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)

Epidemiological data obtained to date show that the delta agent is spread all over the world. In Rumania hepatitis B virus infection is widespread and is associated with a high incidence of chronic liver disease. To determine the prevalence of delta infection, sera from 373 patients with chronic liver disease were tested for HBV markers; 228 were HBsAg positive. Anti-HD was present in 190 sera (83.33%), which reveals a very high incidence and shows a higher frequency of the active forms of the disease. However, in contrast to other studies, we found a high incidence of HDV infection in chronic persistent hepatitis and hepatocellular carcinoma.
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PMID:Prevalence of the hepatitis delta virus in Rumania. 380 80

To establish the impact of transplantation on the course of chronic hepatitis B liver disease we performed a prospective study of the clinical and pathological sequelae of hepatitis B disease in all 22 patients who had renal allografts that functioned for more than 1 year and who were hepatitis B surface antigen (HBsAg)-positive following transplantation. No patient converted to HBsAg-negative. During a mean follow-up of 83 months serial liver biopsies were performed in 20 patients and 1 liver biopsy was available in the remaining 2 patients. Eleven patients died of liver disease, 5 of whom died of hepatic failure, 3 with hepatoma, 2 of gastrointestinal hemorrhage, and 1 of ascites with pleuroperitoneal fistula. Aggressive liver disease was observed in the vast majority of patients: 12 ultimately developed cirrhosis, (mean follow-up 81 months), 6 chronic active hepatitis (mean follow-up 93 months), 3 chronic persistent hepatitis (mean follow-up 89 months), and in 1 patient the presence of HB virus in hepatocytes was the sole morphologic alteration (follow-up 42 months). There was a marked tendency to progression in that 82% of patients with virus only, reactive hepatitis, or chronic persistent hepatitis on initial biopsy subsequently developed chronic active hepatitis or cirrhosis. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Four patients converted to the negative state. Biochemical evidence of persistent liver dysfunction occurred in only 1 patient and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of cirrhosis, leading to death from hepatoma and hepatic failure. This course is worse than that in dialysis patients. Renal transplantation of HBsAg-positive patients with end-stage renal failure may be inadvisable.
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PMID:The impact of renal transplantation on the course of hepatitis B liver disease. 389 Feb 90

Nineteen children with chronic hepatitis related to the hepatitis B virus were followed for an average of 6 years. The determination of the hepatitis B virus DNA in the serum allowed us to know the state of viral replication. Thus three groups of patients could be defined: the first in which replication remained active during the total period of follow-up; the second in which the extinction of replication was observed; the third in which replication was inactive from the beginning of the serological follow-up. Symptoms, high levels of aminotransferases and histologically aggressive lesions, sometimes with cirrhosis, were more frequent in the presence of viral DNA. During the decrease of the replication, a clear-cut and time-limited increase of serum-aminotransferase levels was often noted. After the disappearance of hepatitis B virus DNA in the serum, clinical signs could be found only in children with cirrhosis or hepatocellular carcinoma. Four cases of hepatitis with initial aggressive lesions led to persistent chronic hepatitis without viral DNA in the serum. In all but one of the patients who started with an aggressive form, viral DNA disappeared in the serum. This loss occurred later and only in 2 patients of 5 who presented initially with chronic persistent hepatitis. Thus a long period of follow-up in childhood chronic hepatitis related to B virus shows frequent inactivation of viral replication. This evolution seemed to occur earlier when the initial histological lesions were aggressive as if this aggressiveness favored the elimination of the virus and the presence of specific antibodies in the serum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Course of chronic hepatitis related to B virus in children. Study of serum viral DNA]. 401 86

Serum immunoglobulin G, A, and M and serum antinuclear, mitochondrial, and smooth muscle antibody have been measured in 223 patients with hepatitis-associated antigen (HAA)-positive and -negative acute and chronic liver disease. In patients with acute hepatitis, chronic persistent hepatitis, and primary liver cell carcinoma, these indices failed to show any significant differences. However, in the group with chronic aggressive hepatitis the patients who were HAA negative had significantly higher levels of serum IgG, much higher titres of smooth muscle antibody, and often antinuclear and mitochondrial antibodies which were not found in the HAA-positive patients from this group. This suggests that different pathogenic mechanisms may be operative in HAA-positive and -negative chronic aggressive hepatitis.
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PMID:Serum autoantibodies and immunoglobulins in hepatitis-associated antigen (HAA)-positive and -negative liver disease. 419 47

One hundred consecutive patients with nonautoimmune chronic active hepatitis (51% HBsAg-positive), 50 patients with cirrhosis (38% HBsAg-positive), 25 patients with chronic persistent hepatitis, and 118 patients with hepatoma who were seen at this hospital were reviewed to determine the prevalence and characteristics of glucose intolerance and diabetes in these conditions. Diabetes (fasting serum glucose greater than 7.8 mmol/L, 140 mg/dl on two separate occasions) was present in 8% of patients with chronic persistent hepatitis and mild chronic active hepatitis, 44% of patients with severe chronic active hepatitis, 40% of patients with cirrhosis, and 15% of patients with hepatoma, compared with 7% of all other patients aged 35 yr or over, undergoing liver biopsy. Compared with this high prevalence of diabetes in liver disease, only 3% of diabetic patients referred to the hospital diabetic clinic had chronic hepatitis or cirrhosis. Glucose tolerance was similar in chronic active hepatitis and cirrhosis and was characterized initially by basal hyperinsulinemia, normal basal glucose levels but elevated serum glucose following glucose loading, and evidence of insulin resistance. We suggest that the high prevalence of diabetes in chronic active hepatitis and cirrhosis in Saudi Arabia is due to the insulin resistance of chronic liver disease acting over many years in a population with a high genetic predisposition to diabetes.
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PMID:Diabetes mellitus in chronic active hepatitis and cirrhosis. 608 43

A case is reported in which non-A, non-B posttransfusion hepatitis was followed serially by chronic persistent hepatitis, chronic active hepatitis, and liver cirrhosis that finally developed into hepatocellular carcinoma. The patient died after a 19-year clinical course. During the last 8 years, repeated attempts to identify serum hepatitis B surface antigen, antibody to hepatitis B surface antigen, and antibody to hepatitis B core antigen were consistently negative. Liver biopsy was performed five times during the clinical course, and at autopsy, liver tissue was obtained from four different nontumor regions. These specimens were investigated by a peroxidase immunoenzyme method which failed to detect hepatitis B surface antigen and hepatitis B core antigen. Non-A, non-B posttransfusion hepatitis may become chronic and sometimes may advance to hepatocellular carcinoma.
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PMID:Hepatocellular carcinoma after non-A, non-B posttransfusion hepatitis. 609 43

100 consecutive British chronic carriers of hepatitis B surface antigen seen in a London teaching hospital are described. 77 were male homosexuals and only 19 had either symptoms or signs of chronic liver disease. 27 had normal liver function tests and 69 of the remaining patients had minimal changes, chronic persistent hepatitis, chronic active hepatitis, cirrhosis, or hepatocellular carcinoma diagnosed on liver biopsy. The 4 remaining patients did not have a biopsy but did have abnormal liver function tests. Chronic hepatitis B virus infection was an important cause of these conditions. Most patients showed no clinical, biochemical, or histological change during a mean follow-up period of 44 months, and only 9.7% spontaneously seroconverted from hepatitis B antigen positivity to become anti-hepatitis B e antibody carriers. Although the prognosis is good in the medium term, 7 patients died from hepatocellular carcinoma.
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PMID:Natural history of liver disease in chronic hepatitis B surface antigen carriers. Survey of 100 patients from Great Britain. 611 90

Although we have reached the stage when we can influence viral replication and some aspects of the immune response to the viral antigens, no practical and effective therapeutic regimen has been evolved. The next few years should, however, see considerable advances in this field, perhaps with combined anti-viral and immunostimulant regimens. The need to consider the infectivity of the patient, the risk of developing clinically significant chronic liver disease and the risk of developing clinically significant chronic liver disease and the risk of developing primary liver cell carcinoma in each patient may dictate that different regimens will be needed for HBe antigen-positive and negative carriers and for patients with chronic active or chronic persistent hepatitis and carriers with normal liver histology.
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PMID:Immunological and anti-viral therapy of chronic hepatitis B virus infection. 615 90

Seric alfa-FP has been studied in acute and chronic hepatitis and in hepatocellular carcinoma. Sixty five normal subjects, 62 cirrhoses, 10 active chronic hepatitis, 12 chronic persistent hepatitis, 4 primary biliary cirrhoses and 9 hepatomas have been examined for seric alfa-FP. Abnormal seric alfa-FP (> 10 ng/ml) values agree with literature data. It is likely that hepatocellular regeneration due to viral or inflammatory disorders, can produce formation of alfa-FP and other abnormal proteins fro a depression mechanism of sue regulator gene.
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PMID:[Alpha fetoprotein in non-neoplastic liver diseases]. 616 59

The behaviour of alpha 1 antitrypsin in 76 subjects with cirrhosis of the liver, 14 subjects with chronic persistent hepatitis, 14 subjects with chronic active hepatitis, 8 subjects with toxic hepatitis, 5 subjects with obstructive jaundice, 5 subjects with liver carcinoma. 4 of these groups (cirrhosis, chronic active hepatitis, obstructive jaundice, hepatoma) showed alpha 1 antitrypsin blood levels significantly higher than the control group (82 healthy subjects). Very high alpha 1 antitrypsin blood levels, significantly greater than in cirrhosis, were found in the patients with hepatoma. All these subjects also showed blood levels of alpha fetoprotein higher than 100 ng/ml. The diagnostic meaning of these finding was considered.
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PMID:[Behavior of serum alpha 1-antitrypsin in chronic hepatopathies and its diagnostic significance]. 616 21


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