Objective:The objective of this study is to estimate life expectancies of HIV-positive patients conditional on response to antiretroviral therapy (ART).Methods:Patients aged more than 20 years who started ART during 2000–2010 (excluding IDU) in HIV clinics contributing to the UK CHIC Study were followed for mortality until 2012. We determined the latest CD4+ cell count and viral load before ART and in each of years 1–5 of ART. For each duration of ART, life tables based on estimated mortality rates by sex, age, latest CD4+ cell count and viral suppression (HIV-1 RNA <400 copies/ml), were used to estimate expected age at death for ages 20–85 years.Results:Of 21 388 patients who started ART, 961 (4.5%) died during 110 697 person-years. At start of ART, expected age at death [95% confidence interval (CI)] of 35-year-old men with CD4+ cell count less than 200, 200–349, at least 350 cells/μl was 71 (68–73), 78 (74–82) and 77 (72–81) years, respectively, compared with 78 years for men in the general UK population. Thirty-five-year-old men who increased their CD4+ cell count in the first year of ART from less than 200 to 200–349 or at least 350 cells/μl and achieved viral suppression gained 7 and 10 years, respectively. After 5 years on ART, expected age at death of 35-year-old men varied from 54 (48–61) (CD4+ cell count <200 cells/μl and no viral suppression) to 80 (76–83) years (CD4+ cell count ≥350 cells/μl and viral suppression).Conclusion:Successfully treated HIV-positive individuals have a normal life expectancy. Patients who started ART with a low CD4+ cell count significantly improve their life expectancy if they have a good CD4+ cell count response and undetectable viral load.
Risk if ART is deferred is taken from [328]. The predicted 6-month risk if ART is initiated is based on the assumption that the rate with immediate therapy initiation is one-third the rate without therapy initiation. This (probably conservative) value is based on considering evidence from multiple sources, including references [32,[329][330][331][332][333].BHIVA treatment guidelines 569 r 2008 British HIV Association HIV Medicine (2008) 9, 563-608 but high CD4 percentages, but also may support a decision to start therapy earlier in patients with absolute CD4 counts 4350 cells/mL but with low CD4 percentages {e.g. o14%, where Pneumocystis carinii pneumonia (PCP) prophylaxis is indicated [35]; some studies have indicated increased risk of disease progression in patients with CD4 percentages o15-17% [36]}. Patients with a CD4 count 4350 cells/mLAs detailed above, at CD4 counts 4350 cells/mL, multiple cohort studies have suggested that there might be benefits to ART. This is supported by data from the substudy of patients not on therapy at entry to the SMART study [32]. Some of the previous concerns about earlier initiation of therapy have been reduced because of the availability of simpler, less toxic and better tolerated antiretroviral regimens, improved pharmacokinetic profiles and increasing options after virological failure. For the majority of patients, the absolute risk of deferring therapy until the CD4 count is o350 cells/mL is likely to be low, but in a subgroup at particularly high risk of clinical events that may be preventable by ART, this is not the case. For all these reasons, in a small number of patients, treatment may be started or considered before the CD4 count is below 350 cells/mL, including the following: AIDS diagnosis (e.g. Kaposi's sarcoma); any HIV-related comorbidity; hepatitis B infection, where treatment of hepatitis B is indicated (see hepatitis guidelines); hepatitis C infection in some cases, where treatment for hepatitis is deferred; low CD4 percentage (e.g. o14%, where PCP prophylaxis would be indicated); established CVD or a very high risk of cardiovascular events (e.g. Framingham risk of CVD 420% over 10 years).Additionally, it is likely that successful antiretroviral treatment, by reducing viral load, reduces infectivity irrespective of the current CD4 cell count, and this may be taken into account in deciding on the timing of starting treatment, particularly in discordant couples where the infected partner has a high viral load. This is likely to be an issue in a very small number of patients, and it must be stressed that antiretroviral treatment in this context would be an adjunct rather than an alternative to safer sex.In patients who do not have an AIDS diagnosis or coinfection with hepatitis B or C virus, and whose CD4 counts are above 500 cells/mL, the benefits of starting therapy remain unclear, the risk of deferring therapy is low, and we recommend that they consider enrolment in the START study, where this is an option. ComorbiditiesWhilst it has been clearly shown that...
Switching from a thymidine nucleoside analogue to either tenofovir DF or abacavir leads to significant improvement in limb fat mass over 48 weeks. Tenofovir DF may have modest advantages over abacavir for changes in lipids. Peripheral lipoatrophy, when clinically apparent, resolves slowly following treatment switching.
Background PARV4 is a human parvovirus first detected and cloned from an individual with a HIV seroconversion-like illness and which subsequently persists in lymphoid tissue and bone marrow. In contrast to B19V, PARV4 infections are most frequently detected in injecting drug users (IDUs), particularly those co-infected with HIV-1. To investigate its transmission routes and whether infections are acquired through plasma-derived blood products, we developed a novel anti-PARV4 ELISA to determine seroprevalence in parenterally exposed and non-exposed subjects. Methods PARV4 VP2 was expressed and used as antigen in an indirect ELISA to detect anti-PARV4 IgG. Results All 50 non-parenterally exposed adult controls were anti-PARV4 negative, in contrast to 67% and 33% antibody frequencies in HIV-positive and –negative IDUs respectively. Predominantly parenteral transmission was confirmed by the finding of similar infection frequencies (11/20 and 4/15) among HIV-coinfected and –uninfected haemophiliacs treated with non-virally inactivated FVIII/IX, whereas all but one of their 35 non-haemophiliac siblings were seronegative (despite close household contact). Conclusions This study provides convincing evidence that PARV4 is primarily transmitted parenterally. Evidence for widespread infection of haemophiliacs treated with non-virally inactivated clotting factor creates fresh safety concerns for plasma-derived blood products, particularly as parvoviruses are relatively resistant to virus inactivation.
In patients with virologic suppression who were receiving other PIs, switching to a once-per-day regimen containing atazanavir provided better maintenance of virologic suppression (as demonstrated by significantly lower rates of virologic rebound and treatment failure than those observed with continued unmodified therapy), a comparable safety profile, and improved lipid parameters, compared with those for patients who continued their prior PI-based regimen through 48 weeks.
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