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

Cerebral angiography using a radioactive radiological contrast medium, Thorotrast, was pioneered by Moniz in Portugal in the 1920s. Thorotrast is retained by the reticuloendothelial system, with a biological half-life of several hundred years, so that such patients suffer lifetime exposure to internal radiation. We studied mortality in Portuguese patients who were administered Thorotrast during the period 1928-1959 and in a comparison group of patients who received nonradioactive contrast agents. There were 1096 systemically exposed, 1014 unexposed, and, unique to the Portuguese study, 240 locally exposed Thorotrast patients who were successfully traced and followed up to the end of 1996. Mortality was significantly raised among systemically exposed Thorotrast patients relative to those unexposed for all causes [relative risk (RR) = 2.63], all neoplasms (RR = 6.72), liver cancer (RR = 42.4), chronic liver disease (RR = 5.12), other non-neoplastic diseases of the digestive system (RR = 4.87), neoplastic (RR = 21.9) and non-neoplastic hematological disorders (RR = 6.00), and non-neoplastic diseases of the respiratory system (RR = 4.31). Risks for most of these conditions increased significantly with time since first administration of the contrast medium and with cumulative alpha-particle radiation dose. Mortality was also significantly raised for non-neoplastic disorders of the nervous system (RR = 12.7) and ill-defined conditions (RR = 3.74), but these associations are likely to reflect the initial diagnosis, not Thorotrast exposure, because risks declined significantly with time and/or dose. There were no significant excess deaths from oropharyngeal or nasal cancers, or from any other cause, among patients exposed to Thorotrast locally for visualization of the perinasal sinuses, and no clear trend in risk with time since exposure. This study shows an association between systemic, but not local, exposure to Thorotrast and mortality from liver cancer, chronic liver disease, and neoplastic and non-neoplastic hematological disorders, with risks for these conditions remaining high for over 40 years after administration. Liver conditions, but not hematological disorders, showed a strong and consistent gradient with cumulative alpha-particle radiation dose.
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PMID:Mortality after radiological investigation with radioactive Thorotrast: a follow-up study of up to fifty years in Portugal. 1264 97

Vinyl-chloride monomer (VCM), a human carcinogen, has caused angiosarcoma of the liver. Recent studies have shown that VCM exposure is associated with hepatocellular cancer. In Taiwanese studies, the majority of VCM-exposed workers with liver cancer had history of hepatitis B virus (HBV) infection. To determine the role of HBV on the development of liver cancer in the VCM-exposed workers, we conducted a case-control study from a previously established polyvinyl chloride (PVC) cohort consisting of 4096 male workers from six PVC polymerization plants. A total of 18 patients with liver cancer, and 68 control subjects matched for age and specific plant of employment were selected. Detailed history of the participants that included alcohol consumption status, cigarette use, occupation, and family history of chronic liver disease were obtained using an interviewer-administered questionnaire. When the HBV surface antigen (HBsAg)-negative subjects without history of tank-cleaning were used as the reference, the HBsAg-negative subjects with history of tank-cleaning demonstrated a 4.0-fold greater risk of liver cancer (95% confidence interval: 95% CI = 0.2-69.1). The HBsAg carriers without history of tank-cleaning revealed a 25.7-fold greater risk of liver cancer (95% CI = 2.9-229.4). Whereas the HBsAg carriers with history of tank-cleaning revealed the greatest risk (matched odds ratio (ORm) 396.0, 95% CI = 22.6 -infinity) of developing liver cancer among subjects with different VCM-exposure status and HBsAg status categories. Further analysis showed the interaction term was significant (P < .01). Therefore, our results suggest an interaction between occupational VCM exposure and HBV infection for the development of liver cancer.
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PMID:Interaction of vinyl chloride monomer exposure and hepatitis B viral infection on liver cancer. 1270 41

Telomere maintenance and telomerase reactivation are near universal features of human hepatocellular carcinoma (HCC), yet the shorter telomeres and highly abnormal cytogenetic profiles of HCC suggest that telomere erosion and dysfunction may be operative during the formative stages of tumorigenesis. Previous studies have established that the cancer-enhancing or suppressing impact of telomere dysfunction is highly dependent on several parameters including cell type, tumor stage, and p53 status. Here, to understand better the pathogenetic role of telomere dysfunction in the initiation and progression in human HCC, we have used three mechanistically distinct liver cancer-prone model systems (urokinase plasminogen activator transgenic mice, carbon tetrachloride exposure, and diethylnistrosamine treatment) in the context of successive generations of telomerase-deficient mice null for the telomerase RNA component, mTERC. Across all of the HCC model systems, telomere dysfunction suppressed both the incidence and growth of HCC lesions, a trend that mirrored the level of intratumoral proliferative arrest and apoptosis. On the histological level, telomere dysfunction was associated with a significant increase in the number of early stage neoplastic lesions and a reciprocal decline in the occurrence of high-grade malignancies. These genetic data in the mouse indicate that telomere dysfunction exerts an opposing role in the initiation versus progression of HCC and provide a framework for understanding the intimate link among chronic liver disease, chromosomal instability, and increased HCC in humans.
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PMID:Differential impact of telomere dysfunction on initiation and progression of hepatocellular carcinoma. 1294 29

Liver angioscintigraphy (LAS) is a radio-isotope method for the investigation of liver perfusion and its alteration in various hepatic diseases. It measures the arterial and portal venous fractions of total liver blood flow. The percentage of liver blood flow supplied by hepatic artery is estimated mathematically by the hepatic perfusion index (HPI), normally between 25 % and 40 %. The decrease of portal blood flow in liver cirrhosis is compensated ("buffer" mechanisms) by increased arterial supply, with higher HPI value. For a patient with chronic liver disease, HPI over 50% suggests arterialization of hepatic perfusion, guiding the diagnose to liver cirrhosis. Splenic curve is completing the diagnostic information of the hepatic curve. Corroborated with per rectal scintigraphy and liver SPECT, LAS offers a good hemodynamic staging of chronic inflammatory liver diseases. Malignant tumors (primitive or metastases) increase the arterial supply of the liver and decrease the portal flow, HPI being over 50% (currently 65 % - 90 %). Benign tumors do not change portal/arterial liver blood flow ratio. SPECT or non-scintigraphic morphological investigations increase the diagnostic value of LAS for primitive liver tumors. Liver cancer occurring on cirrhosis is a limitative factor for LAS. Hepatic metastases increase the arterial perfusion (and HPI value) very quickly, before their size allows morphologic imaging diagnosis. LAS is therefore an early method to diagnose liver metastases being especially used in colorectal cancer. Other clinical applications of LAS are: follow up of liver toxicity of drugs, evaluation of portal vein permeability, post surgery follow up of the liver tumor patients.
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PMID:Liver angioscintigraphy: clinical applications. 1505 28

Chronic end stage liver disease is the most frequent indication for liver transplantation. Individuals with end stage cirrhosis, and therefore individuals on liver transplant lists, are at increased risk of developing a hepatic cancer. Those individuals on liver transplant lists also may represent the best group available for evaluating the current methods for screening and surveillance for the development of hepatic cancer as an examination of the explant liver provides a gold standard for tumor assessment. Assuming that only tumor free individuals were screened at the onset of this study, the data obtained enables one to determine the frequency of new hepatic cancers since listing and evaluate the positive and negative predictive values of each assessment method over the surveillance interval. All patients listed for liver transplantation with end stage chronic liver disease, who did not have a hepatoma at the time of transplant listing, were followed and assessed for the development of a hepatic cancer while on the waiting list. The screening techniques utilized included quarterly alpha fetoprotein (alpha FP) determinations and ultrasound (US) studies as well as semi-annual triple phase computed tomography (CT) scans of the liver. alpha FP failed to identify any cases of de novo hepatic cancer in patients waiting for a liver transplant. In contrast, US and especially CT scanning with intravenous contrast identified new hepatic masses. The later method, which identified early enhancing mass lesions, was the more valuable method at identifying masses that subsequently were shown by pathologic examination of the explant liver to be hepatic cancers. However, only 14 of 20 individuals found to have a de novo tumor were identified by this method. Once identified however, the treatments utilized for hepatic tumor ablation while waiting for a transplant appear to be effective with a mean of 57.8+/-8.3% necrosis of the treated masses being identified at the time of explant examination. In conclusion these data suggest that: 1. The development of a hepatocellular carcinoma (HCC) in an individual on a transplant list is not rare and occurs in as many as 20% of cases; 2. The most effective method for the detection of de novo HCC appears to be semi-annual triphasic CT scan with the identification of a new early enhancing lesion; and 3. Once recognized, the presence of the tumor enables the individual to move up on the waiting list as result of the additional model endstage liver disease (MELD) points allowed for individuals with HCCs.
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PMID:The development of de novo hepatocellular carcinoma in patients on a liver transplant list: frequency, size, and assessment of current screening methods. 1510 54

The strategy for treating liver fibrosis in chronic hepatitis patients includes dispelling the etiological factors, inhibiting the inflammatory reaction, decreasing the sedimentation of extracellular matrix, accelerating the degradation of extracellular matrix, improving the microcirculatory and metabolic disturbance, and ameliorating the complicating diseases, etc. Researchers should pay attention to the liver function indexes in chronic liver disease in evaluating the therapeutic effects of anti-fibrosis. Effective etiological treatment should be considered as the first step in treating liver fibrosis in chronic hepatitis patients, and inhibiting the inflammatory reaction is one of the most important tactics for suppressing the development of fibrosis and for decreasing the incidence rate of liver cancer in chronic hepatitis patients. Treatment based on syndrome differentiation, a dynamic therapy aimed at the holistic pathological state, can improve the pathological state of the disease. It is especially important to take the advantages of the integration of traditional Chinese and western medicine in the clinical diagnostic and therapeutic procedure for increasing the therapeutic effect of live fibrosis.
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PMID:[Strategy for treating liver fibrosis by integration of the disease and its syndromes in traditional Chinese medicine]. 1553 14

Protein-energy malnutrition (PEM) is a prevalent observation in cirrhotic patients. In advanced cirrhotic patients with hepatic encephalopathy, dietary protein should be restricted to the low level of 0.5 g/kg/day. In such a strictly protein restricted diet, branched amino acid-enriched nutritious products should be prescribed to improve PEM. Avoidance of day-time or nocturnal fasting by frequent meals and late evening snacks is another recommendation for prevention of PEM. The n-3 polyunsaturated fatty acids (PUFA) modulate lymphocyte proliferation and eicosapetaenoic acid (EPA) up-regulates the metabolic action of insulin. The dietary n-6/n-3 PUFA ratio should be maintained between 2.8 and 3.2 in chronic liver disease. Oxidative stress is suggested as a trigger in the progression of chronic liver disease. Antioxidant vitamins; Vitamins A, E and C and carotenes may be useful to prevent the progression of chronic liver disease. Zinc depression occurs in advanced liver disease and it reduces taste and immune function. A goal of dietary management in chronic liver disease should be preventing PEM and blocking progression to hepatic cancer, and improving quality of life.
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PMID:Chronic hepatic disease and dietary instruction. 1560 46

Hepatitis C virus (HCV) is the leading cause of chronic liver disease worldwide with a prevalence of approximately 14% in Egypt. IL-10 is a cytokine produced by Th2 cells. It down-regulates the proinflammatory response and modulates hepatic fibrogenesis. IL-12 is produced by antigen presenting cells. It promotes Th1 cell response and has many antiviral properties. Data concerning the Th-1/Th-2 balance in chronic hepatitis C (CH-C) are rather conflicting. Using ELISA, we assessed serum IL-10 and IL-12p40 levels in 66 Egyptian patients with HCV-related liver illness (CH-C, cirrhosis, and HCC), and their relationship to disease activity. Our results showed that spontaneous IL-10 was undetectable in patients with CH-C, HCC or controls. Only 5/22 (23%) of patients with cirrhosis showed detectable levels of IL-10. IL-12p40 was elevated in the patient groups compared to controls (p= 0.01, p= 0.01, p= 0.05 in CH-C, cirrhosis and HCC, respectively). The presence of IL-12p40 was associated with HCV level of viremia and serum AST. Serum ALT level was significantly associated with the level of IL-12p40. IL-12p40 was unrelated to liver histology or fibrosis. We concluded that in the Egyptian patients an augmentation of IL-12p40 and a suppression of IL-10 are both found. Whether this pattern is related to HCV genotype 4, or to the presence of schistosomiasis would need to be further investigated.
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PMID:IL-10 and IL-12p40 in Egyptian patients with HCV-related chronic liver disease. 1571 17

HCC is the most frequent primary malignancy of the liver and one of the most common cancers in the world. HCC is substantially a complication of liver cirrhosis, and because HBV and HCV are the predominant causes of chronic liver disease and cirrhosis worldwide, they have a propensity to lead to HCC. Common sites of HCC metastases include the lung, lymph nodes, and portal vein. Bony metastases are rare, and when they do occur the disease is usually far advanced and is associated with clinical manifestations of abdominal pain, weight loss, jaundice, hepato-splenomegaly, ascities, deranged LFTs, and elevated AFP. We report here a patient with asymptomatic advanced HCC, normal LFTs, and normal AFP values presenting with spinal cord compression.
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PMID:Asymptomatic advanced hepatocellular carcinoma presenting with spinal cord compression. 1574 89

Liver fibrosis is a chronic liver disease that will further develop to cirrhosis if severe damage continues to form. A potential treatment for liver fibrosis is to inhibit activated hepatic stellate cell (HSC) proliferation and, subsequently, to induce HSC apoptosis. It has been reported that antioxidants are able to inhibit the proliferation of HSCs. In this study, the aqueous extract of spirulina was chosen as the source of antioxidant to investigate the inhibitory effect on the proliferation of HSC. The growth inhibitory effects of aqueous spirulina and chlorella extract on human liver cancer cells, HepG2, were also studied and compared in pairs. Results indicated that the total phenol content of spirulina was almost five times greater than that of chlorella (6.86 +/- 0.58 vs 1.44 +/- 0.04 mg tannic acid equivalent/g of algae powder, respectively). The antioxidant activity of spirulina determined by the ABTS*+ method was higher than chlorella (EC50: 72.44 +/- 0.24 micromol of trolox equivalent/g of spirulina extract vs 56.09 +/- 1.99 micromol of trolox equivalent/g of chlorella extract). Results of DPPH* assay also showed a similar trend as the ABTS*+ assay (EC50: 19.39 +/- 0.65 micromol of ascorbic acid equivalent/g of spirulina extract vs 14.04 +/- 1.06 micromol of ascorbic acid equivalent/g of chlorella extract). The aqueous extracts of these two algae both showed antiproliferative effects on HSC and HepG2, but spirulina was a stronger inhibitor than chlorella. Annexin-V staining showed that aqueous extract of spirulina induced apoptosis of HSC after 12 h of treatment. In addition, the aqueous extract of spirulina triggered a cell cycle arrest of HSC at the G2/M phase.
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PMID:Antioxidant and antiproliferative activities of Spirulina and Chlorella water extracts. 1588 62


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