Introduction Many, but not all, studies have found a correlation between environmental tobacco smoke (ETS) and acute otitis media (AOM) and other adverse otologic outcomes. Given its high personal and societal costs and the divergent findings of the effect of ETS on middle ear disease, the aim of the current study was to assess the impact and possible determinant factors of ETS on recurrent (two or more) episodes of AOM. Methods The study was performed at Heim Pal Children's Hospital, Ear, Nose and Throat (ENT) Department, Budapest, Hungary. Caregivers of a convenience sample of 412 children attending the ENT outpatient clinic were surveyed via a 22-item questionnaire regarding demographics, socioeconomics, and smoking behaviours of the child's family; as well as caregivers' self report of the number of AOM episodes of the child. Results Of the 412 participants, 155 (38%) children's parents smoked. In bivariate analysis, two or more episodes of AOM correlated with reported hearing problems, day care enrolment, parental employment and increased age of the child. In multivariate logistic regression, parental smoking more than doubled a child's risk for recurrent AOM while increased maternal employment (e.g. part-time or full-time vs. unemployed) boosted risk up to fourfold. Among children whose parents smoked, half-packs of cigarettes smoked per day and day care attendance doubled or nearly tripled, respectively, the risk of recurrent AOM episodes. Conclusions Childhood exposure to ETS is high among an ENT clinic population of Hungarian children. Such exposure correlates with AOM episodes, ENT operations and conductive hearing loss. Data such as these argue for strict laws smoke-free laws not only in Hungary, but also in Europe and around the world.
Objective. In this report, we review the recent literature (ie, past 4 years) to identify advances in our understanding of the middle ear-mastoid-eustachian tube system. We use this review to determine whether the short-term goals elaborated in the last report were achieved, and we propose updated goals to guide future otitis media research.Data Sources. PubMed, Web of Science, Medline.Review Methods. The panel topic was subdivided, and each contributor performed a literature search within the given time frame. The keywords searched included middle ear, eustachian tube, and mastoid for their intersection with anatomy, physiology, pathophysiology, and pathology. Preliminary reports from each panel member were consolidated and discussed when the panel met on June 11, 2015. At that meeting, the progress was evaluated and new short-term goals proposed.Conclusions. Progress was made on 13 of the 20 short-term goals proposed in 2011. Significant advances were made in the characterization of middle ear gas exchange pathways, modeling eustachian tube function, and preliminary testing of treatments for eustachian tube dysfunction.Implications for Practice. In the future, imaging technologies should be developed to noninvasively assess middle ear/eustachian tube structure and physiology with respect to their role in otitis media pathogenesis. The new data derived from these structure/function experiments should be integrated into computational models that can then be used to develop specific hypotheses concerning otitis media pathogenesis and persistence. Finally, rigorous studies on medical or surgical treatments for eustachian tube dysfunction should be undertaken.
Pressure change is faster in smaller MEs than in larger ones. Healthy MEs between 3 and 6 ml are very sensitive to the duration of a potential ET dysfunction to develop ME pathology. In MEs with poor mastoid pneumatization and dysfunctional ET, typical in cholesteatoma cases, mastoid obliteration as surgical reduction of mucosal surface for gas exchange can improve ME gas pressure balance resulting in better long-term outcome.
Cholesteatoma is an epidermoid cyst, which is most frequently found in the middle ear. The matrix of cholesteatoma is histologically similar to the matrix of the epidermoid cyst of the skin (atheroma); their epithelium is characterized by hyperproliferation. The c-MYC protooncogene located on chromosome 8q24 encodes a transcription factor involved in the regulation of cell proliferation and differentiation. Previous studies have found aneuploidy of chromosome 8, copy number variation of c-MYC gene, and the presence of elevated level c-MYC protein in cholesteatoma. In this study we have compared the expression of c-MYC gene in samples taken from the matrix of 26 acquired cholesteatomas (15 children and 11 adults), 15 epidermoid cysts of the skin (atheromas; head and neck region) and 5 normal skin samples (retroauricular region) using RT-qPCR, providing the first precise measurement of the expression of c-MYC gene in cholesteatoma. We have found significantly elevated c-MYC gene expression in cholesteatoma compared to atheroma and to normal skin samples. There was no significant difference, however, in c-MYC gene expression between cholesteatoma samples of children and adults. The significant difference in c-MYC gene expression level in cholesteatoma compared to that of atheroma implies a more prominent hyperproliferative phenotype which may explain the clinical behavior typical of cholesteatoma.
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