Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some studies have suggested that human immunodeficiency virus (HIV) infection modifies the natural history of hepatitis C virus (HCV) infection, accelerating the progression of fibrosis and the development of cirrhosis. Our objective was to evaluate the fibrosis progression rate (FPR) in HCV/HIV-co-infected patients, and to identify factors that may influence it. HCV-mono-infected and HCV/HIV-co-infected patients with a known date of HCV infection (transfusion or injection drug use) and a liver biopsy were included. The FPR was defined as the ratio between the fibrosis stage (Metavir score) and the estimated length of infection in years and the result was reported as fibrosis units per year. The factors studied were gender, age at infection, consumption of alcohol, aminotransferase levels, histological activity grade, HCV genotype and viral load, CD4 cell count, HIV viral load, and the use of antiretroviral therapy. Sixty-five HCV-infected (group 1) and 53 HCV/HIV-co-infected (group 2) patients were evaluated over a period of 19 months. The mean FPR of groups 1 and 2 was 0.086 +/- 0.074 and 0.109 +/- 0.098 fibrosis units per year, respectively (P = 0.276). There was a correlation between length of HCV infection and stage of fibrosis in both groups. The age at infection, the aspartate aminotransferase level (r = 0.36) and the inflammatory activity grade were correlated with the FPR (P < 0.001). No difference in FPR was found between HCV-mono-infected and HCV/HIV-co-infected patients.
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PMID:There is no difference in hepatic fibrosis rates of patients infected with hepatitis C virus and those co-infected with HIV. 1817 24

Viral breakthroughs (VB), defined as having detectable HCV VL while on anti-HCV therapy after achieving maximal suppression, have not yet been characterized with the use of PEG-IFN in HIV/HCV-coinfected patients. We evaluated possible mechanisms for VB among HIV/HCV-coinfected patients receiving PEG-IFN/RBV. Thirty HIV/HCV coinfected patients were treated with PEG-IFN (1.5 mug/kg sc qwk) and RBV (1-1.2 g daily) for 48 weeks. Liver chemistry, HCV VL, genotyping, DNA microarray, and sequencing of HCV E-2 envelope were performed before and during treatment. VB had lower baseline HCV VL but higher ALT and AST than relapsers (ETR) (p < 0.05) and lower CD4+ T lymphocytes (%) than patients with sustained virological responses (SVR), but similar first and second phase HCV viral kinetics (vs. ETR and SVR; p > 0.05). HCV genotypes and envelope sequences were similar for patients with VB pretreatment and at break-through. VB had higher levels of interferon-induced gene (IFIG) expression pretreatment than patients with ETR (p < 0.01). HIV/HCV-coinfected patients have a high rate of VB on PEG-IFN/RBV therapy characterized by higher levels of IFIG expression, immunodeficiency, and hepatic inflammation. Novel strategies are required for the treatment of persons with VB.
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PMID:Immunodeficiency and intrinsic IFN resistance are associated with viral breakthrough to HCV therapy in HIV-coinfected patients. 1818 77

The recent availability of non-invasive tools to measure liver fibrosis has allowed examination of its extent and determination of predictors in all patients with chronic hepatitis C virus (HCV) infection. On the other hand, most information on hepatic fibrosis in HCV/human immunodeficiency virus (HIV)-coinfected patients has been derived from liver biopsies taken before highly active antiretroviral therapy (HAART) was widely available. All consecutive HCV patients with elevated aminotransferases seen during the last 3 years were evaluated and liver fibrosis measured using transient elastography (FibroScan) and biochemical indexes. Patients were split according to their HIV serostatus. A total of 656 (69.6%) HCV-monoinfected and 287 (30.4%) HIV/HCV-coinfected patients were assessed. Mean CD4 count of coinfected patients was 493 cells/muL and 88% were under HAART (mean time, 4.2 +/- 2.4 years). Advanced liver fibrosis or cirrhosis was recognized in 39% of the coinfected and 18% of the monoinfected patients (P < 0.005). A good correlation was found between FibroScan) and biochemical indexes [AST to platelet ratio index (r = 0.405, P < 0.0001), FIB-4 (r = 0.393, P < 0.0001) and Forns (r = 0.407, P < 0.0001)], regardless of the HIV status. In the multivariate analysis, age >45 years, body mass index (BMI) >25 kg/m(2), and HIV infection were independently associated with advanced liver fibrosis or cirrhosis. HIV/HCV-coinfected patients have more advanced liver fibrosis than HCV-monoinfected patients despite the immunologic benefit of HAART.
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PMID:Liver fibrosis on account of chronic hepatitis C is more severe in HIV-positive than HIV-negative patients despite antiretroviral therapy. 1822 3

Suppression of viral replication is followed by increases in CD4+ lymphocytes, and this has been shown to result in decreased susceptibility to opportunists after initiation of highly active antiretroviral therapy (HAART). However, clinical aggravations after the initiation of HAART have been thought to be due to the restored ability to mount an inflammatory response, or the immune reconstitution inflammatory syndrome (IRIS). The degree of IRIS observed in human immunodeficiency virus (HIV)-infected patients following initiation of HAART is variable. This prospective study was aimed at determining the proportion of IRIS and the pattern of opportunistic infections among 186 HIV/AIDS patients receiving HAART between December 2006 and July 2007 at Zewditu Memorial Hospital, Addis Ababa, Ethiopia. The proportion of IRIS was 17.2% (32/186). The mean number of days of IRIS occurrence for each disease ranged from 26 to 122 days with a mean of 80. Opportunistic diseases associated with IRIS were tuberculosis (68.8%, 22/32), herpes zoster rash (12.5%, 4/32), cryptococcosis (9.4%, 3/32), toxoplasmosis (6.3%, 2/32) and bacterial pneumonia (3.1%, 1/32). Compared to baseline readings there were significant increases in CD4 count, aspartate aminotransferase and alanine aminotransferase levels while hemoglobin values decreased during the development of IRIS. In summary, the proportion of IRIS and the pattern of opportunistic infections in HAART-treated patients in Ethiopia mirrored those reported in other countries. Further prospective surveys on epidemiological, immunological, microbial and clinical studies are imperative to assess the proportion and pattern of IRIS and effect of HAART in Ethiopia.
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PMID:Immune reconstitution inflammatory syndrome among HIV/AIDS patients during highly active antiretroviral therapy in Addis Ababa, Ethiopia. 1850 70

Rapid diagnosis is crucial for adequate treatment of disseminated mycobacteriosis. We conducted a retrospective cohort study to identify clinical and laboratorial features of disseminated mycobacteriosis in human immunodeficiency virus (HIV) infected patients that could help to differentiate tuberculosis (TB) from non-tuberculous mycobacteria (NTM) disease. All patients diagnosed from 1996 to 2006 were reviewed. TB was diagnosed in 65 patients and NTM in 31. Patients with TB had higher median levels of aspartate aminotransferase (AST) (69.0 vs. 45.0, P = 0.02) and lactate dehydrogenase (LDH) (725.0 vs. 569.0, P = 0.03). AST and LDH may be valuable tools in differentiating disseminated TB from NTM in HIV-infected patients.
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PMID:Laboratory features for presumptive diagnosis of disseminated tuberculosis in HIV-infected patients. 1892 48

Nevirapine (single dose), commonly used to prevent the mother-to-child transmission of human immunodeficiency virus (HIV) in developing countries, frequently induces viral resistance. Even mutations which occur only in a minor population of the HIV quasispecies (<20%) are associated with subsequent treatment failure but cannot be detected by population-based sequencing. We developed sensitive allele-specific real-time PCR (ASPCR) assays for two key resistance mutations of nevirapine. The assays were specifically designed to analyze HIV-1 subtype A and D isolates accounting for the majority of HIV infections in Uganda. Assays were evaluated using DNA standards and clinical samples of Ugandan women having preventively taken single-dose nevirapine. Lower detection limits of drug-resistant HIV type 1 (HIV-1) variants carrying reverse transcriptase mutations were 0.019% (K103N [AAC]), 0.013% (K103N [AAT]), and 0.29% (Y181C [TGT]), respectively. Accuracy and precision were high, with coefficients of variation (the standard ratio divided by the mean) of 0.02 to 0.15 for intra-assay variability and those of 0.07 to 0.15 (K103N) and 0.28 to 0.52 (Y181C) for inter-assay variability. ASPCR assays enabled the additional identification of 12 (20%) minor drug-resistant HIV variants in the 20 clinical Ugandan samples (3 mutation analyses per patient; 60 analyses in total) which were not detectable by population-based sequencing. The individual patient cutoff derived from the clinical baseline sample was more appropriate than the standard-based cutoff from cloned DNA. The latter is a suitable alternative since the presence/absence of drug-resistant HIV-1 strains was concordantly identified in 92% (55/60) of the analyses. These assays are useful to monitor the emergence and persistence of drug-resistant HIV-1 variants in subjects infected with HIV-1 subtypes A and D.
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PMID:Detection and quantification of minor human immunodeficiency virus type 1 variants harboring K103N and Y181C resistance mutations in subtype A and D isolates by allele-specific real-time PCR. 1943 56

Abnormalities in liver function tests could be produced exclusively by direct inflammation in hepatocytes, caused by the human immunodeficiency virus (HIV). Mechanisms by which HIV causes hepatic damage are still unknown. Our aim was to determine the correlation between HIV viral load, and serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as markers of hepatic damage in HIV naive infected patients. We performed a concordance cross-sectional study. Patients with antiviral treatment experience, hepatotoxic drugs use or co-infection were excluded. We used a Pearson's correlation coefficient to calculate the correlation between aminotransferases serum levels with HIV viral load. We enrolled 59 patients, 50 men and 9 women seen from 2006 to 2008. The mean (+/- SD) age of our subjects was 34.24 +/- 9.5, AST 37.73 +/- 29.94 IU/mL, ALT 43.34 +/- 42.41 IU/mL, HIV viral load 199,243 +/- 292,905 copies/mL, and CD4+ cells count 361 +/- 289 cells/mm(3). There was a moderately strong, positive correlation between AST serum levels and HIV viral load (r = 0.439, P < 0.001); and a weak correlation between ALT serum levels and HIV viral load (r = 0.276, P = 0.034); after adjusting the confounders in lineal regression model the correlation remained significant. Our results suggest that there is an association between HIV viral load and aminotransferases as markers of hepatic damage; we should improved recognition, diagnosis and potential therapy of hepatic damage in HIV infected patients.
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PMID:Correlation between HIV viral load and aminotransferases as liver damage markers in HIV infected naive patients: a concordance cross-sectional study. 1987 52

Hepatitis C virus (HCV) infection is the most important cause of chronic hepatitis, cirrhosis and end-stage liver disease leading to liver transplantation worldwide. Chronic infection by HCV causes liver fibrosis, which is accelerated by unknown mechanisms in patients with human immunodeficiency virus-1 (HIV-1) coinfection. Although the genetic variability of both HCV and HIV has been extensively studied in the context of monoinfections, more limited data is available regarding HCV-HIV coinfection. HCV disease progression among HIV coinfected patients may be influenced not only by demographic, epidemiological and clinical background variables, but also by genetic differences in infecting viruses. To explore this issue, we carried out a study in coinfected patients trying to associate the degree of liver damage to several demographic, clinical, and epidemiological characteristics of the patients, and also to the genetic variability of HCV between patients. For this purpose, we have applied different statistical techniques including the statistical generalized linear model (GLM) framework. The stage of fibrosis was indirectly measured by noninvasive means using the indexes Forns, APRI and FIB-4. HCV genetic variability between patients was estimated by sequencing the core region and by reconstructions of consensus maximum parsimony phylogenetic trees with 50% and 75% bootstrap majority rules. The results showed a direct correlation of the fibrosis biomarkers with the AST/ALT ratio, MoftIDU and with 3a HCV genotype clades, among others.
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PMID:Relating the liver damage with hepatitis C virus polymorphism in core region and human variables in HIV-1-coinfected patients. 2073 59

Nevirapine, a non-nucleoside reverse transcriptase inhibitor (NNRTI), is widely prescribed as a part of the combination therapy of human immunodeficiency virus (HIV) infection because of its efficacy and good tolerability. Here, we report a case of Stevens-Johnson syndrome (SJS) secondary to nevirapine. The patient had a diffuse, exfoliating exanthema with generalized bullous eruptions that involved the face, trunk and both extremities with elevated hepatic alanine aminotransferase and aspartate aminotransferase enzyme activities. The condition improved with stoppage of nevirapine-based highly active antiretroviral therapy (HAART) regimen, so we attributed this adverse event to nevirapine. A strict vigilance of adverse drug reaction is required in HAART.
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PMID:Nevirapine induced Stevens-Johnson syndrome in an HIV infected patient. 2145 32

Primary hepatic lymphoma is a rare presentation of a common disease. Diagnosis is difficult due to the risks of liver biopsy. We report the clinico-pathologic features of this presentation and specifically the utility of image-guided biopsy as a safe method of diagnosis. We retrospectively studied patients diagnosed with 'hepatic lymphoma' at a single center. Twenty-two patients fulfilled the criteria. Median age was 53 years (range 29-87). Nine patients were human immunodeficiency virus (HIV)-positive. The most frequent mode of presentation was with B-symptoms (15/22). All procedures were successful at obtaining diagnostic material with no complications. Six patients had synchronous bone marrow involvement. Nineteen patients received chemotherapy (10 had dose reductions) with an overall response rate of 74%. After a median follow-up of 19 months, 12 patients had died; the median overall survival (OS) was 4 months. Grade 3 or 4 aspartate transaminase (AST) abnormality was associated with very poor outcome. The OS of patients with hepatic lymphoma is poor. However, a response to modern induction therapies may predict a better outcome. The optimal dose adjustment of chemotherapy in this setting is unclear. In patients without readily accessible tissue, an image-guided core biopsy of hepatic lesions is a safe procedure with high diagnostic yield.
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PMID:Clinico-pathologic characteristics of patients with hepatic lymphoma diagnosed using image-guided liver biopsy techniques. 2170 47


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