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

Cirrhosis is a late stage finding in chronic liver diseases of different aetiology. It is defined morphologically as a diffuse process with the presence of fibrosis and structurally abnormal nodules. The consequences of cirrhosis are both, mechanical and functional. The mechanical complications result from intra- and extrahepatic shunting of blood and portal hypertension while the functional relevance bases upon a failure of liver cells to perform their physiological role in metabolism, synthesis and secretion. Beside these complications that are directly linked to liver function cirrhosis in itself is a risk factor for hepatocellular carcinoma.
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PMID:[Pathology of liver cirrhosis and portal hypertension]. 1171 74

Hepatocellular carcinoma mainly affects patients with liver disease and rarely develops in healthy liver. Cirrhosis greatly increases the risk of developing this malignancy and consequently these patients are candidates for close follow-up and surveillance. The most commonly used screening programs are abdominal ultrasonography and serum alpha-fetoprotein determination. Without treatment, the prognosis of hepatocellular carcinoma is poor and mortality continues to be significant even in patients with small tumors detected during follow-up. We present the case of a 71-year-old male patient with alcoholic cirrhosis. The patient was diagnosed during follow-up of a single hepatocellular carcinoma of 4 cm in diameter. Although he refused all treatment, evolution was favorable, serum alpha-fetoprotein levels returned to normal and ultrasonographic images compatible with hepatocellular carcinoma disappeared. Three years after diagnosis, the patient was completely asymptomatic.
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PMID:[Spontaneous regression of hepatocellular carcinoma in a cirrhotic patient]. 1173 Jun 20

Cirrhosis is a diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. The modified Child-Pugh score, which ranks the severity of cirrhosis based on signs and liver function test results, has been shown to predict survival. Strategies have been established to prevent complications in patients with cirrhosis. Esophageal varices can be identified by endoscopy; if large varices are present, prophylactic nonselective beta blocker therapy should be administered. Alpha-fetoprotein testing and ultrasonography can be effective in screening for hepatocellular carcinoma. Vaccines should be administered to prevent secondary infections. The use of nonsteroidal anti-inflammatory drugs should be avoided, and patients should maintain a balanced diet containing 1 to 1.5 g of protein per kg per day. An extensive assessment should be performed before patients with cirrhosis undergo elective surgery. Before advanced liver decompensation occurs, patients should be referred for liver transplantation evaluation. If advanced cirrhosis is present and transplantation is not feasible, survival is between one and two years.
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PMID:Preventive strategies in chronic liver disease: part II. Cirrhosis. 1175 80

Cirrhosis is a diffuse liver disease with premalignant potential in which hepatocellular carcinoma (HCC) frequently develops. The hemodynamics of contrast material are the key to diagnosis of focal liver lesions with computed tomography (CT). Lesions with arterial-dominant vascularity, such as HCC, show brisk enhancement during the arterial phase, whereas lesions with portal blood supply can appear as hyperenhancing lesions in the portal phase. The advent of helical CT has significantly improved the CT examination of the liver because the arterial phase can be displayed independently of the portal phase. The addition of arterial phase imaging to conventional portal phase imaging seems to improve tumor detection and characterization. Although HCC is the single most frequent tumor seen in chronic liver disease, other lesions such as peripheral cholangiocarcinoma and hemangioma should be considered in the differential diagnosis. Optimization of helical CT techniques may allow better detection and characterization of these lesions. In addition to tumor detection, CT plays an important role in preoperative staging of HCC as well as in preoperative assessment of patient candidates to hepatic transplantation. The use of CT angiography with maximum intensity projection techniques may allow for better preoperative work-up and vascular mapping in HCC patients. This article shows the spectrum of helical CT findings in chronic liver disease and specifically in the imaging of HCC and other focal lesions.
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PMID:CT in hepatic cirrhosis and chronic hepatitis. 1186 22

Chronic hepatitis C infection (HCV) accounts for approximately 50% of the cases of hepatocellular carcinoma (HCC) in the United States. Cirrhosis or an advanced stage of fibrosis is the major risk factor of HCC; patients with cirrhosis are recommended to undergo surveillance with alpha-fetoprotein and ultrasound. Alpha interferon (IFN-alpha) is associated with a reduced risk of HCC in patients with chronic infection but insufficient data exist to recommend treatment of patients with cirrhosis and HCV for this reason alone. Resection and liver transplantation are the only "curative" therapies available. Advanced fibrosis or cirrhosis in patients with HCC limits the number of patients for whom resection is applicable. Moreover, the remaining liver is at high risk of developing a second primary tumor. Partial hepatic resection for hepatocellular carcinoma should be restricted to patients with well-compensated cirrhosis (Child's A class). Acceptable parameters include a single lesion not exceeding 5 cm, normal levels of bilirubin, and absence of portal hypertension. Liver transplantation is the best definitive treatment for HCV-infected patients who have small, localized HCC (solitary lesion not greater than 5 cm, or no more than 3 lesions, none of which are greater than 3 cm). Limitations of liver transplantation as a therapy for HCC are the scarcity of donor organs and the prolonged waiting time during which continued tumor growth occurs. Living donors can reduce waiting time and increase the number of patients treatable by transplantation. Chemoembolization and local ablation therapies have not been shown to confer survival benefits as primary treatments for HCC. The potential benefit of these procedures in controlling tumor growth to "bridge" patients to liver transplantation must be further investigated. Similarly, systemic chemotherapy and hormonal therapy do not generally produce a survival advantage. However, recent studies that used octreotide and combination doxorubicin/cisplatin/5-FU/interferon appear to be promising.
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PMID:Hepatitis C and hepatocellular carcinoma. 1205 93

The constellation of histopathologic lesions that characterize alcoholic and nonalcoholic steatohepatitis has been well described and has served as the basis for clinical diagnosis, natural history studies, and experimental models for analyses of etiopathogenesis. The lesions common to both entities include, to varying degrees, steatosis, liver cell ballooning, lobular inflammation with a notable component of polymorphonuclear leukocytes, and a characteristic form of fibrosis that is initially located in the perisinusoidal regions of acinar zone 3. Cirrhosis with or without steatosis or steatohepatitis may occur in both entities. Mallory's hyaline is common but not necessary; megamitochondria and varying amounts of iron may be observed in either process. Hepatocellular carcinoma is a recognized complication of both processes, albeit with greater frequency in the former. Alcoholic hepatitis may present with more severe clinical and histologic manifestations than the nonalcoholic counterpart, including significant morbidity and mortality. The perivenular lesions collectively referred to as sclerosing hyaline necrosis are markers of severity, and are not common in nonalcoholics. In many instances, however, the microscopic lesions of these two processes are similar, likely as a reflection of common pathogenetic pathways, and the distinction between the two is ultimately clinically derived.
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PMID:Alcoholic and nonalcoholic steatohepatitis. 1212 63

One of the main regulatory pathways reported to be altered in hepatocellular carcinoma (HCC) is that of cell cycle control involving RB1 gene-related cell inhibitors. We investigated p14(ARF), p15(INK4B), p16(INK4A), p18(INK4C), and RB1 genes in a series of HCCs and associated cirrhosis with the goal of ascertaining their pattern of inactivation by gene methylation. Thirty-three HCCs, adjacent nonneoplastic cirrhotic tissues, and 6 HCC cell lines were studied. Cirrhoses (25 of 33, 76%), HCCs (31 of 33, 94%), and 3 of 6 (50%) cell lines showed 1 or more methylated genes. Cirrhoses (17 of 33, 51%) had more frequently than HCCs (11 of 33, 33%, P =.01) only 1 methylated gene. With the exception of p18(INK4C) the genes under study showed promoter methylation with frequency ranging from 82% (p16(INK4A) in HCC) to 33% and 39% (p15(INK4B) and p16(INK4A) in cirrhoses). In cases with only 1 methylated gene, p15(INK4B) in cirrhosis (8 of 17, 47%) and p16(INK4A) in HCC (10 of 11, 91%) were the more frequently altered. An optimal correlation was found between p15 and p16 gene methylation and complete protein loss in HCC detected by immunocytochemistry, whereas a partial loss of the same proteins was a feature of methylated cirrhoses. Inactivation by DNA methylation of several genes of the RB1 pathway is common to cirrhosis and HCC. An early pattern of methylatory events (1 methylated gene) is a feature of cirrhosis rather than HCC, whereas an advanced one (> or = 3 methylated genes) is characteristic of malignancy. Early methylation changes seem to involve p15(INK4B) and p16(INK4A) in cirrhosis and p16(INK4A) in HCC. In conclusion, a stepwise progression of methylating events is a feature of the sequence cirrhosis-HCC and contributes to the process of hepatic carcinogenesis with potential clinical implications.
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PMID:Methylation framework of cell cycle gene inhibitors in cirrhosis and associated hepatocellular carcinoma. 1214 52

Cirrhosis predisposes to hepatocellular carcinoma (HCC) which develops by sequential steps of de-differentiation of hepatocytes from regenerative nodules via borderline (dysplastic) nodules to frankly malignant HCC. Effective treatment depends on early recognition of HCC, so the key tasks for imaging are firstly recognising the presence of a suspicious lesion, and secondly differentiating between benign, borderline and malignant nodules. Screening of high-risk cirrhotic patients with sonography and measurement of alpha fetoprotein (AFP) is helpful but will not reliably differentiate small HCC from benign or dysplastic nodules. Large HCCs can usually be recognised by their characteristic morphology on imaging, but the appearances of smaller benign and malignant nodules show considerable overlap on unenhanced sonography, CT and MRI. Increasing degrees of histological malignancy are associated with increasing arterialisation and loss of portal blood supply, so the recognition of HCC requires the use of dynamic imaging with contrast-enhanced CT or T1-weighted MRI with gadolinium enhancement. Sonography with microbubble contrast media now offers another method for detecting arterialised nodules; however, some non-malignant nodules show arterial hypervascularity and a minority of HCCs are hypovascular, so the assessment of perfusion does not conclusively distinguish benign from malignant lesions. Kupffer cell function is another attribute of liver tissue which can be explored using MRI with superparamagnetic iron oxide particles (SPIO). Experience thus far suggests that uptake of SPIO is an effective discriminator between benign and malignant nodules. The combination of SPIO with gadolinium-enhanced MRI offers the opportunity for imaging characterisation of cirrhotic nodules by cellular function as well as by blood supply, and this approach is now proposed as the examination of choice for detecting HCC in cirrhosis.
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PMID:How to detect hepatocellular carcinoma in cirrhosis. 1219 79

Cirrhosis of the liver has to be regarded as a premalignant condition independent of its etiology. The annual risk of developing HCC in cirrhosis is between 1% and 6%. Surveillance-programs have been introduced to detect early stages of HCC in order to improve mortality. However, only controlled trials will answer the question of the efficacy of such programs. Studies on the potential benefit of surveillance-programs comparing survival in surveilled and unsurveilled patients are so far lacking. It seems clear, however, that surveillance-programs can detect small tumors, often unfocal and potentially treatable by a curative approach. Moreover, the etiology (HBV, HCV, genetic hemochromatosis) and activity of liver cirrhosis as measured by serum-transaminases, liver histology (small-cell dysplasia and atypical regenerative nodules), Child-Pugh-stage and the concentration of alpha-fetoprotein at the beginning of a surveillance-program--all these factors reflect a high risk of developing HCC in an individual patient. Until programs are introduced on the basis of randomized, controlled trials of surveillance vs. usual care (with liver-related, specific deaths and all-cause-mortality as end-points) it seems reasonable to screen high-risk patients semi-annually by liver ultrasound and determination of AFP-concentration in the serum.
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PMID:[Hepatocellular carcinoma: risk groups--screening]. 1223 79

Hepatocellular carcinoma (HCC) has a tendency for fatal spontaneous rupture leading to massive hemorrhage. The majority of such ruptures of HCC occur in the liver, while a few previous studies showed that such HCC rupture developed at metastatic sites including the lung, pleura, spleen, and peritoneum. We here report a case of hepatitis C virus-related HCC with spontaneous rupture of a peripancreatic lymph node with HCC metastases. A 61-year-old Japanese man died of hepatic failure after therapy for cirrhosis and HCC for 6 years. At autopsy, the liver showed diffuse multinodular HCC in both lobes. Metastases were found in lumbar vertebral bones and abdominal lymph nodes of the hepatic hilar, peripancreatic and perigastric regions. One lymph node (4 cm in diameter) around the pancreatic head was found ruptured, and blood coagula (100 g) was present around the ruptured node. Pure blood of 2000 ml was noted in the peritoneal cavity. Cirrhosis was not recognized. Histologically, the liver tumors and metastases in the lumbar vertebral bones and abdominal lymph nodes were poorly-differentiated HCC of Edmondson's grade III. The ruptured lymph node was almost replaced by poorly-differentiated HCC, and the ruptured site showed hemorrhage, breakdown of the capsule, and ischemic changes. Non-tumorous liver showed chronic hepatitis C. The immediate cause of death was suggested to be circulatory insufficiency due to rupture of the lymph node and/or hepatic failure. The present case showed that abdominal lymph nodes with HCC metastases may rupture and cause severe hemorrhage in the peritoneal cavity, leading to death.
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PMID:Spontaneous rupture of peripancreatic lymph node with hepatocellular carcinoma metastasis: report of an autopsy case with massive peritoneal bleeding. 1278 8


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