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ABSTRACT: To determine if dexamethasone given to premature infants with bronchopulmonary dysplasia would result in cardiac diastolic dysfunction in early childhood, a topic unstudied in humans.
We compared seven children ages 3 to 8 years born at 26 weeks' gestation and given dexamethasone for bronchopulmonary dysplasia with eight gestation-matched and age-matched control children using echocardiography to assess measures of systolic and diastolic function. All dexamethasone patients had resolved hypertrophic cardiomyopathy.
Dexamethasone patients had the same normal τ and isovolumic relaxation time (24.9 ± 2.8 and 54.6 ± 6.3 ms) as control patients (22.1 ± 3.0 and 48.8 ± 6.7 ms). Peak A velocities were the same in dexamethasone patients as in control patients (59.5 ± 15 versus 49.4 ± 5.8 cm/s, P = .10), resulting in unchanged E:A ratios (1.89 ± 0.57 versus 2.15 ± 0.43, P = .22). Peak E velocity and E-wave deceleration times were not different. We found no significant differences in measures of systolic function (heart rate-corrected velocity of circumferential fiber shortening, wall stress, and ejection fraction). Left ventricular mass was the same between the groups confirming resolution of hypertrophic cardiomyopathy.
These data are consistent with normal myocardial relaxation, suggesting that long-term diastolic function is reassuringly normal in children who received dexamethasone as premature infants with resolution of hypertrophic cardiomyopathy.
The Journal of pediatrics 03/2011; 159(2):227-31. · 4.02 Impact Factor
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Anna Ells,
Duane L Guernsey,
Karin Wallace,
Binyou Zheng, Michael Vincer,
Alexander Allen,
April Ingram,
Orlando DaSilva,
Lee Siebert,
Thomas Sheidow,
Jill Beis,
Johane M Robitaille
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ABSTRACT: To determine whether mutations in the FZD4 gene are a risk factor for developing severe ROP.
Three Canadian tertiary care centers recruited premature infants prospectively and retrospectively, and assigned affectation status based on the maximum degree of severity of ROP recorded in both eyes. Mutation screening of the FZD4 gene was performed using direct sequencing. All sequence changes were evaluated for functional significance.
Two novel FZD4 mutations (Ala370Gly or Lys203Asn) were identified in two infants from the severe ROP group (n=71). No mutation was detected in the mild to no ROP group (n=33), and the two novel mutations were absent in 173 random Caucasian samples. Mutation Ala370Gly was also found in one sibling and one parent of the affected infant, but no signs of familial exudative vitreoretinopathy (FEVR), a condition with phenotypic overlap with ROP known to be caused by FZD4 mutations, were present in either family member.
Mutations in the FZD4 gene in this group of premature infants supports a role for the FZD4 pathway in the development of severe ROP and accounts for approximately 3% of severe ROP in Caucasian premature infants.
Ophthalmic Genetics 03/2010; 31(1):37-43. · 0.93 Impact Factor
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ABSTRACT: To determine the risk of bronchopulmonary dysplasia (BPD) in subgroups of infants with and without patent ductus arteriosus (PDA) who were randomized to indomethacin prophylaxis or placebo, and to examine whether adverse drug effects on edema formation and oxygenation may explain why indomethacin prophylaxis does not reduce BPD.
We studied 999 extremely low birth weight infants who participated in the Trial of Indomethacin Prophylaxis in Preterms (TIPP) and who survived to a postmenstrual age of 36 weeks.
The incidence of BPD in the 2 subgroups of infants with PDA was 52% (55/105) after indomethacin prophylaxis and 56% (137/246) after placebo. In contrast, rates of BPD in the 2 subgroups without a PDA were 43% (170/391) after indomethacin prophylaxis and 30% (78/257) after placebo (P [interaction] = .015). Logistic regression analysis with adjustment for prognostic baseline factors showed that adverse and independent effects of indomethacin prophylaxis on the need for supplemental oxygen and on weight loss by the end of the first week of life may increase the risk of BPD in infants without PDA.
Harmful side effects on oxygenation and edema formation may explain why indomethacin prophylaxis does not prevent BPD even though it reduces PDA.
Journal of Pediatrics 07/2006; 148(6):730-734. · 4.11 Impact Factor
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ABSTRACT: To test whether indomethacin prophylaxis has sex-mediated effects on severe intraventricular hemorrhage (grade III and IV) and on long-term outcomes in extremely-low-birth-weight infants. A secondary analysis was performed in the entire "Trial of Indomethacin Prophylaxis in Preterms study" cohort. The results suggest a weak differential treatment effect of indomethacin by sex.
Journal of Pediatrics 01/2006; 147(6):860-2. · 4.11 Impact Factor
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ABSTRACT: BACKGROUND: It is generally accepted that the risk of cerebral palsy decreases with increasing gestational age of live born infants. However, recent studies have shown that cerebral palsy often has prenatal antecedents including congenital malformations, vascular insults and maternal infection. Cerebral palsy is therefore better viewed as occurring among fetuses, rather than among infants. We explored the epidemiologic implications of this change in perspective. METHODS: We used recently published data from Shiga Prefecture, Japan and from North-East England to examine the pattern of gestational age-specific rates of cerebral palsy under these alternative perspectives. We first calculated gestational age-specific rates of cerebral palsy as per convention, by dividing the number of cases of cerebral palsy identified among live births within any gestational age category by the number of live births in that gestational age category. Under the alternative formulation, we calculated gestational age-specific rates of cerebral palsy by dividing the number of cases of cerebral palsy identified among live births within any gestational age category by the number of fetuses who were at risk of being born at that gestation and being afflicted with cerebral palsy. RESULTS: Under the conventional formulation, cerebral palsy rates decreased with increasing gestational age from 63.9 per 1,000 live births at <28 weeks gestation to 0.9 per 1,000 live births at 37 or more weeks gestation. When fetuses were viewed as potential candidates for cerebral palsy, cerebral palsy rates increased with increasing gestational age from 0.08 per 1,000 fetuses at risk at <28 weeks gestation to 0.9 per 1,000 fetuses at risk at 37 or more weeks gestation. CONCLUSIONS: The fetuses-at-risk approach is the appropriate epidemiologic formulation for calculating the gestational age-specific rate of cerebral palsy from a causal perspective. It shows that the risk of cerebral palsy increases as gestational duration increases. This compelling view of cerebral palsy risk may help refocus research aimed at understanding and preventing cerebral palsy.
BMC Pregnancy and Childbirth 01/2004; 3(1):8. · 2.83 Impact Factor
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ABSTRACT: This study was conducted to determine the rates and risk factors for major disability in very preterm survivors born to residents of Nova Scotia, Canada between 1992 and 1996.
A cohort study was conducted of all 355 infants born to Nova Scotia residents between 22 and 30 weeks gestation. Major disability was defined by mental development index <70, moderate or severe cerebral palsy, bilateral visual acuity <20/200, or deafness requiring bilateral hearing aids. Logistic regression analysis was used to determine which factors were significantly associated with major disability.
Of the infants who survived 1 year and had follow-up data, 21 (8.3%) developed a major disability. Cystic periventricular leukomalacia (PVL), hypernatremia and surgery requiring general anesthesia were independently associated with the development of a major disability.
This study confirms the association between cystic PVL and major disability observed in other studies. Surgery and hypernatremia will be important to verify in future studies since preventive measures may be possible.
Journal of Perinatology 03/2003; 23(2):111-6. · 1.80 Impact Factor
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Pediatric Research - PEDIAT RES. 01/1998; 43.
