The therapeutic benefit of antioxidants on the outcome of acute aluminum phosphide poisoning: a systemic review and meta-analysis.

This systematic review and meta-analysis pool evidence available from clinical trials to verify the effect of antioxidants on the outcome of acute aluminum phosphide (AlP) poisoning. A systematic review complied with "Preferred Reporting Items for Systematic Reviews and Meta-Analyses" (PRISMA) Protocols. Meta-analysis was conducted on 10 studies that fulfill eligibility criteria. Four antioxidants were implemented: N-Acetyl cysteine (NAC), L-Carnitine, Vitamin E, and Co-enzyme Q10 (Co Q10). Risk of bias, publication bias, and heterogeneity were assessed to ensure the results' reliability. Antioxidants significantly decrease mortality of acute AlP poisoning around three folds (OR = 2.684, 95% CI: 1.764-4.083; P < .001) and decrease the need for intubation and mechanical ventilation by two folds (OR = 2.391, 95% CI 1.480-3.863; P < .001) compared with control. Subgroup analysis revealed that NAC significantly decreases mortality by nearly three folds (OR = 2.752, 95% CI: 1.580-4.792; P < .001), and vitamin E significantly decreases mortality by nearly six folds (OR = 5.667, 95% CI: 1.178-27.254; P = .03) compared with control. L-Carnitine showed a borderline significance (P = .050). Co Q10 decreased the mortality compared with the control; however, the difference was not statistically significant (P = .263). This meta-analysis provides solid evidence regarding the efficacy of antioxidants in improving the outcome of acute AlP poisoning with reference to NAC. Wide confidence interval and small relative weight affect reliability regarding vitamin E efficacy. Future clinical trials and meta-analyses are recommended. To our knowledge, no previous meta-analysis was conducted to investigate the efficacy of treatment modalities for acute AlP poisoning.

Exercise Intolerance in Untreated OSA: Role of Pulmonary Gas Exchange and Systemic Vascular Abnormalities.

BACKGROUND: Reduced exercise capacity has been reported previously in patients with OSA hypopnea syndrome (OSAHS), although the underlying mechanisms are unclear. RESEARCH QUESTION: What are the underlying mechanisms of reduced exercise capacity in untreated patients with OSAHS? Is there a role for systemic or pulmonary vascular abnormalities? STUDY DESIGN AND METHODS: This was a cross-sectional observational study in which 14 patients with moderate to severe OSAHS and 10 control participants (matched for age, BMI, smoking history, and FEV1) underwent spirometry, incremental cycle cardiopulmonary exercise test (CPET) with arterial line, resting echocardiography, and assessment of arterial stiffness (pulse wave velocity [PWV] and augmentation index [AIx]). RESULTS: Patients (age, 50 ± 11 years; BMI, 30.5 ± 2.7 kg/m2; smoking history, 2.4 ± 4.0 pack-years; FEV1 to FVC ratio, 0.78 ± 0.04; FEV1, 85 ± 14% predicted, mean ± SD for all) had mean ± SD apnea hypopnea index of 43 ± 19/h. At rest, PWV, AIx, and mean pulmonary artery pressure (PAP) were higher in patients vs control participants (P < .05). During CPET, patients showed lower peak work rate (WR) and oxygen uptake and greater dyspnea ratings compared with control participants (P < .05 for all). Minute ventilation (V·E), ventilatory equivalent for CO2 output (V·E/V·CO2), and dead space volume (VD) to tidal volume (VT) ratio were greater in patients vs control participants during exercise (P < .05 for all). Reduction in VD to VT ratio from rest to peak exercise was greater in control participants compared with patients (0.24 ± 0.08 vs 0.04 ± 0.14, respectively; P = .001). Dyspnea intensity at the highest equivalent WR correlated with corresponding values of V·E/V·CO2 (r = 0.65; P = .002), and dead space ventilation (r = 0.70; P = .001). Age, PWV, and mean PAP explained approximately 70% of the variance in peak WR, whereas predictors of dyspnea during CPET were rest-to-peak change in VD to VT ratio and PWV (R2 = 0.50; P < .001). INTERPRETATION: Patients with OSAHS showed evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction that may explain reduced exercise capacity and increased exertional dyspnea intensity.

Low resting diffusion capacity, dyspnea, and exercise intolerance in chronic obstructive pulmonary disease.

The mechanisms linking reduced diffusing capacity of the lung for carbon monoxide (DlCO) to dyspnea and exercise intolerance across the chronic obstructive pulmonary disease (COPD) continuum are poorly understood. COPD progression generally involves both DlCO decline and worsening respiratory mechanics, and their relative contribution to dyspnea has not been determined. In a retrospective analysis of 300 COPD patients who completed symptom-limited incremental cardiopulmonary exercise tests, we tested the association between peak oxygen-uptake (V̇o2), DlCO, and other resting physiological measures. Then, we stratified the sample into tertiles of forced expiratory volume in 1 s (FEV1) and inspiratory capacity (IC) and compared dyspnea ratings, pulmonary gas exchange, and respiratory mechanics during exercise in groups with normal and low DlCO [i.e.,