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The - SystemChronic Hepatitis Synonyms : 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 :- (source : -) |
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