Maternal and infant use of erythromycin and other macrolide antibiotics as risk factors for infantile hypertrophic pyloric stenosis

Mahon, Barbara E.; Rosenman, Marc B.; Kleiman, Martin B.

doi:10.1067/mpd.2001.117577

Cited by 135 publications

(76 citation statements)

References 13 publications

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“…Possible etiological factors include deficiency of nitric oxide synthase containing neurons, abnormal myenteric plexus innervation, infantile hypergastrinemia and recently exposure to macrolide antibiotics. [3][4][5] Genetic linkage analyses of familial cases with IHPS have suggested five loci that could harbor genes contributing to IHPS; 12q24.2-q24.31, 6 16p13-p12, 7 11q14-q22, 8 Xq23 8 and 16q24. 9 The only gene, so far, that has been implicated with the development of IHPS is the NOS1 gene.…”

Section: Introductionmentioning

confidence: 99%

No association between a promoter NOS1 polymorphism (rs41279104) and Infantile Hypertrophic Pyloric Stenosis

2009

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Infantile hypertrophic pyloric stenosis (IHPS) is a condition affecting infants in the first few months of life. The condition is manifested by persistent vomiting and is caused by a hypertrophied muscle obstructing the gastric outlet. The condition is treated by pyloromyotomy. The incidence is 1-8/1000 births and varies among different populations. The etiology of IHPS is unknown, but both genetic and environmental factors are thought to contribute to the disease. Genetic linkage analysis has so far localized five loci that could harbor genes contributing to IHPS. The only gene implicated in IHPS is the nitric oxide synthase gene (NOS1), in which a single nucleotide polymorphism (rs41279104) in the promoter region has been associated with the disease in 16 patients. In this study, we examined an association of this SNP in 54 familial and 28 sporadic cases with IHPS, and compared the results with normal controls using univariate and multiple logistic regression analysis. We could not confirm any association between the analyzed SNP and infantile hypertrophic pyloric stenosis.

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Section: Introductionmentioning

confidence: 99%

No association between a promoter NOS1 polymorphism (rs41279104) and Infantile Hypertrophic Pyloric Stenosis

2009

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“…In one cohort study, infants receiving erythromycin prophylaxis were found to have greater risk of IHPS (7/157 among those exposed versus 0/125 among those with no erythromycin exposure) (278). In a large retrospective study, Mahon et al evaluated 14,876 infants treated with erythromycin (oral or ophthalmic administration) as well as mothers who received erythromycin during the third trimester to evaluate the risk of IHPS (346). Young infants (especially those less than 2 weeks of age) who received systemic erythromycin had a higher risk of IHPS than those given ophthalmic erythromycin.…”

Section: Postexposure Prophylaxis and Therapeuticsmentioning

confidence: 99%

Pertussis: Microbiology, Disease, Treatment, and Prevention

et al. 2016

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SUMMARYPertussis is a severe respiratory infection caused byBordetella pertussis, and in 2008, pertussis was associated with an estimated 16 million cases and 195,000 deaths globally. Sizeable outbreaks of pertussis have been reported over the past 5 years, and disease reemergence has been the focus of international attention to develop a deeper understanding of pathogen virulence and genetic evolution ofB. pertussisstrains. During the past 20 years, the scientific community has recognized pertussis among adults as well as infants and children. Increased recognition that older children and adolescents are at risk for disease and may transmitB. pertussisto younger siblings has underscored the need to better understand the role of innate, humoral, and cell-mediated immunity, including the role of waning immunity. Although recognition of adult pertussis has increased in tandem with a better understanding ofB. pertussispathogenesis, pertussis in neonates and adults can manifest with atypical clinical presentations. Such disease patterns make pertussis recognition difficult and lead to delays in treatment. Ongoing research using newer tools for molecular analysis holds promise for improved understanding of pertussis epidemiology, bacterial pathogenesis, bioinformatics, and immunology. Together, these advances provide a foundation for the development of new-generation diagnostics, therapeutics, and vaccines.

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“…The MLN gene is considered as an IHPS candidate gene as treatment with the motilin agonist erythromycin in newborn children gives an increased risk for developing IHPS. 31,32 In a previous study, we have investigated the MLN gene as an IHPS candidate gene without finding evidence of association to the disease in that material. 22 However, the MLN gene is located in the candidate region with suggestive linkage on chromosome 6p21, which motivates further studies of this candidate gene.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide linkage analysis in families with infantile hypertrophic pyloric stenosis indicates novel susceptibility loci

et al. 2011

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Infantile hypertrophic pyloric stenosis (IHPS) is a common cause of upper gastrointestinal obstruction during infancy. A multifactorial background of the disease is well established. Multiple susceptibility loci including the neuronal nitric oxide synthase (NOS1) gene have previously been linked to IHPS, but contradictory results of linkage studies in different materials indicate genetic heterogeneity. To identify IHPS susceptibility loci, we conducted a genome-wide linkage analysis in 37 Swedish families. In regions where the Swedish material showed most evidence in favor of linkage, 31 additional British IHPS families were analyzed. Evidence in favor of significant linkage was observed in the Swedish material to two loci on chromosome 2q24 (non-parametric linkage (NPL) ¼3.77) and 7p21 (NPL¼4.55). In addition, evidence of suggestive linkage was found to two loci on chromosome 6p21 (NPL¼2.97) and 12q24 (NPL¼2.63). Extending the material with British samples did not enhance the level of significance. Regions with linkage harbor interesting candidate genes, such as glucagon-like peptide-2 (GLP-2 encoded by the glucagon gene GCG), NOS1, motilin (MLN) and neuropeptide Y (NPY). The coding exons for GLP-2, and NPY were screened for mutations with negative results. In conclusion, we could confirm suggestive linkage to the region harboring the NOS1 gene and detected additional novel susceptibility loci for IHPS.

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Maternal and infant use of erythromycin and other macrolide antibiotics as risk factors for infantile hypertrophic pyloric stenosis

Cited by 135 publications

References 13 publications

No association between a promoter NOS1 polymorphism (rs41279104) and Infantile Hypertrophic Pyloric Stenosis

No association between a promoter NOS1 polymorphism (rs41279104) and Infantile Hypertrophic Pyloric Stenosis

Pertussis: Microbiology, Disease, Treatment, and Prevention

Genome-wide linkage analysis in families with infantile hypertrophic pyloric stenosis indicates novel susceptibility loci

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