Nebulized pentoxifylline for prevention of bronchopulmonary dysplasia in very low birth weight infants: A pilot clinical study

Abstract

Our data show that nebulized PTXF reduces the risk of BPD and may be a potential alternative to steroids in the prevention of this disease.

Bronchopulmonary dysplasia and emphysema: in search of common therapeutic targets

“…Although nitric oxide (NO), which is both a factor with anti-inflammatory properties and a downstream effector of VEGF, improved alveolarization in experimental BPD [62], discrepant findings have been reported for inhaled NO: reduced death and BPD rates were reported in mildly sick preterm infants but, conversely, worsening outcome was reported in very ill VLBW infants [63]. Pentoxifylline, a peripheral vasodilator with anti-inflammatory effects, reduced the risk of BPD by 23% in a pilot study [64]. Blocking the CXC chemokine receptor CXCR2 has been shown to reduce oxygen-radical formation, to prevent neutrophil influx, and to preserve alveolarization in hyperoxia-exposed newborn rats [65].…”

“…antichemokine or receptor blockade in hyperoxia-exposed rats [17,65] pentoxyfilline in VLBW infants [64] No adverse effects observed inhibitory peptide in mouse model [43] curcumin [66], simvastatin [67], lovastatin [68], or HO-1 [69] Retinoids RA in hyperoxic model in rats [82] RA in angiogenic inhibition in mice [83] vitamin A in premature baboons [86] RA in rats and mice with or without inhibited alveolar septation [77,81] RA in mouse models [85] Growth factor supplementation VEGF [54] or FGF7 [98] in hyperoxia-exposed rats HGF [99] or EPO [83] in mouse models VEGF injurious in mouse prenatal lung [51] FGF7 in mouse model, preventive [101] HGF in rats [100] FGF7 in mouse model, curative [101] …”

Advances in emerging treatment options to prevent bronchopulmonary dysplasia

“…In VLBW infants, a pilot RCT of nebulized pentoxifylline versus placebo with 100 participants showed a significant difference in the risk of BPD (OR: 0.32; CIs 0.11 to 0.94; p = 0.039). There were, however, methodological weaknesses in the RCT including the assessors were not blinded to treatment group and there was complete outcome reporting in only 65% of those recruited [77]. When the data were analysed on an intention to treat basis the differences no longer reached statistical significance [78].…”

Genetics of bronchopulmonary dysplasia in the age of genomics

“…TNF-α is mainly produced by mononuclear phagocytes and is a potent mediator of acute inflammation. Levels of TNF-α are increased early on in tracheal aspirates of preterm infants who develop BPD (generally defined here as supplemental oxygen-dependence at 36 weeks of post-menstrual age) and pilot trials indicated a possible clinical therapeutic benefit from TNF-α inhibitors [23]. The TNF-α gene is located in the most polymorphic region of the human genome: the human leukocyte antigen (HLA) locus on chromosome 6.…”