The natural history of HCV infection is quite variable but is notable for a strong propensity to become chronic. Thus, as many as 85% of those individuals infected with HCV develop persistent infection marked by the ongoing presence of HCV RNA in serum for more than 6 months after the onset, although the rate of chronicity appears to be lower among younger individuals.
Some of the factors thought to contribute to severity of chronic chronic hepatitis C include older age at infection, male gender and alcohol consumption. Once cirrhosis has developed, further progression may result in hepatic decompensation or the development of HCC.
Hepatic decompensation in cirrhosis due to hepatitis C is very similar to liver failure associated with other forms of chronic liver disease. Features of decompensation such as ascites, jaundice and bleeding from esophageal varices occur in about 30% of patients with cirrhosis over a period of 10 years. Once features of hepatic decompensation have occurred, the mortality rate from liver disease increases to approximately 10% per year.
For this reason, hepatic decompensation due to hepatitis C represents an indication for liver transplantation.
Cryoglobulinemia is defined by the presence of cryoglobulins in serum. These are abnormal immunoglobulins that characteristically precipitate out in the cold and can redissolve when warmed. Low levels of cryo-globulins can be detected in as many as 40-50% of patients with chronic hepatitis C but are associated with symptoms only rarely, presumably when high levels are present.
Symptoms of cryoglobulinemia include joint aches and skin rashes. The presence of palpable purpura on the lower legs is a characteristic feature of cryoglobulinemia. In as many as 70% of cases, cryoglobulinemia is associated with HCV infection, in the form of type II or 'mixed' cryoglobulinemia.
This may some-times be associated with membranoproliferative glomerulo-nephritis (MPGN) which may result in proteinuria (sometimes severe enough to cause the nephrotic syndrome), hypertension and renal insufficiency. Other complications of cryoglobulinemia include peripheral neuropathy and B-lymphocyte malignancies (rarely). Cryoglobulinemia may be diagnosed by the presence of the typical clinical features with cryoglobulins in serum.
The assay for cryoglobulins in serum is not entirely reliable as it depends on the correct handling of blood specimens. The presence of high titers of rheumatoid factor may also indicate the presence of cryoglobulinemia http://www.nlm.nih.gov/medlineplus/ency/article/000540.htm.
Porphyria cutanea tarda (PCT) is a form of porphyria associated with deficiency of the enzyme uroporphyrinogen decarboxylase. The acquired form is by far the most common and is usually associated with some form of liver disease. In as many as 70% of cases, the underlying liver disease is caused by chronic HCV infection. The clinical features of PCT include photosensitivity with blistering lesions on the hands and facial hirsutism.
Liver biopsy often shows hepatic fibrosis and iron overload in addition to the usual features of chronic hepatitis C. Many other conditions have been linked with chronic HCV infection, although a causal relationship may not have been definitively established. Conditions probably associated with hepatitis C include sialadenitis (sometimes with Sjogren syn-drome), lichen planus and glomerulonephritis not associated with cryoglobulinemia.
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