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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dearth of plasma alpha fetoprotein reference ranges for preterm infants often impairs the clinical interpretation of plasma alpha fetoprotein data collected from ill babies. This study tested our hypothesis that meaningful plasma reference ranges could be established for preterm infants by a simple correction of patient age at sampling date for gestational age deficit at birth. Using a modified radioimmunoassay kit method, determinations of alpha fetoprotein were performed on capillary and venous blood samples collected from 56 babies aged from birth to 5 months with gestational ages ranging from 26 weeks to 43 weeks. Unmodified plasma alpha fetoprotein values were grouped according to patient age and examined statistically using established normal theory methods, but these yielded excessively wide reference intervals and non-Gaussian distribution parameters. Acceptable reference ranges were derived using logarithmic transformation of plasma alpha fetoprotein values and rearrangement against patient age corrected for gestational age deficit. These provisional reference ranges for plasma alpha fetoprotein in preterm (and term) infants are applied to groups of previously meaningless alpha fetoprotein results and used to test the potential usefulness of plasma alpha fetoprotein determination as a diagnostic marker in biliary atresia, hepatitis, and yolk sac derived tumours.
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PMID:Plasma alpha fetoprotein reference ranges in infancy: effect of prematurity. 243 23

Alpha-fetoprotein (AFP) in the sera of 35 LEC (Long-Evans with a cinnamon-like coat color) rats between 7 and 25 weeks of age was evaluated by enzyme-linked immunosorbent assay (ELISA). Elevation of serum AFP and proliferation of oval cells in the liver were observed in most LEC rats, which suffered from acute hepatitis. On the other hand, the serum AFP level was within the normal range before the onset of hepatitis. Immunohistochemical staining for AFP revealed that some of the proliferating oval cells produced AFP. Morphometric analysis of AFP-positive cells and ELISA for serum AFP demonstrated that there was a statistically significant correlation between the number of AFP-positive cells in the liver and the concentration of AFP in the serum. Histological examination revealed the transition and differentiation of the oval cells to small hepatocytes. These results suggested that the phenomena which occurred in LEC rats suffering from acute hepatitis were similar to those that occurred during the early stage of azo dye hepatocarcinogenesis, although the extent of the oval cell proliferation and the elevation of serum AFP in LEC rats were not as great as those in rats treated with azo dye. This is the first report on a rat strain with proliferation of AFP-producing oval cells during its natural history.
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PMID:Elevation of serum alpha-fetoprotein and proliferation of oval cells in the livers of LEC rats. 245 91

This is a retrospective review of 43 patients who had primary liver cancer diagnosed during 1974-1983. Patients' ages ranged from 27 to 84 years (median 52.5). Nine of 39 patients with hepatoma were females, while two of the four patients with cholangiocarcinoma were women. Hepatitis surface antigen was positive in 90% tested, and 62% had cirrhosis. Also, 60-65% were heavy users of alcohol and cigarettes. Alpha-fetoprotein was elevated in one of four white patients, and in six of eight patients of other races (75%). Tissue diagnosis was obtained by peritoneoscopy in 16, by percutaneous biopsy in 7, by laparotomy in 9, and at autopsy in 11. Only one of 11 patients who were explored has his lesion resected. About half of the cases diagnosed antemortem died 1 month or less after diagnosis. The median survival of hepatoma patients who had no specific treatment or systemic chemotherapy was 2 months. Two patients who received chemotherapy in conjunction with occlusion of the hepatic artery lived 16 to 19 months.
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PMID:Primary liver cancer in a referral hospital in Hawaii. 303 54

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

In most cases, primary liver carcinoma in tropical areas remains an hepatoma. The high incidence of this malignant tumor of the liver in some regions, and especially in black Africa, is still unexplained. As compared with the form found either in the European or in the North-African, this hepatoma shows special features since it occurs in younger people (35 years), follows a bursting-out course and is precipitously associated not to an alcoholic cirrhosis but to a post-hepatitic one. An humoral syndrome leading to a presomptive diagnosis consists of hypoglycemia, hypercholesterolemia, hyperlipemia, and high blood level of alcaline phosphatases. In 85% of the cases, these tumors secrete an alpha fetoprotein determined by radioimmunoassay. A major etiologic factor is the oncogenous activity of hepatitis virus B which could be either an induction factor or a "co-factor" which would initiate, facilitate or increase the activity of the carcinogen. In this respect, aflatoxin has to be regarded as a "co-factor" too. The best treatment, when it is possible, is an exeresis carried out through a partial hepatectomy. If such a surgical intervention is unadvisable, chemotherapy is the only possibility. Immunization against viral hepatitis has raised hope for the prophylaxis of hepatoma. But it will not be possible to evaluate it before the year 2.000.
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PMID:[Primary liver cancer in the tropical environment. Classical and current data]. 619 92

The prevalence of serological markers of hepatitis B virus (HBV) infection was investigated in 75 patients with histologically confirmed hepatocellular carcinoma (HCC). Hepatitis Bs-antigen (HBs-Ag) was found in 30.8% and evidence of present or past infection in 61.5%. In a control group of 115 patients with liver cirrhosis of various etiologies in whom evidence of a coexistent HCC was lacking, the corresponding numbers were significantly lower (16.5% and 41.7% resp., p less than 0.05). Below the age of 65 years, markers of present or past HBV-infection were significantly more frequent than in patients above 65 years of age (p less than 0.025). All patients positive for HBs-Ag had an underlying cirrhosis; in seven cases, HCC was found in a non-cirrhotic liver. Alpha-fetoprotein measurements failed to identify patients with HCC in up to 43.6% of the HBs-Ag negative cases. It is concluded that HBV-infection does represent a cofactor in the malignant transformation of the liver, even in areas of lower incidence. Alpha-fetoprotein measurements need to be complemented by other investigations if early recognition of HCC is to lead to better survival.
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PMID:Hepatocellular carcinoma and hepatitis B virus infection. Analysis of 75 cases from Switzerland. 619 40

The histology of 72 livers from 72 children who underwent liver transplantation was reviewed. Nine children (12.5%) had hepatocellular carcinoma (HCC) and/or liver cell dysplasia (LCD) in their native livers. Ages at the time of transplantation ranged from 2 months to 11 years. Primary liver diseases included tyrosinemia (3), biliary atresia (2), chronic active hepatitis B (1), chronic active non-A non-B non-C hepatitis (1), idiopathic neonatal hepatitis (1), and neonatal iron storage disease (1). Explanted livers showed large multifocal HCC in two cases, incidental HCC in three, and dysplastic nodules in four. LCD also was present in three cases in conjunction with HCC. All patients had cirrhosis. Alpha-fetoprotein was measured in six children and was elevated in all six (range, 300 to 1,770,000 ng/mL; normal, 0 to 15 ng/mL). Abdominal computed tomography, ultrasonography, and/or magnetic resonance imaging showed large masses in two cases, but did not detect the tumors of less than 2 cm or the dysplastic nodules in the other seven children. After a follow-up period of 2 months to 3 years (mean, 19.8 +/- 12.1 months), eight children are alive and have no evidence of recurrence. The patient with neonatal iron storage disease died 2 months after transplantation, without evidence of tumor recurrence. The authors conclude that children with end-stage liver disease of diverse causes referred for liver transplantation may have LCD and/or HCC. Serial determination of alpha-fetoprotein and images studies may detect early lesions curable by liver transplantation.
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PMID:Hepatocellular carcinoma and liver cell dysplasia in children with chronic liver disease. 784 22

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The majority of patients who develop HCC have underlying cirrhosis, which suggests that cirrhosis itself represents a preneoplastic condition. Nevertheless, whereas patients with cirrhosis of any origin are at increased risk of developing HCC, those with chronic hepatitis B or C infection seem to be at greatest risk. Patients with cirrhosis resulting from chronic alcohol use, hemochromatosis, autoimmune hepatitis, or alpha-1 antitrypsin deficiency have less risk of developing this cancer, and some hepatic diseases, such as primary biliary cirrhosis and Wilson's disease, do not predispose affected persons to an appreciable risk of developing HCC. Certain histological features, such as liver cell dysplasia and macroregenerative nodules, may represent preneoplastic alterations of hepatocytes, but these changes do not seem to be a necessary step in the evolution of liver cancer. The pathogenesis of HCC is unclear, but seems to involve several steps. Hepatitis B virus infection may result in the malignant transformation of hepatocytes by some directly oncogenic mechanism, whereas other necroinflammatory conditions probably predispose to the development of HCC through the introduction of genetic alterations coupled with a reduction of genetic repair functions. Screening patients at risk for the development of HCC using alpha fetoprotein measurements and ultrasonography is widely practiced despite inconclusive evidence of efficacy. If screening is performed, the program used should be tailored to the perceived risk for a particular patient.
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PMID:Preneoplastic conditions of the liver. 870 61

We experienced six patients with resected hepatocellular carcinoma (HCC) following interferon (IFN) therapy. Hepatitis virus C-RNA in polymerase chain reaction was positive in all patients prior to the IFN therapy. HCV-RNA became negative in two patients following IFN therapy, and was re-positive at the time of detection of HCC. In histological studies prior to the IFN therapy, pre-cirrhosis was diagnosed in four out of six patients and chronic active hepatitis 2B (CAH2B) in one according to the Europian classification. In non-cancerous portion of the liver, cirrhosis developed in five patients, and CAH2B in one. There was no significant correlation among the interval of HCC detection following IFN therapy, tumor size, tumor location, and histological findings. Patients should be carefully followed up by serum alpha fetoprotein levels or ultrasonography of the liver during and following IFN therapy.
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PMID:[Hepatocellular carcinoma following interferon therapy]. 875 58

Hepatocellular carcinoma (HCC) represents the most common form of malignant tumor among males in Thailand, an area endemic for hepatitis B virus (HBV) infection. Various risk factors have been associated with the development of HCC, among them exposure to certain toxins, and infection with hepatitis viruses, in particular HBV, as well as HCV in areas non-endemic for HBV infection. To examine the association of hepatitis viruses with HCC, our group investigated 101 patients who had been clinically, mainly via alpha fetoprotein level, and/or histologically diagnosed with hepatocellular carcinoma. We also examined 200 voluntary blood donors as controls. All subjects underwent serological tests for the presence of hepatitis B surface antigen (HBsAg) and anti-HCV with polymerase chain reaction (PCR) used for the detection of HBV and TT virus (TTV) DNA, and reverse transcription (RT)-PCR for the detection of HCV RNA and HGV RNA. Besides showing a clear preponderance of HCC among males, with a peak incidence the age group 51-70 years, the results obtained in the HCC patients demonstrated that the prevalence of HBV was 65%, four times that of HCV (17%), ten times that of HGV (6%), and seven times that of TTV (9%). In the controls, the prevalence of HBV was 0.5%; that of HCV, 0.5%: that of HGV, 5%; and that of TTV, 7%. These findings confirmed that hepatitis B virus was associated with the development of hepatocellular carcinoma among the Thai population, among whom case histories of chronic hepatitis and cirrhosis have also been encountered quite frequently.
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PMID:Association of hepatitis viruses with hepatocellular carcinoma in Thailand. 1021 23


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