Background: Scant data exist on the normal range of serum gastrin in infants. In phase I and III trials of rabeprazole in gastroesophageal reflux disease, we studied serum gastrin levels in infants 1 to 11 months old, and assessed normal ranges and the effect of acid-suppressive drugs.
Methods: Overall, 349 treatment-naïve or treatment-experienced (previously exposed to proton pump inhibitors and/or H2-receptor antagonists) infants with gastroesophageal reflux disease were screened for baseline serum gastrin. Repeat gastrin was monitored at early termination or end of study, allowing assessment of 1 to 8 week daily rabeprazole (5- or 10-mg) treatment on gastrin levels.
Results: Median (5%–95% range) baseline gastrin was 118 ng/L (39–315) in the treatment-naïve group (n = 251), driven mostly by high levels (121.5 [48–326] ng/L) in the 1- to <4-month-old subgroup. Treatment-experienced infants (n = 98) had elevated baseline gastrin levels (152 [48–487] ng/L; P = 0.0011) with no clear difference between previously proton pump inhibitor–exposed and H2-receptor antagonist–exposed groups. At the end of study, mean (standard deviation) levels were unchanged from baseline in infants withdrawn from rabeprazole to placebo (124  ng/L), but elevated from baseline in those continuing treatment with 5-mg (245  ng/L) and 10-mg (332  ng/L) rabeprazole during the study.
Conclusions: Gastrin levels in treatment-naïve infants were elevated through 8 months of age. Between 8 and 12 months of age, they declined so that the median level was within the upper limit of the normal adult range (<100 ng/L). Previous exposure to acid-suppressive medications and short-term exposure to rabeprazole significantly increased gastrin levels in infants younger than 1 year.
Janssen Research & Development, LLC, Titusville, NJ.
Address correspondence and reprint requests to Dr William Treem, Janssen Research & Development, LLC, 1125 Trenton-Harbourton Rd, Titusville, NJ 08560 (e-mail: firstname.lastname@example.org).
Received 7 January, 2013
Accepted 9 May, 2013
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This article was presented at the 24th meeting of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN), October 18–21, 2012, Salt Lake City, UT.
This study was financially supported by Janssen Research & Development, LLC (previously known as Johnson & Johnson Pharmaceutical Research & Development, LLC) and Eisai Medical Research, Inc. The sponsor also provided a formal review of this manuscript.
This manuscript is based on 2 studies, which are registered at http://www.clinicaltrials.gov as NCT00747526 and NCT00992589.
P.H. and S.S. are employees of Janssen Research & Development LLC (previously known as Johnson & Johnson Pharmaceutical Research & Development, LLC). W.T. is a consultant to Janssen Research & Development LLC.