TCERG1L allelic variation is associated with cisplatin-induced hearing loss in childhood cancer, a PanCareLIFE study

In children with cancer, the heterogeneity in ototoxicity occurrence after similar treatment suggests a role for genetic susceptibility. Using a genome-wide association study (GWAS) approach, we identified a genetic variant in TCERG1L (rs893507) to be associated with hearing loss in 390 non-cranial irradiated, cisplatin-treated children with cancer. These results were replicated in two independent, similarly treated cohorts (n = 192 and 188, respectively) (combined cohort: P = 5.3 × 10−10, OR 3.11, 95% CI 2.2–4.5). Modulating TCERG1L expression in cultured human cells revealed significantly altered cellular responses to cisplatin-induced cytokine secretion and toxicity. These results contribute to insights into the genetic and pathophysiological basis of cisplatin-induced ototoxicity.

Hearing Impairment in Angolan Children with Acute Bacterial Meningitis With and Without Otitis Media and Otorrhea

Background: Bacterial meningitis (BM) is a common cause of hearing loss in childhood. Our aim was to investigate bacterial etiology, hearing impairment, and outcome in childhood BM with vs. without otitis media (OM) in the resource-poor settings of Angola. Methods: Hearing was tested through brainstem-evoked response audiometry (ABR) in 391 (76%) of 512 children with confirmed BM. The bacteria identified from the ear discharge were compared to those from CSF and the relevance of findings was examined in terms of hearing among children with or without OM on day 1 and 7 of hospitalization, and at follow-ups of 1, 3 and 6 month(s).Results: No correlation was found in bacteriology between the ear discharge and CSF, and the most common ear pathogens more likely reflected chronic than acute middle ear infections. On day 7 in hospital, hearing impairment (>40 dB) was common, regardless of whether concomitant OM or not (in 27% vs. 30%, respectively), whereas on day 7, profound hearing loss (>80 dB) was diagnosed slightly more in children without OM 16% vs. 10% accordingly. Any hearing deficit on day 7 was associated with a higher risk of complicated or fatal clinical course (OR 2.76, CI95% 1.43-5.29, P = .002).Conclusion: No significant difference prevailed in hearing thresholds between children with or without OM in hospital on day 7 or at later follow-ups. Any hearing impairment on day 7 associated with a higher risk for complicated clinical course or death. Trial registration: ISRCTN62824827. Registered 22 June 2005, http://www.isrctn.com/ ISRCTN62824827.

Childhood Hearing Loss IN Developing Countries: From Multidisciplinary Team Work to Public Health

This chapter will highlight the common causes of hearing loss in children and emphasize on the fact that most of the hearing loss is due to causes that are preventable. We know that hearing loss in childhood not only impacts on the child’s learning and social interaction with the child’s peers and society, but also has economic implications when the child grows into an adult. Public health awareness is therefore paramount in preventing a large chunk of the hearing gloss and therefore greatly contributes to making sure that the child grows into a productive citizen of the society that the child grows or lives in.

Prevention of Congenital Cytomegalovirus Infection with Vaccines: State of the Art

Cytomegalovirus (CMV) is the most common cause of congenital infection and non-genetic sensorineural hearing loss in childhood. Up to 2% of neonates, with the highest percentages found in developing countries, are congenitally infected with CMV. At birth, most of these infants are asymptomatic. However, approximately 10% have signs and symptoms of the disease, and 40–60% of symptomatic neonates will later develop permanent neurologic sequelae. To reduce congenital CMV (cCMV) infection, a vaccine able to prevent primary infection is essential. In this narrative review, actual ongoing research about the development of a CMV vaccine is discussed. The progressive increase in knowledge on the ways in which the host’s immune system and CMV relate has made it possible to clarify that the development of a vaccine that is certainly capable of reducing the risk of cCMV infection, and preventing both primary and nonprimary infections is extremely difficult. Many of the ways in which the virus evades the immune system and causes cCMV infection are not yet fully understood, especially in cases of nonprimary infection. Moreover, the schedule that should be recommended and that subjects must be vaccinated to obtain the greatest effect have not been precisely defined. Further studies are needed before the problem of cCMV infection and its related challenges can be totally solved.