Hepatic encephalopathy (HE) is defined as a metabolically induced, potentially reversible, functional disturbance of the brain that may occur in acute or chronic liver disease. Standardized nomenclature has been proposed but a standardized approach to the treatment, particularly of persistent, episodic and recurrent encephalopathy associated with liver cirrhosis has not been proposed. This review focuses on the pathogenesis and treatment of HE in patients with cirrhosis. The pathogenesis and treatment of hepatic encephalopathy in fulminant hepatic failure is quite different and is reviewed elsewhere.
Of recent interest has been the description of a serum antibody reacting with the centromere portion of chromosomes in tissue culture cells and found in patients with scleroderma, especially of the CREST type.7'-0 We have looked for anticentromere antibody in serum from 1 10 consecutive patients presenting with PBC, 20 of whom had scleroderma, and from 80 patients with other forms of liver disease, including the autoimmune variety of chronic active hepatitis (CAH).
Materials and methodsThe series comprised 110 consecutive patients with biopsy-proved PBC, of whom 97 (88.2%) were women and 13 (11.8%) were men. Antimitochondrial antibody was present in 94 (85 5%) patients, antinuclear antibody in 11 (10%), and anti-
Combination treatment with pegylated interferon (Peg-IFN) and ribavirin remains the gold standard in the treatment of chronic hepatitis C. This therapy is limited by many side-effects including anaemia, neutropenia and reduced quality of life. The use of adjuvant agents to reduce the frequency of dose reductions because of haematological side-effects has been proven to be effective but there are few reports of what effect the use of these adjuvant therapies is having on sustained virological response (SVR). The aim of the study was to assess the clinical impact on sustained virological response of adjuvant therapies during combination therapy with Peg-IFN and ribavirin for chronic hepatitis C. A total of 132 patients, 96 males, were included in the study. The overall SVR was 66.7%, with 50% of genotype 1/4/6 (n = 27/54) patients achieving SVR and 78.2% of genotypes 2/3. The overall SVR of the treatment naïve patients (83/121) was 68.6%. Fifty-one of these patients were genotype 1 with 49.0% (25/51) of this group achieving SVR. The genotype 2/3 group of treatment naïve patients reached an SVR of 82.9% (58/70). Adjuvant therapy was used in 57 patients (43.8%). With the use of supportive adjuvant therapy, we achieved an overall SVR of 66.7% and in treatment naïve patients 68.6%. In genotype 1 patients, SVR rates of up to 46% have been reported in previous studies without the use of erythropoietin and granulocyte colony stimulating factor. We have demonstrated the SVR for genotype 1 can be improved to 50% overall.
Transjugular intrahepatic portosystemic shunt (TIPS) is an artificially created conduit between the portal and systemic vascular system in the liver performed percutaneously via radiological guidance. It is used mainly in conditions causing portal hypertension and its resulting complications. It reduces portal pressure by diverting portal blood flow into the systemic circulation. Hepatic encephalopathy is the most common complication following TIPS insertion and tends to present fairly early. We describe a case of hepatic encephalopathy as an unusual late complication of TIPS insertion (first presenting six years after) for non-cirrhotic portal hypertension caused by nodular regenerative hyperplasia in an HIV-positive patient on highly active antiretroviral therapy.
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