La oxigenoterapia hiperbárica favorece la recuperación auditiva asociada al aumento de los niveles séricos de IGF-1 y HSP70 en pacientes con hipoacusia súbita neurosensorial idiopática.

Abstract

Introduction

Acute hearing loss adversely affects quality of life; most cases are sensorineural. Sudden loss of sensorineural hearing (which is idiopathic in 90% of cases) is defined as a rapid hearing loss of ≥30 dB in ≥3 contiguous frequencies within ≤72 h [1]. It affects approximately 5–27 per 100,000 people annually, but its incidence has been increasing over the past decades [1–3]. Although its pathogenesis is incompletely understood, the most common triggers involve viral infections, vascular disorders, and autoimmune factors [1, 4].

Functional impairment/loss of cochlear hair cells (HCs) is the most common cause of sensorineural hearing loss, so protection and regeneration of HCs are essential for treatment [5]. There is evidence that insulin-like growth factor 1 (IGF-1) and heat shock protein 70 (HSP70) are associated with HC survival. IGF-1, a vital growth mediator, acts on supporting cells to maintain the number of HCs; exogenous IGF-1 has been reported to promote the regeneration of cochlear afferent synapses [5, 6]. In adult mammals, IGF-1 is primarily produced by the liver, secreted into the plasma, and reaches the inner ear via blood [7]. IGF-1 deficiency may be involved in the pathophysiology of sensorineural hearing loss in Turner syndrome [8]. A cohort study showed that higher serum levels of IGF-1 among individuals aged 50 to 60 years were associated with a decreased risk of hearing loss during a six-year follow-up [9]. However, the characteristics of serum IGF-1 in patients with idiopathic sudden sensorineural hearing loss (ISSHL) remain unclear. Like IGF-1, HSP70 also protects HCs by acting on supporting cells [10]. HSP70 is a stress-inducible heat shock protein that protects HCs from aminoglycosides and cisplatin [11, 12]. In 2006, Park et al. [13] found that serum levels of HSP70 are significantly higher in patients with ISSHL.

Increased oxygen delivery to the inner ear may aid hearing recovery due to the high oxygen demands and relatively limited vascular supply of the cochlea [4]. Hyperbaric oxygen therapy (HBOT) is a therapeutic approach in which the patient breathes 100% oxygen while being exposed to an ambient pressure of >1 atmosphere absolute [14]. Studies have shown that the oxygen tension in the intracochlear perilymph increases significantly during HBOT [15]. Clinically, HBOT is used both as an initial therapy and as a rescue therapy for ISSHL [1]. However, its underlying molecular mechanisms remain unclear. Specifically, it is not known whether HBOT changes the serum IGF-1 and HSP70 levels in patients with ISSHL.

In this study, we found that HBOT changed serum IGF-1 and HSP70 levels in ISSHL patients and explored the molecular mechanisms underlying the HBOT-induced hearing improvements in ISSHL.