Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HIV-VIRAL HEPATITIS CO-INFECTIONS: Several characteristics reveal an HIV-HBV co-infection: high B viral replication, high percentage of patients exhibiting chronic B virus, high risk of cirrhosis, and possibility of B reactivation in severely immunodeficient patients. Regarding HIV-HCV co-infections, there is a greater risk of progression towards cirrhosis. However, anti-retroviral treatment appear to stall the progression of the C-virus hepatic disease. METABOLIC COMPLICATIONS WITH ANTI-RETROVIRAL TREATMENTS: Among the morphological lipodystrophic syndromes, the lipohypertrophic forms must be distinguished from the lipoatrophic forms. Substitution of some antiretroviral molecules is the first measure to be taken, but the results are difficult to assess; other current drug alternatives are unconvincing. The management of hypercholesterolemia and hypertriglyceridemia observed during treatment with antiretrovirals is debatable, and efficacy is not always clearly demonstrated. Regarding hyperlactatemia, potentially the most severe complication of mitochondrial toxicity of antiretroviral treatment, which requires suspension of the nucleoside analogs in severe or moderate symptomatic forms, and simple surveillance and continuation of the treatment in the mild or moderate asymptomatic forms. VIROLOGICAL FAILURE: There are three options possible: continue the same treatment, change it or stop it. Efficacy should be assessed on CD4 and the variations in viral load, rather than on the absolute value of the viral load. IN POOR RESSOURCE SETTINGS: Only a minority of patients has access to antiretroviral treatments. Efforts must be made to continue to search for other forms of management: community measures for prevention and early screening, psychological and nutritional support, prophylactic and treatment strategies for infections or opportunist diseases.
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PMID:[Management of patients infected with HIV]. 1273 13

HIV and HCV share common transmission pathways, but HCV is more efficiently transmitted through blood than with sexual exposure. Thus HCV coinfection is frequent in HIV seropositives, mainly in those with history of injection drug use and/or transfusion. HIV coinfection increases HCV replication rate, the rate of HCV vertical transmission and accelerates the course of hepatitis C towards cirrhosis and hepatocellular carcinoma. The evidence of an effect of HCV on HIV disease progression is less convincing. The results of several studies suggest that HCV coinfection does not hasten the progression of HIV infection towards AIDS. However two recent studies showed that HCV coinfection is independently associated with a lower restoration of CD4 counts during combination antiretroviral treatment. However this finding should be confirmed by additional studies.
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PMID:HIV/HCV co-infection: natural history. 1451 13

Treatment of patients coinfected with HIV and hepatitis C virus is a challenging area for clinicians. We report on a treatment-naive man with advanced AIDS and cirrhosis secondary to hepatitis C, who has been followed from the initial diagnosis. After presentation, he began receiving HAART. During a disseminated Mycobacterium avium complex infection, massive ascites refractory to standard treatment developed. Substitution of nelfinavir for nevirapine in his antiretroviral regimen led to resolution of the ascites. Although excellent virologic control was achieved with HAART, the patient's immunologic response remained blunted until the hepatitis C was successfully treated. This case demonstrates that in some coinfected patients, hepatitis C can be successfully treated at low CD4 cell counts and that hepatitis C may influence the immunologic status of such patients.
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PMID:Successful treatment of hepatitis C in a patient with advanced AIDS and decompensated cirrhosis. 1459 28

Immunological factors are important in the pathogenesis of a wide spectrum of hepatobiliary diseases. Using flow cytometry, we determined the changes in lymphocyte subsets and natural killer cells in 123 individuals (81 patients with liver disease and 42 healthy volunteers). The liver diseases included periportal fibrosis (PPF, 10 patients), liver cirrhosis (LC, 31 patients), and hepatocellular carcinoma (HCC, 40 patients). Schistosomiasis and viral hepatitis B and C were the putative etiological agents of liver diseases. Immunophenotyping by indirect immunofluorescence was conducted using monoclonal antibodies to CD3 (T-lymphocytes), CD4 (helper/inducer T-cells), CD8 (suppressor/cytotoxic T-cells), and CD57 (natural killer cells) cell surface markers. Immunophenotyping of PPF patients showed no significant changes in all markers compared with the healthy controls. However, there was a significant decrease ( P<0.01) in CD3 and CD4 T-cells, and a highly significant increase ( P<0.001) in CD57 T-cells in patients with LC or HCC. In addition, LC and HCC patients showed no significant change in CD8 T-cells compared with controls. In conclusion, the progression of liver diseases is associated with a dysregulation of cellular immune responses. T-lymphocytes and natural killer cells may play a role in the immunopathogenesis of liver cirrhosis and HCC.
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PMID:Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma. 1464 34

The major hepatological consequence of HCV infection is the progression to cirrhosis and its potential complications. Several factors have been clearly shown to be associated with fibrosis progression rate: duration of infection, age, male sex, consumption of alcohol, HIV coinfection and low CD4 count. As age and duration of infection increases, the risk of fibrosis increases and the impact of treatment (IFN) decreases. In conclusion, fibrosis progression has a progressive acceleration, sex, age and consumption of alcohol are strongly involved in this progression; the possibility to assess with non-aggressive biochemical markers the fibrosis stage will probably allow in the future to identify other factors related to fibrosis progression.
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PMID:Risk factors for liver fibrosis progression in patients with chronic hepatitis C. 1509

Liver histology is important for prognosis and treatment strategy in patients with hepatitis C. We report a 10-year experience of transjugular liver biopsy (TJLB) in patients with haemophilia and other congenital bleeding disorders (CBD) in terms of safety, efficiency and therapeutic consequences. TJLB was proposed to patients who were regularly followed for CBD, and were hepatitis C virus (HCV) positive by polymerase chain reaction. Patients with inhibitors or who were human immunodeficiency virus (HIV) positive with CD4 cells <0.2 x 10(9)/l or with evidence of liver failure were excluded. TJLB was performed during a short hospitalization with factor replacement. Between 1992 and 2002, 88 TJLB were performed in 69 of 151 adult HCV patients (39% HIV positive). CBD was haemophilia A in 68% and haemophilia B in 24%. Few mild adverse events were recorded. Histology was assessable in 78 of 88 procedures (89%). Twenty-nine (37%) cases demonstrated minimal change (METAVIR A </= 1 and F </= 1). Extended fibrosis or cirrhosis was recorded in 23 procedures (26%), all in patients whose infection period was longer than 20 years. No relationship between liver histology, HIV status or HCV genotype was found. TJLB appears to be safe and useful in HCV patients with CBD. One-third of patients had minimal histological changes and could avoid systematic anti-HCV treatment.
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PMID:Interest of transjugular liver biopsy in adult patients with haemophilia or other congenital bleeding disorders infected with hepatitis C virus. 1518 Aug 67

The role of lymphocytes in host defence in neoplastic disorders is known. Accumulation of lymphocytes in pleural cavity frequently occurs in different diseases. The aim of the study was to evaluate: 1) the frequency of lymphocyte predominance in different malignant and non-malignant pleural effusions; 2) lymphocyte phenotype and the ratio between helper (CD4+) and cytotoxic/suppressor (CD8+) lymphocytes in malignant and non-malignant effusions. Patients with mesothelioma, lung cancer, lymphoma and metastatic neoplasms were analysed. Analysis was performed on fluids with or without malignant cells. Non-malignant fluids were obtained from patients with: congestive heart failure, liver cirrhosis, pneumonia and tuberculosis. Lymphocytes were the predominant cell type in neoplastic effusions. For further analysis effusions with more than 10% of lymphocytes were included: 12 malignant and 9 non-malignant. For lymphocyte subpopulations analysis, the monoclonal antibodies anti-CD4 and anti-CD8 and APAAP method was used. We observed lower percentage of CD4+ lymphocytes (47%) and higher percentage of CD8+ (39%) lymphocytes in malignant when compared to non-malignant fluids (58% vs 31% respectively). The CD4+/CD8+ ratio was significantly lower in pleural fluid in cases with neoplastic disease when compared to benign cause of pleural involvement (1.03 vs 1.85). Our observations suggest the potential role of lymphocytes, especially CD8+ cells in local response in malignancy in pleural disease.
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PMID:[Lymphocyte and lymphocyte subsets in pleural fluid--comparison of malignant and non-malignant disorders]. 1523 Feb 9

Some hemophilic patients in Japan suffer from infections with both human immunodeficiency virus (HIV) and hepatitis virus because they received contaminated nonheated blood products. Coinfection with HIV appears to accelerate the course of chronic hepatitis. Although powerful antiviral therapy was introduced as HIV treatment and the prognosis of HIV patients was dramatically improved, the risk of rapid progression of hepatitis and carcinogenesis remains for the patients. Recently, we performed surgery for hepatocellular carcinoma (HCC) in two hemophilic patients with HIV and hepatitis C virus (HCV) coinfection. Case 1 was a 52-years-old man who suffered from liver cirrhosis, hypersplenism, and hyperammonemia due to portosystemic shunt. A recent abdominal computed tomography (CT) scan had revealed a low-density area in segment VI of the liver. Splenectomy and partial resection of the liver were performed. Case 2 was a 66-year-old man who had been diagnosed with chronic hepatitis at age 50, and HIV infection at age 52 years. When his serum alpha-fetoprotein level was increased, CT scan of the liver revealed a mass in segment VIII. Subsegmentectmy of the liver was performed. Although the CD4 value in each patient was lower than 200 micro l, the operations were safely carried out and no major complication occurred. Because the chance of encountering HCC patients infected with HIV and HCV is increasing in Japan, we should consider the perioperative care of these patients, as well as the protection of medical workers against HIV infection.
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PMID:Operated hepatocellular carcinoma in two HIV- and HCV-positive hemophilic patients. 1523 96

Persons with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) coinfection are at increased risk for progression to cirrhosis compared with persons with HCV alone, but the reasons for this are unclear. In chronic HCV, the mechanism of liver injury is presumed to be due to HCV-specific T cell destruction of hepatocytes, so it is paradoxical that immunosuppressed hosts have higher rates of fibrosis progression. We examined intrahepatic cellular immune responses to HCV antigens to determine whether there were qualitative or quantitative differences in subjects with and without HIV. Expanded, CD4-enriched, liver-infiltrating lymphocytes from 18 subjects with chronic HCV and 12 subjects with HIV/HCV were cultured in the presence of HCV core protein, nonstructural proteins NS3 and NS5, and recall antigens tetanus toxoid and Candida. Secretion of interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin (IL) 10 was determined using enzyme-linked immunosorbent spot assay. There were no significant differences in liver biopsy grade or stage for HIV/HCV versus HCV groups. There were no significant differences between groups in the secretion of IFN-gamma or TNF-alpha in response to HCV or recall antigens. However, there was a significant increase in IL-10 secretion in response to NS3 and NS5 in subjects with HCV compared with HIV and HCV coinfection. In conclusion, subjects with coinfection have an alteration of intrahepatic HCV-specific IL-10 cytokine response that may have implications for HCV-related disease progression.
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PMID:Comparison of HCV-specific intrahepatic CD4+ T cells in HIV/HCV versus HCV. 1523 95

Hepatitis C virus (HCV) infection is frequent in human immunodeficiency virus (HIV)-infected patients. It is known to have an aggressive course in significantly immunosuppressed patients, and cirrhosis C has become one of the main causes of mortality in HIV-HCV coinfected patients since the improvement of antiretroviral therapy. The reasons for this severe fibrotic evolution are unclear. This prospective study compared chronic HCV lesions, liver immunocompetent cells, fibrosis and liver HCV loads in 2 cohorts of naive patients referred for HCV treatment: 33 HIV-HCV coinfected patients with CD4 >250/microL and 33 HCV-infected patients matched for the main risk factors of fibrosis. Fibrosis, particularly perisinusoidal fibrosis, was more marked in the coinfected patients. This occurred in the absence of a significant difference in disease activity. The number of CD3+ cells in the liver was higher in the HIV-HCV patients than in the HCV patients. Conversely, the number of liver CD4+ cells was lower in HIV-HCV patients than in HCV patients. The numbers of CD8+ and CD68+ cells were similar in the 2 groups. Finally, liver HCV load, assessed by immunostaining and reverse-transcription polymerase chain reaction, was similar in the 2 groups. We conclude that in the population of HIV-HCV coinfected patients with low-level immunosuppression referred for HCV treatment, fibrosis is worse than in HCV patients and the proportion of CD4+ lymphocytes among CD3+ cells is markedly decreased in the liver, whereas intrahepatic viral load is similar. Our data confirm the need to treat such patients against HCV, and suggest that HIV infection could favor fibrosis via the modulation of the intrahepatic immune response.
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PMID:Fibrosis is worse in HIV-HCV patients with low-level immunodepression referred for HCV treatment than in HCV-matched patients. 1534 10


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