Bilateral posterior subcapsular cataracts after inhaled budesonide therapy for bronchopulmonary dysplasia

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LETTER TO THE EDITOR
Bilateral posterior subcapsular cataracts after inhaled budesonide
therapy for bronchopulmonary dysplasia
SERVET OZKIRAZ
1
, ZEYNEL GOKMEN
1
, MEHMET BORAZAN
2
, AYLIN TARCAN
1
,&
BERKAN GURAKAN
1
1
Department of Pediatrics, Baskent University Faculty of Medicine, Ankara, Turkey and
2
Department of Ophthalmology,
Baskent University Faculty of Medicine, Ankara, Turkey
(Received 7 March 2008; revised 26 May 2008; accepted 13 July 2008)
Introduction
Inhaled corticosteroids (ICSs) have been used to
treat or attempt to prevent CLD in the belief that
topical treatment would be associated with fewer
systemic adverse effects. An overview of trials of
inhaled steroids concludes that although there are
short-term beneficial effects with improved lung
function and less need for later systemic steroids,
there are no apparent long-term benefits and no
effects on the mortality or risk of CLD [1].
Excessive doses and prolonged use of corticoster-
oids can impair head growth, neurodevelopmental
outcome, lung structure and long-term survival.
The use of systemic and/or ICSs is a risk factor
for the development of posterior subcapsular
cataracts (PSC) in adults. However, several studies
have suggested that the use of ICSs does not
increase the risk of cataracts in infants or children
[1–3]. We report the development of bilateral
posterior subcapsular cataracts in an infant treated
with inhaled budesonide for bronchopulmonary
dysplasia.
Case report
A 26-week gestational age, 900-g male triplet
infant (intrauterine insemination pregnancy) was
born to a 26-year-old, gravida 2, para 2 mother by
caesarean section. The baby’s Apgar scores at
1 min and 5 min were 3 and 5, respectively.
The prenatal and family histories were unremark-
able. The infant had respiratory distress syndrome,
early neonatal sepsis, patent ductus arteriosus and
necrotising enterocolitis in the neonatal period.
The patient was weaned on postnatal day 28, and
1 day later was begun on a diuretic (furosemide),
inhaled bronchodilator (salbutamol, q.i.d.) and
inhaled BUD 250 mg b.i.d. Stage-2 retinopathy of
prematurity (ROP) was detected at 32 weeks of
age. He was discharged from the NICU with nasal
oxygen, furosemide, inhaled salbutamol and BUD
on postnatal day 85 when the post-conceptional
age was 38 weeks. Oxygen and furosemide was
stopped 2 weeks later. Two months later (4
months after BUD therapy), ROP spontaneously
regressed, but peripherally localised bilateral pos-
terior subcapsular cataracts developed, with no
effect on vision (Figure 1a,b). Plasma electrolyte
levels, liver and kidney function tests, screening for
inborn errors with a tandem mass spectrophot-
ometer, a urine test for reducing substances and
congenital infections (group TORCH) serology
were negative. The only risk factor for cataracts,
which was BUD, was ceased. Ten months after the
cessation of BUD, PSC regressed spontaneously
(Figure 1c,d).
Discussion
Cataracts are classified in accordance with their
anatomic location: the most common types are
Correspondence: Servet Ozkiraz, MD, Ozalan M. Eski Sille Yolu Cad. Sehavet 2 Siteleri, A Blok 116/20, Selcuklu, Konya 42080, Turkey.
E-mail: sozkiraz@yahoo.com
The Journal of Maternal-Fetal and Neonatal Medicine, April 2009; 22(4): 368–370
ISSN 1476-7058 print/ISSN 1476-4954 online Ó2009 Informa Healthcare USA, Inc.
DOI: 10.1080/14767050802320332
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cortical, nuclear and posterior subcapsular. Poster-
ior subcapsular cataracts are the most visually
disabling type and account for the majority of
cataract extractions. Cataracts induced by corticos-
teroid therapy are typically posterior subcapsular.
Several studies have suggested that there is no such
increased risk for infants and children [1–3]. In the
study by Reed et al., there was no increased risk of
cataracts associated with ICS use in a multicentre
randomised trial involving 384 subjects receiving
BDP therapy monitored for 1 year [3]. An open-
label multicentre study of 625 wheezy infants, aged
1–3 years, treated with inhaled fluticasone propio-
nate reported that only 1 patient (male, 44 months)
had a pinhead-sized posterior capsule intraocular
opacity in the left eye. He was taken off fluticasone
propionate and the cataract had disappeared 1 year
later [4]. The CAMP Research Group monitored
the development of PSC in 311 children receiving
long-term treatment with inhaled BUD. At the end
of the 6-year study, only one of the children
receiving BUD developed cataracts. The cataract
was small, did not affect vision testing, and
occurred in a subject who required 36 days of
prednisone therapy as well as supplementary BDP
therapy [5]. Our patient was treated with 500 mg
(b.i.d.) inhaled BUD daily via face mask, with no
systemic corticosteroids. Although the total daily
dose and cumulative dosages were not high, PSC
developed after 4 months of inhaled BUD. PSC was
detected on 6th visit of ophthalmology, and
regressed spontaneously after cessation of BUD.
PSC in our patient could be due to a systemic effect
of BUD, also while inhaling BUD there might have
been some leak around the mask, and BUD might
have affect the eyes directly as a topical agent. This
might be an associated factor of cataract our
patient.
Declaration of interest: Leakage of budesonid
around the mask might have affect the eyes directly
Figure 1. Peripherally localised posterior subcapsular cataracts: (a,c) right eye; (b,d) left eye on slit lamp examination.
Letter to the Editor 369
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as a topical agent, especially in preterm infants. This
might be an associated factor for cataract.
References
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