Liver Disease in Clinical Practice by Tim Cross

Author:Tim Cross
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

Viral genotype is a key factor in determining response to antiviral therapy and affects clinical progression. Genotype 3 infection in particular has a worse prognosis and high risk of complications, such as diabetes.

Presentation

The incubation for HCV infection is between 6 and 10 weeks (WHO data). Eighty per cent of patients are asymptomatic during acute infection. Symptomatic patients present with an insidious onset of acute hepatitis with anorexia, nausea, fatigue and fevers. Jaundice is seen in 25 % of patients. Fulminant hepatitis is extremely rare.

After infection 25 % of patients will clear the virus spontaneously over a period of 2–6 months. The remaining 75 % of patients develop chronic infection.

The majority of chronically infected patients are asymptomatic and have a normal clinical examination or have non-specific symptoms like tiredness and poor concentration (“brain fog”).

Chronic infection is most often picked up through screening of at risk individuals (e.g. at needle exchange programmes or through the incidental finding of abnormal liver function tests). If not picked up incidentally, chronic infection does not normally present until patients develop complications of advanced liver fibrosis such as ascites, variceal bleeding or encephalopathy or impaired synthetic function. Other symptoms and signs are associated with advanced liver disease and include mental disturbance (hepatic encephalopathy), jaundice, abdominal swelling with ascites and peripheral oedema. Up to 19 % of untreated patients with cirrhosis will eventually develop hepatocellular carcinoma.

Extrahepatic manifestations in CHC are relatively common and occur in up to 74 % of patients, although they may not be identified as related to CHC by the patient or their carer. The most common presenting symptoms include arthralgia, paraesthesia and myalgia. Circulating immune complexes, autoimmune processes and mononuclear cell dysfunction are key in the pathogenesis of these non-liver phenomena. Chronic infection is linked to an increase in insulin resistance and type 2 diabetes mellitus. Consequently, infection increases cardiovascular risk, in particular cerebrovascular disease.

Circulating immune complexes may lead to a mixed (type 2a) cryoglobulinaemia that can present in a variety of ways, ranging from asymptomatic detection of circulating mixed cryoglobulin complexes (seen in 40–50 % of CHC patients) to cryoglobulinaemic vasculitis. Serum cryoglobulin and complement levels do not correlate with disease severity. Clinical manifestations include purpuric skin lesions, arthralgia, polyneuropathy and membranoproliferative glomerulonephritis.

CHC infection is associated with autoantibody production, and the many autoimmune diseases have been described. Idiopathic thrombocytopenic purpura (ITP) is an autoimmune condition with antibodies against platelet membrane proteins and frequently seen in conjunction with CHC, in a much higher incidence than the general population.

Links between HCV infection and lung disease have been reported, in particular pulmonary fibrosis. The mechanism of disease, at present, is not fully defined.

Lichen planus is a pruritic dermatological condition from a cell-mediated immune response and is seen with increased incidence in patients with CHC infection, and vice versa.

Other conditions associated with CHC include porphyria cutanea tarda, Sjogren’s syndrome and lymphoproliferative disorders, in particular non-Hodgkin B-cell lymphoma.

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