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  1. Wang J, Sung V, Carew P, Burt RA, Liu M, Wang Y, et al.
    Acad Pediatr, 2019 07;19(5):504-514.
    PMID: 30872125 DOI: 10.1016/j.acap.2019.01.010
    BACKGROUND: Better epidemiologic information on childhood hearing loss would inform research priorities and efforts to prevent its progression.

    OBJECTIVES: To estimate prevalence and secular trends in children's hearing loss.

    DATA SOURCES: We searched MEDLINE and Embase from January 1996 to August 2017.

    STUDY ELIGIBILITY CRITERIA: We included epidemiologic studies in English reporting hearing loss prevalence.

    STUDY APPRAISAL AND SYNTHESIS METHODS: The modified Leboeuf-Yde and Lauritsen tool was used to assess methodological quality. Meta-analyses combined study-specific estimates using random-effects models.

    PARTICIPANTS: Children 0 to 18 years of age.

    RESULTS: Among 88 eligible studies, 43.2% included audiometric measurement of speech frequencies. In meta-analyses, pooled prevalence estimates of slight or worse bilateral speech frequency losses >15 decibels hearing level (dB HL) were 13.1% (95% confidence interval [CI], 10.0-17.0). Using progressively more stringent cutpoints, pooled prevalence estimates were 8.1% (95% CI, 1.3-19.8) with >20 dB HL, 2.2% (95% CI, 1.4-3.0) with >25 dB HL, 1.8% (95% CI, 0.4-4.1) with >30 dB HL, and 0.9% (95% CI, 0.1-2.6) with >40 dB HL. Also, 8.9% (95% CI, 6.4-12.3) had likely sensorineural losses >15 dB HL in 1 or both ears, and 1.2% (95% CI, 0.5-2.1) had self-reported hearing loss. From 1990 to 2010, the prevalence of losses >15 dB HL in 1 or both ears rose substantially (all P for trend

  2. Suaini NH, Koplin JJ, Ellis JA, Peters RL, Ponsonby AL, Dharmage SC, et al.
    J Steroid Biochem Mol Biol, 2014 Oct;144 Pt B:445-54.
    PMID: 25174667 DOI: 10.1016/j.jsbmb.2014.08.018
    We aimed to investigate the relationship between genetic and environmental exposure and vitamin D status at age one, stratified by ethnicity. This study included 563 12-month-old infants in the HealthNuts population-based study. DNA from participants' blood samples was genotyped using Sequenom MassARRAY MALDI-TOF system on 28 single nucleotide polymorphisms (SNPs) in six genes. Using logistic regression, we examined associations between environmental exposure and SNPs in vitamin D pathway and filaggrin genes and vitamin D insufficiency (VDI). VDI, defined as serum 25-hydroxyvitamin D3(25(OH)D3) level ≤50nmol/L, was measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Infants were stratified by ethnicity determined by parent's country of birth. Infants formula fed at 12 months were associated with reduced odds of VDI compared to infants with no current formula use at 12 months. This association differed by ethnicity (Pinteraction=0.01). The odds ratio (OR) of VDI was 0.29 for Caucasian infants (95% CI, 0.18-0.47) and 0.04 for Asian infants (95% CI, 0.006-0.23). Maternal vitamin D supplementation during pregnancy and/or breastfeeding were associated with increased odds of infants being VDI (OR, 2.39; 95% CI, 1.11-5.18 and OR, 2.5; 95% CI, 1.20-5.24 respectively). Presence of a minor allele for any GC SNP (rs17467825, rs1155563, rs2282679, rs3755967, rs4588, rs7041) was associated with increased odds of VDI. Caucasian infants homozygous (AA) for rs4588 had an OR of 2.49 of being associated with VDI (95% CI, 1.19-5.18). In a country without routine infant vitamin D supplementation or food chain fortification, formula use is strongly associated with a reduced risk of VDI regardless of ethnicity. There was borderline significance for an association between filaggrin mutations and VDI. However, polymorphisms in vitamin D pathway related genes were associated with increased likelihood of being VDI in infancy.
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