Bilateral posterior subcapsular cataracts after inhaled budesonide therapy for bronchopulmonary dysplasia

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The Journal of Maternal-Fetal and Neonatal Medicine, April 2009; 22(4): 368–370

LETTER TO THE EDITOR

Bilateral posterior subcapsular cataracts after inhaled budesonide therapy for bronchopulmonary dysplasia

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SERVET OZKIRAZ1, ZEYNEL GOKMEN1, MEHMET BORAZAN2, AYLIN TARCAN1, & BERKAN GURAKAN1 1

Department of Pediatrics, Baskent University Faculty of Medicine, Ankara, Turkey and 2Department 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 corticosteroids 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 unremarkable. 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 posterior 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 spectrophotometer, 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: [email protected] ISSN 1476-7058 print/ISSN 1476-4954 online Ó 2009 Informa Healthcare USA, Inc. DOI: 10.1080/14767050802320332

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Letter to the Editor

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Figure 1. Peripherally localised posterior subcapsular cataracts: (a,c) right eye; (b,d) left eye on slit lamp examination.

cortical, nuclear and posterior subcapsular. Posterior subcapsular cataracts are the most visually disabling type and account for the majority of cataract extractions. Cataracts induced by corticosteroid 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 openlabel multicentre study of 625 wheezy infants, aged 1–3 years, treated with inhaled fluticasone propionate 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

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Letter to the Editor

as a topical agent, especially in preterm infants. This might be an associated factor for cataract. References

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1. Halliday HL. Clinical trials of postnatal corticosteroids: inhaled and systemic. Biol Neonate 1999;76(suppl 1):29–40. 2. Garbe E, Suissa S, LeLorier J. Association of inhaled corticosteroid use with cataract extraction in elderly patients. JAMA 1998;280:539–543.

3. Reed CE, Offord KP, Nelson HS, Li JT, Tinkelman DG. Aerosol beclomethasone dipropionate spray compared with theophylline as primary treatment for chronic mild-to-moderate asthma. J Allergy Clin Immunol 1998;101:14–23. 4. Bisgaard H, Allen D, Milanowski J, Kalev I, Willits L, Davies P. Twelve-month safety and efficacy of inhaled fluticasone propionate in children aged 1 to 3 years with recurrent wheezing. Pediatrics 2004;113:87–94. 5. The Childhood Asthma Management Program Research Group. Long-term effects of budesonide or nedocromil in children with asthma. N Engl J Med 2000;343:1054–1063.

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