Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because primary sclerosing cholangitis (PSC) frequently is associated with inflammatory bowel disease, the phenotypic and functional characteristics of lymphocytes isolated from colonic mucosa were studied in patients with primary sclerosing cholangitis (PSC), patients with ulcerative colitis and patients with other colonic and hepatic disorders. To accomplish this, lymphocytes isolated from colonic biopsies obtained at the time of colonoscopy were expanded in vitro in the presence of interleukin 2 (IL2). Cell propagation was similar in patients with PSC with or without associated inflammatory bowel disease but was diminished significantly when compared to results obtained in patients with ulcerative colitis not associated with PSC. The CD4:CD8 ratio of the propagated lymphocytes was increased in patients with PSC compared to controls. The Leu 19+ subset of cells was also increased in PSC patients. In patients with inflammatory bowel disease, increased cytotoxicity was noted at low effector to target cell ratios with SK-HEP (hepatocellular carcinoma) but not RPMI 7451 (cholangiocarcinoma) targets. No differences between PSC patients and controls were observed for NK sensitive and NK resistant targets. Based upon these studies it can be concluded that: 1) expansion of lymphocytes obtained from endoscopic colonic biopsies using recombinant IL2 represents an alternative method by which intestinal lymphocytes can be studied; 2) natural killer cells are increased in the colonic mucosa of patients with primary sclerosing cholangitis; 3) colonic cytotoxic T lymphocytes may be more active in patients with chronic liver disease and particularly those with associated inflammatory bowel disease.
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PMID:Phenotypic and functional characteristics of colonic lymphocytes isolated from patients with primary sclerosing cholangitis and inflammatory bowel disease. 759 May 74

Intrahepatic cholangiography of primary sclerosing cholangitis (PSC) is characterized by stricture with or without dilation of the biliary tree. To evaluate whether this cholangiographic appearance is present in non-PSC livers as well as the histological features seen in non-PSC livers with this cholangiographic appearance, we performed postmortem intrahepatic cholangiography in 154 liver autopsy specimens. The PSC-like cholangiographic appearance was frequently found in cirrhosis with or without hepatocellular carcinoma (4 of 6, 67%), hepatocellular carcinoma (1 of 1, 100%), adult-type polycystic disease of the liver and kidneys (2 of 3, 67%), submassive hepatic necrosis (2 of 5, 40%), amyloidosis (1 of 2, 50%), and intrahepatic extensive thrombosis (1 of 1, 100%). It was also found but at lower frequency in metastatic carcinomas (3 of 13, 23%) and leukemia/lymphoma infiltration (2 of 12, 17%). Histologically, in livers with such a PSC-like cholangiographic appearance, the intrahepatic bile ducts were compressed by fibrosis, inflammatory infiltrates, liver cysts, cancer cell infiltration, amyloid deposition, or portal thrombi. Dilated ducts had less pronounced changes than strictured ducts. In these hepatobiliary diseases, the changes of intrahepatic bile ducts in the livers without the PSC-like cholangiographic appearance were much less marked than those in the livers with it. These data suggest that the PSC-like intrahepatic cholangiographic appearance is present in several hepatobiliary diseases and that clinicians should take such diseases into consideration if stricture with or without dilation is found on intrahepatic cholangiography.
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PMID:Intrahepatic cholangiographic appearance simulating primary sclerosing cholangitis in several hepatobiliary diseases: a postmortem cholangiographic and histopathological study in 154 livers at autopsy. 904 38

The reason why 10% to 20% of all patients with primary sclerosing cholangitis (PSC) develop cholangiocarcinoma (CC) remains unknown. The aim of this study was to compare the clinical and biochemical presentation in PSC patients with and without hepatobiliary malignancy and to look for risk factors for developing hepatobiliary carcinoma in PSC. All PSC patients (n = 20) with hepatobiliary carcinoma treated at Huddinge Hospital between 1984 and 1995 were age- and sex-matched to 20 PSC patients with end-stage disease without carcinoma. Clinical and biochemical data from four different occasions (time of onset of PSC, 12 and 6 months before and at the time of cancer diagnosis or liver transplantation [Ltx]) were registered. Seventeen patients had CC, 2 had hepatocellular carcinoma (HCC), and 1 had gallbladder carcinoma (GBC). Eighteen of the cancer patients and 19 controls had inflammatory bowel disease (IBD). The number of patients who smoked or were former smokers was significantly higher in the cancer group (P < .0004). The duration of IBD and PSC, extra- and intrahepatic distribution of PSC, surgical and medical treatments did not differ between the two groups. Abdominal pain was the only symptom that was more frequent among cancer patients at the time of cancer diagnosis/Ltx compared with controls. Evaluation of biochemical data did not indicate a more rapid deterioration among cancer patients. The mean value of the tumor marker, CA 19-9, in the cancer group was 700 kU/L; in the control group, it was 46 kU/L (P < .05), although data were only available in 10 cancer patients and 7 controls. Bile duct dysplasia was found in over 60% of patients with PSC and CC in nontumorous liver tissue apart from the tumor. Clinical and biochemical presentation of PSC patients with and without hepatobiliary carcinoma did not differ during the year before cancer diagnosis/Ltx. Smoking seems to be a risk factor for developing hepatobiliary carcinoma in patients with PSC.
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PMID:Risk factors and clinical presentation of hepatobiliary carcinoma in patients with primary sclerosing cholangitis: a case-control study. 946 25

The serum concentrations of CA19-9 and carcinoembryonic antigen (CEA) were measured in 150 consecutive patients with histologically proven liver disease admitted to a liver unit for transplant assessment. A significant proportion of the cases studied had a CA19-9 above the upper limit of the reference range (35 kU/L): alcoholic liver disease (73%), primary sclerosing cholangitis (61%), primary biliary cirrhosis (60%), chronic hepatitis B (71%), chronic hepatitis C (84%), autoimmune hepatitis (36%) and hepatocellular carcinoma (54%). CEA was only elevated in a small proportion of the patients with benign liver disease and the degree of elevation was small (15-37 micrograms/L). Significantly raised CEA was observed in two patients (15%) with hepatocellular carcinoma. Statistically significant correlations were observed between the serum CA19-9 concentration and standard parameters of liver dysfunction: positive correlations with aspartate aminotransferase, alkaline phosphatase and bilirubin and negative correlations with albumin and gamma-glutamyltransferase. Positive relationships were also observed between CA19-9 and both CEA and creatinine. Both increased production of CA19-9 from biliary epithelial cells and decreased clearance due to cholestasis may be contributing to the elevation of CA19-9 in the bloodstream. Our data indicate that caution is needed in the interpretation of CA19-9 results in the presence of liver dysfunction.
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PMID:The effect of benign and malignant liver disease on the tumour markers CA19-9 and CEA. 946 46

Differentiating primary sclerosing cholangitis (PSC) from cholangiocarcinoma (CC) can be a diagnostic challenge with major therapeutic implications. In case of advanced or symptomatic PSC, liver transplantation (OLTx) can be life saving with excellent long-term outcome. However, the outcome of CC diagnosed prior or during OLTx is dismal. PSC is a premalignant condition associated with a risk of developing cholangio- or hepatocellular carcinoma in > 15% of patients. Imaging diagnoses should be integrated into the further clinical data. It is the sudden, rapid and irreversible deterioration of the patient's condition, and the rapid progression of cholangiographic abnormalities, which may strongly point towards a malignancy or a malignant evolution in case of PSC. Brush cytology, (guided) biopsy, and tumor markers such as Ca 19.9 and CEA levels can be of some help, but confirmation of malignancy is often associated with a poor outcome and exclusion from liver transplantation. Clinical deterioration of the PSC patient and signs indicating advanced liver damage are a justification to evaluate patients for liver transplantation. Early transplantation should be considered in appropriate patients.
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PMID:Primary sclerosing cholangitis and cholangiocarcinoma as a diagnostic and therapeutic dilemma. 1043 94

Cholangiocellular carcinomas (CCCs) of the peripheral type (not Klatskin tumors) appear sonographically as solid space-occupying lesions. No typical sonomorphological signs are known. Important hint for the clinician is the knowledge of earlier or accompanying diseases in which CCCs occur more often (primary sclerosing cholangitis, ulcerative colitis, intrahepatic gallstones, parasitic diseases of the bile ducts, choledochal cysts, Caroli's syndrome). Typical Color-Doppler signs are also missing. Definitive diagnostic is left to biopsy. Hepatocellular carcinomas (HCCs) mostly occur in cirrhotic livers. Every newly detected space-occupying lesion in a cirrhotic liver is suspected of HCC until otherwise proven, even when AFP-levels are normal. AFP levels constantly higher than 400 ng/ml make HCC probable, AFP levels of 2000 ng/ml ore more proof HCC. Gray-scale imaging is not uniform and not guiding. Using Color-Doppler nearly all HCCs show markedly hyperperfusion compared to the surrounding liver tissue, vessels are arranged in a chaotic shape. Echo-enhanced Color-Doppler always shows a distinct early arterial hyperperfusion.
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PMID:[Enhanced imaging diagnosis of liver carcinomas. Technical progress is not a substitute for clinical knowledge]. 1085 80

Liver transplantation is the established therapy of choice for endstages of acute and chronic liver diseases of various aetiologies. The place of liver transplantation in the treatment of malignant liver disease, in particular hepatocellular carcinoma, remains, however, debated: liver transplantation for hepatocellular carcinoma achieves 5-year survival similar to that for other indications, and 5-year disease-free survival better than that following "curative" resection, provided certain criteria are fulfilled (one node max. 5 cm in diameter or max. 3 nodes each of max. 3 cm in diameter). This must be weighed against the uncertainties of preoperative staging and the shortage of donor organs. In contrast, cholangiocarcinoma has a poor prognosis after liver transplantation with 3- and 5-year survival rates below 20%. Only small, incidental, peripheral, intrahepatic cholangiocarcinomas in patients with primary sclerosing cholangitis seem to be an exception to this rule. Liver metastases indicate generalised tumour spread, and thus are not an indication for liver transplantation. Liver transplantation may be justified for liver metastases of neuroendocrine gastrointestinal tumours, provided the primary has been curatively resected and there is no extrahepatic spread. Finally, liver-transplanted (immunosuppressed) patients are at increased risk to develop malignant tumours. This includes in particular epithelial skin tumours, (EBV-associated lymphoproliferative diseases and (HHV8-induced) Kaposi's sarcoma.
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PMID:[Liver transplantation and tumors: risk and chance]. 1090 24

Primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC) are chronic progressive cholestatic diseases that frequently lead to biliary cirrhosis. The exact pathogenesis of these diseases remains elusive but is likely immunologically based. Complications range from fatigue and pruritus to end-stage liver disease. The risk of developing hepatocellular carcinoma is low for patients with PBC, whereas cholangiocarcinoma is common in PSC and carries an ominous prognosis. Although ursodeoxycholic acid is effective in slowing the progression of PBC, no effective medical therapy exists for PSC. Liver transplantation is the only option for patients with end-stage liver disease and yields excellent long-term survival in both groups.
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PMID:Biliary tract inflammatory disorders: primary sclerosing cholangitis and primary biliary cirrhosis. 1098 Sep 34

Telomerase, a ribonucleoprotein enzyme associated with cellular immortality, consists of human telomerase RNA component (hTERC), human telomerase protein 1 (hTEP1), and human telomerase reverse transcriptase (hTERT). In this study, the expression of these subunits was examined in non-neoplastic livers [13 cases of chronic viral hepatitis (CVH), 16 of primary biliary cirrhosis (PBC), two of primary sclerosing cholangitis, and six normal livers], using the reverse transcription-polymerase chain reaction (RT-PCR), nested PCR, and in situ hybridization (ISH). Six hepatocellular carcinoma (HCC) cases and one colonic cancer were used as positive controls. Telomeric repeat amplification protocol (TRAP) assay disclosed distinct telomerase activity in all positive controls and weak telomerase activity in non-neoplastic livers in 4 of 13 CVH cases and 5 of 16 PBC cases. By RT- and nested PCR, both hTERC and hTEP1 mRNA were detectable in all non-neoplastic liver tissues; ISH revealed hTERC and hTEP1 mRNA in the periportal and periseptal hepatocytes and inflammatory mononuclear cells in those cases examined. ISH revealed hTERT mRNA only in a few infiltrating mononuclear cells in 3 of 13 CVH and 2 of 16 PBC livers and these five cases were also positive by TRAP assay. In four of these five cases, hTERT mRNA was also detectable by nested PCR, suggesting that hTERT mRNA in the non-neoplastic liver is expressed by infiltrating mononuclear cells. Biliary epithelial cells were totally negative for these human telomerase subunits. Three subunits were constantly detected in all positive controls by ISH as well as by RT- and nested PCR. The finding that hTERC and hTEP1 mRNA, but not hTERT mRNA, were detectable in the non-neoplastic hepatocytes suggests that telomerase is present but not activated and that additional factor(s) are necessary for the expression of hTERT mRNA in the hepatocytes, along with immortalization and neoplastic transformation.
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PMID:PCR and in situ hybridization studies of telomerase subunits in human non-neoplastic livers. 1118 Jan 68

The diagnostic relevance of laparoscopy (LS) and laparoscopic echography (LE) in nodular hepatocellular lesions is studied. LS is done using a R. Wolf laparoscope, and LE--with a 7.5 MHz linear transducer, obtained from the Aloka Company. A total of 250 patients presenting 288 nodular hepatocellular lesions are investigated over 15 years (1983-1998), including: focal nodular hyperplasia (FNH)--1, nodular regenerative hyperplasia (NRH)--1, hepatocellular adenoma (HCA)--1, adenomatous hyperplasia (AH)--38, hepatocellular carcinoma (HCC)--58, Budd-Chiari syndrome--2, primary sclerosing cholangitis (PSCh)--2, and cirrhosis of liver--185. The lesions are distributed according to the updated classification of the International Working Party, published in 1995. In addition to the latter, a case of cholangiocellular adenoma undergoing malignant degeneration and a case presenting carcinoma, giving rise to differential diagnostic difficulties are also described. Some of the aforementioned diseases are reported for the first time in the Bulgarian literature. Emphasis is laid on the practicability of combining endoscopic with imaging diagnostics, attributable to laparoscopic echography and to the advantages of echolaparoscopic biopsy. Almost half of the foci (46.1%) are morphologically verified. The aim of cytological assessment is to establish the malignant character of the lesion, first and foremost, while the histological finding is essential for making a correct diagnosis.
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PMID:[The role of laparoscopy and laparoscopic ultrasonography in the diagnosis and differential diagnosis of nodular hepatocellular lesions]. 1124 62


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