CONTEXT Low oxygen saturation appears to decrease the risk of severe retinopathy of prematurity (ROP) in preterm newborns when administered during the first few weeks after birth. High oxygen saturation seems to reduce the risk at later postmenstrual ages (PMAs). However, previous clinical studies are not conclusive individually. OBJECTIVE To perform a systematic review and meta-analysis to report the association between severe ROP incidence of premature infants with high or low target oxygen saturation measured by pulse oximetry. METHODS Studies were identified through PubMed and Embase literature searches through May 2009 by using the terms “retinopathy of prematurity and oxygen” or “retinopathy of prematurity and oxygen therapy.” We selected 10 publications addressing the association between severe ROP and target oxygen saturation measured by pulse oximetry. Using a random-effects model we calculated the summary-effect estimate. We visually inspected funnel plots to examine possible publication bias. RESULTS Low oxygen saturation (70%–96%) in the first several postnatal weeks was associated with a reduced risk of severe ROP (risk ratio [RR]: 0.48 [95% confidence interval (CI): 0.31–0.75]). High oxygen saturation (94%–99%) at ≥32 weeks’ PMA was associated with a decreased risk for progression to severe ROP (RR: 0.54 [95% CI: 0.35–0.82]). CONCLUSIONS Among preterm infants with a gestational age of ≤32 weeks, early low and late high oxygen saturation were associated with a reduced risk for severe ROP. We feel that a large randomized clinical trial with long-term developmental follow-up is warranted to confirm this meta-analytic result.

Warburg and coworkers (Warburg O, Posener K, Negelein E. Z Biochem 152: 319, 1924) first reported that cancerous cells switch glucose metabolism from oxidative phosphorylation to aerobic glycolysis, and that this switch is important for their proliferation. Nothing is known about aerobic glycolysis in T cells from asthma. The objective was to study aerobic glycolysis in human asthma and the role of this metabolic pathway in airway hyperreactivity and inflammation in a mouse model of asthma. Human peripheral blood and mouse spleen CD4 T cells were isolated by negative selection. T cell proliferation was measured by thymidine incorporation. Cytokines and serum lactate were measured by ELISA. Mouse airway hyperreactivity to inhaled methacholine was measured by a FlexiVent apparatus. The serum lactate concentration was significantly elevated in clinically stable asthmatic subjects compared with healthy and chronic obstructive pulmonary disease controls, and negatively correlated with forced expiratory volume in 1 s. Proliferating CD4 T cells from human asthma and a mouse model of asthma produced higher amounts of lactate upon stimulation, suggesting a heightened glycolytic activity. Lactate stimulated and inhibited T cell proliferation at low and high concentrations, respectively. Dichloroacetate (DCA), an inhibitor of aerobic glycolysis, inhibited lactate production, proliferation of T cells, and production of IL-5, IL-17, and IFN-γ, but it stimulated production of IL-10 and induction of Foxp3. DCA also inhibited airway inflammation and hyperreactivity in a mouse model of asthma. We conclude that aerobic glycolysis is increased in asthma, which promotes T cell activation. Inhibition of aerobic glycolysis blocks T cell activation and development of asthma.

Background-Existing asthma models develop tolerance when chronically exposed to the same allergen.