lactoferrin and Bronchopulmonary-Dysplasia

This study aimed to systematically review and meta-analyze the role of lactoferrin supplementation to prevent late-onset sepsis (LOS) in preterm infants.. Database search include PubMed, Web of Science, and Cochrane central for randomized clinical trial (RCTs). The Cochrane Grading of Recommendations Assessment, Development, and Evaluation methodology was used for summarizing the results.. Ten RCTs involving 3,679 infants were included. Lactoferrin supplementation with or without probiotics decreased all LOS (relative risk [RR]: 0.56; 95% confidence interval [CI]: 0.36-0.86;. Low to moderate quality evidence suggests that lactoferrin supplementation reduces LOS in preterm infants. Further research is needed to improve the certainty in the evidence.

Topics: Administration, Oral; Age of Onset; Bronchopulmonary Dysplasia; Cause of Death; Enteral Nutrition; Enterocolitis, Necrotizing; Humans; Infant; Infant Mortality; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Lactoferrin; Mycoses; Probiotics; Randomized Controlled Trials as Topic; Retinopathy of Prematurity; Sepsis

The focus of this paper is to describe the following: (1) the benefits of implementing feeding guidelines, (2) management practices associated with the prevention of BPD, and (3) management practices associated with prevention of nosocomial infection.

Topics: Anti-Infective Agents; Bronchopulmonary Dysplasia; Cross Infection; Feeding Methods; Female; Fetal Viability; Humans; Immunoglobulins, Intravenous; Infant Nutritional Physiological Phenomena; Infant, Extremely Low Birth Weight; Infant, Newborn; Infant, Very Low Birth Weight; Intensive Care, Neonatal; Lactoferrin; Male; Nutritional Requirements; Practice Guidelines as Topic; Pregnancy; Water-Electrolyte Balance

In a multi-centre randomised controlled trial (RCT), we are assessing whether giving very preterm (i.e., born at < 32 weeks' gestation) infants prophylactic enteral bovine lactoferrin supplementation (150 mg/kg/day) from shortly after birth until 34 weeks' post-menstrual age reduces the incidence of late-onset invasive infection (primary outcome), all-cause mortality, bronchopulmonary dysplasia, necrotising enterocolitis, retinopathy of prematurity, and the duration of antibiotic exposure, intensive care, and hospital admission. The trial is recruiting 2,200 participants from 37 neonatal care centres in the UK over 4 years. We will undertake an economic evaluation within the RCT to evaluate cost-effectiveness and provide an estimate of incremental costs for differences in the pre-specified outcomes in primary and subgroup analyses. If a statistically significant and clinically important effect on the primary outcome is detected, we will seek further funding and approval to assess the impact of enteral lactoferrin supplementation on rates of adverse neuro-developmental outcomes in the participating infants when they are 5 years old.

Topics: Bronchopulmonary Dysplasia; Child, Preschool; Cost-Benefit Analysis; Developmental Disabilities; Dietary Supplements; Enteral Nutrition; Enterocolitis, Necrotizing; Female; Gestational Age; Humans; Infant; Infant Mortality; Infant, Extremely Premature; Infant, Newborn; Infant, Premature, Diseases; Infant, Very Low Birth Weight; Lactoferrin; Male; Multicenter Studies as Topic; Randomized Controlled Trials as Topic

Topics: Blood Banks; Bronchopulmonary Dysplasia; Child Development; Chromosomes, Human, Pair 18; Enterocolitis, Necrotizing; Fetal Blood; Hematinics; Humans; Hypoxia, Brain; Infant; Infant, Newborn; Lactoferrin; Sepsis; Trisomy; Trisomy 18 Syndrome

Bronchopulmonary dysplasia (BPD) is characterized by simplified alveolarization and arrested vascular development of the lung with associated evidence of endothelial dysfunction, inflammation, increased oxidative damage, and iron deposition. Heme oxygenase-1 (HO-1) has been reported to be protective in the pathogenesis of diseases of inflammatory and oxidative etiology. Because HO-1 is involved in the response to oxidative stress produced by hyperoxia and is critical for cellular heme and iron homeostasis, it could play a protective role in BPD. Therefore, we investigated the effect of HO-1 in hyperoxia-induced lung injury using a neonatal transgenic mouse model with constitutive lung-specific HO-1 overexpression. Hyperoxia triggered an increase in pulmonary inflammation, arterial remodeling, and right ventricular hypertrophy that was attenuated by HO-1 overexpression. In addition, hyperoxia led to pulmonary edema, hemosiderosis, and a decrease in blood vessel number, all of which were markedly improved in HO-1 overexpressing mice. The protective vascular response may be mediated at least in part by carbon monoxide, due to its anti-inflammatory, antiproliferative, and antiapoptotic properties. HO-1 overexpression, however, did not prevent alveolar simplification nor altered the levels of ferritin and lactoferrin, proteins involved in iron binding and transport. Thus the protective mechanisms elicited by HO-1 overexpression primarily preserve vascular growth and barrier function through iron-independent, antioxidant, and anti-inflammatory pathways.

Topics: Animals; Animals, Newborn; Bronchopulmonary Dysplasia; Disease Models, Animal; Ferritins; Heme Oxygenase-1; Hemosiderosis; Humans; Infant, Newborn; Iron; Lactoferrin; Lung; Mice; Mice, Transgenic; Oxygen; Pulmonary Edema

To test whether the presence of airway inflammatory markers differentiated babies with hyaline membrane disease (HMD) who recovered (n = 18) from those in whom bronchopulmonary dysplasia (BPD) developed (n = 18), tracheal aspirate samples from 36 newborn infants with HMD who underwent intubation were collected during days 1 to 28 of life and analyzed for the mucosal antimicrobial proteins lactoferrin and lysozyme. For babies with HMD in whom BPD developed, lactoferrin concentrations were decreased during the first 4 days of life (7 +/- 3, 14 +/- 3, 18 +/- 3, and 18 +/- 3 micrograms/ml, respectively) in comparison with those in babies with HMD who recovered (23 +/- 8, 29 +/- 6, 41 +/- 9, and 81 +/- 19 micrograms/ml); group differences reached statistical significance on days 3 and 4 (p less than 0.05). Lysozyme levels in the secretions of babies with BPD were also lower on day 3 (31 +/- 5 micrograms/ml) than in those of babies who recovered (54 +/- 7.5 micrograms/ml). For babies with BPD whose endotracheal tube remained in place beyond day 4, lysozyme levels on days 5 to 12 were significantly lower for those classified as having severe BPD than for those with mild to moderate BPD. Because lysozyme and lactoferrin are products of serous cells found in submucous glands, it seems possible that the relative immaturity of submucous glands may influence the development of BPD.

Topics: Bronchopulmonary Dysplasia; Enteral Nutrition; Gestational Age; Humans; Hyaline Membrane Disease; Infant, Low Birth Weight; Infant, Newborn; Lactoferrin; Muramidase; Trachea