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)

The present paper reviews several studies performed between 1977 and 1986 in Singapore on the 10-year survival outcome of treatment for stage I and II hepatocellular carcinoma (HCC). Of 801 HCC patients evaluated, only 2 survivors (0.3%) remained in complete remission for 13 and 14 years, respectively. One had received four weekly cycles of prednisolone, Adriamycin, vincristine and 5-fluorouracil for an inoperable HCC with a 10-cm diameter, and the other had received localised synchronised hepatic irradiation and Adriamycin. As follow-up, the use of localised hepatic irradiation consisting of 131I-labeled (30 mCi) iodised oil in lipiodol infused via the hepatic artery appeared to benefit patients with small residual tumours but did not affect larger tumours measuring 2 cm in diameter. Prophylactic, intermittent long-term administration of lymphoblastoid interferon-alpha (Wellferon) was carried out in pre-cancerous, high-risk hepatitis B surface antigen (HBsAg)-positive patients with cirrhosis, in immediate male relatives of liver cancer patients, and in persons who had undergone hepatic resection. In the untreated group, 10/162 (6%) cirrhotics, 3/18 (17%) male family members, and 6/10 (60%) post-resection cases developed single or multiple HCCs within 1 year of screening done at 3-month intervals on the basis of alpha-fetoprotein (AFP) levels and real-time hepatic ultrasonography. In contrast, none of the Wellferon-treated group consisting of 518 cirrhotic patients, 82 male relatives of HCC patients and 20 post-resection cases developed HCC. Two HBsAg-positive individuals who had not been treated with interferon (IFN) developed hepatic nodules which that showed dysplasia, AFP elevation and chromosomal changes. These studies demonstrate the poor results of late diagnosis and show that early intervention and prophylaxis with Wellferon can reduce the incidence of HCC in high-risk persons. In addition, transhepatic chemoembolisation and liver resection are suitable methods for treating small HCCs (single or multiple) that are detected by screening. However, some of these early-detected HCCs remain highly malignant. Prophylactic treatment of pre-cancerous conditions appears to be a better option as a long-term programme for HCC.
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PMID:Long-term survival following treatment of hepatocellular carcinoma in Singapore: evaluation of Wellferon in the prophylaxis of high-risk pre-cancerous conditions. 133

Hepatocellular carcinoma (HCC) may uncommonly present with distant metastasis in the absence of a documented neoplasm in the liver. The authors herein describe the case of a 60-year-old man with cirrhosis who developed unilateral enlargement of the breast and a subareolar mass. This problem was clinically thought to represent gynecomastia, but a mammary fine-needle aspiration biopsy demonstrated a malignant epithelial neoplasm composed of large granular amphophilic cells. Bile pigment was visualized in the tumor on aspirate smears and cell block preparations; immunostains showed reactivity for cytokeratin and alpha-fetoprotein, but there was no positivity for epithelial membrane antigen, gross cystic disease fluid protein-15, vimentin, estrogen receptors, progesterone receptors, or S100 protein. These results indicated a diagnosis of metastatic HCC, which was subsequently confirmed by computed tomography of the abdomen.
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PMID:Metastatic hepatocellular carcinoma of the breast, simulating gynecomastia: diagnosis by fine-needle aspiration biopsy. 133 27

This paper reports the application of Cox regression model in prognostic factors analysis of Primary Hepatocellular Carcinoma (PHC), based on the data obtained from 1618 registered of cases PHC and 432 hospitalized patients of PHC in ZhongShan City from 1980 to 1989. The result shows that there is an association between PHC and the following factors: extrahepato metastasis, therapeutic method, clinical stage, alpha-fetoprotein, gamma-glutamyl-transpeptidase, the number of tumors in the liver, the size of the tumor, icteric index and history of cirrhosis. Among these factors, clinical stage III, large liver cancer are unfavorable factors for PHC prognosis, while hepatectomy, hepatic artery catheterization chemotherapy, are favorable prognostic factors.
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PMID:[The analysis of prognostic factors of primary hepatocellular carcinoma with Cox model]. 133 14

Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B1 or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiation-promotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with CCl4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of alpha-fetoprotein or ferritin, nor was there a correlation with alpha-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal EH in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.
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PMID:Serum epoxide hydrolase (preneoplastic antigen) in human and experimental liver injury. 133 49

There is growing interest in screening to detect symptomless hepatocellular carcinoma (HCC), which should be easier to treat than symptomatic tumours. Combined alpha-fetoprotein and ultrasound monitoring can detect HCCs of 1 cm, and Lipiodol retention can be detected in tumours smaller than 1 cm. A number of treatment options are available. Surgical resection may be curative in selected patients with a single small tumour, but the cirrhotic patient is left with a diseased liver and the risk of tumour recurrence or death from underlying liver dysfunction. Orthotopic liver transplantation is a rational treatment for patients with decompensating cirrhosis and a small HCC, but it is expensive and necessitates immunosuppression. A variety of targeted or local therapies, either individually or in combination, can be used to treat HCC. These include percutaneous alcohol injection into an HCC, which may be an alternative to surgical resection. Tumour necrosis can be seen after targeted Lipiodol chemotherapy or radiotherapy. Transcatheter arterial embolisation selectively embolises the feeding artery, and can be combined with Lipiodol chemotherapy. Small tumours are thus amenable to treatment, even in patients who cannot have surgery. Screening and treatment for symptomless HCC seems justified, unless controlled trials teach us differently.
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PMID:Treatment of small hepatocellular carcinomas. 135 2

We evaluated the clinical usefulness of a protein induced by vitamin K absence, antagonist-prothrombin (PIVKA-II), in detecting hepatocellular carcinoma (HCC) specifically in patients with liver cirrhosis, and the possible correlation between levels of PIVKA-II and pathological features of HCC. Plasma levels of PIVKA-II and alpha-fetoprotein (AFP) were measured in 628 patients with various diseases, including 253 with liver cirrhosis and 116 with HCC. PIVKA-II was detected (greater than or equal to 0.1 arbitrary unit/mL) in 54.3% of HCC and the concentration showed a positive correlation with the tumour size. As a screening test for the detection of HCC, PIVKA-II produced values comparable with those of AFP with a sensitivity, specificity and validity of 52.8, 98.8 and 51.6% respectively. Sixteen of 45 patients (37%) with HCC who had low AFP (less than 100 ng/mL) levels were positive for PIVKA-II. No apparent relationship, however, could be found between the levels of PIVKA-II and the aetiology or pathological findings of HCC. These results suggest that PIVKA-II can be a reliable marker for detecting HCC in patients with liver cirrhosis.
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PMID:Plasma abnormal prothrombin (PIVKA-II): a new and reliable marker for the detection of hepatocellular carcinoma. 137 40

We determined the plasma levels of urokinase-type plasminogen activator (u-PA) antigen and alpha-fetoprotein (AFP) in 44 patients with different stages of liver cirrhosis and in 29 patients with liver cirrhosis-based primary liver cancer at the time of first clinical detection of the malignant disease. Sensitivity values of u-PA and AFP in detecting primary liver cancer were 57 and 62%, respectively, and specificity values were 95 and 86%, respectively. A combination of both markers led to a significant increase of sensitivity to 89.7%. The specificity of the combination of both markers was 97.3%. In tumor patients with unilocular disease and tumor patients with multicentric disease and/or metastatic spread, similar sensitivity values could be obtained with both markers. Therefore, a combination of u-PA and AFP can increase the accuracy of detection of primary liver cancer, especially in chronic liver diseases known to be predisposing for primary liver cancer, e.g., liver cirrhosis of long duration.
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PMID:Determination of plasma urokinase-type plasminogen activator antigen in patients with primary liver cancer: characterization as tumor-associated antigen and comparison with alpha-fetoprotein. 137 29

Clinical and experimental evidence indicates that estrogens are involved in the control of hepatocyte proliferation both in normal and in neoplastic conditions. Thirty-two cirrhotic patients with unresectable or otherwise untreatable hepatocellular carcinoma were allocated to receive either tamoxifen (30 mg/day) or no treatment. The patients in the two groups were matched for age, male/female ratio, Child-Pugh class, approximate tumor volume (US and CT scan), and etiology of the underlying cirrhosis. Survival of the tamoxifen-treated patients (life-table, Wilcoxon-Breslow) was significantly prolonged (P = 0.0038), with 35% (vs 0%) survival at 12 months. No difference was observed between males and females or between alcoholic and nonalcoholic cirrhosis. In 40% of tamoxifen-treated patients, the levels of alpha-fetoprotein declined. In conclusion, the antiestrogen tamoxifen appears to be effective in the palliative treatment of hepatocellular carcinoma. An initial decline in alpha-fetoprotein levels may represent an early favorable prognostic sign.
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PMID:Prospective controlled trial with antiestrogen drug tamoxifen in patients with unresectable hepatocellular carcinoma. 137 60

The patterns of sequential fluctuation of serum alpha-fetoprotein levels were analysed in 218 patients with liver cirrhosis in whom the serum alpha-fetoprotein levels were regularly and serially measured for more than 1 year. In the group of patients with persistently abnormal high values (greater than 50 ng/mL) over a follow-up period of more than 1 year, the incidence of the subsequent development of hepatocellular carcinoma was statistically and significantly higher (44%) compared to the other groups which showed normal (less than 20 ng/mL) or low abnormal levels (21-50 ng/mL) (16%), and transient abnormal high levels (greater than 50 ng/mL for a period of less than 1 year, mostly within 5 months) or fluctuated repeatedly between normal and transient abnormal high levels (23%). Hepatocellular carcinoma developed in 48 patients more than 2 years after the diagnosis of liver cirrhosis, and the fluctuating patterns of serum alpha-fetoprotein levels were analysed in these patients. The serum alpha-fetoprotein levels in 10 of these 48 patients stayed below 50 ng/mL until about 2.0-10.0 months before the detection of hepatocellular carcinoma and then increased steadily until the time of hepatocellular carcinoma detection. In these 10 patients, the monthly increasing ratios were approximately 1.6-4.8 times the previous values.
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PMID:A retrospective study on the patterns of sequential fluctuation of serum alpha-fetoprotein level during progression from liver cirrhosis to hepatocellular carcinoma. 137 64

The authors describe a case of HBsAg positive liver cirrhosis and elevated alpha-fetoprotein value (AFP) where imaging techniques failed to detect focal liver changes. Diagnosis of hepatocellular carcinoma was reached by ultrasound-guided fine needle aspiration biopsy of portal vein thrombosis.
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PMID:Diagnosis of hepatocellular carcinoma by fine needle biopsy of portal vein thrombosis. 137 76


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