The efficacy and therapeutic mechanisms of continuous renal replacement therapy (CRRT) for improvement of oxygenation in acute respiratory distress syndrome (ARDS) remain controversial. These questions were addressed by retrospective analysis of severe ARDS patients admitted to the pediatric intensive care unit of our hospital from 2009 to 2015 who received high-volume continuous veno-venous hemofiltration during mechanical ventilation. There was a significant improvement in partial oxygen pressure/fraction of inspired oxygen (PaO2/FiO2) 24 hours after CRRT onset compared with baseline (median change = 51.5; range = −19 to 450.5; P < .001) as well as decreases in FiO2, peak inspiratory pressure, positive end-expiratory pressure, and mean airway pressure (P < .05). The majority of patients had a negative fluid balance after 24 hours of CRRT. White blood cell (WBC) count decreased in the subgroup with high baseline WBC count (P < .05). PaO2/FiO2 was higher in ARDS patients with extrapulmonary etiology than in those with pulmonary etiology (P < .05). Improvement in oxygenation is likely related to both restoration of fluid balance and clearance of inflammatory mediators.
BackgroundRecent studies have proved that autophagy dysfunction in proinflammatory cells is involved in tissue damage and an excessive inflammatory response in sepsis. In the present study, we identified that the human antimicrobial peptide LL-37 facilitates resistance to DNase II-induced mitochondrial DNA (mtDNA) degradation and subsequent autophagy.Material/MethodsWe found higher serum levels of LL-37 in patients with severe sepsis compared to that in patients with mild sepsis. Neutrophils isolated from mice with sepsis after treatment with Cramp-mtDNA produced an excess of proinflammatory cytokines, including IL-1β, IL-6, IL-8, MMP-8, and TNF-α. Cramp-mtDNA in the lung samples from model animals with sepsis was detected by immunohistochemical staining.ResultsExogenous delivery of Cramp-mtDNA complex significantly exacerbated lung inflammation but the antibody against Cramp-mtDNA attenuated the excessive inflammatory response in LPS-induced acute lung injury. The expression of proinflammatory cytokines in lungs was upregulated and downregulated after treatment with the complex and antibody, respectively. LC-3 expression in 16HBE cells increased after LPS induction, irrespective of stimulation with LL-37.ConclusionsThese data show that LL-37 treatment worsens local inflammation in sepsis-induced acute lung injury by preventing mtDNA degradation-induced autophagy.
Pulmonary Agenesis (PA) is a rare congenital malformation of lung development, and patients with comorbid Pulmonary Hypertension (PH) have substantially increased morbidity and mortality risks. We describe five pediatric cases born with unilateral PA who developed PH. By integrating our findings with those of 7 previously published case reports, we aim to provide a more complete description of disease features, prognosis, and the most effective treatment strategies. We found that male PA patients and those with right-side agenesis were more likely to develop PH. Moreover, half of these comorbid patients had congenital heart disease with left-to-right shunt. Early diagnosis and treatment, including surgical and medical interventions, are critical for preservation of cardiopulmonary function. All PA cases should receive regular cardiopulmonary function tests starting at an early age.
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