Four children with a median age of 10.3 years (range 6.5-11.2 years) were included in the study. Their clinical immune categories were: A1 (n=2), A2 (n=1), and B3 (n=1). Treatment of all four patients was with zidovudine (AZT)+lamivudine (3TC)+ritonavir (RTV). At the end of the first STI, VL was a median 214000 copies/ml (range 27400-616000), corresponding to 5.3 log(10) (range 4.4-5.8). At the end of the second STI, VL was a median 72400 copies/ml (range 17800-126000) or 4.7 log(10) (range 4.2-5.1), which corresponds to a rebound 0.6 log(10) lower than the first. At the end of the third STI, VL was a median 28200 copies/ml (range 5370-140000) or 4.45 log(10) (range 3.7-5.1), a rebound 0.85 log(10) lower than the first. All rebounds were followed by a decrease in the VL to undetectable levels during the treatment periods. CD8+ T lymphocyte counts increased during viral rebounds and an initial decrease in CD4+ T lymphocyte counts was followed by a tendency to increase even exceeding CD8+ T cell counts. Only one event of transitory severe immunosuppression occurred. There were no symptoms related to the HIV infection.
A prospective study was conducted on 57 pregnant women to investigate the effect of antiretroviral drugs (ARV) on the carbohydrate metabolism during pregnancy. The women were divided into three groups: ZDV Group, 20 HIV-1 infected women taking ZDV; TT Group, 25 patients on triple antiretroviral treatment (ZDV + 3TC + NFV); and Control Group, 12 pregnant women. Blood samples were obtained during the first visit for the determination of fasting plasma glycemia, when the patients were also submitted to a 75 g oral glucose test (OGTT-75g). These procedures were performed four times along pregnancy.
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Lamivudine (LAM) resistance is common on lamivudine monotherapy for chronic hepatitis B. This study examined the safety and efficacy of telbivudine (LDT) given with adefovir (ADV) versus ADV monotherapy in patients with chronic, lamivudine-resistant HBV infection.
This article provides an extensive review of the evidence on the combination of ABC 600 mg and 3TC 300 mg. Specifically, it discusses the chemistry-- including the phrarmacodynamics, resistance to treatment, pharmacokinetics and metabolism--and formulations available. It also looks at clinical efficacy, including safety and tolerability.
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The aim of this study was to assess the effects of anti-tumour necrosis factor (TNF) agents on hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-negative and anti-hepatitis B core (HBc)-positive patients (HBV occult carriers) with rheumatic diseases.
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Fifty enrolled patients with CHB were evenly divided into 2 groups: a group treated with of lamivudine (LAM) (100 mg/day) plus adefovir (ADV) (10 mg/day) combination, and a group treated with entecavir (ETV) (0.5 mg/day). Serum levels of ALT, AST, creatinine, bilirubin, HBsAg, HBeAg and HBV viral load, and genotypic resistance were analyzed at 0, 12, 24, 52, and 104 weeks. HBV DNA levels were determined by real-time PCR and HBsAg and HBeAg by chemiluminescence. Serum levels of ALT, AST, creatinine, and bilirubin were measured by an automatic biochemical analyzer. Data analysis was performed with SPSS 12.0 software.
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We determined the frequency with which human immunodeficiency virus (HIV) peripheral blood mononuclear cell cultures convert from positive to negative in subjects enrolled in a substudy of AIDS Clinical Trials Group (ACTG) 320, which compared the efficacy of treatment with a combination of indinavir, zidovudine, and lamivudine (indinavir arm) to that of a combination of zidovudine and lamivudine (dual-nucleoside arm). All subjects included for study had positive baseline HIV cultures. Cultures were performed in real time with 10(7) fresh patient peripheral blood mononuclear cells, using the ACTG consensus method. We found lower rates of positive HIV cultures in the indinavir treatment arm than in the dual-nucleoside treatment arm (64 versus 96% at week 24, P < 0.001). Within the indinavir arm of the study, we found that positive cultures were less likely to occur in samples with a plasma HIV type 1 (HIV-1) RNA level of <500 copies/ml than in those with a level of >or=500 copies/ml (44 versus 90%, P < 0.001). In addition, HIV cultures from samples with HIV-1 RNA levels of >or=500 copies/ml turned positive 8.5 days earlier, on average, than those from samples with levels of <500 copies/ml (P < 0.001). However, 38% of samples with plasma RNA levels of <50 copies/ml still were positive for HIV by culture. Thus, the rates of HIV isolation by standard culture procedures decrease as the plasma viral load decreases below 1,000 copies/ml; however, HIV isolates were still obtained from a substantial proportion of subjects with RNA levels of <50 copies/ml. The delay in the time required for HIV cultures to turn positive should be considered when attempting to obtain an HIV isolate from patients with suppression of plasma viral load.
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To investigate the variability of the main immunodominant motifs of hepatitis B virus (HBV) core gene by ultra-deep-pyrosequencing (UDPS).
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To determine the concentrations of nevirapine (NVP), lamivudine (3TC) and stavudine (D4T) in seminal and blood plasma in HIV-1-infected men.
Chronic hepatitis B virus (CHB) infection is a major cause of cirrhosis and hepatocellular carcinoma. Nucleoside analogs (NAs) are popularly used to treat chronic hepatitis B virus (HBV) infections; however, the anti-HBV effect is attenuated by drug-resistant viral mutations selected during long-term antiviral therapy. The timely analysis of drug-resistance mutations is essential in order to adjust treatment regimes. In this study, a T1699C substitution was introduced into the x gene of pHBV1.3 to generate an additional XhoI site, termed pHBV1.3‑XhoI, which is a nonsense mutation and does not influence protein expression, HBV replication ability, or NA susceptibility. Based on co-transfection with weak or non-replicative HBV plasmids and pHBV1.3-XhoI or pHBV1.3 and -XhoI-P-null plasmids into hepatocellular carcinoma cells, PCR was used to amplify 1176‑bp segments of T/C1699 using the isolated HBV encapsulated DNA as a template, modified by XhoI digestion and subjected to agarose gel electrophoresis. Different bands composed of different virions were used to distinguish the replication capacities of the plasmids. Our results demonstrated no significant effects when different virions co-existed. A novel resistance test method was developed by co-transfection with pHBV1.3-XhoI and -rtL180M/M204V and treatment with various NA concentrations. Different bands composed of pHBV1.3-XhoI or -rtL180M/M204V were used to distinguish NA susceptibility. The bands composed of pHBV1.3 were more sharply reduced by lamivudine (LMV) than -rtL180M/M204V. The data demonstrate that the method established in our study may be used for the analysis of drug-resistant phenotypes at the cellular level.
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The patient was suffering from post-hepatitis liver cirrhosis, CHILD stage B, with underlying chronic hepatitis B and C coinfection.
Persistent genital human immunodeficiency virus type 1 (HIV-1) shedding among women receiving antiretroviral therapy (ART) may present a transmission risk. We investigated the associations between genital HIV-1 suppression after ART initiation and adherence, resistance, pretreatment CD4 cell count, and hormonal contraceptive use. First-line ART was initiated in 102 women. Plasma and genital HIV-1 RNA levels were measured at months 0, 3, and 6. Adherence was a strong and consistent predictor of genital HIV-1 suppression (P < .001), whereas genotypic resistance was associated with higher vaginal HIV-1 RNA level at month 6 (P = .04). These results emphasize the importance of adherence to optimize the potential benefits of ART for reducing HIV-1 transmission risk.
We retrospectively studied 62 patients (49 males; median age 54 years) with chronic HBV-related liver disease who were treated with lamivudine and who had at least 1-year on-treatment follow-up. Patients were subdivided according to the lamivudine dosage: 25 patients were treated with lamivudine 300 mg qd for two weeks, then shifted to 100mg qd (high-dose group) and 37 patients were treated with the standard dose of 100mg qd (standard-dose group).
Chemotherapy can cause hepatitis flare-up through viral reactivation in patients who have had contact with hepatitis viruses. Few data are available on the genotype of the reactivated viruses.
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We describe a 39-year-old man with hepatitis B virus-(HBV) related chronic hepatitis who presented with nephrotic syndrome and decompensated cirrhosis. A kidney biopsy revealed membranoproliferative glomerulonephritis (MPGN) which was thought to be related to the HBV infection. Because interferon-alpha therapy was generally not recommended in patients with advanced liver disease, we chose lamivudine as an alternate treatment for the HBV-associated glomerulonephritis (GN). After 3-month treatment with oral lamivudine, resolution of the renal disease dramatically occurred together with improvement in liver function. To our knowledge, this is the first case of HBV-associated MPGN successfully treated with oral lamivudine therapy. The possible role of lamivudine in the treatment of HBV-associated GN is discussed.
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Genotyping of 50 consecutive specimens each from blood donors and VCT clients during 2005-2006 showed no mutations associated with HIVDR in the reverse transcriptase or protease regions of the HIV pol gene. These results are categorized by the WHO HIV drug resistance threshold survey method as representing a low prevalence (<5%) of transmitted HIV drug resistance.
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This study was to evaluate the antiviral efficacy and safety in nucleoside naive Chinese patients with chronic hepatitis B (CHB) treated with entecavir (ETV) or lamivadine (LVD).
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Long-term administration of i.m. HBIG saves up to 60% of the usual costs for i.v. prophylaxis of HBV reinfection in patients after OLT. In combination with lamivudine, long-term i.m. HBIG therapy is as efficient as i.v. HBIG treatment, but its lower costs clearly favour its use in preventing HBV reinfection after OLT.
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in this pilot study, abacavir/lamivudine plus raltegravir was effective and generally well-tolerated over 48 weeks with modest changes in fasting lipids.
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About half of the patients had switched to tenofovir+ zidovudine/lamivudine/abacavir for simplification purposes or toxicity while the other half had experienced virologic failure. 80/122 (66%) responded. Median viral load decreased to 78 copies/ml at week 48; median CD4 count increased to 321 cells/mm(3). Of the 42 virologic failures, only 3 patients failed after week 24. 24/35 patients who had been on a non-suppressive zidovudine/lamivudine/abacavir-only regimen at baseline and added tenofovir to intensify, responded. 41/53 patients who switched from any nucleoside reverse transcriptase inhibitor-only regimen improved or maintained suppression. Genotypes were available for 85/122 patients. The only predictor of virologic failure was the combination 41L+210W+215Y/F mutational pattern. 16 of the patients who failed on tenofovir+ zidovudine/lamivudine/abacavir therapy selected new primary nucleoside reverse transcriptase inhibitor resistance mutations that they previously did not have. 48/85 (56%) patients with genotype tests had at least 3 (3-10; median 4) nucleoside reverse transcriptase inhibitor resistance-associated mutations in the past.
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The evolution of a sexually transmitted multiresistant HIV-1 in a linked transmission chain was followed for 33 months to assess its potential to persist in the absence of treatment. The multiresistant HIV reverted slowly to wild type in reverse transcriptase (positions 44, 67, 74, 118) rendering the virus only susceptible to lamivudine/emtricitabine. Persistence of the replication-competent resistant HIV increases its potential to spread further and strengthens the importance of resistance testing in newly infected patients.
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The efficacy of anti-viral therapy for chronic hepatitis B virus (HBV) is lost upon the emergence of resistant virus. Using >500 patient HBV isolates from several entecavir clinical trials, we show that phenotypic susceptibility correlates with genotypic resistance and patient virologic responses.
TDF susceptibilities of lamivudine-resistant clones (rtL180M/M204V) and lamivudine plus entecavir-resistant clones (rtL180M/S202G/M204V) were similar to wild type clones in vitro. However, lamivudine plus adefovir-resistant clones (rtA181T/N236T) acquired tolerance to TDF, and the rtN236T mutation was considered to be a causal substitution for TDF resistance. Furthermore, genotypic differences in TDF susceptibility were also observed between genotypes A and C in vitro, and the differences could be confirmed in vivo (p = 0.023).
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To examine T-cell repertoire modifications, the evolution of T-helper (TH)1/TH2 cytokine imbalance and modifications in chemokine receptor expression when the viral load is decreased by 2-3 log10 copies/ml under highly active antiretroviral therapy (HAART).
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A total of 78 patients with compensated CHB (Group A) were maintained on either adefovir 10 mg daily (n = 38) or placebo (n = 40) while continuing lamivudine. An additional 38 patients with decompensated cirrhosis or post liver transplantation (Group B) received lamivudine plus adefovir. The primary endpoint was HBV DNA response at year 2.
The purpose of the study is to analyse the prevalence of hepatitis B virus (HBV) infection and its incidence of reactivation among multiple myeloma (MM) patients treated in the era of novel therapy in an endemic Asian setting.
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In this 48-week, prospective, open-label, randomized study, patients were either switched to once-daily LPV/r, tenofovir (TDF), and lamivudine (3TC) (QD arm) or remained on their existing regimen (control arm). The primary endpoint of the study was the proportion of patients maintaining virologic suppression following 48 weeks of treatment.
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Monitoring of renal function becomes increasingly important in the aging population of HIV-1 infected patients. We compared Cockroft & Gault (C&G), Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), Modification of Diet in Renal Disease (MDRD), Cystatin C- and 24 h urine-based estimated GFR (eGFR) with the gold standard, measured GFR (mGFR) using [125I]-iothalamate.