Optimal First-Line Therapy for Acute Low-Tone Sensorineural Hearing Loss

Abstract

Background and Objectives: We aimed to analyze treatment outcomes following different initial management approaches and confirm treatment regimens for acute low-tone sensorineural hearing loss (ALHL) that would yield the best results. Subjects and Methods: We retrospectively analyzed the medical records of 106 patients with ALHL who visited a university hospital's otology clinic from March 2013 to June 2019. Pure-tone averages at the initial visit and at 2 and 4 weeks after the initial visit were evaluated. Results: Forty-nine patients were enrolled in this study; of them, 41 (83.7%) exhibited complete recovery (CR) at 2 weeks and 43 (87.8%) exhibited CR at 1 month after the initial visit. Regression analysis revealed that CR at 2 weeks after the initial visit was associated with diuretic use [Exp(B): 10.309, 95% confidence interval (CI): 1.007-100]. An initial daily low-dose steroid use was marginally significant [Exp(B): 1.042, 95% CI: 0.997-1.092; p=0.066]. Isolated diuretic use [Exp(B): 25.641, 95% CI: 1.121-90.909; p=0.039] was an independent, good prognostic factor at 1 month after the initial visit. However, other treatment regimens did not affect the final results. Conclusions: A combination of initial daily administration of ≤30 mg prednisolone plus diuretics was sufficient as the first-line treatment for ALHL. High-dose steroids and salvage intratympanic steroid injections can be applied as a second choice; however, the predicted outcome would not be good in that case.

Prognosis of Acute Low‐Tone Hearing Loss Without Vertigo: A Scoping Review

“…One additional study 17 was identified within the references of one of the full‐texts and manually added to the full‐text review. Among all full‐texts reviewed, 41 studies 3–8,10,13,16–18,22–51 were determined to meet the study inclusion and exclusion criteria and these studies subsequently underwent data extraction (Figure 1).…”

Application of Human Stem Cells to Model Genetic Sensorineural Hearing Loss and Meniere Disease

“…Despite the extensive occurrence of genetic SNHL in the world, there are no Food and Drug Administration (FDA)-approved cellular or molecular therapies [4,50]. Current treatments for human SNHL and MD are medical therapy using steroids, hearing aids, surgery to correct the cause of the hearing loss, or cochlear implants [84][85][86][87][88][89]. Though these devices offer significant relief of the moderate and severe SNHL by amplifying sound or directly electrically stimulating the auditory nerve, they have significant limitations in terms of speech discrimination in complex acoustic environments [90].…”

“…The major achievements in disease modeling using a hiPSC-derived inner ear for genetic SNHL include the genes MYO7A, MYO15, and MERRF in HCs [70,89,90], and GJB2 and SLC26A4 (Pendred syndrome) in SCs [106,[123][124][125] (Table 2). These studies have defined the molecular mechanisms involving each gene and showed the cellular effects of each mutation.…”

Application of Human Stem Cells to Model Genetic Sensorineural Hearing Loss and Meniere Disease

“…Despite the extensive occurrence of genetic SNHL in the world, there are no Food and Drug Administration (FDA)-approved cellular or molecular therapies [ 4 , 50 ]. Current treatments for human SNHL and MD are medical therapy using steroids, hearing aids, surgery to correct the cause of the hearing loss, or cochlear implants [ 83 , 84 , 85 , 86 , 87 , 88 , 89 ]. Though these devices offer significant relief of the moderate and severe SNHL by amplifying sound or directly electrically stimulating the auditory nerve, they have significant limitations in terms of speech discrimination in complex acoustic environments [ 90 ].…”

“…The major achievements in disease modeling using a hiPSC-derived inner ear for genetic SNHL include the genes MYO7A, MYO15, and MERRF in HCs [ 70 , 89 , 90 ], and GJB2 and SLC26A4 (Pendred syndrome) in SCs [ 106 , 120 , 121 , 122 , 123 , 124 ] ( Table 2 ). These studies defined the molecular mechanisms involving each gene and showed the cellular effects of each mutation.…”