Influence of enteral feeding and anemia on tissue oxygen extraction after red blood cell transfusion in preterm infants.
Biomarker Discovery and Utility in Necrotizing Enterocolitis.
Clinics in perinatology
2019; 46 (1): 1–17
Understanding factors that impact tissue oxygen extraction may guide red blood cell (RBC) transfusion decision making in preterm infants. Our objective was to assess the influence of enteral feeding and anemia on cerebral and mesenteric oxygen saturation (Csat and Msat) and fractional tissue oxygen extraction (cFTOE and mFTOE) over the entire time course of RBC transfusion.Preterm, very low-birth-weight infants receiving RBC transfusions at a single center were enrolled. Near-infrared spectroscopy sensors measured Csat and Msat levels from an hour before transfusion to 24 hours after. During this period, changes in Csat, Msat, cFTOE, and mFTOE were described, and their association with enteral feeding status and pretransfusion degree of anemia were assessed using generalized estimating equations.RBC transfusion data from 31 preterm infants were included. Infants receiving enteral feeds exhibited lower pretransfusion Msat. Infants with pretransfusion hematocrit greater than 30% exhibited higher pretransfusion Csat and lower pretransfusion cFTOE. Such differences in baseline measurements persisted through 24 hours after transfusion. However, no statistically significant differences in oxygenation measures over time by enteral feeding or anemia status were identified.Compared to NPO, enteral feeding was associated with lower Msat; anemia (hematocrit ≤30%) was associated with lower Csat and higher cFTOE. Over the time course of RBC transfusion, trajectories of Csat, Msat, cFTOE and mFTOE did not differ by enteral feeding or anemia status.
View details for DOI 10.1111/trf.15680
View details for PubMedID 31984520
Prenatal and postnatal inflammation-related risk factors for retinopathy of prematurity.
Journal of perinatology : official journal of the California Perinatal Association
Necrotizing enterocolitis (NEC) is a devastating disease of prematurity, with no current method for early diagnosis. Diagnosis is particularly challenging, frequently occurring after the disease has progressed to the point of significant and often irreversible intestinal damage. Biomarker research has tremendous potential to advance clinical management of NEC and our understanding of its pathogenesis. This review discusses the need for novel biomarkers in NEC management, evaluates studies investigating such biomarkers, and explains the difficulties associated with translating biomarker discovery into clinical use.
View details for PubMedID 30771811
Tissue plasminogen activator for neonatal coronary thrombosis presenting with mitral valve regurgitation and impaired ventricular function.
Congenital heart disease
2017; 12 (3): 270–74
To evaluate the relationship between prenatal and postnatal inflammation-related risk factors and severe retinopathy of prematurity (ROP).The study included infants born <30 weeks in California from 2007 to 2011. Multivariable log-binomial regression was used to assess the association between prenatal and postnatal inflammation-related exposures and severe ROP, defined as stage 3-5 or surgery for ROP.Of 14,816 infants, 10.8% developed severe ROP. Though prenatal inflammation-related risk factors were initially associated with severe ROP, after accounting for the effect of these risk factors on gestational age at birth through mediation analysis, the association was non-significant (P = 0.6). Postnatal factors associated with severe ROP included prolonged oxygen exposure, sepsis, intraventricular hemorrhage, and necrotizing enterocolitis.Postnatal inflammation-related factors were associated with severe ROP more strongly than prenatal factors. The association between prenatal inflammation-related factors and ROP was explained by earlier gestational age in infants exposed to prenatal inflammation.
View details for PubMedID 30932029
The influence of prior oral contraceptive use on risk of endometriosis is conditional on parity.
Fertility and sterility
2014; 101 (6): 1697–1704
Neonatal coronary thrombosis is a rarely reported disorder, with variable outcomes described. This study assessed the feasibility and safety of an institutional protocol using tissue plasminogen activator (tPA) administration for the treatment of neonatal coronary artery thrombi.They reviewed the outcome of three neonates with clinical evidence of myocardial infarction secondary to coronary thrombosis. All three underwent the tPA treatment protocol.The three described cases presented at 5 hours, 15 hours, and 10 days of life. The patients identified underwent the tPA protocol at least once. There was clinical evidence of improvement in coronary flow, as well as demonstration of increased left ventricular function and decreased mitral regurgitation. No major adverse events occurred.Thrombolytic therapy with this tPA protocol may be safe and effective in treating neonates with coronary thrombosis.
View details for DOI 10.1111/chd.12432
View details for PubMedID 28140523
Explaining regional disparities in traffic mortality by decomposing conditional probabilities.
Injury prevention : journal of the International Society for Child and Adolescent Injury Prevention
2011; 17 (2): 84–90
To estimate the influence of prior oral contraceptive pill (OCP) use on future diagnosis of endometriosis in young women.Prospective cohort study, the Australian Longitudinal Study on Women's Health.Community-based sample.9,585 women age 18-23 at study onset.None.Risk of self-reported endometriosis estimated with Cox proportional-hazards regression with time-dependent covariates.Compared with never users, endometriosis hazard ratios in nulliparous women with <5 years and ≥ 5 years of OCP use (preceding diagnosis) were 1.8 (95% CI, 1.30-2.53) and 2.3 (95% CI, 1.59-3.40), respectively. Similar risk was seen in both women reporting infertility and unsure fertility. In parous women with <5 years of use, the hazard ratio for endometriosis was 0.41 (95% CI, 0.15-0.56) and for ≥ 5 years of use was 0.45 (95% CI, 0.16-1.23). Women reporting early noncontraceptive OCP use had a twofold higher risk (odds ratio 2.07; 95% CI, 1.72-2.51).Prior OCP exposure reduces the risk of diagnosis of endometriosis in parous women but increases it among nulliparous women; these associations appear unaffected by fertility status. An increased risk of endometriosis diagnosis seen in women reporting early noncontraceptive OCP use may explain some of the positive OCP risk seen in nulliparous women.
View details for DOI 10.1016/j.fertnstert.2014.02.014
View details for PubMedID 24666753
In the USA, the mortality rate from traffic injury is higher in rural and in southern regions, for reasons that are not well understood.For 1754 (56%) of the 3142 US counties, we obtained data allowing for separation of the deaths/population rate into deaths/injury, injuries/crash, crashes/exposure and exposure/population, with exposure measured as vehicle miles travelled. A 'decomposition method' proposed by Li and Baker was extended to study how the contributions of these components were affected by three measures of rural location, as well as southern location.The method of Li and Baker extended without difficulty to include non-binary effects and multiple exposures. Deaths/injury was by far the most important determinant in the county-to-county variation in deaths/population, and accounted for the greatest portion of the rural/urban disparity. After controlling for the rural effect, injuries/crash accounted for most of the southern/northern disparity.The increased mortality rate from traffic injury in rural areas can be attributed to the increased probability of death given that a person has been injured, possibly due to challenges faced by emergency medical response systems. In southern areas, there is an increased probability of injury given that a person has crashed, possibly due to differences in vehicle, road, or driving conditions.
View details for DOI 10.1136/ip.2010.029249
View details for PubMedID 21212443
View details for PubMedCentralID PMC3446824