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

Transfusion of whole blood or blood components is the mainstay of treatment in patients with beta-thalassemia and hemophilia. Owing to the scarcity of reports regarding the frequency of transfusion-transmitted hepatitis virus infections in thalassemia patients, the frequency of such infections was studied in India in 40 multi-transfused thalassemia patients (26 males, 14 females; mean age 8.1 +or- 5.3 years, range 1-35) with no clinical or biochemical evidence of liver disease. The enzyme-linked immunosorbent assay (ELISA) technique (Abbott) was used for all tests. The patients had received an average of 80 units (range 10-250) of blood. A majority of these units had been screened for hepatitis B surface antigen (HBsAg) using RPHA. HBsAg antibodies were present in 18 (45%), antihepatitis C virus (HCV) in 7 (17.5%), and antihuman immunodeficiency virus in 1 (2.5%) case, respectively. Of 18 HBsAg positive patients, antidelta and anti-HCV antibodies were present in 3 and 4 patients, respectively; 1 patient had both the antibodies. 4 of 40 (10%) patients had evidence of both hepatitis B virus (HBV) and HCV infection. In a US study, the frequencies of HBsAg and anti-HBs positively among thalassemics were 4.5% and 43.5%, respectively. In contrast, 90% of hemophiliacs show serological evidence of HBV infection. Routine screening of blood donors by CEP or RPHA technique was started in the hospital blood bank 7 years ago. The sensitivity of these techniques is much lower than that of RIA and ELISA and a majority of the patients has received initial blood transfusions before HBsAg screening was started. The study indicated that more than 50% of multi-transfused thalassemia patients showed serological evidence of one or more HBV, HCV, HDV, and HIV infection. Thus, screening of blood units for HBV, HCV, and HIV infections to be used for thalassemic patients and vaccination of thalassemic patients against hepatitis B is imperative.
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PMID:Frequency of hepatitis B, C and D and human immunodeficiency virus infections in multi-transfused thalassemics. 142 37

Trimethoprim and trimethoprim-sulphamethoxazole (co-trimoxazole) are often prescribed in HIV patients treated with zidovudine. The pharmacokinetics of zidovudine, after a dose of 3 mg kg-1 by constant rate intravenous infusion over 1 h were evaluated in nine HIV patients in an open, randomized, three-phase crossover study, without and with trimethoprim (150 mg) and trimethoprim-sulphamethoxazole (160 and 800 mg). The metabolic clearance of zidovudine was not significantly influenced by trimethoprim-sulphamethoxazole and trimethoprim. However, the renal clearance of zidovudine was decreased by 58 and 48%, respectively, and that of its glucuronide by 27 and 20% (P < 0.05). The fraction of the dose excreted as the parent compound fell by 47 and 39% and the metabolic ratio by 48 and 43% (P < 0.05). This kinetic drug interaction, apparently due solely to trimethoprim, may only be clinically important when hepatic glucuronidation is also impaired by liver disease or inhibited by other drugs.
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PMID:Trimethoprim, alone or in combination with sulphamethoxazole, decreases the renal excretion of zidovudine and its glucuronide. 149 87

Involvement of the liver with the same opportunistic organisms and neoplasms affecting other organs has been recognized since the beginning of the AIDS epidemic. In this overview of hepatic histopathologic features in AIDS, we review the range of opportunistic infections and neoplasms accompanying HIV infection. Hepatic disease may result from viral, bacterial, protozoal, or fungal infection, or secondary to drugs and neoplasms. Liver involvement in AIDS usually reflects disseminated rather than primary disease. CMV and mycobacteria are the most common organisms in liver identified in biopsy and autopsy studies. A variety of nonspecific features, including steatosis, granulomas, and sinusoidal abnormalities may also be seen. HIV-1 itself was recently identified in the liver. Speculation regarding the significance of this finding has been discussed in this review. Hepatitis B, C, and D may also complicate the course of disease in patients with AIDS. Hepatitis B behaves differently in the population with AIDS than in immunocompetent patients. We concluded our review with a discussion of the present recommendations regarding the use of liver biopsies in these patients. This topic continues to be widely debated in the literature.
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PMID:Hepatic histopathology in the acquired immunodeficiency syndrome. 163 22

We assessed the prevalence and clinical significance of antibodies to hepatitis C virus among a cohort of 148 patients with chronic hepatitis B virus infection. Sixteen patients (11%) had anti-hepatitis C virus detectable by enzyme-linked immunoassay. The results from eight of these patients were positive by recombinant immunoblot assay. The results of recombinant immunoblot assay testing were not consistent; therefore the analysis of the patients' data was based on anti-hepatitis C virus enzyme-linked immunoassay results. Patients with chronic hepatitis B with anti-hepatitis C virus were more likely to be cirrhotic (44% vs. 21%) and to have decompensated liver disease (24% vs. 6%). Hepatitis B virus replication appeared to be suppressed in patients with both infections as measured by hepatitis B virus-associated DNA polymerase activity (mean = 2,055 vs. 2,555 cpm). Human immunodeficiency virus infection was more common in the anti-hepatitis C virus positive group (36% vs. 11%). Thus hepatitis C virus appears to suppress hepatitis B virus replication and to cause more severe liver disease in patients with chronic hepatitis B infection.
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PMID:The significance of antibody to hepatitis C virus in patients with chronic hepatitis B. 164 40

To determine whether the abnormalities of cell-mediated immunity described in chronic D hepatitis are associated with hepatitis D virus (HDV) infection or concomitant human immunodeficiency virus (HIV) infection, serologic and tissue hepatitis B virus (HBV) and HDV markers and T lymphocyte subsets were studied in serum samples from 38 patients with chronic D hepatitis, 26 of whom had HIV infection. Patients with chronic D hepatitis and HIV infection had significantly lower peripheral blood T4:T8 ratios resulting from a significant increase in T8+ (suppressor/cytotoxic) cells, while numbers of T lymphocyte subsets were normal in cases with chronic D hepatitis only. HIV+ patients showed an increase in HBV replication (identified by hepatitis B core antigen in liver and hepatitis B e antigen and HBV DNA in serum) and in HDV replication (tissue D antigen and HDV RNA) without evidence of more active liver disease. Probably the immunologic disturbances detected in chronic D hepatitis are secondary to HIV infection, do not contribute to the pathogenesis of liver injury, and are associated with increased viral B and D replication.
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PMID:Influence of human immunodeficiency virus infection on cell-mediated immunity in chronic D hepatitis. 167 49

The implications of testing all blood donations in the UK for antibody to hepatitis C virus (HCV) are considered. Although the risks of serious liver disease arising from transfusion-transmitted HCV are relatively low in the UK, the cost of such screening will be high in terms of financial outlay and lost donations. In the UK, at least, screening of all blood donations for anti-HCV is unlikely to be as cost effective as screening for HBsAg or anti-HIV.
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PMID:Hepatitis C virus screening: UK Blood Transfusion Service on the threshold. 172 56

We have studied the potential thrombogenicity of two different heat-treated prothrombin complex concentrates (PCC) in patients with Haemophilia B. Seven patients were studied on nine separate occasions. Four of the patients had chronic hepatitis C (HCV) associated liver disease and three were HIV-antibody positive. The PCCs were Profilnine (Alpha Therapeutics, Thetford, UK) and 9A (Bio-Products Laboratory, Elstree, UK) and the dose administered ranged from 35 to 60 U/kg. Blood samples were taken on ten separate occasions; twice before the infusion and at 15, 40, 60, 75 and 120 min and 4, 8 and 24 h after the infusion of PCC. Investigations included prothrombin time, kaolin cephalin clotting time, thrombin time, fibrin(ogen) degradation products, factor VIII, factor IX, antithrombin III and fibrinopeptide A (FPA). Fibrinopeptide A rises were seen following two of six infusions of 9A and one of three infusions of Profilnine. On all three occasions the rise in FPA was transient, returning to baseline levels within 120 min. Plasma beta-thromboglobulin (BTG) was assayed in three patients and in one patient, the rise in FPA was followed by an increase in BTG. No other changes were observed and there were no clinical features of disseminated intravascular coagulation. Our results indicate that even with normal clinical doses of PCC, intravascular thrombin generation can occur in patients with Haemophilia B. However, this effect is inconsistent both with respect to PCC batch and patient, but may occur in the absence of HIV infection and HCV liver disease.
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PMID:Potential thrombogenicity of heat-treated prothrombin complex concentrates in Haemophilia B. 178 33

Severe chronic active hepatitis, defined as the presence of a fivefold increase in serum aminotransferases and a twofold rise in gamma globulin for at least 10 weeks, is considered a progressive immunological liver disease requiring corticosteroid treatment, particularly when serum autoantibodies and a severe lymphoplasmacellular periportal infiltrate are found in the liver biopsy specimen. A 38 year old man who fulfilled the criteria for severe chronic active hepatitis is described. His sex, his homosexuality, and the presence of antibodies against HIV, however, led to the suspicion of a coinfection with hepatitis C virus (HCV) rather than autoimmune disease. The rapid and complete response to alpha interferon treatment and a recently available positive antibody test for HCV supported this view. These findings indicate that a HCV related chronic active hepatitis can present as the severe autoimmune type of chronic active hepatitis. Moreover, as in HBV infection, the response to treatment differs from that of autoimmune severe chronic active hepatitis.
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PMID:Severe chronic active hepatitis (autoimmune type) mimicked by coinfection of hepatitis C and human immunodeficiency viruses. 195 76

The effect of human immunodeficiency virus (HIV) infection on type and severity of liver disease was studied in 61 HIV-positive patients who did not have AIDS and in 45 AIDS patients. Liver biopsies revealed viral hepatitis in 12 of 18 non-AIDS patients but in only 4 of 34 AIDS patients (P less than .0005, Fisher's exact test). Acute, non-A non-B, and chronic active hepatitis B were seen exclusively in the non-AIDS group; however, chronic persistent hepatitis B was seen in both groups. In 9 of 18 AIDS patients intra vitam liver histopathology established diagnoses of opportunistic infections or tumors. Tissue reaction to certain pathogens, such as hepatitis B virus, mycobacteria, and cryptococci, seems to be milder in AIDS patients than in others who are HIV positive or the expected reaction of the normal host. This is likely because of impaired cell-mediated immunity in patients with advanced HIV disease.
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PMID:Hepatic involvement in patients with human immunodeficiency virus infection: discrepancies between AIDS patients and those with earlier stages of infection. 201 Jun 40

56 haemophiliacs selected on the basis of HIV-1 antibody status, liver disease grade and mean annual dose of clotting factor concentrate used were studied. Spontaneous and stimulated IgG and IgM production in vitro were measured. HIV-1 infection was associated with increased spontaneous immunoglobulin production and an impaired response to pokeweed mitogen and Staph Aureus protein A. Implying a shift in the proportions of partially and fully activated B cells. In the absence of HIV-1 infection there was a shift to a greater proportion of partially activated B cells in patients with severe liver disease. The remainder had in vitro immunoglobulin production comparable to controls. B cell abnormalities occur early in the course of HIV-1 infection. Liver disease and not clotting factor concentrate treatment cause B cell abnormalities in the absence of HIV-1 infection in haemophilia.
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PMID:B cell dysfunction in haemophilia in the absence and presence of HIV-1 infection. 202 40


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