Value of the neutrophil-to-lymphocyte ratio in chronic obstructive pulmonary disease complicated with pulmonary hypertension.

OBJECTIVE: To investigate the relationship between the neutrophil-to-lymphocyte ratio and chronic obstructive pulmonary disease complicated with pulmonary hypertension (COPD + PH). METHODS: We retrospectively analyzed clinical data from 242 COPD patients at our hospital from July 2018 to July 2019. Patients underwent examinations including blood analysis, C-reactive protein, N-terminal brain natriuretic peptide (BNP), pulmonary function, and cardiac color ultrasound. RESULTS: Patients were divided into the COPD and COPD + PH groups using pulmonary arterial pressure (<50 and ≥50 mmHg, respectively). Compared with the COPD group, the COPD + PH group had greater pulmonary arterial pressure, smoking history, neutrophil-to-lymphocyte ratio (NLR), C-reactive protein, BNP, Chronic Obstructive Pulmonary Disease Assessment Test score, and right atrium and ventricular diameters, but smaller body mass index, forced vital capacity, lymphocyte count, and left ventricular diameter. BNP and NLR had positive effects on PH; forced vital capacity had a negative impact. Moreover, BNP (area under the curve [AUC] = 0.748, sensitivity = 0.692, specificity = 0.701) and NLR (AUC = 0.679, sensitivity = 0.831, specificity = 0.452) had predictive value for PH, and both were positively correlated with PH. CONCLUSIONS: NLR is associated with COPD + PH, and may be useful for its diagnosis.

Posttreatment With LYRM03 Protects Rats From Acute Lung Inflammation Induced by Lipopolysaccharide via Suppressing the NF-κB/MyD88/TLR4 Axis.

BACKGROUND: 3-amino-2-hydroxy-4-phenyl-valyl-isoleucine (LYRM03) has been shown to be beneficial in a rat model of acute lung injury (ALI). Nonetheless, the pharmacologic action of LYRM03 interference has not been demonstrated to occur through oxidative stress and apoptosis in a rat lipopolysaccharide (LPS)-induced ALI model, and the potential pathogenic mechanism needs to be clarified. Our research intended to explore the mechanism of action using an in vivo rat LPS-induced ALI model and highlight the associated pathogenesis. METHODS: Sprague-Dawley rats were randomly assigned to the following five groups: Sham; LPS (5 mg/kg); LPS + LYRM03 (5 mg/kg); LPS + LYRM03 (10 mg/kg); and LPS + LYRM03 (20 mg/kg). Pulmonary injury indicators were documented at 24 h after LPS-induced ALI. Morphologic alterations, such as the extent of the injury, were determined using hematoxylin-eosin staining. Furthermore, expression levels of oxidative stress indicators (malondialdehyde, superoxide dismutase, and glutathione peroxidase) and inflammatory molecules (tumor necrosis factor-α, interleukin-8, and interleukin-6) in circulation were observed. The production of apoptosis-associated proteins (poly ADP-ribose polymerase, c-caspase 3, B-cell lymphoma-2, and Bcl2 associated X), inflammatory mediators (high mobility group box-1, toll-like receptor 4, nuclear factor-kappa B p65, and myeloid differentiation primary response 88), and inhibitor of kappa B-α were determined through Western blotting. Real-time polymerase chain reaction was applied to assess the messenger RNA expression of the inflammatory mediators. RESULTS: The LPS-treated group exhibited a remarkable increase in the extent of the pulmonary injury, oxidative stress indicator secretion, inflammatory molecule release, and inflammatory mediator production and an increase in the inhibitor of kappa B-α levels relative to the Sham group. The LYRM03 (5 and 10 mg/kg)-treated groups exhibited a remarkable decrease relative to the LPS group. In addition, treatment with LYRM03 (20 mg/kg) powerfully limited the extent of the injury and demonstrated anti-inflammatory actions. CONCLUSIONS: The results of this investigation indicated that treatment with LYRM03 plays a role in lung defense by inhibiting the NF-κB/MyD88/TLR4 pathway.

Neuromuscular electrical stimulation improves exercise capacity in adult patients with chronic lung disease: a meta-analysis of English studies.

BACKGROUND: Neuromuscular electrical stimulation (NMES) has been suggested as an alternative rehabilitative therapy to enhance exercise performance and skeletal muscle function in adult patients with chronic lung disease. However, the results of individual studies have been inconsistent. We performed a meta-analysis to evaluate the effectiveness of NMES with regard to increasing exercise capacity, quadriceps strength, muscle mass, cross-sectional area, and quality of life and decreasing dyspnea in adult patients with chronic lung disease. METHODS: A systematic search was conducted of the PubMed, Cochrane Library and EMBASE databases for randomized controlled trials (RCTs) published in English-language journals before January 2018. Data were extracted using standardized forms, and the weighted mean difference (WMD) or standardized mean difference (SMD) with 95% confidence intervals (CIs) was calculated. RESULTS: Eleven RCTs involving 368 patients were included in this meta-analysis. The pooled results showed that NMES significantly improved the 6-min walk distance (WMD: 37.93 m, 95% CI: 19.53-56.33 m; P<0.0001; P for heterogeneity =0.11; I2=47%) but not the incremental shuttle walk test (WMD: 18.18 m, 95% CI: -79.41 to 115.77 m, P=0.72; P for heterogeneity <0.0001, I2=94%) or endurance shuttle walk test (ESWT) (WMD: 96.73 m, 95% CI: -45.58 to 239.03 m, P=0.18; P heterogeneity =0.22, I2=34%). Moreover, NMES was associated with a significant improvement in quadriceps strength (SMD: 1.14, 95% CI: 0.86-1.43, P<0.00001; P heterogeneity =0.02, I2=58%). CONCLUSIONS: This systemic review and meta-analysis provided evidence supporting the beneficial role of NMES in improving exercise capacity in patients with chronic respiratory disease.