Data_Sheet_1_Severity of frailty using modified Thai frailty index, social factors, and prediction of mortality among community-dwelling older adults in a middle-income country.PDF

BackgroundFrailty has been increasingly recognized as a public health problem for aging populations with significant social impact, particularly in low- and middle-income countries. We aimed to develop a modified version of the Thai Frailty Index (TFI) and explore the association between different frailty statuses, socioeconomic factors, and mortality in community-dwelling older people from a middle-income country.MethodsThe data from participants aged ≥60 years in the Fourth Thai National Health Examination Survey were used to construct the 30-item TFI. Cutoff points were created based on stratum-specific likelihood ratio. TFI ≤ 0.10 was categorized as fit, 0.10–0.25 as pre-frail, 0.25–0.45 as mildly frail, and >0.45 as severely frail. The association of frailty status with mortality was examined using Cox proportional hazard models.FindingsAmong 8,195 older adults with a mean age of 69.2 years, 1,284 died during the 7-year follow-up. The prevalence of frailty was 16.6%. The adjusted hazard ratio (aHR) for mortality in pre-frail was 1.76 (95% CI = 1.50–2.07), mildly frail 2.79 (95% CI = 2.33–3.35), and severely frail 6.34 (95% CI = 4.60–8.73). Having a caretaker in the same household alleviated mortality risk for severely frail participants with an aHR of 2.93 (95% CI = 1.92–4.46) compared with an aHR of 6.89 (95% CI = 3.87–12.26) among those living without a caretaker.InterpretationThe severity of frailty classified by the modified TFI can predict long-term mortality risk for community-dwelling older adults. Identification of severely frail older people to provide appropriate care might alleviate mortality risk. Our findings can inform policymakers to appropriately allocate services in a resource-limited setting.</p

A Randomized Clinical Trial Testing the Anti-Inflammatory Effects of Preemptive Inhaled Nitric Oxide in Human Liver Transplantation

<div><p>Decreases in endothelial nitric oxide synthase derived nitric oxide (NO) production during liver transplantation promotes injury. We hypothesized that preemptive inhaled NO (iNO) would improve allograft function (primary) and reduce complications post-transplantation (secondary). Patients at two university centers (Center A and B) were randomized to receive placebo (n = 20/center) or iNO (80 ppm, n = 20/center) during the operative phase of liver transplantation. Data were analyzed at set intervals for up to 9-months post-transplantation and compared between groups. Patient characteristics and outcomes were examined with the Mann-Whitney U test, Student t-test, logistic regression, repeated measures ANOVA, and Cox proportional hazards models. Combined and site stratified analyses were performed. MELD scores were significantly higher at Center B (22.5 vs. 19.5, p<0.0001), surgical times were greater at Center B (7.7 vs. 4.5 hrs, p<0.001) and warm ischemia times were greater at Center B (95.4 vs. 69.7 min, p<0.0001). No adverse metabolic or hematologic effects from iNO occurred. iNO enhanced allograft function indexed by liver function tests (Center B, p<0.05; and p<0.03 for ALT with center data combined) and reduced complications at 9-months (Center A and B, p = 0.0062, OR = 0.15, 95% CI (0.04, 0.59)). ICU (p = 0.47) and hospital length of stay (p = 0.49) were not decreased. iNO increased concentrations of nitrate (p<0.001), nitrite (p<0.001) and nitrosylhemoglobin (p<0.001), with nitrite being postulated as a protective mechanism. Mean costs of iNO were $1,020 per transplant. iNO was safe and improved allograft function at one center and trended toward improving allograft function at the other. ClinicalTrials.gov with registry number 00582010 and the following URL:<a href="http://clinicaltrials.gov/show/NCT00582010" target="_blank">http://clinicaltrials.gov/show/NCT00582010</a>.</p></div

Patient and Surgery Demographics for Center B Cohort.

<p>Values show median (range). P-values calculated from unpaired t-test for placebo vs. iNO.</p

The Distribution, Frequency and Type of Hepatobiliary Complications.

<p>Center A.</p><p>Placebo: allograft dysfunction (1), primary graft non-function (1), reduced portal vein flow (1), hepatic artery bleeding (2).</p><p>iNO: allograft dysfunction (1), hepatic artery bleeding (1).</p><p>Center B.</p><p>Placebo: 1-month:primary graft dysfunction (1), reduced hepatic artery blood flow (1), biliary leak (1), 6-months:biliary stricture (2), 9-months:rejection (1), hepatic artery stenosis (1), death (1).</p><p>iNO: 9-months:hepatic artery stenosis (1), death (1).</p

Patient and Surgery Demographics for Center A Cohort.

<p>Values show median (range). P-values calculated from unpaired t-test for placebo vs. iNO. N = 20 except An = 19. Bn = 18.</p

Effects of iNO on liver nitrite levels pre- (LB1) and post-reperfusion (LB2).

<p>Nitrite was measured in paired liver biopsies and data normalized to protein. No significant differences in nitrite levels were observed pre- vs. post-reperfusion or between placebo and iNO treatments.</p

iNO therapy did not affect hospital or ICU length of stay.

<p>Kaplan-Meier plots shown and with P-values from Cox proportional hazards models adjusting for MELD, cold ischemic time, weight, BMI, warm ischemic time or donor age within each center. Placebo = ○, iNO = ▪.</p

Effects of iNO on plasma and RBC nitroso species.

<p>Plasma nitroso (Panel A) or RBC nitroso (Panel B) were measured and normalized to protein and heme, respectively. Data show measurements from paired arterial and venous samples collected at different times during the intraoperative period (□ = placebo; • = iNO). The first time point denotes pre-initiation of placebo or iNO. The third and fourth data points represent pre- and 1 h post-reperfusion samplings. Data show mean ± SEM (n = 19–20).</p

Changes in metHb and nitrogen dioxide (NO₂) as a function of blood draw (BD) in placebo (○) or iNO (▪) groups.

<p>Data are mean ± SEM (n = 20 for each group, except UAB placebo where n = 19 and UW iNO where n = 17–20. *P<0.0001 by 2-way ANOVA with Bonferroni multiple comparisons post-test.</p

Individual responses to iNO on TUNEL staining pre- and post-reperfusion.

<p>Panel A and B show changes in TUNEL positive nuclei in hepatic central vein area and panels C and D in the hepatic triad area for Center A (panel A and B) and Center B (panel C and D) cohorts. Indicated P-values determined by Wilcoxon rank-sum (n = 18–20).</p