Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.
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PMID:Viral hepatitis and cirrhosis. 16 21

A 65 year old woman with lupoid hepatitis developed hepatocellular carcinoma which was diagnosed at an early stage. She had no history of blood transfusion and serum hepatitis B virus markers were negative. Prednisolone and 6-mercaptopurine were administered for the treatment of lupoid hepatitis. A hepatocellular carcinoma was detected by the elevation of serum alpha-fetoprotein and imaging studies. A tumour, 1.4 cm in diameter, was located in the lateral segment of the left hepatic lobe. It was resected by hepatic subsegmentectomy. Histological study showed a hepatocellular carcinoma of Edmondson type II against a background of posthepatitic cirrhosis. The patient was in good condition 2.5 years after the operation.
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PMID:Resected case of hepatocellular carcinoma associated with lupoid hepatitis. 256 48

Immune complexes were investigated in the clinical course of 35 patients with the liver disease diagnosed by clinical and laboratory criteria, including the liver biopsy. Immune complexes were assayed by use of radio-labelled polyclonal rheumatoid and C1q as reactants with immune complexes. Although the highest amounts of immune complexes were determined in a few number of sera from patients with primary biliary cirrhosis, significantly higher amounts of immune complexes were observed in sera from patients with fulminant hepatitis, liver cirrhosis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma. However, no significant increase in immune complexes was seen in the clinical course of patients with chronic aggressive hepatitis (2A), chronic persistent hepatitis and acute hepatitis. Clinical follow-up studies of patients with higher amounts of immune complexes showed significant changes in the amounts of immune complexes in parallel with clinical, biochemical and immunological variables. The ultracentrifugal analysis demonstrated that immune complexes involved in the liver disease seemed to be larger than 19s in the size, since their concentration fluctuated according to the clinical course, although smaller complexes sedimenting at 7s and those between 8s and 19s were recognized without any significant changes in the clinical course.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 7. Immune complexes in the clinical course and their ultracentrifugal analysis. 626 81

Anti-liver-specific membrane lipoprotein (anti-LP-1) and anti-Tamm-Horsfall glycoprotein (anti-THGP) rabbit antibodies were found to bind to Chang liver cells, a cultured human hepatocyte cell line, and PLC/PRF/5, a hepatoma cell line. The antibodies bound were determined by an immunofluorescence staining and a semiquantitative 125I-protein A binding assay. The 125I-protein A binding assay was successfully adapted to determine anti-hepatocyte plasma membrane antibodies in sera of patients with lupoid hepatitis and chronic active hepatitis. The percentage of 125I-protein A bound in 10 normal subjects were 1.5 +/- 0.4 (mean +/- standard deviation) for PLC/PRF/5 and 1.6 +/- 0.6 for Chang liver cell, while those in 2 patients with lupoid hepatitis were 7.2 +/- 0.3, 5.9 +/- 0.1, and those in 8 patients with chronic active hepatitis 3.9 +/- 1.3, 3.2 +/- 1.5, respectively. Furthermore, a blocking study revealed that LP-1 and THGP were partially involved in antigen sites recognized with anti-hepatocyte plasma membrane antibodies in sera of a patient with lupoid hepatitis. The retaining ability of antibody binding to the hepatocytes after the absorption with non-hepatocyte cells suggested the presence of antibodies specific for the hepatocyte plasma membrane in the patient's serum.
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PMID:Hepatocyte plasma membrane antigens. I. Determination of antibodies bound to the hepatocyte plasma membrane by 125I-protein A binding assay. 631 64

We prospectively analysed the liver histology and clinical data of 45 patients with a clinical diagnosis of chronic hepatitis. There was more chronic active hepatitis than chronic persistent hepatitis. In both, there were more men than women except in the subgroup of lupoid hepatitis, where all were women. As a group, chronic persistent hepatitis patients tended to have less severe abnormalities in biochemical liver function tests. Chronic hepatitis B infection accounted for 38% (17/45) of all patients. Of these, 53% (9/17) were Maori or Polynesian, although they only account for approximately 1/5 of the European population in Auckland. This correlated with the known high hepatitis B surface antigen carrier frequency in the Maori and Polynesian and the high incidence of primary hepatocellular carcinoma in this ethnic group. The present study also showed there are relatively few chronic active hepatitis patients, those with immunological abnormalities (lupoid hepatitis, 5/45), who are likely to respond to steroid treatment.
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PMID:A clinical-pathological study on chronic hepatitis in Auckland. 659 Oct 11

Inhibition assay of 125I-C1q binding to IgG-p-azobenzamidoethyl Sepharose 6B (IgG-Sepharose) by immune complexes was developed for the detection of circulating soluble immune complexes in the liver disease and was compared with polyclonal rheumatoid factor (pRF) binding inhibition assay and with C1q binding assay. The C1q inhibition assay was proved to be very sensitive, reproducible and rapid. Sucrose density gradient ultracentrifugal analysis showed that the assay could detect aggregates of human IgG (AHGG) larger than 19s. C1q inhibition activity (C1qIA) correlated with severity of the liver disease, defined by histological criteria. The highest C1qIA was observed in sera of patients with primary biliary cirrhosis, followed by liver cirrhosis, fulminant hepatitis, chronic aggressive hepatitis (2B), lupoid hepatitis and hepatocellular carcinoma in the order. There were correlations of C1qIA with serum gamma-globulin levels, sero-positivity for rheumatoid factor and hepatitis B surface antigen, and significant correlations existed also among pRFIA, C1qIA and C1qBA. Ultracentrifugal analysis of sera from patients with the liver disease showed that ClqIA demonstrated two sizes of immune complexes, 7s and larger than 19s, while complexes larger than 8s were seen in pRFIA.
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PMID:Studies on circulating soluble immune complexes of the liver disease. 6. Comparative studies of 125I-pRF inhibition assay, 125I-Clq inhibition assay and 125I-Clq binding assay. 697 71

An 81-year-old woman in whom liver dysfunction had been pointed out 3 years previously was diagnosed as having liver cirrhosis due to lupoid hepatitis. Considering the poor prognosis of cirrhosis and her age, immunosuppressive therapy was not adopted. Nine months later, a small liver tumor was found by ultrasonography and was diagnosed as hepatocellular carcinoma (HCC). The tumor was treated with transcatheter arterial embolization, but grew continuously. She also developed gingival lymphoma that was successfully treated. Three years after initial diagnosis of lupoid hepatitis, she died of hepatic failure. An autopsy was performed and confirmed the clinical diagnosis, liver cirrhosis with HCC. HCC is regarded as a rare complication of lupoid hepatitis, but cases of HCC complicating lupoid hepatitis may increase with progress in treatment methods and elongation of survival. The present case suggests that any malignancy can be developed in long-term surviving patients with lupoid hepatitis.
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PMID:Autopsy case of hepatocellular carcinoma associated with lupoid hepatitis and complicated by malignant lymphoma. 839 33

A 66-year-old woman was diagnosed as having lupoid hepatitis due to the presence of hypergammaglobulinemia, lupus erythematosus cells, and positivity for antinuclear, anti-DNA, and anti-smooth muscle antibodies. None of the serum hepatitis B markers were positive. Symptomatic relief was obtained by prednisolone administration. Five years after the diagnosis of lupoid hepatitis, hepatocellular carcinoma (HCC) was detected by ultrasonography and computed tomography, after which hepatectomy was performed. Although transcatheter arterial embolization was done on two occasions and repeat hepatectomy was performed twice for recurrent HCC, her liver function remained good with the prednisolone treatment. Antibody for hepatitis C virus has been negative since our first check in 1992. As of this writing, the patient has been alive and well 6 years and 2 months after the first hepatectomy. There have been no previous reports of 6-year survival after hepatectomy for HCC associated with lupoid hepatitis.
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PMID:Hepatocellular carcinoma associated with lupoid hepatitis: a review of Japanese reports. 855 6