Mechanisms involved in hearing disorders of thyroid ontogeny: a literature review

Abstract

Endocochlear, retrocochlear and/or central origin hearing damage may be related to the absence of appropriate levels of thyroid hormone during morphogenesis and/or auditory system development. Hearing disorders related to the thyroid are not well studied, despite speculation on the pathophysiological mechanisms. The objective of this review was to characterize the main pathophysiological mechanisms of congenital hypothyroidism and to evaluate the relationship with central and peripheral hearing disorders. We conducted a literature review using the databases MedLine, LILACS, Cochrane Library, SciELO, Institute for Scientific Information (ISI), Embase, and Science Direct between July and September on 2016. We identified the studies that address hearing disorder mechanisms on the congenital hypothyroidism. Congenital hypothyroidism may have clinical and subclinical manifestations that affect the auditory system and may be a potential risk factor for hearing impairment. Hearing impairment can severely impact quality-of-life, which emphasizes the importance of monitoring and evaluating hearing during the clinical routine of these patients.

Figure 1. The role of T3 in human auditory system formation and development. In the foetal period, the primary auditory responses and the hearing sensitivity progressively matures until early childhood. During the first quarter, the embryo depends totally on the mother’s thyroid hormones, which are produced in small amounts during the second half of gestation. After birth occurs, there is an increase in the T4 and T3 levels in the newborn. Adapted from Ng and cols., 2013 (23).