17 research outputs found
HIV RNA measurement in dried blood spots of HIV-infected patients in Thailand using Abbott m2000 system
No full textWorld Health Organization recommends using dried blood spots (DBS) for HIV RNA viral load (VL) measurement whenever plasma processing is not convenient or feasible. DBS collected from 80 treatment-naïve HIV-infected patients presenting in three hospitals of two different regions of Thailand were shipped to a central laboratory along with corresponding plasma specimens. Viral load was measured in both DBS and plasma using the Abbott m2000 system. HIV RNA levels were strongly correlated (r = 0.94) with a mean of differences of 0.23 log10 copies/mL. Using the 1,000 copies/mL cut-off, the sensitivity of DBS was 97% (95%CI, 91–100%) and specificity was 75% (95%CI, 19–99%). DBS are useful to scale-up HIV RNA VL testing in settings with limited access to VL testing.</div
Predictors of 5-year mortality in HIV-infected adults starting highly active antiretroviral therapy in Thailand.
No full textOBJECTIVE: To estimate the early and long-term mortalities and associated risk factors in adults receiving highly active antiretroviral therapy (HAART) in Thailand. DESIGN: A prospective observational cohort study. METHODS: Previously untreated adults starting HAART in 2002-2009 were followed-up in 43 public hospitals. Kaplan-Meier probability of survival was estimated up to 5 years of therapy. Factors associated with early (≤6 months) and long-term (>6 months) mortalities were assessed using Cox regression analyses. RESULTS: A total of 1578 adults received HAART (74% women; median age, 33 years; CD4 cell count, 124/mL), with a median follow-up of 50 months (interquartile range, 41-66). Eighty-nine patients (6%) died (37 occurred ≤6 months and 52 occurred >6 months) and 183 (12%) were lost to follow-up. Probability of survival [95% confidence interval (CI)] was 97.5% (96.7% to 98.2%) at 6 months, 96.6% (95.6% to 97.4%) at 1 year, and 93.5% (91.9% to 94.8%) at 5 years. Probability of being alive and on follow-up was 80.8% (78.5% to 82.8%) at 5 years. Early mortality was associated with anemia [adjusted hazard ratio (aHR) 3.6, 95% CI: 1.7 to 7.5] and low CD4 count (aHR 1.6, 95% CI: 1.1 to 2.2 per 50 cells decrease) at treatment initiation. Long-term mortality was associated with persistent anemia (aHR 4.9, 95% CI: 2.1 to 11.6), CD4 increase from baseline 1000 copies per milliliter (aHR 2.8, 95% CI: 1.3 to 6.1) at 6 months of HAART; male gender; and calendar year of enrollment. CONCLUSIONS: Early mortality was associated with anemia and severe immunosuppression at initiation of therapy. Long-term mortality was associated with persistent anemia, CD4 count increase, and virological response at 6 months of therapy over baseline characteristics, highlighting the importance of laboratory monitoring
HIV RNA measurement in dried blood spots of HIV-infected patients in Thailand using Abbott m2000 system - Fig 1
No full text(A) Regression analysis of HIV RNA levels in paired plasma and DBS specimens from 80 participants. (B) Bland-Altman analysis of agreement between HIV RNA levels in 80 paired plasma and DBS specimen. The horizontal lines represent the mean difference and +2 standard deviations (SD).</p
Baseline characteristics of study population.
No full textBaseline characteristics of study population.</p
New-Onset Diabetes and Antiretroviral Treatments in HIV-Infected Adults in Thailand
No full textBACKGROUND: Use of several antiretrovirals (ARVs) has been shown to be associated with a higher risk of diabetes in HIV-infected adults. We estimated the incidence of new-onset diabetes and assessed the association between individual ARVs and ARV combinations, and diabetes in a large cohort in Thailand. METHODS: We selected all HIV-1-infected, nondiabetic, antiretroviral-naive adults enrolled in the Program for HIV Prevention and Treatment cohort (NCT00433030) between January 2000 and December 2011. Diabetes was defined as confirmed fasting plasma glucose >/= 126 mg/dL or random plasma glucose >/= 2 00 mg/dL. Incidence was the number of cases divided by the total number of person-years of follow-up. Association between ARVs and ARV combinations, and new-onset diabetes was assessed using Cox proportional hazards models. RESULTS: Overall, 1594 HIV-infected patients (76% female) were included. Median age at antiretroviral therapy initiation was 32.5 years. The incidence rate of diabetes was 5.0 per 1000 person-years of follow-up (95% confidence interval: 3.8 to 6.6) (53 cases). In analyses adjusted for potential confounders, exposure to stavudine + didanosine [adjusted hazard ratio (aHR) = 3.9; P = 0.001] and cumulative exposure >/= 1 year to zidovudine (aHR = 2.3 vs. no exposure; P = 0.009) were associated with a higher risk of diabetes. Conversely, cumulative exposure >/= 1 year to tenofovir (aHR = 0.4 vs. no exposure; P = 0.02) and emtricitabine (aHR = 0.4 vs. no exposure; P = 0.03) were associated with a lower risk. CONCLUSIONS: The incidence of diabetes in this predominantly female, young, lean population was relatively low. Although stavudine and didanosine have now been phased out in most antiretroviral therapy programs, our analysis suggests a higher risk of diabetes with zidovudine, frequently prescribed today in resource-limited settings
Switching HIV Treatment in Adults Based on CD4 Count Versus Viral Load Monitoring: A Randomized, Non-Inferiority Trial in Thailand
No full textBackground
Viral load (VL) is recommended for monitoring the response to highly active antiretroviral therapy (HAART) but is not routinely available in most low- and middle-income countries. The purpose of the study was to determine whether a CD4-based monitoring and switching strategy would provide a similar clinical outcome compared to the standard VL-based strategy in Thailand.
Methods and Findings
The Programs for HIV Prevention and Treatment (PHPT-3) non-inferiority randomized clinical trial compared a treatment switching strategy based on CD4-only (CD4) monitoring versus viral-load (VL). Consenting participants were antiretroviral-naïve HIV-infected adults (CD4 count 50–250/mm3) initiating non-nucleotide reverse transcriptase inhibitor (NNRTI)-based therapy. Randomization, stratified by site (21 public hospitals), was performed centrally after enrollment. Clinicians were unaware of the VL values of patients randomized to the CD4 arm. Participants switched to second-line combination with confirmed CD4 decline >30% from peak (within 200 cells from baseline) in the CD4 arm, or confirmed VL >400 copies/ml in the VL arm. Primary endpoint was clinical failure at 3 years, defined as death, new AIDS-defining event, or CD4 400 copies/ml at switch was 7.2 months (5.8–8.0) in VL versus 15.8 months (8.5–20.4) in CD4 (p = 0.002). FDO scores were not significantly different at time of switch. No adverse events related to the monitoring strategy were reported.
Conclusions
The 3-year rates of clinical failure and loss of treatment options did not differ between strategies although the longer-term consequences of CD4 monitoring would need to be investigated. These results provide reassurance to treatment programs currently based on CD4 monitoring as VL measurement becomes more affordable and feasible in resource-limited settings.
Trial registration
ClinicalTrials.gov NCT0016268
Resistance mutations found at first ARV switch (CD4 arm).
No full text<p>This table includes all 16 participants in the CD4 arm who had VL >400 copies/ml at the time of switching.</p>a<p>Duration of replication before measurement of genotype may be shorter than duration before ARV drug switching.</p>b<p>These two participants both had Y181C mutations at baseline and were the only two of the participants switching to second-line regimens with major baseline NNRTI resistance mutations.</p
Kaplan Meier curve of occurrence of clinical failure.
No full text<p>Kaplan Meier curve of occurrence of clinical failure.</p
Resistance mutations found at first ARV switch (VL arm).
No full text<p>This table shows 18 patients randomized to the VL arm who reached switching criteria of >400 copies/ml. The last samples collected before switch were genotyped. One participant with extensive PI resistance in the pretreatment specimen is omitted from this table.</p>a<p>“Duration of replication before genotype” is defined as time from first detection of VL >400 copies/ml to genotyping. This may be shorter than the duration before ARV drug switching.</p>b<p>These two participants were not included in calculations related to ARV drug switches since, although they met VL criteria for switching during the study, they both switched after the end of the study (April 1, 2010).</p
Characteristics of the patients at baseline, according to randomization arm.
No full texta<p>There were eight protocol deviations reported related to inclusion criteria: One patient was not ARV naive, one woman was pregnant, one was chronically infected with hepatitis C, two had hemoglobin level <8.0 g/dl, two had absolute neutrophil count <1,000 cells/mm<sup>3</sup>, one had serum creatinine above 1.0× ULN.</p
