Tenofovir, ritonavir-boosted atazanavir, and ritonavir-boosted lopinavir use were independent predictors of chronic renal impairment in HIV-positive persons without preexisting renal impairment. Increased tenofovir discontinuation rates with decreasing eGFR may have prevented further deteriorations. After discontinuation, the ARV-associated incidence rates decreased.
Objectives To describe the CD4 cell count at the start of combination antiretroviral therapy (cART) in low-income (LIC), lower middle-income (LMIC), upper middle-income (UMIC) and high-income (HIC) countries. Methods Patients aged ≥16 years starting cART in a clinic participating in a multi-cohort collaboration spanning six continents (International epidemiological Databases to Evaluate AIDS and ART Cohort Collaboration) were eligible. Multi-level linear regression models were adjusted for age, gender and calendar year; missing CD4 counts were imputed. Findings 379,865 patients from nine LIC, four LMIC, four UMIC and six HIC were included. In LIC the median CD4 cell count at cART initiation increased by 83% from 80 to 145 cells/μl between 2002 and 2009. Corresponding increases in LMIC, UMIC and HIC were from 87 to 155 cells/μl (76% increase), 88 to 135 cells/μl (53%) and 209 to 274 cells/μl (31%). In 2009, compared to LIC, median counts were 13 cells/μl (95% CI -56 to +30) lower in LMIC, 22 cells/μl (-62 to +18) lower in UMIC and 112 /μl (+75 to +149) higher in HIC. They were 23 cells/μl (95% CI +18 to +28) higher in women than men. Median counts were 88 cells/μl (95% CI +35 to +141) higher in countries with an estimated national cART coverage >80%, compared to countries with <40% coverage. Conclusions Median CD4 cell counts at start of cART increased 2000-2009 but remained below 200 cells/μl in LIC and MIC and below 300 cells/μl in HIC. Earlier start of cART will require substantial efforts and resources globally.
The burden of HCV-related liver disease has increased markedly. Although the proportion diagnosed was high, treatment uptake remained low, with no increase over the last 7 years. Reducing the HCV burden in Australia requires scale-up of interferon-free HCV therapies.
Background: Limited empirical evidence exists for hepatitis C virus (HCV) treatment-asprevention. The Surveillance and Treatment of Prisoners with hepatitis C (SToP-C) study assessed HCV treatment-as-prevention in four Australian prisons.Methods: SToP-C is a non-randomised trial, including a pre/post analysis within a prospective longitudinal cohort of people incarcerated in two maximum-(male) and two medium-security prisons (one male, one female). All prison inmates at least 18 years were eligible for enrolment.Participants were enrolled from late-2014 to 2019. Following HCV testing, participants were monitored for risk behaviors and HCV, among three sub-populations: 1) uninfected (HCV antibody negative); 2) previously infected (HCV antibody positive, HCV RNA negative); 3) infected (HCV antibody and HCV RNA positive). Uninfected and previously infected (at-risk) participants were followed every 3-6 months for HCV primary infection and re-infection, respectively. Infected participants were assessed for treatment, initially standard of care treatment (by prison health services), followed by direct-acting antiviral (DAA) treatment scale-up from mid-2017 (12 weeks sofosbuvir/velpatasvir, through SToP-C). Participants were followed until study closure in November 2019. The primary study outcome was HCV incidence compared between pre-and post-treatment scale-up periods among participants at risk of HCV primary infection or re-infection. The trial was registered with ClinicalTrials.gov (identifier: NCT02064049) Findings: Of 3,691 participants enrolled, 719 (19%) had detectable HCV RNA and 2,965 were at-risk of primary infection (n=2,240) or re-infection (n=725) at baseline. DAA treatment was initiated in 349/499 eligible participants during the treatment scale-up period. Among at-risk population with longitudinal follow-up (n=1,643; median age 33 years; 82% male), 31% reported injecting drug use in prison. HCV incidence declined by 48%, from 8.31 to 4.35/100 person-years between pre-and post-treatment scale-up periods [Incidence Rate Ratio (IRR): 4 0.52, 95%CI: 0.36, 0.78]. Incidence of primary infection declined from 6.64 to 2.85/100 personyears (IRR: 0.43, 95%CI: 0.25, 0.74), while incidence of re-infection declined from 12.36 to 7.27/100 person-years (IRR: 0.59, 95%CI: 0.35, 1.00). Among participants reporting injecting drug use in the current imprisonment, incidence of primary infection declined from 39.08 to 14.03/100 person-years (IRR: 0.36, 95%CI: 0.16, 0.80), and incidence of re-infection declined from 15.26 to 9.34/100 person-years (IRR: 0.61, 95%CI: 0.34, 1.09). Adjusted analysis indicated a significant reduction in HCV risk between pre-and post-treatment scale-up periods (adjusted Hazard Ratio: 0.50, 95% CI: 0.33, 0.76).Interpretation: DAA treatment scale-up was associated with reduced HCV incidence in prison, indicative of HCV treatment-as-prevention. The findings support broad DAA treatment scale-up among incarcerated populations.
BackgroundLife expectancy has increased for newly diagnosed HIV patients since the inception of combination antiretroviral treatment (cART), but there remains a need to better understand the characteristics of long-term survival in HIV-positive patients. We examined long-term survival in HIV-positive patients receiving cART in the Australian HIV Observational Database (AHOD), to describe changes in mortality compared to the general population and to develop longer-term survival models.MethodsData were examined from 2,675 HIV-positive participants in AHOD who started cART. Standardised mortality ratios (SMR) were calculated by age, sex and calendar year across prognostic characteristics using Australian Bureau of Statistics national data as reference. SMRs were examined by years of duration of cART by CD4 and similarly by viral load. Survival was analysed using Cox-proportional hazards and parametric survival models.ResultsThe overall SMR for all-cause mortality was 3.5 (95% CI: 3.0–4.0). SMRs by CD4 count were 8.6 (95% CI: 7.2–10.2) for CD4<350 cells/µl; 2.1 (95% CI: 1.5–2.9) for CD4 = 350–499 cells/µl; and 1.5 (95% CI: 1.1–2.0) for CD4≥500 cells/µl. SMRs for patients with CD4 counts <350 cells/µL were much higher than for patients with higher CD4 counts across all durations of cART. SMRs for patients with viral loads greater than 400 copies/ml were much higher across all durations of cART. Multivariate models demonstrated improved survival associated with increased recent CD4, reduced recent viral load, younger patients, absence of HBVsAg-positive ever, year of HIV diagnosis and incidence of ADI. Parametric models showed a fairly constant mortality risk by year of cART up to 15 years of treatment.ConclusionObserved mortality remained fairly constant by duration of cART and was modelled accurately by accepted prognostic factors. These rates did not vary much by duration of treatment. Changes in mortality with age were similar to those in the Australian general population.
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