Corticosteroid Therapy for Hearing and Balance Disorders
This review addresses the current status of steroid therapies for hearing and vestibular disorders and how certain misconceptions may be undermining the efficacy in restoring normal ear function, both experimentally and clinically. Specific misconceptions addressed are that steroid therapy is not effective, steroid‐responsive hearing loss proves an underlying inflammatory problem in the ear, and steroids only have application to the hearing disorders listed below. Glucocorticoid therapy for hearing and balance disorders has been employed for over 60 years. It is recommended in cases of sudden hearing loss, Meniére's disease, immune‐mediated hearing loss, and any vestibular dysfunction suspected of having an inflammatory etiology. The predominant steroids employed today are dexamethasone, prednisone, prednisolone, and methylprednisolone. Despite years of use, little is known of the steroid responsive mechanisms in the ear that are influenced by glucocorticoid therapy. Furthermore, meta‐analyses and clinical study reviews occasionally question whether steroids offer any benefit at all. Foremost in the minds of clinicians is the immune suppression and anti‐inflammatory functions of steroids because of their efficacy for autoimmune hearing loss. However, glucocorticoids have a strong binding affinity for the mineralocorticoid (aldosterone) and glucocorticoid receptors, both of which are prominent in the ear. Because the auditory and vestibular end organs require tightly regulated endolymph and perilymph fluids, this ion homeostasis role of the mineralocorticoid receptor cannot be overlooked in both normal and pathologic functions of the ear. The function of the glucocorticoid receptor is to provide anti‐inflammatory and antiapoptotic signals by mediating survival factors. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.
Document Type: Research Article
Affiliations: 1: Oregon Hearing Research Center, Department of Otolaryngology/Head & Neck Surgery, Oregon Health & Science University, Portland, Oregon, USA 2: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden
Publication date: November 1, 2012