Hepatitis, Viral: C
D E FI N I T ION
Hepatitis caused by infection with hepatitis C virus (HCV), often following a
chronic course ( 80% cases).
AETIOLOGYHCV
is a small, enveloped, single-stranded RNA virus of the flavivirus family.
As it is an RNA virus, fidelity of replication is poor and mutation rates are high, resulting in
different HCV genotypes, and even in a single patient, many viral quasi-species may be
present.
Transmission
: Occurs via the parenteral route, and at-risk groups include recipients of blood
and blood products prior to blood screening, IV drug users, non-sterile acupuncture and
tattooing, those on haemodialysis and health care workers. Sexual and vertical transmission
is uncommon (1–5%, " risk in those co-infected with HIV).
Pathology/Pathogenesis
: Although HCV is hepatotropic, it is not thought that the virus is
directly hepatotoxic, rather that the humoral and cell-mediated response leads to hepatic
inflammation and necrosis. On liver biopsy, chronic hepatitis is seen and a characteristic
feature is lymphoid follicles in the portal tracts. Fatty change is also common and features
of cirrhosis may be present.
EPIDEMIOLOGY
Common. Prevalence is 0.5–2% in developed countries, with higher
rates in certain areas (e.g. Middle East) because of poor sterilisation practices. Different HCV
genotypes have different geographical prevalence.
HISTORY
Ninety per cent of acute infections are asymptomatic with<10% becoming jaundiced with a
mild flu-like illness.
May be diagnosed after incidental abnormal LFT or in older individuals with complications of
cirrhosis.
EXAMINATION
There may be no signs or may be signs of chronic liver disease in long-standing infection.
Less common extra-hepatic manifestations include:
. skin rash, caused by mixed cryoglobulinaemia causing a small-vessel vasculitis; and
. renal dysfunction, caused by glomerulonephritis.
INVESTIGATIONS
Blood:
HCV serology
: Anti-HCV antibodies, either IgM (acute) or IgG (past exposure or chronic).
Reverse-transcriptase PCR
: Detection and genotyping of HCV RNA. Used to confirm antibody
testing; also recommended in patients with clinically suspected HCV infection but
negative serology.
LFT
: Acute infection causes " AST and ALT, mild " bilirubin. Chronic infection causes 2–8 times
elevation of AST and ALT, often fluctuating over time. Sometimes normal.
Liver biopsy
: To assess degree of inflammation and liver damage as transaminase levels bear
little correlation to histological changes. Also useful in diagnosing cirrhosis as patients
with cirrhosis will require monitoring for hepatocellular carcinoma.
MANAGEMENT
Prevention
Screening of blood, blood products and organ donors, needle exchange schemes
for IV drug abusers, instrument sterilization. No vaccine available at present.
Medical:
Acute
No specific management and mainly supportive (e.g. antipyretics, antiemetics,
cholestyramine). Specific antiviral treatment can be delayed for 3–6 months.
Hepatitis, Viral: C (continued)
Chronic
Combined treatmentwith pegylated interferon-a (cytokine which augments natural
antiviral mechanisms) and ribavirin (guanosine nucleotide analogue) is the treatment
strategy of choice
. HCV genotype 1 or 4: 24–48 weeks
. HCV genotype 2 or 3: 12–24 weeks
Monitoring of HCV viral load is recommended after 12 weeks of treatment to determine
efficacy of treatment. Regular ultrasound of liver may be necessary if the patient has
cirrhosis.
COMPLICATIONS
Fulminant hepatic failure in acute phase (0.5%), chronic HCV carriage,
cirrhosis and hepatocellular carcinoma. Less common are porphyria cutanea tarda, cryoglobulinaemia
and glomerulonephritis.
PROGNOSIS
Approximately eighty per cent of exposed progress to chronic HCV infection,
and of these, 20–30% develop cirrhosis over 10–20 years.
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