Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 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

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

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

A review of the histopathology and demonstration of alpha-interferon with a monoclonal anti-alpha-interferon antibody reagent were carried out in 71 consecutive cases of acute and chronic hepatitis, and also in some cases of cirrhosis and HCC. The main cells expressing alpha-interferon were lymphocytes, plasma cells, fibroblasts and polymorphonuclears. There was no evidence for local alpha-interferon production near the site of virus replication in hepatitis B infection. Eleven cases of hepatitis were positive for alpha-interferon. The carrier state showed the highest positive rate in the different types of hepatitis. The positive rate in acute and chronic persistent hepatitis was lower than that in carrier state but higher than that in cirrhosis and HCC. The alpha-interferon positive cells were mainly located in the portal area and in the fibrotissue band around the necrotic and/or carcinomatous cells. These suggest that the function of the interferon system was related mainly to the pathological changes of liver tissue. Early use of interferon might be of therapeutic value to protect liver tissue from injury and to improve the interferon response of the host.
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PMID:[Detection of alpha-interferon positive cells in liver tissue from patients with hepatitis]. 839 41

Soluble HLA-class I and CD8 molecules were determined by sandwich ELISA in patients with viral-induced hepatic disorders. As a whole, the patients with hepatic disorders (acute hepatitis: AH; chronic hepatitis: CH; liver cirrhosis: LC; hepatocellular carcinoma: HCC) showed higher sHLA-class I and sCD8 levels than normal controls (P < 0.001). AH patients had the highest sHLA-class I levels (mean, 3513 +/- 2112 ng/ml), followed by CH (2896 +/- 1290 ng/ml), LC (2293 +/- 1266 ng/ml), and HCC (2221 +/- 1212 ng/ml) sCD8 levels wer highest in AH, followed by HCC, LC, and CH, in that order. Among histologically defined C virus-positive patients, sHLA-I levels were higher in those with chronic active hepatitis (CAH) 2A (3802 +/- 1124 ng/ml) than in those with chronic persistent hepatitis (CPH; 2200 +/- 711 ng/ml; P < 0.01), the levels then decreased as the disease progressed (CAH2B, 3564 +/- 1783 ng/ml, LC, 2376 +/- 1265 ng/ml). In contrast, sCD8 values showed little difference among the disorders. sHLA-class I levels showed a positive correlation with sCD8 values both in whole patients and in patients with AH (P < 0.01), but no correlation was shown, in any patients, with biochemical parameters such as GPT and GOT. These findings, taken together, suggest that hepatic destruction is not the only cause of sHLA-class I production, but that sHLA-class I levels, together with sCD8 levels, may reflect immunological activity in hepatic disorders.
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PMID:Serum concentrations of soluble HLA-class I and CD8 forms in patients with viral hepatic disorders. 921 47