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)

Primary liver cancer, particularly HCC, is increasing in certain countries, notably Japan. Although hepatitis B virus has been etiologically linked to hepatocarcinogenesis and integration of its DNA into hepatocyte chromosomal DNA has been emphasized, other etiologic factors seem to have an interplay with virus infection. Histopathology of HCC has geographic variations. An expanding encapsulated HCC is most common in Japan, whereas it is nearly nonexistent in the West; such regional differences can only be explained by differences in the major etiologic factors. Early detection of HCC is now possible with ultrasound examination combined with AFP measurement, and this strategy has been executed with success in the Far East where HCC is endemic among cirrhotics. The speed of tumor growth can be measured with accuracy by ultrasound examination. Preneoplastic or early lesions of HCC in a cirrhotic liver seem to be adenomatous hyperplastic nodules or foci, and the conventional histological criteria for malignant liver cells do not seem applicable to such lesions. Although advanced cirrhosis is a real deterrent for hepatic surgery, hepatic resection affords a better survival compared with any nonsurgical therapeutic modality. Transcatheter arterial embolization is one of the current preferences of the hepatologist for inoperable patients. Lastly, a new staging scheme has been proposed for the assessment of prognosis and for comparison of efficacy of various therapeutic modalities.
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PMID:Primary liver cancer. Quadrennial review lecture. 301 22

The pathologic findings of 232 consecutive cases of hepatocellular carcinoma (HCC) autopsied during the past ten years at Kurume, Japan, were analyzed from the point of view of global epidemiology, in relation to clinical feature, and in regard to incidence, age, sex, etiologic factors, size of liver, changes in noncancer parenchyma, gross type of tumor, extrahepatic metastases, intravascular and intraductal growths, cancer cell histology, hepatitis B surface antigen (HBsAg) in hepatocytes and cancer cells, liver cell dysplasia, and frequency and clinicopathologic characteristics of minute HCC. Furthermore, postmortem hepatic arteriography and portography were done in 152 livers for comparison with gross anatomy and celiac angiograms. It was found that: (1) epidemiologically, HCC in Japan is distinct from that in the West that it is frequently encapsulated, livers are generally small because of frequent and advanced cirrhosis and small cancer, minute HCC, is not uncommon at autopsy, cirrhosis most commonly associated is the one with thin stroma and medium size nodules, and micronodular cirrhosis is very rare despite frequent alcohol abuse; (2) HCC is increasing in incidence; (3) HBsAg is frequently found in parenchyma; (4) liver cell dysplasia is indirectly related to HBsAg with no evidence for premalignancy; (5) the lung is the most frequent site of metastasis but peritoneal dissemination is unusual; (6) intraportal tumor growth is very common and the hepatic vein is less frequently affected; (7) growth in the major bile duct is frequently associated with intraportal growth and clinically presents as obstructive jaundice; and (8) tumor is supplied solely by arteries and celiac arteriograms are closely correlated with gross pathologic findings.
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PMID:Pathology of hepatocellular carcinoma in Japan. 232 Consecutive cases autopsied in ten years. 629 17

The concentrations of N-terminal peptide of type III procollagen in the sera of patients with various cancers were measured by radioimmunoassay. The mean value (with standard deviation) in the control group was 9.9 +/- 2.6 ng/ml. Serum levels exceeding 15 ng/ml were defined as positive, and it was found that 94% of 18 patients with primary liver cancer with cirrhosis, 88% of 8 patients with primary liver cancer without cirrhosis, 77% of 13 patients with metastatic liver cancer, 86% of 7 patients with recurrent breast cancer, 86% of 8 patients with colonic cancer, 75% of 8 patients with pancreatic cancer, 70% of 23 patients with stomach cancer, 51% of 35 patients with lung cancer, and 54% of 28 patients with uterine cancer showed positive levels. The concentrations showed great intersubject variations, probably reflecting the activity of tumor growth and/or invasion. The concentrations in the sera of patients with primary liver cancer with cirrhosis were generally higher than those in patients with liver cirrhosis alone or primary liver cancer without cirrhosis. This result suggested that the growth of primary liver cancer complicated by cirrhosis might be detected by serial measurements of this peptide in the serum of patients with liver cirrhosis. Present data suggested that this peptide is not cancer-specific, but assay of the peptide might be of value as an auxiliary means of detecting and monitoring various cancers, especially liver cancer.
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PMID:High concentrations of N-terminal peptide of type III procollagen in the sera of patients with various cancers, with special reference to liver cancer. 673 30

Twenty-five cases of small hepatocellular carcinoma (HCC; diameter < or = 30 mm) were evaluated for overall morphologic features and growth patterns. The tumors often showed a well-differentiated, normotrabecular histologic pattern and insidious interstitial invasion, which resembled benign hepatocytes scattered in connective tissues. As the tumor grew, a less-differentiated tumor area became predominant. Portal tracts included in small HCC nodules were quantitatively assessed, revealing that they progressively reduced in number with tumor growth. The tumor margin was often reported to be unclear. The present results indicate that the histologic grade of tumor differentiation, capsular formation, existence of liver cirrhosis and patterns of interstitial invasion are important factors for determining the nature of the margin. The score of argyrophilic nuclear organizer regions (AgNOR) was examined in 5 cases showing typical interstitial invasion with the insidious type. In each case, the AgNOR score of the invading tumor cells was lower than that of tumor cells within the HCC nodules, but higher than benign hepatocytes in cirrhotic parenchyma. It clarified that the growth activity of well-differentiated HCC was rather suppressed upon their interstitial invasion.
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PMID:Growth patterns and interstitial invasion of small hepatocellular carcinoma. 764 31

To investigate the influence of alcohol intake on tumor growth of hepatocellular carcinoma (HCC) in patients with type C cirrhosis, we examined the tumor volume doubling time (TVDT) of 35 nodules from 35 cases of HCC, calculated through ultrasonographic imaging. The patients were divided into two groups according to their drinking habit; 21 habitual drinkers (alcohol group; 80g ethanol/day for 5 years), and 14 patients without alcohol abuse (non alcoholic group). The average value of TVDT in the alcoholic group was 78 +/- 47 days, although that of the non alcoholic group was 142 +/- 60 days. A statistically significant difference (p < 0.01) was found between the two groups. Of the 21 habitual alcohol drinkers, 8 refrained from drinking after detection of HCC; their TVDT was about 30 days shorter than those who continued alcohol intake. In conclusion we found that alcohol intake was closely related to the tumor growth of HCC in patients with type C cirrhosis.
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PMID:Effect of alcohol on tumor growth of hepatocellular carcinoma with type C cirrhosis. 883 93

Angiogenesis occurs in response to tissue damage, and is of vital importance for tumor growth and metastasis. Basic fibroblast growth factor (bFGF), a well-known angiogenic factor, has been suggested to be a useful diagnostic marker in certain hypervascular tumors. However, the relevance of its detection has not been well evaluated in patients with hepatocellular carcinoma (HCC) and benign chronic liver diseases. In the current study, immunoassay of bFGF was performed on serum samples from 39 patients with HCC, 21 with liver cirrhosis, 22 with chronic hepatitis and 40 normal subjects. The serum bFGF level was significantly increased in patients with liver cirrhosis and HCC when compared with those with chronic hepatitis or normal subjects (all p-values < 0.001). However, no difference was observed between the groups with liver cirrhosis and HCC (p > 0.05). If we set 9.6 pg/ml (mean + 3 standard deviations of bFGF in the control group) as the upper limit of normal serum level of bFGF, elevated bFGF concentrations were noted in 9.1%, 42.9% and 51.3% of patients with chronic hepatitis, liver cirrhosis and HCC respectively. In non-cancer patients, the coexistence of acute illness (p = 0.000) was an independent factor related to the elevation of serum bFGF. On the other hand, a multivariate analysis demonstrated that both advanced stage of cancer (p = 0.026) and coexistence of acute illness (p = 0.000) influence the serum level of bFGF in patients with HCC. We conclude that serum bFGF levels are significantly higher in patients with HCC and are positively correlated with advanced tumor stage. Nevertheless, elevation of serum bFGF may also be observed in a significant number of patients with liver cirrhosis. Therefore, measurement of serum bFGF alone cannot be satisfactory as a tumor marker for diagnosis of HCC. In addition, it is important to point out that coexistence of acute illness may be a crucial confounding factor in the diagnosis or monitoring of any cancer by the estimation of serum bFGF.
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PMID:Implications of serum basic fibroblast growth factor levels in chronic liver diseases and hepatocellular carcinoma. 925 19

The treatment of patients with compensated liver cirrhosis and small hepatocarcinomas remains controversial. Whereas partial hepatectomy (PH) is currently recommended, the role of orthotopic liver transplantation (OLT) has become progressively accepted. We used the techniques of decision analysis to measure the clinical benefits and the economic consequences of immediate resection versus transplantation in patients with compensated cirrhosis and who were diagnosed with small hepatocellular carcinoma (HCC). We restricted our analysis to patients with resectable carcinomas, which is either solitary tumor (< or = 5 cm in diameter), or multiple tumors (up to 3), none being > 3 cm in diameter and, in both cases, no tumor invasion of blood vessels. We took into account the risks of tumor spreading and dissemination and/or development of decompensated cirrhosis while waiting for donor organs because organ shortage is presented as the main obstacle to transplantation in these patients. Our analysis suggests that orthotopic liver transplantation (OLT) offers a substantial survival benefit compared with resection, ranging from a minimum of 1 year to a maximum of 4.7 years depending on treatment-related survival rates. However, the magnitude of this benefit relies on the availability of an organ donor; therefore, if the waiting period exceeds 6 to 10 months, depending on tumor growth pattern, the increase in life expectancy provided by transplantation is overwhelmed by the risks that patients face while waiting for transplantation. Consequently, partial resection becomes the preferred strategy. The predicted marginal cost-effectiveness ratios of transplantation compared with resection would range between $44,454 and $183,840 per additional year gained mainly influenced by the time delay before getting a transplant. We conclude that compared with partial hepatectomy (PH), OLT for resectable hepatocarcinoma(s) offers substantial survival benefit among well-targeted subgroups of patients as long as an organ donor is available within a maximal 6 to 10 months time delay, which is a plausible scenario in most centers with a liver transplant program. However, the marginal cost-effectiveness ratios incurred by this strategy are higher than that of many other current medical interventions.
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PMID:Partial hepatectomy or orthotopic liver transplantation for the treatment of resectable hepatocellular carcinoma? A cost-effectiveness perspective. 969 9

Hepatocellular carcinoma (HCC) presenting as obstructive jaundice due to intrabile duct tumor growth is being reported with increasing frequency. We describe our clinical experiences and evaluate the results of different operative procedures for this disease. A retrospective study was undertaken to review 18 patients with obstructive jaundice by tumor emboli from HCC during a 15-year period of time. We reviewed clinical features, types of operative procedures, operative findings, and survival in the patients. All patients on initial examination had recurrent episodic jaundice or cholangitis. Types of surgical procedures were choledochotomy with T-tube drainage alone in nine patients, choledochotomy with T-tube drainage followed by hepatectomy in six, and T-tube drainage followed by transcatheter hepatic arterial chemoembolization in the remaining three patients. Liver cirrhosis was the associated disease in 15 (83.3%). There were three postoperative deaths (16.7%). The mean survival time for nine patients with external drainage alone was 4.5 months. For the three patients with T-tube drainage and transcatheter hepatic arterial chemoembolization, mean survival time was 11 months. Six patients who had undergone hepatectomy had a better postoperative survival time, with 1 surviving for more than 3 years and another alive for 70 months, without evidence of recurrence at the moment. Jaundice is not necessarily a harbinger of advanced disease and a contraindication for surgery. Managed properly, these patients will have satisfactory palliation and occasional cure.
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PMID:Obstructive jaundice caused by tumor emboli from hepatocellular carcinoma. 1023 Dec 5

A 62-year-old Japanese man with hepatitis B virus-related liver cirrhosis revealed alpha-fetoprotein (AFP) elevation. Dynamic computed tomography, taken at this time, showed a liver tumor in the anterior segment. As the patient refused any further medical treatment, he was observed in an outpatient clinic. The size of the tumor reduced and the serum level of AFP decreased gradually without any treatment. Twelve months after the initial diagnosis, the tumor could not be detected by computed tomography (CT) scan, and the level of AFP had declined to the normal range. Blood supply is essential for tumor growth and an arterioportal shunt near the tumor may change the dynamics of blood flow to the tumor. The shunt found in this patient was thought to be one of the causative factors leading to regression, but it could not be denied that immunological mechanisms may have played an important role in the spontaneous regression of hepatocellular carcinoma.
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PMID:Spontaneous regression of hepatocellular carcinoma. 1043 23

Dipeptidyl peptidase (DPP) IV has roles in T-cell costimulation, chemokine biology, type-II diabetes and tumor biology. Fibroblast activation protein (FAP) has been implicated in tumor growth and cirrhosis. Here we describe DPP8, a novel human postproline dipeptidyl aminopeptidase that is homologous to DPPIV and FAP. Northern-blot hybridization showed that the tissue expression of DPP8 mRNA is ubiquitous, similar to that of DPPIV. The DPP8 gene was localized to chromosome 15q22, distinct from a closely related gene at 19p13.3 which we named DPP9. The full-length DPP8 cDNA codes for an 882-amino-acid protein that has about 27% identity and 51% similarity to DPPIV and FAP, but no transmembrane domain and no N-linked or O-linked glycosylation. Western blots and confocal microscopy of transfected COS-7 cells showed DPP8 to be a 100-kDa monomeric protein expressed in the cytoplasm. Purified recombinant DPP8 hydrolyzed the DPPIV substrates Ala-Pro, Arg-Pro and Gly-Pro. Thus recombinant DPP8 shares a postproline dipeptidyl aminopeptidase activity with DPPIV and FAP. DPP8 enzyme activity had a neutral pH optimum consistent with it being nonlysosomal. The similarities between DPP8 and DPPIV in tissue expression pattern and substrates suggests a potential role for DPP8 in T-cell activation and immune function.
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PMID:Cloning, expression and chromosomal localization of a novel human dipeptidyl peptidase (DPP) IV homolog, DPP8. 1101 66


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