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Query: UMLS:C0345904 (liver cancer)
15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent technical and clinical advances in MR of the liver are reviewed with special reference to the role of MR as a primary screening technique for detection of space-occupying lesions, especially metastases. The major current problem in upper abdominal MR imaging is physiologic motions, and this appears to have been effectively solved by newly introduced pulse-sequence and timing-parameter strategies. Short-TR/TE spin-echo sequences with extensive signal averaging and heavy T1-weighting produce images with exceptional anatomic detail and liver-cancer contrast differences. With this sequence superior sensitivity for liver-cancer detection has been shown in quantitative signal-difference to noise comparisons with other pulse sequences and in clinical comparisons with CT. MR discovered 14% more individual metastases and 3% more patients with liver cancer than CT in a blinded comparative study of 142 patients undergoing both exams. MR also showed greater specificity (98%) than CT (91%) in distinguishing patients without liver metastases. Differentiation of hemangioma from metastases was possible with greater than 90% specificity by using heavily T2-weighted sequences. Use of a fast-scan, gradient-recalled echo technique can also produce good-quality, multislice, T1-weighted studies of the liver in 20 sec--a breath-hold. MR contrast agents (such as gadolinium-DTPA and reticuloendothelial-system-specific, superparamagnetic ferrite-iron-oxide particles) offer further promise for enhanced sensitivity for liver-cancer detection. When optimal pulse sequences are employed, MR can now be appropriate as a primary screening method for detecting liver neoplasms.
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PMID:Leo J. Rigler lecture. MR imaging of the liver. 349 Jul 43

Primary hemochromatosis is a genetic disorder rarely recognized in childhood; its long-term consequences include cirrhosis and liver cancer. We report a family with primary hemochromatosis affecting three generations, including a 7-year-old child and a 29-month-old child; these are the youngest children with primary hemochromatosis yet reported. The pathophysiology, genetics, and clinical findings of this disorder are reviewed. Serum ferritin and transferrin saturation are useful screening tests; definitive diagnosis, however, depends on determination of hepatic iron content. A plan for evaluating and treating affected patients is proposed. Physicians caring for children must learn to recognize this potentially treatable disorder.
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PMID:Primary hemochromatosis in childhood. 365 74

We analyzed survival and causes of death among 163 patients with primary hemochromatosis diagnosed between 1959 and 1983. The mean follow-up period was 10.5 +/- 5.6 years (+/- S.D.). Cumulative survival was 92 per cent at 5 years, 76 per cent at 10 years, 59 per cent at 15 years, and 49 per cent at 20 years. Life expectancy was reduced in patients with cirrhosis of the liver as compared with those without cirrhosis (P less than or equal to 0.05), in patients with diabetes mellitus as compared with those without diabetes (P less than or equal to 0.002), and in patients who could not be depleted of iron during the first 18 months of venesection therapy as compared with those who could be depleted (P less than or equal to 0.001). Prognosis was not influenced by sex (P less than or equal to 0.5). Patients without cirrhosis had a life expectancy that was not different from that expected in an age- and sex-matched normal population. Analysis of the causes of death in 53 patients, as compared with the normal population, showed that liver cancer was 219 times more frequent among the patients (16 patients), cardiomyopathy was 306 times more frequent (3 patients), liver cirrhosis was 13 times more frequent (10 patients), and diabetes mellitus was 7 times more frequent (3 patients). Death rates for other causes, including extrahepatic carcinomas (seven patients), were not different from the rates expected. We conclude that patients with hemochromatosis diagnosed in the precirrhotic stage and treated by venesection have a normal life expectancy, whereas cirrhotic patients have a shortened life expectancy and a high risk of liver cancer even when complete iron depletion has been achieved.
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PMID:Survival and causes of death in cirrhotic and in noncirrhotic patients with primary hemochromatosis. 405 6

Using hexachlorocyclohexane (BHC) as a model histopathological, histoenzymological, biochemical, and electrophoretic studies were undertaken to find out certain parameters for early diagnosis of liver cancer. In addition, cytogenetic studies were carried out to evaluate the effect of BHC feeding on mitotic and meiotic divisions. The results of these investigations suggest that there is a significant change in liver weight in experimental group. Histologically, liver cells follow a definite sequential cellular alteration ultimately leading to liver tumor. Histochemically, well defined pattern of glycogen accumulation and iron distribution in hepatocytes was observed. The electron-microscopic observation demonstrated prominently the proliferation of agranular endoplasmic reticulum in early stages. The distribution of certain enzymes linked with plasma membrane, lysosomes, and mitochondria showed the functional alteration of these organelles both in neoplastic nodules and tumours induced by BHC. The biochemical changes observed in gluconeogenic enzymes (G6Pase and F1,6dipase) and dehydrogenases (LDH, ICDH, and MDH) at different duration of exposure to BHC indicated decrease in enzyme activity of both gluconeogenic pathway and tricarboxylic acid cycle, linked with energy metabolism. These changes tend to recover with discontinuation of BHC but 8 months continuous feeding produces irreversible changes in G6Pase activity. Using polyacrylamide gel electrophoresis technique a change in serum proteins and LDH isoenzymes was observed. However, extrapolation of these findings to human situation needs more extensive studies, taking into account all possible variables, such as the DDT and BHC load in our environment and the body burden resulting there from.
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PMID:Experimental studies on insecticides commonly used in India. 616 13

The clinical tolerability and diagnostic value of Resovist as a new superparamagnetic iron oxide contrast medium was studied in 30 patients with malignant focal liver lesions (28 metastases, 2 HCC) within a phase II multicenter study. Magnetic resonance imaging (MRI) was performed at 1.0 Tesla with T1-weighted FLASH- and T2-weighted spin echo sequences before and following intravenous injection of Resovist at three different dose groups (4, 8 and 16 mumol Fe/kg). Liver signal intensity was significantly reduced on post-contrast images, while malignant focal liver lesions showed no signal changes. Resovist improved tumor liver contrast and lesion-conspicuity, especially for lesions smaller than 1 cm. The dose of 8 mumol Fe/kg was sufficient to achieve diagnostic tumor-liver contrast. Compared to images directly after injection, the number of detected lesions did not improve until 70 min later. There were no significant changes in vital signs (heart rate, blood pressure) or laboratory values until 72 h post-injection.
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PMID:[New super-paramagnetic iron particles for MRI. Phase II study of malignant liver tumors]. 756 92

Iron was systematically studied in the nontumorous liver of 24 patients with hepatocellular carcinoma (HCC) developed on a noncirrhotic liver compared with 4 control groups (cirrhosis with and without HCC, liver metastasis, and normal liver) matched according to age, sex, and presence of chronic alcoholism. Assessment of liver iron was made by (1) histology according to iron distribution and quantification (total iron score: 0 to 60), and (2) biochemistry (liver iron concentration-N < 36 mumol/g) with calculation of the hepatic iron index (liver iron concentration/age). Patients with hepatocellular carcinoma developed on a noncirrhotic liver presented with (1) histological iron in 83%; (2) parenchymal iron excess significantly more frequent (90%) than in controls; (3) total iron score (15 +/- 12) and liver iron concentration (81 +/- 96) significantly greater than in controls; and (4) hepatic iron index significantly increased (1.4 +/- 1.5) when compared with control groups, except for the hepatocellular carcinoma complicating cirrhosis group (0.9 +/- 1.1). This study (1) shows a mild but unquestionable parenchymal iron excess in the nontumorous liver of most patients presenting with hepatocellular carcinoma developed on a noncirrhotic liver and, at a lesser extent, on cirrhosis, (2) should incite others to study the putative role of iron in the development of liver cancer both in patients with cirrhosis and those without it, whatever the cause of the underlying liver disease, and (3) add argument to take into account and to treat any liver iron excess, even when mild.
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PMID:Increased liver iron stores in patients with hepatocellular carcinoma developed on a noncirrhotic liver. 763 11

In order to clarify the factors contributing to the signal intensities (SIs) of HCC on T1-weighted images, the amount of water, lipid, copper (Cu), iron (Fe), and manganese (Mn) was determined in HCC and surrounding hepatic parenchyma of 13 patients. The relationships among these findings, the histopathologic findings, and the SIs of T1-weighted images were evaluated. Among the 13 HCC, 3 had a high SI, 5 were isointense, and 5 had a low SI on T1-weighted images compared to the surrounding hepatic parenchyma. The paramagnetic ions which contributed to the SI patterns were assumed to be Cu in HCC (38.0 +/- 62.4 micrograms/g ww), and Fe in the liver (61.1 +/- 42.4 micrograms/g ww) and HCC (40.0 +/- 34.3 micrograms/g ww). In 8 HCC with high- or isointensity, 2 were grades I, 5 were grade II, and one was grade III according to the Edmondson-Steiner's histopathologic classification. It is concluded that the SI patterns alone can not be a sign of low grade malignancy because of the existence of Fe in livers and HCC.
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PMID:MR imaging of hepatocellular carcinoma. Correlation of metal content and signal intensity. 771 Jul 97

A population-based cohort of 120 Danish men, discharged with a hospital diagnosis of primary hemochromatosis from 1977 to 1989, was followed up to 1989 for subsequent cancer risk. Nineteen subjects (including 6 with primary liver cancers) were excluded from the analysis, either because they died within the same month of hemochromatosis diagnosis or because they had cancer prior to diagnosis of hemochromatosis. Among the 101 remaining subjects, 4 primary liver cancers occurred one year or more after the diagnosis of hemochromatosis, far surpassing the expected number based on incidence rates from the Danish population (standardized incidence ratio 92.9, 95% confidence interval 25.0 to 237.9). The excess of liver cancer was associated with cirrhosis and included cholangiocarcinoma as well as hepatocellular carcinoma. Significantly elevated risks were also observed for non-hepatic cancers (13 cases; SIR 3.5, 95% CI 1.9 to 6.0), notably esophageal cancer (2 cases; SIR 42.9, 95% CI 4.8 to 154.9) and skin melanoma (2 cases; SIR 27.8, 95% CI 3.1 to 100.3). The results of this population-based study are in accordance with the hypothesis that patients with primary hemochromatosis have a substantial risk of primary liver cancer. Further studies of hemochromatosis may be useful in clarifying the relation of non-hepatic malignancies to body iron stores in the general population.
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PMID:Cancer risk following primary hemochromatosis: a population-based cohort study in Denmark. 782 8

5-Aminolevulinic acid (ALA), a heme precursor accumulated in acute intermittent porphyria (AIP) and lead poisoning, undergoes metal-catalyzed oxidation in air-equilibrated solutions buffered at neutral pH, yielding free radicals (O2, HO. and ALA.). The capacity of ALA to release iron from horse spleen and rat liver ferritin in vitro and to concomitantly initiate liposome lipid peroxidation was characterized. ALA induced iron release from ferritin in normally aerated solutions, in a dose (0.05-1 mM)- and time (0-120 min)-dependent manner; no reaction occurs under nitrogen. Superoxide dismutase partially inhibited (50% at 100 U/ml) iron release by 0.5 mM ALA, whereas the addition of catalase (50 U/ml) had no effect under these conditions. In phosphatidylcholine: cardiolipin (80:20) liposomes, and in the presence of 2 microM EDTA, ALA (0.025-1 mM) per se had a subtle effect on lipid peroxidation, while after addition of ferritin (0.25 mg/ml) there was a significant increase in lipid peroxidation as evaluated by dose-dependent formation of 2-thiobarbituric-reactive substances and diene conjugation. In vivo, iron accumulation in the liver of ALA-treated rats was observed. Altogether, these data demonstrate the ability of ALA-generated free radicals to release iron from ferritin and to affect iron metabolism in vivo. ALA-mediated iron release from ferritin, therefore, may aggravate oxidative damage to cell components and contribute to the pathology observed in AIP (eg., primary liver cancer) and lead poisoning.
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PMID:5-Aminolevulinic acid induces iron release from ferritin. 784 Jun 72

Sublobular nodules of hepatocytes free of iron or exhibiting much less iron than the surrounding parenchyma, referred to in this study as iron-free-foci, are frequently found in the livers of patients with genetic hemochromatosis complicated by hepatocellular carcinoma. To test the hypothesis that such nodules are preneoplastic lesions, iron-free foci were sought in the initial liver biopsy specimens of 185 patients with untreated and uncomplicated genetic hemochromatosis. Iron-free foci were found in 14 (7.6%) patients, all men, aged from 38 to 76 yr, with heavy iron overload and with fibrosis or cirrhosis. Twelve patients with iron-free foci were followed for 0.9 to 15 yr (7 +/- 6 yr). In six (50%), HCC developed, compared with 2 (8%) from a control group consisting of 24 patients without IFF matched according to age, sex, degree of fibrosis, liver iron amount and follow-up duration. The mean number of iron-free foci per iron-free foci-positive specimen was 3.2 +/- 2.1. Ten patients had dysplastic aspects in their iron-free foci, and four had intrahepatocytic iron-positive inclusions at the periphery of iron-free foci. Proliferative cell nuclear antigen was positive in 75% of iron-free foci and in 24% +/- 21% of hepatocyte nuclei in iron-free foci. This study clearly demonstrates that iron-free foci are proliferative lesions and strongly suggests that such nodules are preneoplastic foci. Therefore the finding of IFF in the initial liver biopsy specimen from a patient with genetic hemochromatosis should lead to regular screening for hepatocellular carcinoma.
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PMID:Preneoplastic significance of hepatic iron-free foci in genetic hemochromatosis: a study of 185 patients. 790 16


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