A multicenter study was set up to elucidate the environmental and medical risk factors contributing to age-related hearing impairment (ARHI). Nine subsamples, collected by nine audiological centers across Europe, added up to a total of 4,083 subjects between 53 and 67 years. Audiometric data (pure-tone average [PTA]) were collected and the participants filled out a questionnaire on environmental risk factors and medical history. People with a history of disease that could affect hearing were excluded. PTAs were adjusted for age and sex and tested for association with exposure to risk factors. Noise exposure was associated with a significant loss of hearing at high sound frequencies (>1 kHz). Smoking significantly increased high-frequency hearing loss, and the effect was dose-dependent. The effect of smoking remained significant when accounting for cardiovascular disease events. Taller people had better hearing on average with a more pronounced effect at low sound frequencies (<2 kHz). A high body mass index (BMI) correlated with hearing loss across the frequency range tested. Moderate alcohol consumption was inversely correlated with hearing loss. Significant associations were found in the high as well as in the low frequencies. The results suggest that a healthy lifestyle can protect against age-related hearing impairment.Electronic supplementary materialThe online version of this article (doi: 10.1007/s10162-008-0123-1) contains supplementary material, which is available to authorized users.

Age-related hearing impairment (ARHI) is the most prevalent sensory impairment in the elderly. ARHI is a complex disease caused by an interaction between environmental and genetic factors. The contribution of various environmental factors has been relatively extensively studied. In contrast, investigations to identify the genetic risk factors have only recently been initiated. In this paper we describe the results of an association study performed on 2418 ARHI samples derived from nine centers from seven European countries. In 70 candidate genes, a total of 768 tag single nucleotide polymorphisms (SNPs) were selected based on HAPMAP data. These genes were chosen among the monogenic hearing loss genes identified in mice and men in addition to several strong functional candidates. After genotyping and data polishing, statistical analysis of all samples combined resulted in a P-value that survived correction for multiple testing for one SNP in the GRHL2 gene. Other SNPs in this gene were also associated, albeit to a lesser degree. Subsequently, an analysis of the most significant GRHL2 SNP was performed separately for each center. The direction of the association was identical in all nine centers. Two centers showed significant associations and a third center showed a trend towards significance. Subsequent fine mapping of this locus demonstrated that the majority of the associated SNPs reside in intron 1. We hypothesize that the causative variant may change the expression levels of a GRHL2 isoform.

OBJECTIVE:In this study, we determined the prevalence of hearing loss in 157 children with proven congenital cytomegalovirus (cCMV) infection. We looked at possible risk determinants for developing hearing loss and proposed recommendations for screening and follow-up in the newborn.METHODS: In a prospective 22-year study, 157 children with proven cCMV infection were evaluated for sensorineural hearing loss (SNHL). The development of SNHL was correlated with the type of maternal infection (primary versus nonprimary), the gestational age of maternal primary infection, imaging findings at birth, and the presence of symptomatic or asymptomatic infection in the newborn.RESULTS: Of all children, 12.7% had SNHL, and 5.7% needed hearing amplification because of SNHL. Improvement, progression, and fluctuations of hearing thresholds were seen in 45%, 53.8%, and 5.7% of the children, respectively. Hearing loss was more common in the case of a symptomatic infection at birth (P 5 .017), after a maternal primary infection in the first trimester of pregnancy (P 5 .029), and in the presence of abnormalities on a neonatal brain ultrasound and/or MRI (P , .001).CONCLUSION SNHL is a common sequela in children with cCMV infection. Risk factors for SNHL were primary maternal infections before the 14th week of pregnancy, the presence of a disseminated infection at birth, and imaging abnormalities in the newborn. These children may benefit from a more thorough investigation for SNHL than children who do not present with those risk factors.WHAT'S KNOWN ON THIS SUBJECT: Hearing loss is 1 of the most common sequelae in children with a congenital cytomegalovirus infection.WHAT THIS STUDY ADDS: Incidences of hearing loss and the need for hearing rehabilitation in children with congenital cytomegalovirus infection are discussed. We describe risk indicators for late-onset hearing loss.

In allergic rhinitis, cross-linking of IgE molecules upon allergen contact induces degranulation of mast cells and basophils within the mucosal tissue and results in the release of typical mediators, which consecutively induce the well-known symptoms. Omalizumab counteracts these interactions by reducing serum levels of free IgE. Therapy targeted at IgE also interferes with its binding to the low-affinity receptors inhibiting the amplification of the Th₂-type response. Treatment of allergic rhinitis with anti-IgE has been shown to be safe and to reduce specific symptoms. Furthermore, the combination of omalizumab with specific immunotherapy may not only increase efficacy but also safety in selected patients. Therefore, we reviewed previously published studies on omalizumab therapy in allergic rhinitis, either as monotherapy or in combination with immunotherapy. In patients with nasal polyps, a local multiclonal IgE response has recently been described, initiated by Staphylococcus aureus-derived enterotoxins, which at least modifies the inflammatory reaction within the tissue. Evidence accumulates that these enterotoxins act as superantigens resulting in a multiclonal T- and B-cell activation with massive IgE formation within the airways. Because of the multiclonality, a range of allergens could possibly maintain a constant degranulation of mast cells present in the polyp tissue, which may contribute to disease severity. We here discuss a proof-of-concept treatment trial with omalizumab in nasal polyposis, which – in case of a positive therapeutic response – would also pave the way for anti-IgE treatment approaches for severe non-atopic lower airway disease.

This study does not support a role for selenium in protection against asthma, but effect modification and confounding cannot be ruled out.