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

Data provided by 51 voluntary blood donors identified as asymptomatic HBsAg carriers five to ten years (mean = 7.5 years) before their inclusion in the study are analysed towards their long-term evolution. HBsAg clearance was estimated 2.5% yearly and 83.9% of those remaining positive showed the classical non-replicative serological pattern; another 12.9% were negative for both HBeAg-Anti HBe (seroconversion window?), one of them presenting raised ASAT-ALAT levels and enhanced histological activity (lobular chronic hepatitis). Neither alpha-fetoprotein seric levels (RIA) nor liver ultrasonography demonstrated hepatocellular carcinoma suspicion signs in 35 HBsAg positive cases to this methods; ASAT-ALAT levels raised over two fold the normal superior limit in only 11.4%, and neither aggressive chronic liver disease nor hepatocyte dysplasia was showed in 17 biopsied cases (70.6% normal; 23.6% chronic reactive or chronic persistent hepatitis; 5.8% chronic lobular hepatitis). One out of five patients biopsied with a seven years interval showed histologic worsening.
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PMID:[Long-term course in asymptomatic carriers of HBsAg in an area of low prevalence of hepatocarcinoma]. 248 74

We reviewed 40 liver biopsy specimens from 36 patients with non-A, non-B (NANB) hepatitis by light microscopy to characterize the histopathologic features associated with this condition. NANB hepatitis had been acquired from intravenous drug use (6 patients), transfusion (11 patients), sporadic (13 patients), and other routes (6 patients). The major pathologic diagnoses included acute hepatitis, chronic persistent hepatitis, chronic lobular hepatitis, chronic active hepatitis with or without cirrhosis, and hepatocellular carcinoma. Histopathologic changes seen in varied combinations in these specimens included acidophilic degeneration of hepatocytes (100%), fat (85%), formation of portal tract lymphoid aggregates or follicles (52%), bile duct damage (30%), and multinucleate giant hepatocytes (25%). Prominence of sinusoidal cells was variable, but often striking. Hepatocyte atypia (liver cell dysplasia) was noted in 17 specimens. These histologic parameters appear to be diagnostically useful when applied in appropriate clinical settings and will require reevaluation when serologic tests for NANB hepatitis become available.
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PMID:Non-A, non-B hepatitis: characterization of liver biopsy pathology. 250 Apr 77

Hereditary tyrosinemia type I presents with either acute hepatic failure in the neonatal period or later in infancy with progressive liver dysfunction secondary to cirrhosis. The inevitably fatal outcome in those children with the chronic form has been transformed with the advent of liver transplantation. Native livers from five children who received allografts were studied pathologically and compared with earlier hepatic biopsies in two of these patients that had been performed several years before transplantation. Our findings support the conclusion that a sequence of morphologic changes from the initial micronodular cirrhosis through an intermediate mixed cirrhotic pattern to macronodular cirrhosis occurs. The micronodular phase is transitory, over a period of only a few months, since mixed micronodular macronodular cirrhosis was already present in the livers of children who received transplants by 11 months of age. Focal hepatocellular dysplasia was present in one of the livers with mixed cirrhosis but was not identified in the other two cases. Macronodular cirrhosis accompanied two cases of hepatocellular carcinoma in this study. In order to preclude the latter complication, liver replacement is necessary before the age of 2 years.
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PMID:Hereditary tyrosinemia type I (chronic form): pathologic findings in the liver. 253 31

A hepatocellular carcinoma (HCC) measuring 0.2 cm in diameter was found in the center of an adenomatous hyperplasia (AH) measuring 1.7 cm in diameter in a cirrhotic liver. The liver cells of the AH showed a marked fatty change and contained many Mallory bodies. The AH and HCC were studied in relation to liver cell dysplasia in 108 surgically resected livers. The AH was mainly associated with fully developed cirrhosis in 5 (71%) of the 7 cases. The liver cell dysplasia, however was accompanied largely by fibrosis and early-stage incomplete septal cirrhosis in 10 (67%) of the 15 cases. As far as the active inflammatory change was concerned, a fairly active inflammation was found in only 3 (20%) of the 15 livers with liver cell dysplasia, but in 4 (57%) of the 7 livers with AH.
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PMID:Hepatocellular carcinoma in adenomatous hyperplasia of the liver. 253 56

Liver cell dysplasia (LCD) has been recognised for many years in association with hepatocellular carcinoma (HCC). The presence of LCD relates to cirrhosis, particularly macronodular, as well as HBsAg positivity in many countries. These relationships have not previously been recognised in southern Africa. This study of LCD in 160 rural and urban black patients with proven HCC records a significant difference between the prevalence of dysplasia in rural HBsAg-positive and -negative cases: 75.6% in HBsAg+ individuals vs. 29.4% of those negative for HBsAg (P less than 0.01). Furthermore a significant relationship is reported between dysplasia and macronodular cirrhosis, LCD being observed in 62.9% of those with macronodular cirrhosis vs. 29.5% of non-cirrhotics (P less than 0.001). In addition there was evidence for a relationship between severity of dysplasia and domicile (rural greater than urban), age (being more extensive in younger patients), and ongoing viral replication (82.3% of patients showing the highest grade of dysplasia were found to be serum HBeAg+ and/or tissue HBcAg+ cf. 3.7% with absent or low-grade dysplasia). It is apparent that in southern Africa the presence of dysplasia in HBsAg+ individuals implies that HCC should be actively excluded in these patients and that they should thereafter be carefully monitored for the development of a tumour.
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PMID:Liver cell dysplasia accompanying hepatocellular carcinoma in southern Africa. Differences between urban and rural populations. 254 Nov 97

Hepatocellular carcinoma is closely associated with cirrhosis, but it also develops, although much less frequently, in a noncirrhotic liver. It is suspected, without supporting evidence, that hepatocellular carcinoma has a different etiology when associated and not associated with chronic liver disease. In this study, 66 noncirrhotic cases found among 618 autopsies for hepatocellular carcinoma (10.7%) were analyzed retrospectively. The noncirrhotic liver was histologically unremarkable in 3 cases and in the histologically evaluable 56 cases it had fibrosis of varying degrees or mild cellular infiltrate, or both, in the portal tract. There was one liver that had portal venous changes compatible with those in idiopathic portal hypertension (Banti's syndrome). In these noncirrhotic livers, the parenchymal cells were generally unremarkable except for liver cell dysplasia that was seen in 26.8%. Serum hepatitis B surface antigen was positive in only 7.4% in contrast to 26.6% in cirrhotic cases. Three histologically unremarkable cases had no clinical or histologic evidence of chronic liver disease; two involved painter-plasterers and one a farmer. The liver weight in these cases ranged from 4400 to 6180 g. In contrast, the average liver weight in cirrhotic cases was 1998 g. Noncirrhotic patients when compared with cirrhotic patients had better liver function tests and much less frequent varices. It was concluded that approximately 11% of hepatocellular carcinoma cases in Japan are noncirrhotic, the majority having some histologic changes in the portal tracts suggestive of past or ongoing chronic liver disease, and that there are rare cases that have no histologic changes in the liver.
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PMID:Hepatocellular carcinoma without cirrhosis in Japanese patients. 254 16

Non-neoplastic morphologic changes in various types of cirrhosis were evaluated in relationship to the presence or absence of hepatocellular carcinoma (HCC), using autopsy livers from Hokuriku (Japan) and Los Angeles (USA). Macronodular cirrhosis was closely related to HCC in B-viral cirrhosis, alcoholic cirrhosis and cirrhosis of uncertain type. Liver cell dysplasia was most frequently seen in cases with and without HCC in B-viral cirrhosis but was significantly more frequent with HCC in cases of alcoholic cirrhosis and cirrhosis of uncertain type. Nodular bulging activity within regenerative nodules was closely related to HCC in alcoholic cirrhosis. A positive relationship between HCC and Mallory bodies was found in non-alcoholic cirrhosis. These data suggest that patients with macronodular cirrhosis, liver cell dysplasia, nodular bulging activity and Mallory bodies may have an increased risk of developing, or having HCC dependent on the etiology of cirrhosis. The geography and race differences had some relationship to the incidence of HCC.
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PMID:Risk lesions in cirrhosis and development of hepatocellular carcinoma: an autopsy study. 254 32

In the light of recent findings concerning the importance of intermediate alpha 1-antitrypsin deficiency in the development of chronic liver disease and of hepatocellular carcinoma, we report the case of a 56-year-old woman affected by cirrhosis with significant features of liver cell dysplasia associated with intermediate alpha 1-antitrypsin deficiency (protease inhibitor SZ phenotype). In our paper we emphasize the importance of a precocious diagnosis and identification of individuals carrying the Z allele, also heterozygous.
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PMID:Alpha-1-antitrypsin protease inhibitor SZ phenotype and liver cirrhosis. 278 75

We have examined the relationship between hepatitis B virus infection and hepatocellular carcinoma in a series of 50 British patients with histologically-proven hepatocellular carcinoma. Serum HBsAg was detected in 10 patients (20 per cent), and of the remainder, 21 per cent of those tested had serological evidence of past hepatitis B virus exposure. None of nine tumour specimens from serum HBsAg negative patients had detectable HBV-DNA integration into the tumour cell genome. The presence or absence of serum HBsAg was of no prognostic significance in British patients with hepatocellular carcinoma. Liver cell dysplasia, a possible pre-malignant lesion, was noted in 53 per cent of patients who had had liver biopsies before the diagnosis of hepatocellular carcinoma, and in 79 per cent of biopsies taken at the time of diagnosis of hepatocellular carcinoma. The presence of liver cell dysplasia was not more common in serum HBsAg positive patients.
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PMID:Hepatocellular carcinoma and the hepatitis B virus: a study of British patients. 282 69

The livers of 345 autopsy cases of chronic liver disease were examined for macroregenerative nodule (MRN), a large nodular lesion more than 10 mm in diameter. A total of 86 lesions of MRN was found in 49 cases (14.2%): 32 were from 191 cases of hepatocellular carcinoma (HCC), 16 were from 148 cases of cirrhosis only, and one was from six cases of chronic hepatitis. The incidence (19.6%) and the size (12.1 mm) of MRN in macronodular type of cirrhosis were significantly higher and larger than those in other types of cirrhosis. Also, the average size of MRN lesions of cases with HCC (12 mm) was significantly larger than that of cases with cirrhosis only (10.5 mm). The incidence of liver cell dysplasia (LCD) in cases of MRN (67.3%) was significantly higher than that in cases without MRN (40.9%). The MRN lesions were divided into Type I and Type II, the latter having proliferative foci distinguishable from the surrounding tissue. Three of them contained atypical cells regarded as cancer. Type II lesions were larger in size, and cases with multiple MRN lesions were seen more frequently in cases of HCC. The average age of the patients with Type II lesion was 5 years older than those with Type I lesions. These findings suggest that MRN should not be ignored in the morphogenesis of HCC.
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PMID:Macroregenerative nodule of the liver. A clinicopathologic study of 345 autopsy cases of chronic liver disease. 282 60


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