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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alpha-fetoprotein (AFP) was assessed in 159 subjects with chronic liver disease, incl. 125 chronic HBsAg carriers (42 suffered from cirrhosis of the liver) and in 34 HbsAg negative cirrhotic patients. In the group of 83 patients with chronic hepatitis B a slightly elevated AFP value was recorded in 7.2%, however, during the check-up examination it was already normal. During a one-year follow up hepatocellular carcinoma (HCC) was revealed in 4 of 42 HBsAg positive cirrhoses (9.5%) and in 2 of 34 (5.9%) HBsAg negative cirrhoses, the difference was not, however, significant. Five patients with HCC had markedly elevated or rising AFP value, one patient had abnormal AFP level despite advanced HCC. All cases of HCC were diagnosed late, in one patient radical treatment was not successful. We conclude that to improve the adverse prognosis of patients with HCC it is necessary to follow-up prospectively all patients with cirrhosis of the liver by sonography twice a year and examine after the same time intervals serum AFP to detect early stages HCC where there is still some chance of successful treatment.
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PMID:Assessment of alpha-fetoprotein in chronic HBsAg carriers and in HBsAg negative cirrhosis of the liver. 752 85

The differential diagnosis of an abdominal mass in an infant or young child includes hepatoblastoma. This rare embryonal neoplasm of the liver is linked to several congenital abnormalities and may be associated with maternal occupational exposure to metal fumes, petroleum products, or paints. Alpha-fetoprotein is a useful tumor marker that may also be elevated with hepatocellular carcinoma. The relatively better prognosis of hepatoblastoma, if completely resected, mandates its differentiation from hepatoma. The fetal subtype of hepatoblastoma seems to represent a "favorable" histology pattern.
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PMID:Hepatoblastoma: a rare pediatric neoplasm. 767 85

A family displaying hereditary persistence of alpha-fetoprotein (HPAFP) in adult life was detected in an antenatal screening programme for spina bifida. RFLP linkage analysis shows that the trait is linked with the albumin-AFP locus. The molecular mechanism responsible for the post-natal repression of the AFP gene is unknown. We wished to determine the molecular mechanism underlying HPAFP in this family. Sequence analysis of the 5'-flanking sequences of their gene revealed a GA substitution at position -119 associated with the trait. This substitution occurs in a potential HNF I binding site, and increases the similarity of the sequence to a consensus HNF I recognition site. In a competitive gel retardation assay the mutant sequence binds HNF I alpha more tightly than the wild type sequence. Furthermore, 5'-flanking sequences of the human AFP gene containing the G-->A substitution direct a higher level of CAT expression in transfected human hepatoma cells than the wild type sequences. We conclude that the G-->A substitution at position -119 of the AFP gene is the mutation causing HPAFP in this family. These results highlight the importance of this HNF I binding site in the developmental regulation of the AFP gene.
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PMID:A G-->A substitution in an HNF I binding site in the human alpha-fetoprotein gene is associated with hereditary persistence of alpha-fetoprotein (HPAFP). 768 42

Alpha-fetoprotein reactive to Pisum sativum agglutinin levels (AFP-R-PSA) was measured in sera from 124 patients with hepatocellular carcinoma (HCC) and 54 patients with benign liver diseases (BLD). The level of AFP-R-PSA in the HCC group (42% +/- 22%) was significantly higher than that in the BLD group (10% +/- 8%). When an AFP-R-PSA level above 25% was used as a value highly suggestive of HCC, the sensitivity of the test was 82%, the specificity was 96%, the accuracy was 86%, and the positive prediction value was 98%. The positive rates of AFP-R-PSA in HCC patients with a serum AFP level below 100 micrograms/L and with a serum AFP level below 400 micrograms/L were 78% and 84%, respectively. Corresponding value was 74% for 31 patients with a tumor size less than 5cm. If AFP was combined with AFP-R-PSA, the detection rate of small HCC in this study would be increased from 32% to 87%. These data indicate that measurement of AFP-R-PSA is useful for the differentiation of BLD and for the early diagnosis of HCC.
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PMID:Alpha-fetoprotein reaction to Pisum sativum agglutinin in differentiation of benign liver diseases from hepatocellular carcinoma. 769 3

There is not yet an effective standard therapy for severe advanced hepatocellular carcinoma (HCC). We attempted continuous local arterial infusion chemotherapy using 5-fluorouracil (5-FU) and cisplatin (CDDP) with an implanted reservoir for these patients, and evaluated its efficacy. Twenty-one HCC patients received continuous arterial infusion of 5-FU and CDDP for 1 week, followed by a 1-week no-infusion period; this regimen was repeated 1-32 times, and patients were observed for 36-549 days. The 1-year survival rate was 61.1%, and alpha fetoprotein levels decreased in 13 patients. All could continue as outpatients for 94.0% of the entire course of therapy. Because CDDP amplifies the effect of 5-FU as a biochemical modulator, and because continuous infusion strengthens the effect of 5-FU and reduces the side effects of CDDP, we consider this therapy to be effective for patients with severe advanced HCC, prolonging survival and improving the quality of life.
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PMID:The efficacy of continuous local arterial infusion of 5-fluorouracil and cisplatin through an implanted reservoir for severe advanced hepatocellular carcinoma. 777 43

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

We report a non alcoholic, Chinese, 65 years old male that presented in august, 1992 with painful hepatomegaly of rapid installation and malaise. Ultrasound examination revealed multiple substitution images, diagnosed histologically as hepatoma. Serum alpha fetoprotein was 6600 U/ml. Malaise increased and the patient died two months later. This patient had a porphyria cutanea tarda and a chronic hepatitis diagnosed 6 years before. He also had positive titers for hepatitis C virus antibodies. In patients with porphyria cutanea tarda, hepatoma frequency is 400 fold higher and hepatitis C virus infection is highly prevalent. Thus, the surveillance of these patients with periodic alpha feto protein determinations and abdominal ultrasound examinations is recommended, specially in those infected by hepatitis C virus.
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PMID:[Porphyria cutanea tarda, chronic liver disease caused by the C virus and hepatocarcinoma. Clinical case]. 791 41

721 patients with liver cirrhosis were regularly screened by sonography and determination of alpha fetoprotein during a period of eleven years (1.1.1982-1.1.1993). In 137 of them hepatocellular carcinoma (HCC) was diagnosed; 28 (20.4%) had a unilocular HCC with a diameter up to 5 cm. Diagnosis was regularly verified by sonographic guided puncture, in rare cases by laparoscopy and biopsy. Beside a diameter of 5 cm the tumor should be localized at least 5 mm from the main structures in the hilus, and not in the centre of the liver; furthermore multilocular hepatocellular carcinomas and intra- and extrahepatic metastases were contraindications. Child-Pugh-classification should be A+B and urea synthesis rate at least 6 g per day. In 21 patients (75%) a portal hypertension was diagnosed; 19 (68%) had bled from esophageal varices; in case of one bleeding a therapeutic sclerotherapy and in case of recurrent variceal hemorrhage an elective shunt operation were performed. Surgical resection was carried out with controlled hypotension and temporary occlusion of the hepatoduodenal ligament. Tumor was removed by segmentectomy or bisegmentectomy and in rare cases by enucleation. There were 3 clinical deaths (10.7%); causes of death were liver failure and (2) sepsis (1). All patients could be followed up to January 1, 1993; there were 12 further deaths of liver failure, tumor recurrence or second tumor. 13 patients are still living. Thus the live expectancy for one year was 80, for 5 years 50 and for 10 years 30%. There is no doubt, that it is possible to detect hepatocellular carcinoma in patients with liver cirrhosis early by regular sonography and determination of alpha-fetoprotein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Single hepatocellular carcinoma (phi < or = 5 cm) in liver cirrhosis. Early diagnosis and surgical removal]. 826 41

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 report herein the case of a 35-year-old woman with aplastic anemia who developed hepatocellular carcinoma after long-term therapy with oxymetholone. She was treated with 60 mg/day of oxymetholone for 3 years (total dose 64.8 g). Alpha-fetoprotein, hepatitis B surface antigen, and hepatitis C antibody were all negative, but serum titers of carcinoembryonic antigen and carbohydrate antigen were elevated. Lateral segmentectomy of the liver was performed. The histopathological findings were compatible with those of multiple hepatocellular carcinoma without liver cirrhosis. Three years since the operation, the patient is doing well and no signs of tumor recurrence have been detected. According to our review of Japanese cases of hepatocellular carcinoma associated with anabolic steroid therapy, in all instances the tumors developed after long-term administration of anabolic steroids for hematologic diseases. In patients under long-term anabolic steroid therapy, routine screening of the liver by ultrasonography and computed tomography should be performed to detect liver tumors in the early stages.
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PMID:Hepatocellular carcinoma associated with anabolic steroid therapy: report of a case and review of the Japanese literature. 872 41


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