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June
2007: VOLUME
4, NUMBER 10
[Editor's
Note: Clinicians concerned about caring for their patients with influenza
are invited to link to our sister e-publication, eInfluenza
Review, to access the current (May 2007) accredited program on Pediatric
Influenza Prevention.]
Antioxidants
and Other Novel Treatments for BPD
This month eNeonatal Review is
unveiling our new look as well as several new features:
- Our revised Newsletter
Archive has been updated and expanded to view by volume and title.
It contains all our previous issues and provides a full two years
of available CME/CE accredited programs. Coming soon will be a keyword
search.
- You can now link to the Post
Test directly from each email newsletter by using the buttons
on the right.
Thank you for your continued
support. With almost 7000 subscribers,
we’re now one of the largest
online Neonatal resources. Let
us know what you think of eNeonatal Review by sending us an email.
In
This Issue...
Bronchopulmonary
dysplasia (BPD) is a chronic lung disease that primarily affects premature
infants who are treated with supplemental oxygen and ventilatory support
for a primary respiratory disorder[1-4], and is primarily
characterized by abnormalities
of lung growth, including angiogenesis and alveolarization. Although
multifactorial in origin, reactive oxygen species (ROS) from hyperoxia
and inflammation, volutrauma, and genetic predisposition are thought
to play important rolesin the development of BPD[3,5-9]. The condition is associated
with significant long-term complications, including wheezing, asthma,
repeated respiratory infections, and neurodevelopmental impairments.
Recently, an NIH /FDA consensus panel reviewed pharmacologic interventions
that need to be studied in very low birth weight (VLBW) infants[10].
In this issue, we review novel
therapeutic strategies for the prevention and treatment of BPD, including
inhaled nitric oxide (iNO) directed at decreasing pulmonary vasoconstriction
as well as ameliorating intrapulmonary and systemic inflammation, explorations
into vitamin A, recombinant human superoxide dismutase (rhSOD), and
anti-transforming growth factor beta (TGF-β) antibodies to specifically
reduce the oxidant injury and inflammation associated with BPD. |
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Course
Directors
Edward
E. Lawson, MD
Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Christoph
U. Lehmann, MD
Assistant Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Lawrence
M. Nogee, MD
Associate Professor
Department of Pediatrics
- Neonatology
The Johns Hopkins
University
School of Medicine
Mary
Terhaar
Assistant Professor
Undergraduate Instruction
JHU School of Nursing
Robert
J. Kopotic, MSN, RRT, FAARC
Director of Clinical
Programs
ConMed Corporation |
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GUEST
AUTHORS OF THE MONTH |
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Commentary & Reviews:
Jonathan
M. Davis,
MD
Professor
of Pediatrics
Tufts
University School of Medicine
Chief
of Newborn Medicine
Associate
Director
Clinical
Research Center The Floating Hospital for Children
Tufts – New England Medical Center
Boston,
MA |
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Commentary & Reviews:
Juliette
C. Madan, MD, MS
Assistant
Professor of Pediatrics
Tufts
University School of Medicine
Assistant
Pediatrician
Division
of Newborn Medicine
Tufts – New England Medical Center
Boston,
MA |
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Guest
Faculty Disclosure
No faculty member has indicated that they have received financial support for consultation, research or evaluation or has a financial interest relevant to this literature review.
Unlabeled / Unapproved Uses
The following faculty members have disclosed that their presentation will reference unlabeled/unapproved use of drugs or products:
Jonathan M. Davis, MD
Inhaled nitric oxide, caffeine
Course
Directors' Disclosures |
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The
Johns Hopkins University School of Medicine and The Institute for
Johns Hopkins Nursing take responsibility for the content, quality,
and the scientific integrity of this CE activity.
At the conclusion of this activity, participants should be
able to: |
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Discuss
the uses of inhaled nitric oxide for the prevention of BPD |
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Describe
the uses of targeted antioxidant and anti-inflammatory therapies
to prevent or treat BPD |
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Explain
the importance of long-term follow-up and evaluation of functional
outcomes in determining the efficacy of treatments for BPD |
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COMPLETE
THE POST TEST
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below. This will take you to the post-test.
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Complete the post-test and course
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Step
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Print out your certificate.
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Visit
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gained through this program or click on the link below to go directly
to the post-test.
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Despite
intensive study and multiple
attempts to develop specific
therapies to prevent or ameliorate
BPD, little success has actually
been achieved. Part of the
difficulty involves the optimal
definition of BPD. Current
definitions include oxygen
requirements at 36 weeks
corrected gestational age
(CGA), which may not adequately
predict the later pulmonary and neurodevelopmental outcomes that are
of greater importance. For instance, in a 1999 study, administration
of vitamin A to VLBW infants was shown to result in a small but significant
(7%) reduction in the incidence of BPD at 36 weeks CGA[11].
However, Ambalavanan and
colleagues (reviewed herein)
followed these infants to
18-22 months CGA and were
unable to demonstrate any
improvements in clinical
respiratory status from vitamin
A. This is surprising in
view of the extensive scientific
data indicating that vitamin
A protects the preterm lung
from the damaging effects of hyperoxia and mechanical ventilation.
In contrast, we demonstrated (study reviewed herein) that repeated
doses of intratracheal recombinant human superoxide dismutase (rhSOD
- an important antioxidant enzyme) administered to critically ill VLBW
infants did not result in significant differences in pulmonary outcome
at 36 weeks CGA (although severe ROP was markedly reduced). However,
at one year corrected age, rhSOD-treated infants did show significant
improvements in clinical pulmonary status, with the most dramatic changes
seen in infants <27
weeks gestation).
While the beneficial effects
of iNO have been established
in full term infants with severe
respiratory failure, its use
in preterm infants is more controversial.
Three recent trials studied different
iNO intervention strategies (different
dosing, timing, and duration
of exposure) to prevent BPD (the
Kinsella and Ballard trials are
reviewed herein). However, each
of these trials used a different
definition of BPD (oxygen requirements
at 36 weeks CGA, either alone
or with/without a physiologic
oxygen challenge test or radiographic
criteria). A previous study was
unable to demonstrate any beneficial
effects of iNO in a population
of seriously ill VLBW infants[12],
Kinsella and associates (using
an early, low dose treatment
component) demonstrated a significant
reduction in BPD in larger infants,
although iNO significantly reduced
severe neurologic injury in the
entire cohort. In contrast, Ballard
and colleagues (using a later,
higher dose treatment strategy)
demonstrated a significant reduction
in the incidence of BPD in their
entire birth cohort, with infants
enrolled between 7-14 days of
age having a significantly better
outcome than infants enrolled
between 15-21 days. Although
longer term outcome studies still
need to be completed, it appears
that the early use of low dose
iNO may prevent severe brain
injury, while higher doses started
by one week of life may be efficacious
in the prevention of BPD.
While caffeine is routine for
treatment of apnea of prematurity, Schmidt and associates demonstrated
that the early use of caffeine significantly reduced death or BPD in
VLBW infants[13] (a study reviewed in the October 2006 issue
of eNeonatal
Review). The long term follow-up from this trial will be of utmost
importance in determining whether pulmonary and neurodevelopmental outcomes
associated with caffeine are also significantly improved. Finally, multiple
growth factors and cytokines affecting lung development are present
in the fetal lung. This delicate balance may be significantly altered
in response to preterm birth, infection, hyperoxia and mechanical ventilation.
Nakanishi and colleagues (reviewed herein) administered anti-TGF-β to
mice exposed to chronic hyperoxia (a model with similar characteristics
to BPD) and found that these antibodies significantly reduced inflammation
and lung injury while improving lung growth and clinical outcome. This
important study demonstrates both the importance of TGF-β signaling
in the pathogenesis of hyperoxic injury in the newborn lung and its
relationship to disrupted terminal lung development.
BPD continues to be an important
cause of long-term pulmonary
dysfunction in VLBW infants. While several therapies, both novel and
more established, have the potential to significantly ameliorate this
condition, we need to be cautious in our interpretation of preliminary
data until longer-term results are available (e.g., wheezing, asthma,
respiratory infections, hospitalizations). This is especially true since
these studies employed a slightly different definition of BPD (defined
above) and 36 weeks CGA represents just a single moment in time. While
we need to revisit these studies to more fully understand the efficacy
of some treatments, there is justifiable optimism regarding future development
of others.
References
| 1. |
Kinsella
JP, Greenough A, Abman SH. Bronchopulmonary
dysplasia. Lancet 2006; 367:1421-31.
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| 2. |
Avery
ME, Tooley WH, Keller JB, et al. Is
chronic lung disease in LBW infants preventable? A survey of eight
centers. Pediatrics 1987; 79:26-30. |
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| 3. |
Jobe
AH. The
new BPD: an arrest of lung development. Pediatr Res 1999;46:641-43. |
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| 4. |
Bancalari
E, Abdenour GE,
Feller R, Gannon
J. BPD: clinical presentation. J Pediatr 1979; 95:819-23. No
URL Available |
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| 5. |
Hallman
M, Haataja K. Genetic
influences and neonatal lung disease. Sem Neonatol 2003; 8:19-27. |
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| 6. |
Coalson
JJ. Pathology
of new bronchopulmonary dysplasia. Semin Neonatol 2003; 8:73-81. |
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| 7. |
Berman
W Jr, Katz R, Yabek SM, Dillon T, Fripp RR, Papile LA. Long
term follow-up of BPD. J Pediatr 1986; 109:45-50. |
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| 8. |
Martin
RJ, Mhanna MJ, Xaxhiu MA. The
role of endogenous and exogenous nitric oxide on airway function.
Semin Perinatol 2002;2:432-8. |
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| 9. |
Bland
RD, Albertine KH, Carlton DP, MacRitchie AJ. Inhaled
nitric oxide effects on lung structure and function in chronically
ventilated preterm lambs. Am J Respir Crit Care Med 2005; 172:899-906. |
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| 10. |
Walsh
MC, Szefler S, Davis J, et al. Summary
proceedings from the bronchopulmonary dysplasia working group.
Pediatrics 2006;117:52-6.. |
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| 11. |
Tyson
JE, Wright LL, Oh W, et al. Vitamin
A supplementation for ELBW infants. N Engl J Med. 1999; 340:1962-1968.
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| 12. |
Van
Meurs KP, Wright
LL, Ehrenkranz
RA, et al. Inhaled
nitric oxide
for premature
infants with severe respiratory failure.
N Engl J Med
2005;353:13-22.
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| 13. |
Schmidt
B, Roberts R, Davis P, et al. Caffeine
therapy for apnea of prematurity. New Engl J Med 2006; 354:
2112-21. |
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EARLY
iNO THERAPY FOR THE PREVENTION OF BPD |
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Kinsella
JP, Cutter GR, Walsh WF, Gerstmann DR, Bose CL, Hart C, Sekar
KC, Auten RL, Bhutani VK, Gerdes JS, George TN, Southgate WM,
Carriedo H, Couser RJ, Mammel MC, Hall DC, Pappagallo M, Sardesai
S, Strain JD, Baier M, Abman SH. Early inhaled nitric
oxide therapy in premature newborns with respiratory failure. N
Engl J Med 2006; 355:354-64.
(For non-journal subscribers, an additional fee may apply
for full text articles.) |
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Kinsella
and colleagues recently
completed a multicenter, randomized trial involving 793 newborns
who were 34 weeks gestation or less at birth and had respiratory
failure requiring mechanical ventilation. Premature newborns, stratified
into 3 birthweight categories (500-749 grams, 750-999 grams, or 1000
to 1250 grams), randomly received either iNO (5 ppm) or placebo gas
within 48 hours of birth for 21 days or until extubation. Primary
outcome was a combination of death or BPD at 36 weeks CGA; secondary
outcomes included severe IVH (grades III or IV), PVL, or ventriculomegaly.
The results in the
entire cohort of 500-1250 gram infants showed no difference in the
overall risk of the combined outcomes. However, iNO significantly
decreased the risk of BPD by 50%, and the combined risk of death
or BPD by 40% in the subgroup of patients with birthweights of 1000-1250
grams (BPD 29.8% in the iNO group vs. 59.6% in the placebo group).
Of note, the secondary outcomes of brain injury (IVH, PVL, ventriculomegaly)
were decreased in the overall population of 500-1250 gram infants
(brain injury 17.5% in iNO group vs. 23.9% in placebo group, p=0.03).
Importantly, iNO therapy was not associated with increased risks
of pulmonary hemorrhage or other adverse events.
This important study
addresses concerns about early iNO therapy in the VLBW population
related to the potential risk for neonatal brain injury, pulmonary
hemorrhage, and death. While iNO has beneficial vasoactive and anti-inflammatory
effects, it is thought to adversely affect platelet adhesion. The
authors theorize that iNO may reduce neutrophil accumulation in infants
with RDS, and may also reduce oxidant stress by modulating inflammatory
cytokines and cell apoptosis. They also hypothesize that iNO may
modulate systemic circulation of cytokines that can injure distant
organs through reduction in lung-derived cytokines. Of particular
note is the authors’ finding that the use of iNO, with median iNO
exposure of 14 days, appears safe in this VLBW population, even when
used within the first 48 hours of life when risk for neurologic injury
is highest. |
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Ballard
RA, Truog WE, Cnaan A, Martin RJ, Ballard PL, Merrill JD, Walsh
MC, Durand DJ, Mayock DE, Eichenwald EC, Null DR, Hudak ML, Puri
AR, Golombek SG, Courtney SE, Stewart DL, Welty SE, Phibbs RH, Hibbs
AM, Luan X, Wadlinger SR, Asselin JM, Coburn CE for the NO CLD Study
Group. Inhaled nitric oxide in preterm infants undergoing
mechanical ventilation. N Engl J Med 2006; 355:343-53.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Ballard
and colleagues conducted a randomized, stratified, double-blind, placebo-controlled
trial of iNO at 21 centers involving infants of birthweights of 1250
grams or less who required ventilatory support between the ages of 7
and 21 days. iNO was started at 20 ppm for 48-96 hours, then decreased
weekly to 10, 5 and 2 ppm for a minimum duration of 24 days (as long
as infants required intubation). The primary study outcome of interest
was survival without BPD at 36 weeks gestation; secondary outcomes included
duration of oxygen therapy/duration of hospitalization. Of particular
interest were the long term pulmonary outcomes including need for rehospitalization
and respiratory support (mechanical ventilation/CPAP and oxygen supplementation)
at 40, 44, 52, and 60 weeks postmenstrual age.
Among 294 infants receiving iNO
and 288 receiving placebo, the iNO group had a significantly increased
rate of survival without BPD at 36 weeks gestation (43.9% vs. 36.8%
in placebo group, p<0.05). The infants who received iNO also were
discharged sooner and received supplemental oxygen for a shorter period
of time. There were no short term safety concerns relative to rates
of NEC, sepsis, PDA requiring therapy, ROP, or neurologic findings on
ultrasound. Subgroup analysis demonstrated that iNO was more beneficial in infants enrolled between ages 7 to 14 days compared to those infants enrolled between days of life 15 to 21.
The decision was made to delay
enrollment in the study until 7 days of life secondary to concerns about
potential brain injury with early use. The authors believed that later
and more prolonged therapy would prevent lung injury from hyperoxia
and improve surfactant function, lung growth, angiogenesis, and alveolarization.
Further long-term neurodevelopmental
follow-up to the Kinsella and Ballard trials will provide important
information for practitioners regarding the long-term safety of this
specific treatment. |
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CYTOKINE-DIRECTED
THERAPIES |
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Nakanishi
H, Sugiura T, Streisand JB, Lonning SM, Roberts Jr. JD. TGF-β neutralizing
antibodies improve pulmonary alveologenesis and vasculogenesis in
the injured newborn lung. Am J Phyisiol: Lung Cell Mol
Physiol. 2007 Apr 13; [Epub ahead of print].
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Pulmonary
injury, associated with the disruption of alveologenesis in the developing
lung, is known to cause BPD in premature infants. TGF-β is an important
regulator of cellular differentiation and early lung development, and
levels of TGF-β are increased in various forms of lung injury.
Although the role of TGF-β in the pathogenesis of BPD has been
studied, its role in inhibiting terminal lung development is not well
understood. In this study, the authors theorized that oxygen-induced
injury in the maturing lung is associated with TGF-β mediated disruption
of alveologenesis and microvascular development. They tested the hypothesis
that TGF-β neutralizing antibodies would attenuate TGF-β signaling,
and promote alveolar development using a newborn mouse model of BPD.
Upregulation of TGF-β signaling results in increased nuclear localization
of a protein called phospho-Smad2. In this study, the investigators
found that treatment with TGF-β neutralizing antibodies attenuated
nuclear localization of phospho-Smad2
in response to hyperoxia in pulmonary cells. Of note, the use of TGF-β neutralizing antibodies
also improved quantitative indicators of alveologenesis, extracellular
matrix assembly, and microvascular lung development in the injured and
developing lung. Interestingly, the use of these antibodies demonstrated
improved overall somatic growth in hyperoxic mouse pups, with no increase
in inflammatory markers.
The changes demonstrated in this
hyperoxia model of BPD included: improved microvascular development,
alveolar septal elastin organization, and improved overall alveologenesis.
This important animal study demonstrates the potential benefit of anti-TGF-β antibodies
in preventing lung injury in developmental diseases of the lung in premature
infants. |
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ANTIOXIDANT
THERAPIES: VITAMIN A |
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Ambalavanan
N, Tyson JE, Kennedy KA, Hansen NI, Vohr BR, Wright LL, Carlo WA
and the NICHD NRN. Vitamin A supplementation for extremely
low birth weight infants: outcome at 18 to 22 months. Pediatrics
2005; 115: e249-e254.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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VLBW
infants are often deficient in vitamin A (retinol), which may increase
the risk for BPD. While randomized controlled trials and a systematic
review have indicated that vitamin A supplementation decreases BPD and/or
death[1,2,3], the long-term effects of vitamin A supplementation
had not been reported previously. Goals of the present study investigated
the longer-term risks and benefits of vitamin A supplementation, including
rates of death, neurodevelopmental impairment (NDI), pulmonary complications,
and re-hospitalizations at 18-22 months CGA among infants who were previously
enrolled in the NICHD vitamin A trial[1]. The primary outcome
for this study was NDI (defined as one or more of the following conditions:
MDI or PDI <70, CP, blindness, or hearing impairment) or death. The
follow-up visit evaluated information regarding number of re-hospitalizations,
respiratory medication use, and the need for oxygen at home or in a
chronic care facility.
A total of 807 infants participated
in the original vitamin A trial. 85% of the survivors were assessed
at 18-22 months CGA. For all measurements of NDI, no significant differences
between the treatment groups were found. Of note, there were no differences
and no evidence of benefit from vitamin A supplementation on long-term
pulmonary morbidity after discharge. The patients who developed BPD
at 36 weeks CGA were more likely to have NDI at follow-up, with rates
of 54% in the BPD group vs 37% in infants who did not have BPD (RR:
1.48, CI: 1.22-1.80, p <0.001).
The prior vitamin A randomized controlled trial had shown
clear benefit to an intervention directed toward decreased rates of
BPD (55% vs. 62%, RR 0.89, 95% CI 0.80-0.99)[1]; however,
in Ambalavanan’s long-term follow-up study, the pulmonary benefits were
not evident. In fact, the trends related to pulmonary morbidity demonstrated
a borderline significant result, with the vitamin A group being more
likely to require diuretics at follow-up (RR 2.80, CI: 0.91-8.64, p
= 0.06). In addition, there were more patients from the vitamin A group
who required oxygen for home use, were still receiving oxygen therapy
at >6 months of age, and still required oxygen at the 18-22 month
follow-up. These findings reinforce the importance of direct long-term
pulmonary morbidity and neurodevelopmental outcomes evaluation as opposed
to evaluating the outcome of a diagnosis of BPD at 36 weeks’ corrected
age.
References
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ANTIOXIDANT
THERAPIES: RECOMBINANT SOD |
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Davis
JM, Parad RB, Michele T, Allred E, Price A, Rosenfeld W; for the
North American Recombinant Human CuZnSOD Study Group. Pulmonary
outcome at one year corrected age in infants treated at birth with
recombinant human superoxide dismutase. Pediatrics 2003;111:469-76.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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View
journal abstract |
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View
full article |
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Preterm
infants have been shown to be relatively deficient in pulmonary antioxidant
enzyme activity with a maturation pattern similar to pulmonary surfactant,
of particular importance since preterm infants are routinely exposed
to hyperoxia (even room air is hyperoxic compared to in utero oxygen
tensions) and damage from reactive oxygen species have been implicated
in the pathogenesis of BPD. To examine whether treatment of premature
infants with recombinant human superoxide dismutase (rhSOD) reduces
BPD and improves pulmonary outcome at 1 year corrected age, 302 infants
(600-1200 grams birth weight) were randomized to receive either intratracheal
rhSOD (5 mg/kg in 2 mL/kg saline) or placebo every 48 hours (as long
as intubation was required) for up to 1 month of age.
There were no differences between
groups in the incidence of death
or the development of BPD – defined
as oxygen requirement with an
abnormal chest radiograph at
28 days of life (required by
the FDA) or at 36 weeks CGA.
However, in follow-up at a median of 1 year CGA, 37% of placebo-treated
infants had repeated episodes of wheezing or other respiratory illness
severe enough to require treatment with asthma medications, such as
bronchodilators and/or corticosteroids, compared with 24% of rhSOD-treated
infants, a 36% reduction (p<0.05).
In a subset of infants <27 weeks gestation, 42% treated with placebo
received asthma medications compared
with 19% of rhSOD treated infants,
a 55% decrease. Infants <27 weeks
gestation who received rhSOD
also had a 55% decrease in emergency department visits and a 44% decrease
in subsequent hospitalizations.
These data indicate that treatment
at birth with rhSOD may reduce early pulmonary injury, resulting in
improved clinical status when measured at 1 year corrected age. Future
trials are currently being planned to examine the impact of prophylactic,
intratracheal administration of rhSOD in VLBW infants on clinical pulmonary
outcome at 1 year corrected age. |
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At
the conclusion of this activity, participants should be able to:
|
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Discuss
the uses of inhaled nitric oxide for the prevention of BPD |
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|
Describe
the uses of targeted antioxidant and anti-inflammatory therapies
to prevent or treat BPD |
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|
Explain
the importance of long-term follow-up and evaluation of functional
outcomes in determining the efficacy of treatments for BPD |
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or any other
relationship
a faculty member
or provider has
with the manufacturer(s)
of any commercial
product(s) discussed
in an educational
presentation.
The Course Directors
reported the
following:
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|
Edward
E. Lawson, MD has indicated a financial relationship
of grant/research support from the NIH. He also receives financial/material
support from Nature Publishing Group as the Editor of the Journal
of Perinatology. |
|
|
|
Christoph
U. Lehmann, MD has indicated no financial relationship
with commercial supporters. |
|
|
|
Lawrence
M. Nogee, MD has received grant support from the National
Institute of Health. |
|
|
|
Mary
Terhaar has indicated no financial relationship with
commercial supporters. |
|
|
|
Robert
J. Kopotic, MSN, RRT, FAARC has indicated a financial
relationship with the ConMed Corporation. |
Guest
Authors Disclosures |
|
| Disclaimer
Statement — back
to top |
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| The
opinions and recommendations expressed by faculty and other experts
whose input is included in this program are their own. This enduring
material is produced for educational purposes only. Use of Johns
Hopkins University School of Medicine name implies review of educational
format design and approach. Please review the complete prescribing
information of specific drugs or combination of drugs, including
indications, contraindications, warnings and adverse effects before
administering pharmacologic therapy to patients. |
|
© 2007
JHUSOM, IJHN, and eNeonatal Review
Created by DKBmed. |
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COMPLETE
THE POST TEST
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1.
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Step
2.
If you have participated in a Johns Hopkins
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Step
3.
Complete the post-test and course evaluation.
Step
4.
Print out your certificate.
Respiratory Therapists
Visit
this page to confirm that your state will accept the CE Credits gained
through this program or click on the link below to go directly to the post-test.
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