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

Spontaneous bacterial peritonitis is a well-known entity, with a reported incidence of 15-20% in advanced cirrhotic patients. Escherichia coli and Klebsiella pneumoniae are the most common causes of spontaneous bacterial peritonitis; Brucella is extremely rare. We aimed to present one case of such a rare condition in a cirrhotic patient who also had hepatocellular carcinoma. Routine laboratory tests, abdominal ultrasonography and peritoneal fluid examinations were studied in a cirrhotic patient with ascites. Peritoneal fluid white blood cell count was 1300/mm3, with lymphocyte predominance (80%). Peritoneal fluid and blood culture both yielded Brucella melitensis. The patient also had a mass in the right lobe of the liver confirmed as hepatocellular carcinoma by biopsy. Brucella should be suspected as a cause of spontaneous bacterial peritonitis in cirrhotic patients with no response to standard spontaneous bacterial peritonitis treatments and with immunodeficiency such as hepatocellular carcinoma.
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PMID:Spontaneous bacterial peritonitis due to Brucella Melitensis in a cirrhotic patient. 1625 87

We have previously shown that hepatocytes exposed to hepatitis C virus (HCV) and human immunodeficiency virus (HIV) envelope proteins undergo apoptosis. In this article, we further elucidate the signaling mechanisms that mediate this effect. We found that, in human hepatocellular carcinoma (HepG2) cells, HCV E2 protein and HIV glycoprotein (gp) 120 significantly up-regulated the Fas ligand (FasL) and enhanced the formation of the Fas death-inducing signaling complex downstream of Fas receptor activation. Moreover, after stimulation with HCV E2 and HIV gp120, enhanced expression of caspases 2 and 7 and increased caspase 3 activity were observed. In addition, we showed up-regulation of the proapoptotic molecule Bid and its association with caspase 8 after treatment with these envelope proteins. We also found that HCV E2 and HIV gp120 induced a partial translocation of Bid to the mitochondria, which resulted in the release of cytochrome C and the apoptosis-inducing factor. Thus, the results of this study suggest that FasL and Bid play an important role in HCV and HIV envelope protein-induced apoptosis.
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PMID:Molecular mechanism of hepatic injury in coinfection with hepatitis C virus and HIV. 1626 11

The human and monetary costs of chronic hepatitis C and the complications arising from this disease, including hepatocellular carcinoma and liver transplantation, emphasize the increased urgency to treat hepatitis C virus (HCV)-infected patients earlier in the course of their disease. The current standard of treatment for patients chronically infected with HCV is combination therapy with pegylated interferon plus ribavirin. Among undertreated groups of patients are those with persistently normal alanine aminotransferase levels, those coinfected with human immunodeficiency virus and HCV, and nonresponders to previous treatment with standard interferon. This review summarizes the rationale for earlier treatment of chronic HCV infection, as well as evidence showing that patients who do not achieve a virologic response on treatment may derive benefit from treatment, including improved histologic characteristics and delayed progression of disease.
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PMID:An urgency to identify and treat chronic hepatitis C. 1628 Sep 65

Hepatocellular carcinoma (HCC) resulting from chronic infection with hepatitis B or C virus (HBV, HCV) is a significant health problem. Concurrent infection with human immunodeficiency virus (HIV) may accelerate the progression from cirrhosis to HCC. Current guidelines advise screening patients with cirrhosis at 6-month intervals using ultrasonography and measurement of alpha-fetoprotein levels. In early-stage HCC, resection and liver transplantation are curative, as is percutaneous ethanol injection for small tumours in patients who are not candidates for surgery. HIV-infected patients do not qualify for liver transplantation. For late-stage HCC, chemoembolization can improve survival. Prevention of hepatitis and cirrhosis are key goals in reducing the impact of HCC. Numerous issues in HCC prevention, diagnosis, and management still remain to be resolved through large-scale, randomized clinical trials.
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PMID:Management of hepatocellular carcinoma in human immunodeficiency virus-infected patients. 1635 82

A retrospective review was performed of patients diagnosed with Pneumocystis carinii pneumonia (PCP) from 1994 to 2003 at the Prince of Wales Hospital in Hong Kong. Eighteen patients were identified. Six (33.3%) were co-infected with human immunodeficiency virus (HIV). The remaining 12 non-HIV-infected patients had underlying diseases: three post-renal transplant recipients, three with haematological malignancies, two with auto-immune diseases, two with renal diseases, one with hepatocellular carcinoma and one with congenital cytomegalovirus disease. Cytomegalovirus co-infection was observed in four patients. All patients received cotrimoxazole therapy, with intolerance observed in four of them, including one with glucose-6-phosphate dehydrogenase deficiency, two with repeated vomiting and one with renal impairment. Overall crude mortality was 33.3%. The results suggested that, apart from being a common infection for patients with HIV infection, PCP can occur during the course of many immunosuppressive diseases and therapies. The mortality of PCP was high despite appropriate treatment. Chemoprophylaxis should be considered in populations at risk.
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PMID:Pneumocystis carinii pneumonia in Hong Kong: a 10 year retrospective study. 1638 34

Prior to the introduction of viral inactivation techniques in the mid-1980s, the vast majority of patients with hemophilia who received plasma-derived clotting factor concentrates were exposed to and infected with the hepatitis C virus (HCV), a lipid-enveloped bloodborne pathogen. Hemophilia patients may also have been co-infected with the human immunodeficiency virus (HIV) after receiving contaminated blood products. HCV mono-infection has a very slow progression, but patients with hemophilia who are co-infected with HCV and HIV can exhibit a comparatively rapid progression of liver disease. Potential complications of chronic HCV infection are subsequent cirrhosis with hepatic failure and the ultimate onset of hepatocellular carcinoma. The treatment of either of these may involve orthotopic liver transplantation. Liver biopsy and morphologic evaluation of tissue remain the current "gold standard" by which the severity of HCV-induced liver disease can be reliably assessed. Although there has been a reluctance to perform invasive percutaneous liver biopsies in patients with hemophilia, available evidence suggests that they appear to be safe and they certainly provide greater specificity and sensitivity than radiographic techniques such as computerized tomography or magnetic resonance imaging. Treatment of HCV-infected patients is targeted towards preventing the progression of early cirrhosis and end-stage liver disease. The current standard of care for individuals with hemophilia has generally been considered to be the combination of standard interferon-alpha (IFN-alpha) with ribavirin for at least 6 months. Data concerning the use of PEGylated IFN, substituting for standard IFN-alpha, are now emerging, although relatively little of this information relates specifically to hemophilia patients with liver disease. Nevertheless, the favorable data from large non-hemophilia-related HCV disease with early cirrhosis have been extrapolated to the hemophilia scenario, and there has been no evidence in the limited number of hemophiliacs treated in this way to refute this conclusion.
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PMID:Update on liver disease in hemophilia patients. 1642 78

High rates of coinfection with human immunodeficiency virus-1 (HIV) and the hepatitis B virus (HBV) are commonly found in at risk populations due to their shared parenteral route of transmission. Although the increasingly widespread use of highly active antiretroviral therapy (HAART) has prolonged survival for those with HIV, it has also increased the potential for morbidity and mortality from other diseases and opportunistic infections. Liver-related illness is a leading cause of morbidity and mortality in those infected with HIV and HBV is responsible for a vast proportion of this, especially in regions of high HBV prevalence. HIV/HBV coinfected patients may exhibit atypical serological markers of HBV infection, hindering appropriate diagnosis. They may experience faster progression to cirrhosis, decompensation, and hepatocellular carcinoma than HBV-monoinfected patients. Rates of response to vaccine against HBV are abrogated in those with HIV, facilitating the spread of the virus. Treatment of HBV must be monitored for resistance, although newer agents appear to have less risk of resistance development. Moreover, treatment of HIV with antivirals must be monitored closely for liver toxicity. Because liver damage with HBV occurs via the immune response to the virus, liver damage is possible with HAART-mediated immune reconstitution. Although liver transplant is not commonly undertaken in HIV-positive patients, centers undertaking transplantation report improved survival and low rates of HBV recurrence.
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PMID:Management of hepatitis B virus in HIV-positive patients. 1655 8

Hepatitis B virus (HBV) and Hepatitis C virus (HCV) are major causes of liver disease. Chronic infection with these viruses often leads to chronic liver disease, including cirrhosis or primary hepatocellular carcinoma (HCC). Concern is growing among patients and health care workers about possible transmission of bloodborne pathogens during medical procedures. This fear has primarily been focused on nosocomial transmission of human immunodeficiency virus (HIV), but other bloodborne infectious agents may also be transmitted during procedures. Chief among these are the hepatitis viruses, particularly HBVand HCV, both of which are significantly more widespread than HIV Circumstantial evidence suggests that hemodialysis, per se, is an important risk factor for infection with HCV.
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PMID:Hepatitis and transfusions. 1664 31

Composite promoters combining the prostate-specific antigen (PSA) enhancer core element with promoter elements derived from gene coding for human prostate-specific transglutaminase gene, prostate-specific membrane antigen gene, prostate-specific antigen, rat probasin or phosphoglycerate kinase were characterized for their ability to specifically express the enhanced green fluorescent protein (EGFP) gene in prostate versus non-prostate cancer cell lines when transferred with a human immunodeficiency virus-1-based lentiviral vector. By themselves minimal proximal promoter elements were found to inefficiently promote relevant tissue-specific expression; in all the vectors tested, addition of the PSA enhancer core element markedly improved EGFP expression in LnCaP, a cancer prostate cell line used as a model for prostate cancer. The composite promoter was inactive in HuH7, a hepatocarcinoma cell line used as a model of neighboring non-prostate cancer cells. Among the promoters tested, the combination of the PSA enhancer and the rat probasin promoter showed both high specificity and a strong EGFP expression. Neither a high viral input nor the presence of the cPPT/CTS sequence affected composite promoter behavior. Our data suggest that composite prostate-specific promoters constructed by combining key elements from various promoters can improve and/or confer tissue specific expression in a lentiviral vector context.
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PMID:Use of the PSA enhancer core element to modulate the expression of prostate- and non-prostate-specific basal promoters in a lentiviral vector context. 1674 21

Hepatitis C virus (HCV) infection is a major cause of morbidity and mortality in hemophiliacs who received nonvirucidally treated large-pool clotting factor concentrates before 1986. In fact, although many hemophiliacs infected with HCV have a slow progression of liver disease, in a minority of them hepatitis evolves toward end-stage liver disease and hepatocarcinoma. Moreover, a significant percentage of HCV-infected hemophiliacs were also coinfected with human immunodeficiency virus (HIV), which can accelerate the progression of liver disease. Thus, the aim of anti-HCV therapy is to interrupt the chronic infection in order to prevent the progression of hepatitis to cirrhosis, liver decompensation, cancer and, ultimately, death. In this review we present the literature data on anti-HCV treatment in hemophiliacs. Combination therapy with interferon (IFN) and ribavirin has improved the poor results obtained with IFN monotherapy and has become the standard treatment of chronic hepatitis C. Given the positive results obtained with pegylated interferon plus ribavirin in nonhemophiliacs, ongoing trials are evaluating this promising therapy in HCV-chronically infected hemophilic patients; preliminary results show a sustained response rate similar to that in patients without coagulopathy. Finally, based on the encouraging results in coinfected nonhemophiliacs, anti-HCV treatment should also be considered for those HIV-positive hemophiliacs in whom anti-retroviral treatment has stabilized the HIV infection.
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PMID:Treatment of hepatitis C in hemophiliacs. 1683 39


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