Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Homozygous alpha 1-antitrypsin deficiency (PiZZ phenotype) is known to be associated with increased risk of cirrhosis and primary liver cancer. Although a relationship between heterozygous alpha 1-antitrypsin deficiency and chronic liver disease was suggested recently, it is still a matter of controversy whether such patients are at increased risk of liver cancer. The goal of this study was to determine the prevalence of heterozygous alpha 1-antitrypsin deficiency of different phenotypes among patients with primary hepatobiliary cancers. We studied 82 patients with primary hepatobiliary cancer; 59 had hepatocellular carcinoma and 23 had bile duct carcinoma. alpha 1-Antitrypsin quantitation and phenotyping were performed in each patient using standard methods. The distribution of the various Pi phenotypes was compared with that found in a normal population and reported elsewhere. Odds-ratio and chi 2 tests were used to measure the relative risk and the significance of association, respectively, between primary hepatobiliary cancers and heterozygous alpha 1-antitrypsin deficiency. Four patients in each of the cancer groups were heterozygous. Among the hepatocellular carcinoma patients, three had the PiMS phenotype and one had the PiMZ phenotype. Of these four heterozygous patients, only two had cirrhosis; one had cryptogenic cirrhosis and the other had hepatitis B virus-related cirrhosis. One noncirrhotic patient with a PiMZ phenotype had a fibrolamellar carcinoma. Of the four patients with bile duct carcinoma, three had the PiMS phenotype and one had the PiMZ phenotype. Of the four heterozygous patients, two had primary sclerosing cholangitis without associated inflammatory bowel disease and one patient had had previous biliary operations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of increase in heterozygous alpha 1-antitrypsin deficiency phenotypes among patients with hepatocellular and bile duct carcinoma. 131 55

PAP technique and rabbit anti-X serum were used to detect the X protein in tumor and nontumor liver tissues from 34 patients with HCC. The positive rate of the X protein in both tissues were 94.1% and 84.4% respectively. Of the 34 patients with HCC, 27 were complicated by liver cirrhosis, in whom 92.6% were X protein positive in liver cells. It was found that almost all of the liver cells adjacent to the tumor tissue showed strong positive staining. The high frequency and predominant expression of X protein in HCC and liver cirrhosis tissues indicated that X protein may play an important role in hepatocarcinogenesis. X protein was detected in 17.2% of the patients with CAH, which suggested the risk of transformation from CAH to cirrhosis and/or HCC. X protein was first found in bile duct epithelial cells in 59.4% of the patients with HCC, and 6 of 34 HCC were combined with bile duct carcinoma, and some cancer cells were found positive for X protein. It seems that X protein may also be a potential factor in the oncogenesis of bile duct carcinoma.
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PMID:[Expression of hepatitis B virus X protein in tumor and nontumor tissues of patients with hepatocellular carcinoma (HCC)]. 132 50

Macroregenerative nodules, also called nodules of adenomatous hyperplasia, have been well documented in Japan. Extensive studies support the hypothesis that in the Japanese population these lesions represent a possible pathway for hepatocarcinogenesis. However, reporting of these lesions in non-Japanese populations has so far been rare. We examined 44 sequential cirrhotic hepatectomy specimens from adult patients who underwent orthotopic liver transplantation at our institution. All livers were serially sectioned every 0.5 cm. Macroregenerative nodules were defined as regenerative nodules at least 1 cm in diameter. Forty-eight macroregenerative nodules were found in 11 livers (25% of livers). The antecedent diseases in these livers included hepatitis C (3), alcoholism (2), primary biliary cirrhosis (2) (one with iron overload), cryptogenic cirrhosis (2), hepatitis B (1) and alpha 1-antitrypsin deficiency (1). The macroregenerative nodules often differed from the surrounding nodular parenchyma in color, texture or the degree to which they bulged beyond the cut liver surface. Three livers contained grossly apparent hepatocellular carcinomas. Microscopically, macroregenerative nodules could be classified as those with (type 2) and without (type 1) dysplasia. Four livers had type 1 lesions, two had type 2 lesions and five had lesions of both types. We found 36 type 1 lesions in all and 12 type 2 lesions, 3 containing foci of microscopic carcinoma. All hepatocellular carcinomas arose in livers containing macroregenerative nodules (either type). Liver cell dysplasia, large-cell or small-cell, was observed in cirrhotic nodules of 27 livers. Microscopic or macroscopic hepatocellular carcinoma occurred in three livers with large-cell but not small-cell dysplasia and in one liver without dysplasia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Macroregenerative nodules and hepatocellular carcinoma in forty-four sequential adult liver explants with cirrhosis. 132 12

A 61-year-old male was admitted because of hemoptysis. He had a 9 year history of liver cirrhosis associated with HB viral chronic hepatitis. Physical examination revealed no abnormalities. Laboratory investigations revealed positive HBs antigen with normal alpha-fetoprotein. Chest X-ray film showed large mediastinal lymph nodes and an endobronchial polypoid mass in the distal end of the right main bronchus. The right main PA was narrowed due to compression by the mediastinal mass. Bronchoscopic examination revealed a polypoid mass in the right main bronchus. The biopsy specimen was histologically diagnosed as undifferentiated large cell carcinoma. The patient developed respiratory failure, and died 3 weeks after admission. Autopsy revealed a small liver cancer of 1.3 cm diameter within the cirrhotic liver, associated with a small abdominal lymph node metastasis and large mediastinal lymph node swellings. Thromboembolism in the bilateral main pulmonary arteries was concluded to be the cause of death. The mediastinal mass which directly invaded into the right main bronchus had a close histological similarity with the liver cancer, showing undifferentiated carcinoma cells with bizarre nuclei and abundant cytoplasm. An immunohistological study revealed cells positive for alpha-fetoprotein in the mediastinal lymph nodes. The patient was diagnosed as having small liver cancer with mediastinal lymph node metastases. A survey of the literature revealed only a few cases of advanced hepatoma associated with prominent mediastinal metastases. This is the first reported case of small liver cancer presenting with large mediastinal lymph node metastases.
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PMID:[A case of small liver cancer presenting as a huge mediastinal mass]. 132 37

This study discusses four children of hepatocellular carcinoma (HCC) who were asymptomatic HBsAg carriers or had HBsAg-positive chronic hepatitis for 3 to 11 years before the occurrence of the carcinoma. Three of these four patients were positive for anti-HBe at 3 to 5 years before the diagnosis of hepatocellular carcinoma. Autopsy findings disclosed liver cirrhosis in all the four patients. To the best of our knowledge few reports have documented children in HBsAg carrier status or with HBsAg-positive hepatitis prior to the development of hepatocellular carcinoma. It is emphasized that HBsAg-positive children, with or without detectable hepatic lesions in routine examinations, have a possibility of developing HCC, and should be carefully monitored for long periods.
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PMID:Hepatocellular carcinoma in children with hepatitis B surface antigen. 133 50

Point-mutational activation of the c-Ki-ras proto-oncogene has been shown to be rare in human hepatocellular carcinoma, the most common primary liver cancer and one usually associated with chronic viral infection. To reveal the association of c-Ki-ras activation with cholangiocarcinogenesis under different etiological backgrounds, the incidence of point mutation at codons 12 and 13 of the c-Ki-ras proto-oncogene was examined in three groups of human liver cancers with differentiation to biliary epithelial cells: Group 1, cholangiocellular carcinoma in Japanese with normal livers; Group 2, cholangiocellular carcinoma in Thais who had lived in an area where the liver fluke Opisthorchis viverrini is endemic; and Group 3, combined hepatocellular-cholangiocellular carcinoma, a rare type showing features of both hepatocellular and biliary epithelial differentiation, in Japanese with chronic viral hepatitis with or without cirrhosis. The polymerase chain reaction and direct sequencing of its product were used to detect the mutation. Point mutation at codon 12 of the c-Ki-ras gene was detected in five (56%) of nine cases in Group 1. In contrast, the mutation was not detected in any of the cases in Groups 2 and 3. Therefore, point-mutational activation of c-Ki-ras did not seem to be involved in the development of primary liver cancers associated with apparent chronic irritation of liver cells or biliary epithelial cells caused by exogenous liver-fluke or viral infection. On the other hand, point-mutational activation of the c-Ki-ras proto-oncogene may be involved in cholangiocarcinogenesis in liver without preexisting liver-fluke or viral infection.
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PMID:Cholangiocarcinomas in Japanese and Thai patients: difference in etiology and incidence of point mutation of the c-Ki-ras proto-oncogene. 133 66

The results of liver transplantation for hepatocellular carcinoma are disappointing. Thus, in 11 patients transplanted for hepatocellular carcinoma on cirrhosis, the actuarial survival rate at 3 years was 20 percent, with a postoperative mortality of 27 percent and 4 deaths caused by recurrence of the malignancy. These poor results contrast with those we obtained after liver transplantation for cirrhosis and finding of incidental hepatocellular carcinoma in the resected part of the liver. Out of 6 patients with incidental carcinoma only 1 died postoperatively (16.6 percent), and no case of recurrent malignancy was observed. These results confirm that the malignancy recurrence rate is high after transplantation for large carcinoma. On the other hand, the absence of recurrence after transplantation for incidental hepatocellular carcinoma encourages us to look for small carcinomas on cirrhosis.
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PMID:[Liver transplantation for hepatocellular carcinoma. Mid-term results]. 133 83

The authors applied a silver colloid technique to identify Argyrophilic Organiser Region (AgNOR) to 8 groups of hepatic lesions: alcoholic hepatitis with dysplasia (3 cases); chronic active hepatitis with dysplasia (4 cases); cirrhosis with dysplasia (5 cases); focal nodular hyperplasia (4 cases) and hepatocellular carcinomas (3 cases of grade I, 3 cases of grade II and 5 cases of grade III of Edmondson). Four cases of non-specific reactive hepatitis were used as control. This work suggests the simplicity and utility of simultaneous application of clumps per cell, AgNORs per clump and total AgNORs counts in the evaluation of neoplastic and preneoplastic lesions of the liver. The results show, in hepatocellular carcinomas, a relationship between the number of clumps, the AgNORs per clump, the total number of AgNORs and the grading of Edmondson. The nodular lesions that can be considered in the differential diagnosis with carcinoma are sufficiently well discriminated using the two parameters AgNORs per clump and total number of AgNORs.
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PMID:Hepatocellular carcinoma and preneoplastic lesions of the liver: evaluation of argyrophilic nucleolar organizer regions (AgNORs). 133 18

Super-selective hepatic arteriography was performed in 40 patients with liver neoplasma by injecting H2O2. The final diagnosis were as follows: 23 hepatic cases of carcinoma, 14 patients had cavernous hemangioma, 1 case of hepato-cirrhosis and 2 cases excluding neoplasma. According the contrast, the entrance of H2O2 into neoplasma could be divided into four types: rapid-filling, middle speed-filling, low speed-filling, enclostic but no entering. The acoustic contrast technique, pathological basis, and qualitative diagnosis were also discussed.
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PMID:[Transcatheter hepatic arteriography combined with ultrasound in the diagnosis of space occupying lesions]. 133 16

Alagille's syndrome or arteriohepatic dysplasia has been described in Cuba in nine patients between nine months and 12 years of age (8 males and one female). Among the clinical features we found five major abnormalities: chronic cholestasis with neonatal jaundice (9/9), peculiar facies (9/9), peripheral pulmonary artery hypoplasia associated with cardiac murmur (6/9), butter-fly-like arch defects (4/9), and posterior embryotoxon (6/7). Two children had a severe xanthomatosis. Laparoscopy showed green hepatomegaly depending on the degree of cholestasis, and only one patient had incipient signs of micronodular cirrhosis. Liver histology showed a paucity of interlobular bile ducts. Survival was of 60%. One patient survived more than 30 years. Four patients died of liver carcinoma (unique report in infants), broncho-pneumonia, acute renal failure, and sudden death respectively. Among the minor features were mental retardation (5/9), a peculiar voice (3/9), growth retardation observed in some of our patients. This is the first report on Alagille's syndrome in Latin America, because so far reports have come only from Europe and North America.
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PMID:[Alagille's syndrome in Cuba. A report of 9 cases]. 134 Aug 42


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