A global measure of patient-reported outcomes after injury - life back on track.

PURPOSE: Assess the psychometric properties of the Life Back on Track (LBoT) measure, a novel self-reported single-item global measure of the trajectory of wellbeing after a transport accident. MATERIALS AND METHODS: Evaluated the validity, reliability, sensitivity, and responsiveness using four survey waves (n = 1556 in wave 1), and two repeated cross-sectional surveys (n = 5238) and (n = 1964), of individuals injured in a transport accident in Victoria. RESULTS: There were statistically significant differences in the distribution of the LBoT scores by the respondent depression or pain scores, return to work status, financial ability to get by, ability to cope, and ability to bounce back (all p < 0.001). The LBoT measure was a statistically significant (p < 0.001) and reasonable predictor of future work status, and was moderately correlated (>0.67) with the EQ-5D-3L (concurrent validity). Retest reliability (ICC ≥0.76) and sensitivity (effect sizes >1.52) were supported, and it was moderately responsive to change (standard response mean statistics 0.4-0.8). CONCLUSIONS: LBoT is a valid measure to track the individual's trajectory of subjective wellbeing in the context of recovery after a trauma, and is potentially useful as an indicator to track the performance of commissioned providers, and to monitor or evaluate the value of service outcomes.Implications for RehabilitationThere is a demand to develop a simple metric to measure the impact of injury, the effectiveness of rehabilitation and the degree of recovery from trauma.Life Back on Track (LBoT) is a valid single-item measure to track an individual's trajectory of subjective wellbeing after trauma.It has the potential to complement clinical measures where a routine collection of a simple measure is desirable.It is suitable as an indicator of service outcomes for organisations that commission services.

Planned multiple exposures to autologous virus in HIV type 1-infected pediatric populations increases HIV-specific immunity and reduces HIV viremia.

We tested to determine if planned multiple exposures to autologous HIV in pediatric patients with HIV-1 infection will induce cellular immunity that controls viremia. A prospective multicenter study of aviremic pediatric patients on highly active antiretroviral therapy who underwent progressively longer antiretroviral treatment interruptions in cycles starting with 3 days, increasing by 2 days in length each consecutive cycle, was conducted. Eight individuals became viremic and reached Cycle 13 or greater with an "off-therapy" interval of >or=27 days. HIV-specific interferon-gamma (IFN-gamma) production to inactivated HIV and vaccinia vectors expressing gag, env, nef, and pol increased (>10-fold) from baseline in six of eight subjects. The HIV-specific lymphoproliferative response as measured by the median stimulation index (SI) increased in the treatment group from 1 at baseline to 16, 12, 4, and 3 at Cycles 7, 10, 13, and 17, respectively. Median plasma RNA levels peaked at Cycle 7 (4.45 log) and declined to levels <10(4) cp/ml after Cycle 10 (4.1, 3.5, and 3.4 at Cycles 10, 13, and 17). In a subset of five patients who reached Cycle 17, HIV-specific IFN-gamma frequencies were 4- to 30-fold higher and median RNA levels were 0.32-2.10 (median 1.3) log lower than at comparable days off treatment at Cycle 8 (17 days off therapy). A second group of children, not undergoing drug interruption, did not develop significant increases in either HIV-specific IFN-gamma production or SI. Increased HIV-specific immune responses and decreased HIV RNA were seen in those children who have had >10 cycles of antiretroviral discontinuations of increasing durations acting as autologous virus vaccinations. Other studies may have failed due to an insufficient number of exposures to HIV; most of the studies had fewer than six drug interruptions.

Structured treatment interruptions (STIs) in HIV-1 infected pediatric populations increases interferon gamma production and reduces viremia.

We assessed the effect of progressively longer antiretroviral structured treatment interruptions (STIs) starting with 3 days, increasing by 2 days in length each cycle on HIV-specific immune responses. As well, we correlated these responses with control of HIV viremia. Eight individuals became viremic and reached cycle 13 with an STI of > or =27 days. HIV-specific gamma-interferon production to inactivated HIV and vaccinia vectors expressing gag, env, nef, and pol increased (>10-fold) in six of eight subjects. Median plasma RNA levels peaked @ cycle 7 and declined to levels <10(4)cp/ml after cycle 10. In a subset of five who reached cycle 17, HIV-specific IFN-gamma frequencies increased from cycle 8 to cycle 17 with evidence of improved virologic control over comparable periods off antiretroviral therapy. This allowed us to conclude that exposure to autologous virus increased HIV-specific immune responses and decreased HIV RNA were seen in those who have had >13 interruptions, with STI intervals that exceeded 27 days.