Lower foetal haemoglobin levels at 31- and 34-weeks post menstrual age is associated with the development of retinopathy of prematurity : PacIFiHER Report No. 1 PacIFiHER Study Group (Preterm Infants and Fetal Haemoglobin in ROP).
Journal
Eye (London, England)
ISSN: 1476-5454
Titre abrégé: Eye (Lond)
Pays: England
ID NLM: 8703986
Informations de publication
Date de publication:
02 2021
02 2021
Historique:
received:
22
11
2019
accepted:
27
04
2020
revised:
24
04
2020
pubmed:
16
5
2020
medline:
22
6
2021
entrez:
16
5
2020
Statut:
ppublish
Résumé
Previous studies have suggested that lower mean foetal haemoglobin (HbF) levels is associated with an increased risk for developing retinopathy of prematurity (ROP). Lower HbF levels may lead to high oxygen exposure to the developing retina thereby increasing the risk of acute ROP. In this study, we characterize the temporal relationship of HbF levels and the development of ROP. This is a single institution prospective observational cohort study. Preterm infants (born <31 weeks gestational age or <1500 g) with HbF measured at birth (cord blood), 31-, 34-, and 37-weeks post menstrual age (PMA); and at least one ROP exam, were enrolled. A total of 60 preterm infants (28 females, 47%) were enrolled. At 31-, 34-, 37-weeks PMA, infants with ROP (mild = Type 2 or less severe and severe = Type 1 ROP) had statistically lower percentages of HbF than infants with no ROP (28.2 ± 15 and 9.7 ± 2.9 vs 67.1 ± 29.6; p < 0.0001; 23.3 ± 14.7 and 32.5 vs 60.1 ± 25; p < 0.005; 31.9 ± 15.8 and 41.6 vs 60.2 ± 20.0; p < 0.0019). Infants with HbF levels in the lowest tercile at 31-weeks PMA were 7.6 times more likely to develop mild and severe ROP (95% CI 2.1-24.0, p value = 0.0006) and this risk increased to 12.3 times (95% CI: 2.6-59.0, p value = 0.0017) at 34-weeks PMA. Low HbF levels at 31- and 34-weeks PMA are associated with significantly increased risk of developing ROP. The decrease in HbF precedes the development of ROP and may be important in its pathogenesis.
Sections du résumé
BACKGROUND/OBJECTIVES
Previous studies have suggested that lower mean foetal haemoglobin (HbF) levels is associated with an increased risk for developing retinopathy of prematurity (ROP). Lower HbF levels may lead to high oxygen exposure to the developing retina thereby increasing the risk of acute ROP. In this study, we characterize the temporal relationship of HbF levels and the development of ROP.
SUBJECTS/METHODS
This is a single institution prospective observational cohort study. Preterm infants (born <31 weeks gestational age or <1500 g) with HbF measured at birth (cord blood), 31-, 34-, and 37-weeks post menstrual age (PMA); and at least one ROP exam, were enrolled.
RESULTS
A total of 60 preterm infants (28 females, 47%) were enrolled. At 31-, 34-, 37-weeks PMA, infants with ROP (mild = Type 2 or less severe and severe = Type 1 ROP) had statistically lower percentages of HbF than infants with no ROP (28.2 ± 15 and 9.7 ± 2.9 vs 67.1 ± 29.6; p < 0.0001; 23.3 ± 14.7 and 32.5 vs 60.1 ± 25; p < 0.005; 31.9 ± 15.8 and 41.6 vs 60.2 ± 20.0; p < 0.0019). Infants with HbF levels in the lowest tercile at 31-weeks PMA were 7.6 times more likely to develop mild and severe ROP (95% CI 2.1-24.0, p value = 0.0006) and this risk increased to 12.3 times (95% CI: 2.6-59.0, p value = 0.0017) at 34-weeks PMA.
CONCLUSIONS
Low HbF levels at 31- and 34-weeks PMA are associated with significantly increased risk of developing ROP. The decrease in HbF precedes the development of ROP and may be important in its pathogenesis.
Identifiants
pubmed: 32409707
doi: 10.1038/s41433-020-0938-5
pii: 10.1038/s41433-020-0938-5
pmc: PMC8027597
doi:
Substances chimiques
Fetal Hemoglobin
9034-63-3
Types de publication
Journal Article
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
659-664Références
Ashton N, Ward B, Serpell G. Role of oxygen in the genesis of retrolental fibroplasia; a preliminary report. Br J Ophthalmol. 1953;37:513–20.
doi: 10.1136/bjo.37.9.513
Ashton N, Ward B, Serpell G. Effect of oxygen on developing retinal vessels with particular reference to the problem of retrolental fibroplasia. Br J Ophthalmol. 1954;38:397–432.
doi: 10.1136/bjo.38.7.397
IC M. The mode of development of the vascular system of the retina with some observations on its significance for certain retinal disorders. Trans Ophthalmol Soc. 1948;68:137–80.
Patz A, Eastham A, Higginbotham DH, Kleh T. Oxygen studies in retrolental fibroplasia. II. The production of the microscopic changes of retrolental fibroplasia in experimental animals. Am J Ophthalmol. 1953;36:1511–22.
doi: 10.1016/0002-9394(53)91779-6
Patz A. The role of oxygen in retrolental fibroplasia. Trans Am Ophthalmol Soc. 1968;66:940–85.
pubmed: 4888959
pmcid: 1310320
Pierce EA, Avery RL, Foley ED, Aiello LP, Smith LE. Vascular endothelial growth factor/vascular permeability factor expression in a mouse model of retinal neovascularization. Proc Natl Acad Sci USA. 1995;92:905–9.
doi: 10.1073/pnas.92.3.905
Sonmez K, Drenser KA, Capone A Jr, Trese MT. Vitreous levels of stromal cell-derived factor 1 and vascular endothelial growth factor in patients with retinopathy of prematurity. Ophthalmology. 2008;115:1065–70. e1061.
doi: 10.1016/j.ophtha.2007.08.050
Erdol H, Hacioglu D, Kola M, Turk A, Aslan Y. Investigation of the effect of hemoglobin F and A levels on development of retinopathy of prematurity. J AAPOS. 2017;21:136–40.
doi: 10.1016/j.jaapos.2017.03.006
Stutchfield CJ, Jain A, Odd D, Williams C, Markham R. Foetal haemoglobin, blood transfusion, and retinopathy of prematurity in very preterm infants: a pilot prospective cohort study. Eye. 2017;31:1451–5.
doi: 10.1038/eye.2017.76
Fierson WM, American Academy of Pediatrics Section on O, American Academy of O, American Association for Pediatric O, Strabismus, American Association of Certified O. Screening examination of premature infants for retinopathy of prematurity. Pediatrics. 2013;131:189–95.
doi: 10.1542/peds.2012-2996
International Committee for the Classification of Retinopathy of P. The international classification of retinopathy of prematurity revisited. Arch Ophthalmol. 2005;123:991–9.
doi: 10.1001/archopht.123.7.991
Christiansen SP, Dobson V, Quinn GE, Good WV, Tung B, Hardy RJ, et al. Progression of type 2 to type 1 retinopathy of prematurity in the early treatment for retinopathy of prematurity study. Arch Ophthalmol. 2010;128:461–5.
doi: 10.1001/archophthalmol.2010.34
Wimberley PD. Fetal hemoglobin, 2,3-diphosphoglycerate and oxygen transport in the newborn premature infant. Scand J Clin Lab Invest Suppl. 1982;160:1–149.
pubmed: 6182604
Stockman JA 3rd, Garcia JF, Oski FA. The anemia of prematurity. Factors governing the erythropoietin response. N Engl J Med. 1977;296:647–50.
doi: 10.1056/NEJM197703242961202
Bunn HF, Briehl RW. The interaction of 2,3-diphosphoglycerate with various human hemoglobins. J Clin Invest. 1970;49:1088–95.
doi: 10.1172/JCI106324
Di Fiore JM, Walsh M, Wrage L, Rich W, Finer N, Carlo WA, et al. Low oxygen saturation target range is associated with increased incidence of intermittent hypoxemia. J Pediatr. 2012;161:1047–52.
doi: 10.1016/j.jpeds.2012.05.046
Di Fiore JM, Bloom JN, Orge F, Schutt A, Schluchter M, Cheruvu VK, et al. A higher incidence of intermittent hypoxemic episodes is associated with severe retinopathy of prematurity. J Pediatr. 2010;157:69–73.
doi: 10.1016/j.jpeds.2010.01.046
Poets CF. Intermittent hypoxemia/bradycardia and the developing brain: how much is too much? Commentary on M.B. Schmid et al.: Cerebral oxygenation during intermittent hypoxemia and bradycardia in preterm infants (Neonatology 2015;107:137-146). Neonatology. 2015;107:147–9.
doi: 10.1159/000369775
Pillekamp F, Hermann C, Keller T, von Gontard A, Kribs A, Roth B. Factors influencing apnea and bradycardia of prematurity - implications for neurodevelopment. Neonatology. 2007;91:155–61.
doi: 10.1159/000097446
Bancalari E, Claure N. Oxygenation targets and outcomes in premature infants. JAMA. 2013;309:2161–2.
doi: 10.1001/jama.2013.5831
Polin RA, Bateman D. Oxygen-saturation targets in preterm infants. N Engl J Med. 2013;368:2141–2.
doi: 10.1056/NEJMe1305534