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Chronic Hepatitis

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Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs,

A diagnosis of chronic hepatitis should be made firmly once liver disease has been present on clinical or other grounds (e.g., biochemical abnormalities, viral markers etc.) for at least 6 months. Until recently chronic hepatitis was classified into persistent (milder disease) and active (more serious disease). However, clinical course and prognosis of chronic hepatitis mainly depend on the cause and the current trend is to specify the aetiology together with pathohistologic findings if known (e.g., chronic hepatitis C with mild periportal ‘piecemeal?necrosis and no evidence of fibrosis, idiopathic chronic hepatitis with significant bridging necrosis and development of some fibrous septa). 

The major causes of chronic hepatitis are hepatitis B and C viruses, but it is unclear what is responsible for persistent damage of the liver. It appears that direct viral damage is less important factor than damage caused by activation of the immune system against viral infection. Idiopathic cases in absence of viral infection or other toxic cause may be induced by an autoimmune process as there is substantial evidence of immunologic hepatocellular injury and damage. However, direct proof of this link is still missing as autoantibodies against liver cells have not been demonstrated (activated lymphocytes are probably more important for hepatocyte destruction).

Clinical features:  < BACK TO TOP >

           About 1/3 of cases follow acute hepatitis, but most develop insidiously without acute hepatitis.

           Clinical features may vary and many patients are asymptomatic and liver involvement is discovered incidentally by the testing of blood; this is especially the case in chronic hepatitis C.

           Sometimes patients present with fatigue, arthralgia, poor appetite, nausea, fatty food intolerance, upper abdominal discomfort, especially over the liver, or even low-grade fever.

           Jaundice is variable; it could be absent or of various intensity.

           Idiopathic, presumably autoimmune form, occurs more frequently in young women, with involvement of other organs in form of acne, amenorrhoea (absence of menstruation), ulcerative colitis, pulmonary fibrosis, glomerulonephritis, haemolytic anaemia and hypothyroidism.

           The clinical course is also highly variable; patients may experience spontaneous remission or may have mild disease without progression for years; some patients have rapidly progressive disease and develop cirrhosis within a few years.

           Patients with long-standing HBV or HCV infection are at a substantially increased risk for hepatocellular carcinoma.

Diagnosis:  < BACK TO TOP >

           Physical examination is usually normal but may show slight tenderness over the liver and slight hepatomegaly (enlargement of the liver).

           Hepatocellular damage is reflected in variably increased aminotransferase (ALT and AST), plasma bilirubin (usually both conjugated and unconjugated) and alkaline phosphatase (moderate cholestasis); hypoalbuminaemia occurs with more advanced liver damage.

           In viral chronic hepatitis it is possible to detect HBsAg, HBeAg and HBV-DNA (markers of hepatitis B infection), or and HCV-RNA (markers of hepatitis C virus infection); anti-HCV antibody is not protective and its presence indicates active infection.

           Autoimmune form is suggested when markers of viral infection are absent and markers of autoimmunity may be present such as antinuclear antibodies, anti smooth muscle antibodies (anti-actin), rheumatoid factor, antimitochondrial antibodies, as well as elevated levels of IgG.

           Percutaneous liver biopsy is essential for assessment and prognosis of hepatocellular damage.

           In Wilson’s disease it is usual to find low blood copper level, low serum ceruloplasmin (copper binding protein in blood), raised urinary copper excretion and excess of hepatic copper in biopsy samples.

           In haemochromatosis serum ferritin is greatly increased, as well as the plasma iron with increased saturation of transferrin (above 50%, normally around 30%); if necessary liver biopsy will demonstrate iron overload.

Management  < BACK TO TOP >

           Management generally has to target the cause of chronic hepatitis.

           Chronic viral hepatitis is treated with a combination of interferon alpha [Roferon, Intron-A] given by injection and oral ribavirin [Rebetol], which is a synthetic guanosine nucleoside analogue. This regime given over 6-12 months leads to long-term clearance of signs of hepatitis viruses and improvement in liver inflammation in around 40% of treated patients (interferon alone is effective in only 20% of cases).

           Autoimmune chronic hepatitis is treated with corticosteroids (they are contraindicated in viral hepatitis). Initially, prednisolone [Delta-Cortef, Panafcortelone, Solone] is given in larger doses, and later maintenance therapy with smaller doses is required for at least 2 years. Immunosuppressive drugs such as azathioprine [Imuran] may be added to corticosteroid schedule.

           Liver transplantation is an option in end stage with 80% 7 years survival. Unfortunately viral infection universally recurs and affects the transplanted liver; this is more prominent in chronic hepatitis B then in C.

Prognosis  < BACK TO TOP >


Nutrition < BACK TO TOP >

Nutrition that alleviate or prevent Chronic Hepatitis :-

Herbs < BACK TO TOP >

Herbs that alleviate or prevent Chronic Hepatitis :-

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