It is estimated that 82% of the 227 000 people living with hepatitis C in Australia have been diagnosed.4 However, many of these people have either not been informed of their diagnosis or are not aware of the implications of chronic viral hepatitis. Before 2016, fewer than one in four Australians with chronic hepatitis C had been treated and approximately one in five were undiagnosed. Because hepatitis C is a major cause of chronic liver disease, cirrhosis and liver cancer, it is essential that all people with chronic infection are identified so that treatment can be provided.
Anyone at risk of contracting a blood-borne infection should be tested for hepatitis C, as should anyone with evidence of chronic liver disease or abnormal liver enzymes.2 Injecting drug users should be a major focus for testing as they represent approximately 80% of infected people. Other important groups include migrants from high-prevalence countries or regions such as Egypt, Pakistan, Mediterranean and eastern European countries, Africa and Asia.
Patients should be screened using a serological test for anti-hepatitis C antibodies. If screening is positive, diagnosis requires confirmation of infection using a polymerase chain reaction (PCR)-based assay to detect hepatitis C RNA. If viral RNA is present, genotype and viral load testing should be performed to determine the appropriate treatment regimen and duration. The Figure shows a simplified schema for the management of patients with chronic hepatitis C.3 Patients who have antibodies to hepatitis C but test negative for viral RNA (confirmed on two occasions at least one month apart) do not have chronic hepatitis C. They may have spontaneously cleared infection, been previously successfully treated, or have a false positive antibody result.
All patients should be assessed for liver disease and comorbidities. Having a history of excessive alcohol intake, being overweight or obese, and having type 2 diabetes or other liver disease significantly increase the chance that an individual has advanced fibrosis or cirrhosis. Laboratory testing should include assessment of renal function, blood glucose, other blood-borne infections such as HIV and hepatitis B, liver enzymes and full blood count. An elevated aspartate aminotransferase (AST) and low platelet count are suggestive of advanced fibrosis or cirrhosis.
Fibrosis assessment is essential before starting antiviral treatment as the results can change after treatment and people at risk of long-term complications such as hepatocellular carcinoma can be missed. Many people with a low risk of advanced fibrosis, such as younger patients with a short duration of infection or people without a history of excessive alcohol intake or metabolic risk factors, can be assessed using simple validated serum-based scores such as the APRI score (AST to Platelet Ratio Index)5 and Hepascore.6 A low score excludes cirrhosis, and patients with a high score (e.g. an APRI score ≥1) have an increased likelihood of cirrhosis and should be assessed further.
Patients requiring more accurate assessment of liver fibrosis than can be determined by serum markers may benefit from transient elastography (Fibroscan).7 Fixed machines in liver clinics, or portable machines in community settings, offer rapid, accurate and noninvasive assessment of fibrosis. Access to transient elastography is increasing and can generally be arranged through the local health district or other providers. As with serum markers, a low score is very accurate for excluding cirrhosis, but a median liver stiffness of at least 12.5 kPa is associated with a significantly higher chance of cirrhosis. These patients require specialist review and long-term surveillance for hepatocellular carcinoma and other liver disease complications.