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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of recurrence of hepatitis B virus (HBV) following orthotopic liver transplantation (OLT) is as high as 80% when no attempt at prevention has been considered. HBV reinfection is associated with the reappearance of hepatitis B surface antigen (HBsAg) and HBV DNA in serum and, in most cases, with rapid severe graft damage. Immunoprophylaxis using polyclonal anti-HBs immunoglobulins reduces the risk of recurrence but this long-term therapy remains highly expensive. In this report, we use fresh frozen plasma (FFP) with high titers of anti-HBs immunoglobulins in an attempt to reduce HBV recurrence. From July 1987 to September 1993, 11 patients underwent OLT for HBV-related liver disease (18% of our OLT patients). FFP were administered to 6 patients continually for 7 to 46 months. Only one patient, under long-term immunosuppressive treatment before OLT, was reinfected 7 months after OLT. Rapid development of graft failure was observed with histologic manifestations of a fibrosing cholestatic hepatitis, leading to patient death after 12.5 months with concomitant bacterial infection. In this protocol, the rate of reappearance of HBsAg was 17%, a figure which can be favorably compared with other reports. All patients were subsequently tested for HCV and HIV and remained negative. In conclusion, FFP with high titers of anti-HBs immunoglobulins is at least as effective as polyclonal anti-HBs immunoglobulins in reducing the rate of HBV recurrence following OLT. The estimated cost of this new immunoprophylaxis method is less than 10% of the classical prophylaxis based on purified human polyclonal anti-HBs immunoglobulins.
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PMID:[Prevention of viral recurrence following liver transplantation for post-hepatitis B and B-delta cirrhosis]. 819 Dec 67

Hepatic involvement was investigated in 31 children with perinatal HIV-1 infection, who were followed for 2-82 months (mean 30.5). Liver disease, as revealed by increased aminotransferase levels, liver biopsy or necroscopy, was diagnosed in 18 children (58%), of which 7 (22.5%) had acute hepatitis and 11 (35.5%) showed chronic liver disease. Overall, 40 persistently active or recurrent viral infections, as demonstrated by positive culture and/or detection of serum DNA, specific IgM, IgA and high levels of IgG, were revealed in the children with liver disease, while 12 similar infections were detected in 13 children without liver disease (p < 0.001). In particular, the children with liver disease showed a significantly (p < 0.002) higher incidence of cytomegalovirus (CMV) infections than children without liver disease (13 versus 3). Moreover, hepatitis C and B virus infections were revealed only in children with liver disease (5 and 1 patients, respectively). Clinical outcome showed a significantly (p < 0.001) higher mean survival in the children without liver disease than those with liver disease (47.5 versus 18.2 months). In fact, nine of the children with liver disease (50%) died, as opposed to only one of the children without liver disease (7.7%; p = 0.01). Based on these findings, liver disease is indicative of a poor prognosis in children with HIV infection, being related to the presence of multiple active viral infections.
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PMID:Multiple viral infections in HIV-infected children with chronically-evolving hepatitis. 826 Aug 69

Human immunodeficiency virus (HIV)-related liver disease is frequently diagnosed. We report a study about 100 liver biopsy samples (LB) in patients with HIV infection. The aim of the study has been to analyze the liver biopsy yield when a systemic disease (group A) or a chronic liver disease (group B) are suspected. Tuberculosis, all of them disseminated, was the most common finding in group A biopsy samples, and a 81% yield was obtained. Chronic active hepatitis was the most common finding group B, and profitability reached 90%. We conclude that LB is the elective method to diagnose systemic disease, in patients previously selected according to their clinical findings, and that final diagnoses and safe.
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PMID:[Liver disease in patients with human immunodeficiency virus infection. Study of 100 biopsies]. 835 88

IgA nephropathy (IgAN) is characterized by the presence of IgA and C3 deposits in the mesangium. Mesangial IgA is mostly dimeric IgA1 with a J chain, lacking a secretory component. In view of the recent demonstration of elevated serum levels of secretory component and secretory IgA in liver disease and HIV infection associated with hyper-IgA, we measured the serum secretory component in 50 IgAN patients and 45 controls. Free secretory component and secretory IgA and IgM levels were determined by enzyme-linked immunosorbent assay. Normal or low levels were found patients. These data support previous work suggesting that in IgAN circulating and probably mesangial IgA do not originate from the epithelial compartment of the mucosal immunoglobulins as it is the case in other hyper-IgA diseases.
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PMID:Serum secretory IgA and IgM and free secretory component in IgA nephropathy. 853 52

Autoimmune hepatitis is an inflammatory disease of the liver of unknown etiology that progresses toward cirrhosis and liver failure and is generally responsive to immunosuppressive treatment. The presence of anti-smooth muscle antibodies with anti-actin specificity and of anti-liver kidney microsomal antibodies defines two distinct subgroups of the disease. An autoantibody against liver cytosolic antigens has recently been described. Management of autoimmune hepatitis relies on immunosuppressive therapy with steroids alone or combined with azathioprine. When the disease is poorly controlled, despite good patient compliance to therapy, cyclosporin should be recommended. Progressive liver disease in chronic hepatitis B in adults has been associated with the presence of precore mutants of hepatitis B virus. In children, the presence of precore mutants seems not to affect the rate of seroconversion to anti-hepatitis B e antigen. However, high viremic levels of precore mutants are associated with persistent viral replication and liver disease. Interferon alfa seems to be less effective in children than in adults in the treatment of chronic hepatitis B; however, it hastens the seroconversion rate to anti-hepatitis B e antigen, accelerating the spontaneous clearance of the virus in children with already low levels of viral replication. Blood transfusions, especially those received in the perinatal period, are the single most important source of infection with hepatitis C in childhood. HIV coinfection is a major risk factor for vertical transmission of hepatitis C virus in pregnant women. Chronic hepatitis C in children is usually an asymptomatic disease associated with mild to moderate fluctuation of aminotransferase activities and histologic features of mildly active hepatitis. Severe active hepatitis and cirrhosis are infrequent during childhood and adolescence. Interferon may have a place in the treatment of chronic hepatitis C in children.
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PMID:Chronic hepatitis in children. 854 54

A case/control study was conducted in Bujumbura, Burundi, from 1991 to 1992 to assess the relationship between chronic liver disease and hepatitis C virus (HCV). Patients presenting chronic liver disease (n = 80) were selected based on clinical, laboratory, ultrasonographic, and/or endoscopic findings. Patients with AIDS or hepatocellular carcinoma were excluded. Controls (n = 159) matched with regard to age and sex were recruited from outpatients who had blood tests at a liver disease clinic. Patients and controls were tested for anti-HCV antibodies by ELISA and LIA. Screening for hepatitis B virus (HBs antigen, anti-HBs and anti-HBc antibodies) and human immunodeficiency virus (HIV) was achieved by ELISA with confirmation of HIV infection by LIA. The incidence of anti-HCV antibodies was significantly higher in patients (55.0%) than controls (33.3%) (p < 0.001). The incidence of HBs antigens was significantly higher in patients (28.8%) than controls (7.5%) (p < 0.0001). The incidence of anti-HIV antibodies was not significantly different in the two groups. Multifactorial analysis indicated that anti-HCV antibodies and HBs antigens were risk factors for chronic liver disease, but did not detected a significant interaction between these two risk factors. Prevention of hepatitis C and B would reduce the incidence of chronic liver disease but cost currently limits widespread use of this approach.
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PMID:[Relationship between chronic liver diseases and hepatitis C in Burundi adults]. 855 18

From November 1993 to December 1994, the seroprevalence of anti-HCV, HBsAg was studied among 346 HIV-infected persons (asymptomatic HIV-infected persons and AIDS patients) and 1,023 subjects from the general population (including 119 cord blood samples). The prevalence of anti-HCV, HBsAg among HIV-infected patients aged 15-45+ years was 11.0 and 11.6 per cent respectively which is significantly higher than the comparable levels for the general population (1.9% and 4.7%) in the age group 15-44 years. There was no statistically significant association of anti-HCV and HBsAg prevalence among 200 asymptomatic HIV-infected carriers and 146 AIDS patients. Assays for anti-HCV among blood donors are highly recommended to reduce the development of liver disease or cirrhosis in the immediate future.
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PMID:Seroprevalence of anti-HCV among HIV-infected persons and general population. 857 73

We have undertaken a comprehensive study of hepatitis C virus (HCV) genotype and its clinical significance in haemophilic patients. 189 HCV RNA positive were typed, using the Simmonds classification scheme, by restriction fragment length polymorphism (RFLP) in an amplified segment of the 5' non-coding region of the HCV genome. Type 1 was found in 121 (64.0%), type 2 in 23 (12.2%), type 3 in 36 (19.0%), type 4 in 3 (1.6%), type 5 in 2 (1.1%) and mixed infection in 3 (1.6%). There were no type 6 infections and one patient (0.5%) could not be typed. Genotype was not associated with diagnosis, age, or with HIV infection. Type 1 was associated with higher serum HCV RNA levels, and with a poor response to interferon. Progression to hepatic decompensation has been seen less frequently in those with type 3 compared to type 1 infection (p = 0.07). Three out of eleven patients studied over a longer time course showed a change in genotype, the remainder were persistently infected with HCV type 1. In conclusion, HCV genotype has clinical relevance in the management of haemophilic patients. Those with type 1 are probably more likely to develop serious liver disease and since they respond poorly to interferon-alpha, should be considered for new treatment strategies aimed at sustained clearance of HCV RNA.
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PMID:Chronic hepatitis C virus infection in haemophilic patients: clinical significance of viral genotype. 860 6

All patients with a positive reaction to the tuberculin skin test should be evaluated for weight loss, night sweats, fever, chronic cough and other signs of active tuberculosis. Chest radiographs should also be obtained in these patients. All converters receiving isoniazid should be examined monthly for signs of hepatitis and neurotoxicity. Liver function tests should be obtained at initiation of isoniazid therapy and again during the first two to four months in patients age 35 or older or with a history of alcoholism, liver disease or intravenous drug use. All cases of active tuberculosis should be reported to the local public health department. Most patients with active tuberculosis should receive isoniazid, rifampin, ethambutol and pyrazinamide daily for two weeks, followed by directly observed administration twice weekly for six additional weeks. If sputum cultures show no resistance after two months of therapy, pyrazinamide and ethambutol may be discontinued, with isoniazid and rifampin taken for an additional 16 weeks. Patients with human immunodeficiency virus infection or acquired immunodeficiency syndrome should receive the initial treatment for at least nine to 12 months, and isoniazid and rifampin for at least six months after culture conversion has occurred.
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PMID:Outpatient management of tuberculosis. 862 77

Chronic liver disease due to hepatitis C virus (HCV) infection is a major problem in hemophiliacs. Recent reports suggested that hemophiliacs coinfected with hepatitis C virus and human immunodeficiency virus (HIV) have an increased incidence of liver failure but the mechanism of accelerated liver injury is not clear. We tested plasma from 100 hemophiliacs for anti-HCV by second generation ELISA, anti-HIV by EIA, and HCV RNA and HIV RNA by branched DNA and polymerase chain reaction assays to determine if hemophiliacs coinfected with HCV and HIV have higher HCV RNA levels and more active liver disease. Seventy-nine (79%) patients were anti-HCV positive, of whom 85% were HCV RNA positive. None of the anti-HCV-negative patients had detectable HCV RNA in plasma. Forty-two (42%) patients were anti-HIV positive, of whom 47% had detectable HIV RNA. All the anti-HIV-positive patients were also anti-HCV positive. The prevalence of both anti-HCV and anti-HIV increased significantly with age. There was no difference in HCV RNA levels between anti-HIV-positive and anti-HIV-negative patients (mean: 21 +/- 4 vs 18 +/- 5 Meq/ml), although HCV RNA levels were significantly higher in anti-HIV-positive patients with CD4 counts < 200/mm3 (P = 0.008). There was an inverse correlation between HCV RNA levels and CD4 counts but no correlation was found between HCV RNA and serum aminotransferase levels. We found a high prevalence of HCV and HIV coinfection in our hemophiliacs. Hepatitis C virus replication appears to be increased in patients with severe immunodeficiency secondary to progressive HIV infection. However, there was no correlation between HCV RNA and serum ALT level, suggesting that HCV is not directly cytopathic.
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PMID:Effect of human immunodeficiency virus infection on hepatitis C virus infection in hemophiliacs. 865 62


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