.
