Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-nine liver disease patients (7 chronic persistent hepatitis, CPH; 10 chronic active hepatitis, CAH; 13 liver cirrhosis, LC; 9 primary hepatocellular carcinoma, PHC, without LC; and 10 PHC with associated LC) and 20 controls were assessed for their serum alpha-L-fucosidase (ALF) and alpha-fetoprotein (AFP) levels and several routine liver injury parameters. Tumor diameter in those with hepatic cancer was assessed by angio-CT. Only ALF and AFP were significantly greater in patients with PHC and PHC + LC patients as compared to patients with LC alone. At an accepted cutoff level of 500 ng/ml, the AFP level provided 43% false negative tests. On the other hand, an ALF level exceeding 740 mumol/hr/ml provided a sensitivity of 84% with a specificity of 94%. No relationship between the ALF level and Child's criteria or with any liver injury parameter was evident. Considering all individual values, the ALF, rather than the AFP, correlated with tumor size. This finding suggests the ALF level may be of value in the early detection of PHC as well as in the follow-up of patients treated for PHC.
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PMID:Serum alpha-L-fucosidase. A more sensitive marker for hepatocellular carcinoma? 171 99

Six acute phase proteins (haptoglobin, alpha 1-acid glycoprotein, alpha 1-antitrypsin, alpha 2-macroglobulin, C reactive protein and transferrin) have been measured in the sera of chronic liver disease (CLD) patients with different aetiology (viral, autoimmune and alcoholic) and histology (steatosis, chronic persistent hepatitis, chronic active hepatitis, cirrhosis), and in patients with liver cancer. 1) The most striking changes concerned alpha 2-macroglobulin (increased) and haptoglobin (decreased) levels. 2) Transferrin was lower in alcoholic liver disease than in viral CLD, CRP was lower in autoimmune than in viral or alcoholic CLD, and alpha 1-acid glycoprotein was lower in viral and alcoholic CLD than in autoimmune CLD. Acute phase protein assay may prove useful in differential diagnosis, particularly when specific markers are not available (autoimmune, non A, non B, alcoholic liver diseases). 3) No significant differences related to aetiology (B, non A non B, D viruses) were observed in viral CLD. 4) Patients who progressed to CLD after acute viral hepatitis type B or non A non B did not show different APP levels from those who had recovered when tested 8-12 months after the acute phase. 5) The pattern of APP changes observed in primary liver cell carcinoma was different from both the cirrhotic pattern and the pattern presented by other tumours with or without liver metastasis.
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PMID:Acute phase proteins in chronic and malignant liver diseases. 245 53

During the last eighteen years (1970-1987) at the Infectious Diseases Clinic of the University of Pavia, Ospedale Policlinico S. Matteo, IRCCS, Pavia (referral Center for hepatitis in our district: 502534 inhabitants) we observed 4238 patients (2706 M = 63.8%; 1532 F = 36.2%) admitted with presumptive diagnosis of hepatitis. The male to female sex ratio was 1.78 and average age was 38 (1-90) years. Acute viral hepatitis was diagnosed in 3238 patients (76.4%), 1960 of which were males (60.5%) and 1278 (39.5%) females, with an average age of 35 (1-88) years. The possible route of transmission was: drug addition in 487 patients (15%), blood transfusion in 464 (14.3%), other (sexual, professional, familiar) in 332 (10.3%), unknown in 1955 (60.4%). Chronic hepatitis (CH) was diagnosed according to the European Association for the Study of the Liver (EASL) and to the International Association for the Study of the Liver (IASL) in 848 patients (20%), 704 M(83%) and 144 F (17%) with an average age of 48 (2-90) years. 463 patients (54.5%) were biopsied during admission, 385 (45.5%) received definitive diagnosis by clinical and previous histologic records. CAH was found in 268 (57.9%), CPH in 161 (34.8%) and CLH in 20 (4.3%) patients. Other liver diseases (steatosis, cirrhosis, HCC) were identified in 152 subjects (3%). The prevalence of A, B, NANB and Delta hepatitis virus and HI virus in the acute disease was respectively of 5.4%, 54.8%, 33.9%, 0.28% and 0.77%. In CH the HBV aetiology accounted for 49.1%, NANB virus for 44.5%, co/super infection with HDV for 15%. Among factors involved in pathogenesis of chronic hepatitis we focused attention on drug addition which was found in 129 (28.7%) patients, blood transfusion in 70 (15.6%), HIV infection in 35 of 166 (21.1%). The data still demonstrate the high prevalence of HBV aetiology of CH and existence of co-factors in the pathogenesis of chronicity. The lack of markers for NANB infection persists as the main problem in the diagnosis of liver disease. This work was supported by grant 40% from M.P.I.: "Epatiti virali acute e croniche"....
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PMID:The spectrum of chronic hepatitis in the last two decades in a university hospital for infectious diseases. 249 35

The high rate of infection with hepatitis B virus in certain defined populations in industralized countries and among the general population in many non-industrialized countries stresses the need for hepatitis B vaccines. Hepatitis B, one of at least six different forms of viral hepatitis, may progress to chronic liver disease, including chronic persistent hepatitis, chronic active hepatitis, cirrhosis and primary liver cancer. Primary liver cancer is one of the ten most common cancers in the world today. Immunization against hepatitis B is required therefore for groups at high risk of infection according to epidemiological patterns, socioeconomic factors, cultural and sexual practices and the environment.
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PMID:Hepatitis B vaccines. 295 11

The attempt to divide the large group of chronic HBsAg carriers into "healthy" vs. those with chronic hepatitis of various intensities is sometimes difficult. The major problems are overlap in clinical manifestations, hepatic test results and histologic as well as virologic features. Nevertheless, this separation is not only conceptually important, but may also be useful in patient management, particularly because of the risk of transition to cirrhosis and HCC. Although at least 75% of patients with HCC associated with HBV have cirrhosis, the time point at which the cirrhosis developed is not established, particularly since the vast majority of chronic HBsAg carriers fall into the "healthy" category. Important unanswered questions are, therefore: how often do "healthy" carriers develop cirrhosis and/or HCC, including the time relations between the two? Does the transformation to HCC result from one or several identifiable acute events in the "healthy" carrier (or in mild CPH) or is it a gradual process of progressing chronic hepatitis B in which intercurrent exacerbations may still play a role? Do the quantitative observations as to the relation between persistent HBV infections and HCC in the East apply to Western countries? Our hypothesis concerning pathogenesis is based on pathologic, molecular, clinical and epidemiologic observations and concepts, and is supported by studies of hepadna virus-infected animals. This thesis proposes that integration of HBV DNA into host chromosomes in acute or chronic hepatitis or during the "healthy" carrier state corresponds to an initiation event similar to that described in chemical carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of the hepatitis B virus carrier state to hepatocellular carcinoma. 303 25

Long term follow up of 16 homosexual men and 78 intravenous drug abusers who were chronic carriers of hepatitis B surface antigen (HBsAg) showed fundamental differences between the two groups. Viral replication, expressed by the presence of hepatitis B e antigen, lasted for four years or more in 10 out of 14 (71%) of the homosexual men whereas it was not present in 43 out of 73 (59%) of the drug addicts within one year. This shows a difference in the immunological response between homosexual HBsAg carriers and addicts that is not related to infection with human T cell lymphotropic virus type III. Severe histological damage such as chronic aggressive hepatitis, cirrhosis, or primary liver cancer was found in more than half of the homosexual men who underwent biopsy examinations. In drug addicts chronic persistent hepatitis was a regular finding in the absence of markers of delta infection, but in those addicts infected with the delta agent the degree of liver damage was comparable with that found in homosexual men.
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PMID:Long term follow up of chronic hepatitis B virus infection in intravenous drug abusers and homosexual men. 308 9

In a retrospective study a total of 754 sera from 397 hepatitis patients were assayed for delta antigen and antibody by radioimmunoassay. The study included patients of all age groups (3 months up to 85 years) whose first serum sample, taken from 1978 until January 1984, was positive for HBsAg. Clinically the patients could be subdivided into three major groups: 311 sera were from 181 patients with acute hepatitis, 296 from 135 CPH/CAH patients, including a few cases of liver cirrhosis and 3 cases of HCC, and 147 sera were from 81 asymptomatic carriers. Delta markers were found in 30 patients (7.6%). 20 of these were under the age of 30, and 13 presented with acute, often fulminant hepatitis or (in a minority of cases) exacerbations of preexisting HBV infection. Only two symptomless carriers had anti-delta. It seems of particular interest that all 10 cases where delta antigen could be demonstrated in the first serum sample presented with acute, often fulminant hepatic disease and 9 had anti-HBc-IgM antibodies. Where a second sample could be tested (5 cases), seroconversion to anti-delta was always demonstrated. Delta superinfection could be shown in 2 cases where anti-delta antibodies appeared more than a year after HBsAg positivity was first detected.
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PMID:[Delta hepatitis in Switzerland. Determination of delta antigens and delta antibodies in 397 HBsAg-positive patients (1978-1984)]. 647 32

Chronic delta infection occurs in Greece in about 10 to 15% of HBsAg+ subjects, being largely unrelated to parenteral transmission and/or to drug addiction. The observed cases exhibited histological changes ranging from chronic persistent hepatitis to chronic active hepatitis, cirrhosis, and even hepatocellular carcinoma on cirrhosis. The male/female ratio of patients with delta Ag + CLD was 3.8:1 and their mean age 40 years. They were younger compared to delta Ag-/HBsAg+ CLD and they presented with a wide spectrum of symptoms and signs. About 25% of the patients were oligosymptomatic or asymptomatic and about 40% manifested their disease as an episode of acute hepatitis with protracted or relapsing course followed by chronicity. Biochemical changes appeared to be more severe than in delta Ag-/HBsAg + CLD. The natural history was frequently characterised by a progressive course, terminating, in about 15 years, to death from cirrhosis and liver failure, although remissions occasionally occurred. HCC also developed but probably less frequently than in HBsAg positive, delta Ag negative CLD. Whether the natural course of delta Ag+ CLD can be modified by any form of treatment remains to be proved.
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PMID:Delta antigen positive chronic liver disease in Greece: clinical aspects and natural course. 666 75

In Japanese blood donors, positivity for antibodies to hepatitis C virus (HCV) ranges from 0.2% in subjects under 20 to 3.9% in those over 50 years. It is estimated that at least 2.3 million Japanese have contracted HCV infection through contaminated blood. HCV carrier state was confirmed by polymerase chain reaction for HCV-RNA in subjects positive for antibodies to more than one viral protein (70% of cases). Subjects positive for core antibody alone, however, were found to be HCV-RNA negative with normal liver function, and are considered to have only a past history of HCV infection (30% of cases). Acute hepatitis C progresses to chronic infection in about 90% of cases. In comparison with hepatitis B, chronic hepatitis C leads more frequently to cirrhosis and liver cancer, and rarely remits spontaneously. In typical HCV infection, aminotransferase activities fluctuate markedly in the early stages, then become relatively stable for 10 years or more, with chronic persistent hepatitis shown by histological examination. Thereafter, aminotransferase activities may change dramatically, with progression to chronic active hepatitis and rapid development of cirrhosis and hepatocellular carcinoma. On average, it takes about 30 years for chronic hepatitis C to progress from initial infection to cirrhosis and cancer, but the disease progresses much more rapidly in elderly patients.
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PMID:Epidemiology and long term prognosis of hepatitis C virus infection in Japan. 768 12

During the period 1982-1990, 544 patients with clinical evidence of liver disease were admitted to King Fahd University Hospital, Al-Khobar, Saudi Arabia. Besides routine laboratory and sonographic investigations, all were subjected to either a needle liver biopsy, laparoscopy or a laparotomy. The tissue diagnoses were as follows: liver cirrhosis 17.3%, periportal fibrosis 14.3%, metastatic cancer 12.9%, primary hepatoma (hepatocellular carcinoma: HCC) 12.1%, hepatic granuloma 11.2%, chronic active hepatitis 7.7%, chronic persistent hepatitis 2.2%, fatty liver 7.2%, hydatid liver disease 4.6% and others 2.8%. In 7.7% the histology was normal. These results will be discussed and compared with results reported in local and international literature.
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PMID:Pattern of chronic liver disease in the eastern province of Saudi Arabia. A hospital-based clinicopathological study. 789 3


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