Institutional members access full text with Ovid®

Share this article on:

Histamine-2 Receptor Blockers Alter the Fecal Microbiota in Premature Infants

Gupta, Raegan W.*; Tran, Lynn; Norori, Johana; Ferris, Michael J.§; Eren, A. Murat||; Taylor, Christopher M.; Dowd, Scot E.#; Penn, Duna*

Journal of Pediatric Gastroenterology and Nutrition: April 2013 - Volume 56 - Issue 4 - p 397–400
doi: 10.1097/MPG.0b013e318282a8c2
Original Articles: Gastroenterology

Objectives: Bacterial colonization is considered a major risk factor for necrotizing enterocolitis (NEC). The objective of the present study was to test the hypothesis that histamine-2 receptor (H2-) blockers alter colonic bacterial colonization by analyzing and comparing the fecal microbiota in premature infants with and without H2-blocker therapy using sensitive molecular biological techniques.

Methods: Seventy-six premature infants ≤1500 g or <34 weeks gestation were enrolled in this case-controlled, cross-sectional study. Stool samples were collected from 25 infants receiving H2-blockers and 51 babies who had never received them. Following DNA extraction and PCR amplification of 16S rRNA, 454 pyrosequencing was undertaken and the resulting sequences were subjected to comparison with published sequence libraries.

Results: Proteobacteria and Firmicutes were the major phyla contributing to fecal microbial communities. Microbial diversity was lower, relative abundance of Proteobacteria (primarily of the family Enterobacteriaceae) was increased, whereas that of Firmicutes was decreased in the stools of infants receiving H2-blockers compared with those who had never received them.

Conclusions: Although not designed to look specifically at the effect of H2-blockers on the incidence of NEC, our study suggests that their use lowers fecal microbial diversity and shifts the microfloral pattern toward Proteobacteria. These alterations in fecal microbiota may predispose the vulnerable immature gut to necrotizing enterocolitis and suggest prudence in the use of H2-blockers in the premature infant.

*Department of Pediatrics, Division of Neonatology, Louisiana State University Health Sciences Center, New Orleans

Pediatrix Medical Group of Louisiana, Baton Rouge General Hospital Medical Center, Baton Rouge

Research Institute for Children, Children's Hospital

§Departments of Pediatrics and Microbiology Immunology and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA

||Josephine Bay Paul Center for Comparative Molecular Biology and Evolution, Marine Biological Laboratory, Woods Hole, MA

Department of Computer Science, University of New Orleans, LA

#MR DNA Molecular Research LP, Shallowater, TX.

Address correspondence and reprint requests to Raegan W. Gupta, MD, Department of Pediatrics, Division of Neonatology, Children's Hospital of New Orleans, 200 Henry Clay Avenue, New Orleans, LA 70118 (e-mail: rwetze@lsuhsc.edu).

Received 4 June, 2012

Accepted 29 November, 2012

The authors received support from T.G. and Doris Solomon Family Foundation Endowed Chair, LSUHSC Dept. of Pediatrics and Research Institute for Children, Louisiana Vaccine Center-South Louisiana Institute for Infectious Disease Research (Louisiana Board of Regents).

The authors report no conflicts of interest.

Copyright 2013 by ESPGHAN and NASPGHAN