Gastric Acid Inhibition for Fat Malabsorption or Gastroesophageal Reflux Disease in Cystic Fibrosis: Longitudinal Effect on Bacterial Colonization and Pulmonary Function
Received 2 January 2009; received in revised form 28 May 2009; accepted 17 June 2009. published online 17 August 2009.
Refers to article:
Bronchiectasis in Infants and Preschool Children Diagnosed with Cystic Fibrosis after Newborn Screening
, 21 July 2009
Stephen M. Stick, Siobhain Brennan, Conor Murray, Tonia Douglas, Britta S. von Ungern-Sternberg, Luke W. Garratt, Catherine L. Gangell, Nicholas De Klerk, Barry Linnane, Sarath Ranganathan, Phillip Robinson, Colin Robertson, Peter D. Sly, Australian Respiratory Early Surveillance Team for Cystic Fibrosis (AREST CF)
The Journal of Pediatrics
November 2009 (Vol. 155, Issue 5, Pages 623-628.e1) Abstract |
Full Text |
Full-Text PDF (452 KB)
Objectives
To investigate bacterial colonization and pulmonary function longitudinally in patients with cystic fibrosis (CF) receiving drugs for gastric acid (GA) inhibition for fat malabsorption or for gastroesophageal reflux disease (GERD).
Study design
A retrospective cohort study of 218 pediatric patients with CF was performed. Multilevel modeling was used to perform longitudinal analysis of forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), maximum expiratory flow at 50% of FVC (MEF50), and maximal mid-expiratory flow between 25% and 75% of FVC (MMEF25-75). Cox regression was used to calculate Pseudomonas aeruginosa- and Staphylococcus aureus-free survival.
Results
Patients with CF and GA inhibition had a significantly smaller yearly decline of MEF50 and MMEF25-75 compared with control subjects. Other pulmonary function parameters and P aeruginosa or S aureus acquisition or colonization were not different from that of control subjects. GERD was associated with a significantly reduced pulmonary function (FEV1 and FVC) and an earlier acquisition of P aeruginosa and S aureus.
Conclusions
GA inhibition did not affect pulmonary function or bacterial acquisition and therefore is not contraindicated in patients with CF. GA inhibition might improve pulmonary function with time, because the decline of MEF50 and MMEF25-75 was less pronounced. GERD was associated with a reduced pulmonary function and an earlier acquisition of P aeruginosa and S aureus. Therefore the diagnosis and treatment of GERD should be aggressively pursued in patients with CF.
aDepartment of Pediatric Gastroenterology, University Medical Center Utrecht, Utrecht, the Netherlands
bDepartment of Pediatric Pulmonology, University Medical Center Utrecht, Utrecht, the Netherlands
cJulius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands
Reprint requests: H.P.J. van der Doef, MD, Department of Pediatric Gastroenterology [KE.04.133.1], University Medical Center Utrecht, Postbox 85090, 3508 AB Utrecht, The Netherlands.
Dr van der Doef was supported by a grant from the Wilhelmina Research Fund (OZF 2005/04). The authors declare no conflicts of interest.
ABSTRACT