4.5 Article

Lenticulostriate Vasculopathy in Very-Low-Birth-Weight Preterm Infants: A Longitudinal Cohort Study

Journal

CHILDREN-BASEL
Volume 8, Issue 12, Pages -

Publisher

MDPI
DOI: 10.3390/children8121166

Keywords

lenticulostriate vasculopathy; prematurity; very-low-birth-weight; cranial ultrasound

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LSV is common in very-low-birth-weight preterm infants, with linear-type presentation being most common. Perinatal characteristics, placental pathologies, and neonatal morbidities were similar between infants with and without LSV, but prolonged oxygen usage was identified as an independent risk factor for late-onset LSV development. Further research on the long-term clinical impacts of LSV is needed.
Background: The pathogenesis and clinical significance of lenticulostriate vasculopathy (LSV) are unclear. Our study aimed to determine the prevalence, presentation, and evolution of LSV, and the perinatal risk factors associated with LSV among very-low-birth-weight (VLBW) preterm infants. Methods: One-hundred-and-thirty VLBW preterm infants were retrospectively enrolled in this study. Serial cranial ultrasound examinations were performed regularly from birth until a corrected age of 1 year. Infants with LSV were assigned to early-onset (<= 10 postnatal days) and late-onset (>10 postnatal days) groups. Data describing the infants' perinatal characteristics, placental histopathology, and neonatal morbidities were collected, and the groups were compared. Results: Of the VLBW infants, 39.2% had LSV before they were 1 year old. Linear-type LSV was the most common presentation, and >50% of the infants had bilateral involvement. LSV was first detected at 112 +/- 83 postnatal days, and its detection timing correlated negatively with gestational age (GA) (R-2 = 0.153, p = 0.005) and persisted for 6 months on average. The infants with and without LSV had similar perinatal characteristics, placental pathologies, cytomegalovirus infection rates, and clinical morbidities. The late-onset LSV group comprised 45 (88.2%) infants who had a significantly higher rate of being small for gestational age (SGA) and used oxygen for longer than the infants without LSV. After adjusting a multivariable regression model for GA and SGA, analysis showed that the duration of oxygen usage was an independent risk factor for late-onset LSV development in VLBW infants (odds ratio: 1.030, p = 0.032). Conclusion: LSV may be a nonspecific marker of perinatal insult to the developing brains of preterm infants. Prolonged postnatal oxygen usage may predispose VLBW preterm infants to late-onset LSV development. The long-term clinical impacts of LSV should be clarified.

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