今日の臨床サポート

老人性難聴

著者: 山岨達也 東京大学医学部附属病院 耳鼻咽喉科・聴覚音声外科

監修: 森山寛 東京慈恵会医科大学附属病院

著者校正/監修レビュー済:2021/02/10
患者向け説明資料

概要・推奨   

  1.  軽度難聴でも生活上の不自由を感じる場合、早期の補聴器装用を勧める。
  1.  補聴器については補聴器相談医に紹介する。
  1.  補聴効果の乏しい場合は人工内耳の適応があり、専門医に紹介する。
薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
山岨達也 : 特に申告事項無し[2021年]
監修:森山寛 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 定期レビューを行い、疾患頻度をupdateした。また、語音聴取成績、補聴器装用のタイミング、人工内耳手術の適応について修正した。
 

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 老人性難聴とは高齢者にみられる聴力の生理的な年齢変化により生じる難聴、すなわち加齢に伴って徐々に進行する両側性感音難聴である[1]
  1. 純音聴力検査では高音域から聴力閾値が上昇し、徐々に低・中音域まで障害される。
 
老人性難聴(軽度難聴 高音急墜型)

高音急墜型感音難聴のオージオグラム(軽度難聴)

出典

img1:  著者提供
 
 
 
老人性難聴(軽度難聴 高音漸傾型)

高音漸傾型感音難聴のオージオグラム(軽度難聴)

出典

img1:  著者提供
 
 
 
老人性難聴(中等度難聴 水平型・高音漸傾型)

水平型感音難聴のオージオグラム(中等度難聴)

出典

img1:  著者提供
 
 
 
  1. 聴覚情報の中枢処理の遅延、音源定位の悪化などが特徴である[2][3]
  1. 騒音下での聴取が困難となり、難聴が進むと子音の弁別に困難を覚え、さらに進行すると母音の弁別も困難となりコミュニケーションが高度に障害される[2][3]
  1. 難聴の発現時期や程度には個人差が大きい。同年代では女性が男性より難聴が軽い傾向にある[1]
  1. 頻度については65歳以上の25~40%、75歳以上の40~66%、85歳以上の80%以上と推定されている[4]
  1. わが国での老人性難聴の正確な頻度は不明であるが、良聴耳の平均聴力が25 dB を超えたものと定義すると、65歳以上で1,900万人が罹患していると推定される。
問診・診察のポイント  
問診
  1. 難聴の有無、その経緯、性状

これより先の閲覧には個人契約のトライアルまたはお申込みが必要です。

最新のエビデンスに基づいた二次文献データベース「今日の臨床サポート」。
常時アップデートされており、最新のエビデンスを各分野のエキスパートが豊富な図表や処方・検査例を交えて分かりやすく解説。日常臨床で遭遇するほぼ全ての症状・疾患から薬剤・検査情報まで瞬時に検索可能です。

まずは15日間無料トライアル
本サイトの知的財産権は全てエルゼビアまたはコンテンツのライセンサーに帰属します。私的利用及び別途規定されている場合を除き、本サイトの利用はいかなる許諾を与えるものでもありません。 本サイト、そのコンテンツ、製品およびサービスのご利用は、お客様ご自身の責任において行ってください。本サイトの利用に基づくいかなる損害についても、エルゼビアは一切の責任及び賠償義務を負いません。 また、本サイトの利用を以て、本サイト利用者は、本サイトの利用に基づき第三者に生じるいかなる損害についても、エルゼビアを免責することに合意したことになります。  本サイトを利用される医学・医療提供者は、独自の臨床的判断を行使するべきです。本サイト利用者の判断においてリスクを正当なものとして受け入れる用意がない限り、コンテンツにおいて提案されている検査または処置がなされるべきではありません。 医学の急速な進歩に鑑み、エルゼビアは、本サイト利用者が診断方法および投与量について、独自に検証を行うことを推奨いたします。

文献 

著者: George A Gates, John H Mills
雑誌名: Lancet. 2005 Sep 24-30;366(9491):1111-20. doi: 10.1016/S0140-6736(05)67423-5.
Abstract/Text The inevitable deterioration in hearing ability that occurs with age--presbycusis--is a multifactorial process that can vary in severity from mild to substantial. Left untreated, presbycusis of a moderate or greater degree affects communication and can contribute to isolation, depression, and, possibly, dementia. These psychological effects are largely reversible with rehabilitative treatment. Comprehensive rehabilitation is widely available but underused because, in part, of social attitudes that undervalue hearing, in addition to the cost and stigma of hearing aids. Remediation of presbycusis is an important contributor to quality of life in geriatric medicine and can include education about communication effectiveness, hearing aids, assistive listening devices, and cochlear implants for severe hearing loss. Primary care physicians should screen and refer their elderly patients for assessment and remediation. Where hearing aids no longer provide benefit, cochlear implantation is the treatment of choice with excellent results even in octogenarians.

PMID 16182900  Lancet. 2005 Sep 24-30;366(9491):1111-20. doi: 10.1016/・・・
著者: Bevan Yueh, Nina Shapiro, Catherine H MacLean, Paul G Shekelle
雑誌名: JAMA. 2003 Apr 16;289(15):1976-85. doi: 10.1001/jama.289.15.1976.
Abstract/Text CONTEXT: Hearing loss is the third most prevalent chronic condition in older adults and has important effects on their physical and mental health. Despite these effects, most older patients are not assessed or treated for hearing loss.
OBJECTIVE: To review the evidence on screening and management of hearing loss of older adults in the primary care setting.
DATA SOURCES AND STUDY SELECTION: We performed a search from 1985 to 2001 using MEDLINE, HealthSTAR, EMBASE, Ageline, and the National Guideline Clearinghouse for articles and practice guidelines about screening and management of hearing loss in older adults, as well as reviewed references in these articles and those suggested by experts in hearing impairment.
DATA EXTRACTION: We reviewed articles for the most clinically important information, emphasizing randomized clinical trials, where available, and identified 1595 articles.
DATA SYNTHESIS: Screening tests that reliably detect hearing loss are use of an audioscope, a hand-held combination otoscope and audiometer, and a self-administered questionnaire, the Hearing Handicap Inventory for the Elderly-Screening version. The value of routine screening for improving patient outcomes has not been evaluated in a randomized clinical trial. Screening is endorsed by most professional organizations, including the US Preventive Services Task Force. While most hearing loss in older adults is sensorineural and due to presbycusis, cerumen impaction and chronic otitis media may be present in up to 30% of elderly patients with hearing loss and can be treated by the primary care clinician. In randomized trials, hearing aids have been demonstrated to improve outcomes for patients with sensorineural hearing loss. Nonadherence to use of hearing aids is high. Prompt recognition of potentially reversible causes of hearing loss, such as sudden sensorineural hearing loss, is important to maximize the possibility of functional recovery.
CONCLUSION: While untested in a clinical trial, older adults can be screened for hearing loss using simple methods, and effective treatments exist and are available for many forms of hearing loss.

PMID 12697801  JAMA. 2003 Apr 16;289(15):1976-85. doi: 10.1001/jama.28・・・
著者: Tatsuya Yamasoba, Shinichi Someya, Chikako Yamada, Richard Weindruch, Tomas A Prolla, Masaru Tanokura
雑誌名: Hear Res. 2007 Apr;226(1-2):185-93. doi: 10.1016/j.heares.2006.06.004. Epub 2006 Jul 25.
Abstract/Text Mitochondrial DNA (mtDNA) mutations/deletions are considered to be associated with the development of age-related hearing loss (AHL). We assessed the role of accumulation of mtDNA mutations in the development of AHL using Polg(D257A) knock-in mouse, which exhibited increased spontaneous mtDNA mutation rates during aging and showed accelerated aging primarily due to increased apoptosis. They exhibited moderate hearing loss and degeneration of the hair cells, spiral ganglion cells and stria vascularis by 9 month of age, while wild-type animals did not. We next examined if mitochondrial damage induced by systemic application of germanium dioxide caused progressive hearing loss and cochlear damage. Guinea pigs and mice given germanium dioxide exhibited degeneration of the muscles and kidney and developed hearing loss due to degeneration of cochlear tissues, including the stria vascularis. Calorie restriction, which causes a metabolic shift toward increased energy metabolism in some organs, has been shown to attenuate AHL and age-related cochlear degeneration and to lower quantity of mtDNA deletions in the cochlea of mammals. Together these findings indicate that decreased energy metabolism due to accumulation of mtDNA mutations/deletions and decline of respiratory chain function play an important role in the manifestation of AHL.

PMID 16870370  Hear Res. 2007 Apr;226(1-2):185-93. doi: 10.1016/j.hear・・・
著者: Shinichi Someya, Jinze Xu, Kenji Kondo, Dalian Ding, Richard J Salvi, Tatsuya Yamasoba, Peter S Rabinovitch, Richard Weindruch, Christiaan Leeuwenburgh, Masaru Tanokura, Tomas A Prolla
雑誌名: Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19432-7. doi: 10.1073/pnas.0908786106. Epub 2009 Nov 9.
Abstract/Text Age-related hearing loss (AHL), known as presbycusis, is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. The molecular mechanisms underlying AHL are unknown, and currently there is no treatment for the disorder. Here we report that C57BL/6J mice with a deletion of the mitochondrial pro-apoptotic gene Bak exhibit reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, and prevention of AHL. Oxidative stress induces Bak expression in primary cochlear cells, and Bak deficiency prevents apoptotic cell death. Furthermore, a mitochondrially targeted catalase transgene suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Oral supplementation with the mitochondrial antioxidants alpha-lipoic acid and coenzyme Q(10) also suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Thus, induction of a Bak-dependent mitochondrial apoptosis program in response to oxidative stress is a key mechanism of AHL in C57BL/6J mice.

PMID 19901338  Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19432-7. ・・・
著者: Shinichi Someya, Tatsuya Yamasoba, Richard Weindruch, Tomas A Prolla, Masaru Tanokura
雑誌名: Neurobiol Aging. 2007 Oct;28(10):1613-22. doi: 10.1016/j.neurobiolaging.2006.06.024. Epub 2006 Aug 4.
Abstract/Text Presbycusis is characterized by an age-related progressive decline of auditory function, and arises mainly from the degeneration of hair cells or spiral ganglion (SG) cells in the cochlea. Here we show that caloric restriction suppresses apoptotic cell death in the mouse cochlea and prevents late onset of presbycusis. Calorie restricted (CR) mice, which maintained body weight at the same level as that of young control (YC) mice, retained normal hearing and showed no cochlear degeneration. CR mice also showed a significant reduction in the number of TUNEL-positive cells and cleaved caspase-3-positive cells relative to middle-age control (MC) mice. Microarray analysis revealed that CR down-regulated the expression of 24 apoptotic genes, including Bak and Bim. Taken together, our findings suggest that loss of critical cells through apoptosis is an important mechanism of presbycusis in mammals, and that CR can retard this process by suppressing apoptosis in the inner ear tissue.

PMID 16890326  Neurobiol Aging. 2007 Oct;28(10):1613-22. doi: 10.1016/・・・
著者: Shinichi Someya, Wei Yu, William C Hallows, Jinze Xu, James M Vann, Christiaan Leeuwenburgh, Masaru Tanokura, John M Denu, Tomas A Prolla
雑誌名: Cell. 2010 Nov 24;143(5):802-12. doi: 10.1016/j.cell.2010.10.002.
Abstract/Text Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals.

Copyright © 2010 Elsevier Inc. All rights reserved.
PMID 21094524  Cell. 2010 Nov 24;143(5):802-12. doi: 10.1016/j.cell.20・・・

ページ上部に戻る

戻る

さらなるご利用にはご登録が必要です。

こちらよりご契約または優待日間無料トライアルお申込みをお願いします。

(※トライアルご登録は1名様につき、一度となります)


ご契約の場合はご招待された方だけのご優待特典があります。

以下の優待コードを入力いただくと、

契約期間が通常12ヵ月のところ、14ヵ月ご利用いただけます。

優待コード: (利用期限:まで)

ご契約はこちらから