METHODS: This is a retrospective study performed in a vascular surgery unit in a tertiary hospital on patients who underwent AKAs over 1 year, from July 2021 until June 2022. Patient demographic data, WIfI scoring, outcome of AKAs, and patency of profunda femoris and internal iliac artery (IIA) were collected. To minimize confounding, a single vascular surgeon performed all computed tomography imaging reviews and arterial measurements. Approval for this study was obtained from the National Research Registry, NMRR ID-23-01865-KQ4 (investigator initiated research).
RESULTS: Ninety patients underwent AKA over 1 year, from July 2021 until June 2022. Occluded IIA in the presence of patent profunda femoris did not affect the wound healing of the AKA stump. There was significant association between WIfI scoring and mortality. Patients with a WIfI scoring of 3 to 4 were observed to have a higher mortality rate compared with patients with normal healing: 47 (72.0%) vs. 4 (80.0%); P = 0.021.
CONCLUSIONS: In this study, the IIA patency shows no statistically significant effect on AKA stump healing; however, the small number of patients is a drawback of the study. This study also demonstrates that the WIfI score can be a prognostic factor for mortality in patients undergoing AKA.
METHODS: HIV+ patients from the Australian HIV Observational Database (AHOD) and the TREAT Asia HIV Observational Database (TAHOD) meeting specific criteria were included. In these analyses Asian and Caucasian status were defined by cohort. Factors associated with a low CD4:CD8 ratio (cutoff <0.2) prior to ART commencement, and with achieving a normal CD4:CD8 ratio (>1) at 12 and 24 months post ART commencement were assessed using logistic regression.
RESULTS: There were 591 patients from AHOD and 2,620 patients from TAHOD who met the inclusion criteria. TAHOD patients had a significantly (P<0.001) lower odds of having a baseline (prior to ART initiation) CD4:CD8 ratio greater than 0.2. After 12 months of ART, AHOD patients were more than twice as likely to achieve a normal CD4:CD8 ratio compared to TAHOD patients (15% versus 6%). However, after adjustment for confounding factors there was no significant difference between cohorts in the odds of achieving a CD4:CD8 ratio >1 (P=0.475).
CONCLUSIONS: We found a significantly lower CD4:CD8 ratio prior to commencing ART in TAHOD compared to AHOD even after adjusting for confounders. However, after adjustment, there was no significant difference between the cohorts in odds of achieving normal ratio. Baseline CD4+ and CD8+ counts seem to be the main driver for this difference between these two populations.
METHODS: Treatment modification was defined as a change of two antiretrovirals, a drug class change or treatment interruption (TI), all for >14 days. We assessed factors associated with CD4 changes and undetectable viral load (UVL <1,000 copies/ml) at 1 year after second-line failure using linear and logistic regression, respectively. Survival time was analysed using competing risk regression.
RESULTS: Of the 328 patients who failed second-line ART in our cohorts, 208 (63%) had a subsequent treatment modification. Compared with those who continued the failing regimen, the average CD4 cell increase was higher in patients who had a modification without TI (difference =77.5, 95% CI 35.3, 119.7) while no difference was observed among those with TI (difference =-5.3, 95% CI -67.3, 56.8). Compared with those who continued the failing regimen, the odds of achieving UVL was lower in patients with TI (OR=0.18, 95% CI 0.06, 0.60) and similar among those who had a modification without TI (OR=1.97, 95% CI 0.95, 4.10), with proportions of UVL 60%, 22% and 75%, respectively. Survival time was not affected by treatment modifications.
CONCLUSIONS: CD4 cell improvements were observed in those who had treatment modification without TI compared with those on the failing regimen. When no other options are available, maintaining the same failing ART combination provided better VL control than interrupting treatment.