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Genetic Testing for Hearing Loss

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Objectives

 Indications for a genetic evaluation for hearing loss  Common genetic syndromes associated with hearing

loss

 Benefits and limitations of genetic testing for hearing

loss

(3)

Why have a genetic evaluation ?

 Why did it happen ?  Can it happen again ?

(4)

Etiology

of Hearing Loss

(5)
(6)

40% of deafness is “non-genetic” BUT

 Teratogens

 known genetic susceptibility  Congenital/perinatal infections

 not all that are exposed have effects; genetic variation?  Prematurity

 hyperbilirubinemia  low birthweight

 NICU, ventilation

 what is the underlying cause of LBW, neonatal distress?  Ototoxic medications

 known genetic susceptibility  Meningitis

(7)

Terminology

 DFN (for DeaFNess)

 DFNA - autosomal dominant  DFNB - autosomal recessive  DFN - X-linked

(8)
(9)

Autosomal Recessive Nonsyndromic Hearing Loss

 Congenital severe to profound type is most common  Genetic studies have identified >60 different loci, with

genes identified for only some of the loci

(10)
(11)

DFNB1

GJB2 gene codes for Connexin 26 protein GJB6 gene codes for Connexin 30 protein

 Most common cause of nonsyndromic, autosomal

recessive, congenital hearing loss (50%)

 Overall Connexin 26 mutations accounts for 20% of

patients with nonsyndromic sensorineural hearing loss

98% of individuals with DFNB1 have two GJB2

mutations

(12)

CX 26 CX 30 CX 26 CX 30

Compound Heterozygosity

(Digeneic Inheritance)

(13)

Connexin 26 (DFNB1 / GJB2)

 Phenotype

 non-syndromic

 normal vision and vestibular

function

 non-progressive (2/3)  hearing loss = mild to

profound with intra- and inter- familial variability

 few kindreds are progressive

and asymmetric

 2 common mutations :

 35delG (85% N. Europeans)  167delT (Jewish)

 235delC mutation (Chinese)

(14)

DFNB1 testing strategy

 First screen for 35delG deletion in Connexin 26  If negative or find only one mutation

 DNA sequencing of Connexin 26

DFNB1 is not complete unless screening for the splice site

mutation (exon 1 of GJB2) and the large GJB6-containing deletions is included

 If DNA sequencing of Connexin 26 is normal

 Targeted mutation analysis of Connexin 30

 Two large deletions GJB6-D13S1830 and GJB6-D13S1854  GJB6-D13S1830 is the most common GJB6 mutation associated

(15)
(16)

List of autosomal recessive hearing loss loci

Locus Name Gene Symbol Onset Type

DFNB1 GJB2 Prelingual 1 Usually stable

GJB6

DFNB2 MYO7A Prelingual, postlingual Unspecified DFNB3 MYO15 Prelingual Severe to profound; stable DFNB4 SLC26A4 Prelingual, postlingual Stable, progressive DFNB6 TMIE

Prelinqual Severe to profound; stable DFNB7/11 TMC1

DFNB8/10 TMPRSS3 Postlingual 2, Prelingual Progressive, stable

DFNB9 OTOF Prelingual Usually severe to profound; stable DFNB12 CDH23 Prelingual Severe to profound; stable DFNB16 STRC Prelingual Severe to profound; stable DFNB18 USH1C Prelingual Severe to profound; stable DFNB21 TECTA Prelingual Severe to profound; stable DFNB22 OTOA Prelingual Severe to profound; stable DFNB23 PCDH15 Prelingual Severe to profound; stable DFNB24 RDX Prelingual Severe to profound; stable DFNB25 GRXCR1 Prelingual Moderate to profound; progressive DFNB28 TRIOBP Prelingual Severe to profound; stable DFNB29 CLDN14 Prelingual Severe to profound; stable DFNB30 MYO3A Prelingual Severe to profound; stable DFNB31 DFN31 Prelingual —

DFNB32/82 GPSM2 Prelingual Severe to profound; stable DFNB35 ESRRB Unknown Severe to profound DFNB36 ESPN Prelingual —

DFNB37 MYO6 Prelingual —

(17)
(18)

Autosomal Dominant NSHL

 Usually post-lingual

 Usually progressive (onset in 2nd or 3rd decades)  Accounts for 15% of cases of nonsyndromic hearing

loss

 In general, onset is postlingual and is progressive  Some forms also include vestibular dysfunction  Over 40 genes have been identified

(19)
(20)

Mitochondrial gene associated with HL

 12S rRNA gene mutation

 A1555G confers a sensitivity to aminoglycosides

HL within days of even a single dose

 40% of those not exposed develop HL by 30 years of age

 Isolated sensorineural hearing loss.

 Variable age of onset: congenital - 7th decade.  Flat, sloping or high frequency hearing loss.  Progressive hearing loss.

 Mild-to-profound sensorineural hearing loss with or

without a history of aminoglycoside exposure, or

 Hearing loss that appears to be consistent with

(21)
(22)

Syndromic Hearing Loss

 Is more than one organ system involved?

 Are there similar issues in family members?

(23)

Genetic Syndromes with Hearing Loss as a

Major Feature

 Alport

Branchial-Oto-Renal

 Jervell and Lange-Nielsen  Neurofibromatosis type 2  Pendred

(24)

Branchio-oto-renal Syndrome (BOR)

 Estimated to occur in 2%

of children with

congenital hearing loss

 Ear: pits/tags,

abnormalities of the

external, middle, or inner ear

 Hearing loss: can be mild

to profound,

sensorineural, conductive, or mixed

 Branchial arch: sinus or

cyst in neck

 Renal: agenesis,

hypoplasia, or dysgenesis

(25)

Stickler Syndrome

 Characterized by cleft

palate, micrognathia, severe myopia, retinal detachments, cataracts, short stature, and

hypermobility

 SNHL in about 40%,

conductive can also be seen

 Most autosomal dominant,

although can be recessive

 Mutations in one of four

collagen genes (COL2A1)

 At risk for retinal

detachment, arthritis

(26)

3

34 27 16

Accident Seizures

Vision prob Deaf in one ear

Thick glasses,

hearing aids, joint prob

(27)

Waardenburg Syndrome

 Accounts for 3% of childhood

hearing impairment

 Incidence is 1 in 4000 live

births

 AD – PAX 3 gene mutation  May have unilateral or

bilateral SNHL

 Pigmentary features include:

 white forelock

 heterochromia irides

 premature graying

 vitiligo

 Craniofacial features include:

 dystopia canthorum (lateral

displacement of inner canthus of eye)

 broad nasal root and synophrys

 (people may dye their hair –

therefore ask specifically about white forelock)

(28)

Alport Syndrome

 Hearing, vision, and renal involvement

 Blood in urine (hematuria) often first symptom

 Typically progresses to renal failure

 HL may not become evident until the second decade of

life, 80-90% by age 40

 Anterior lenticonus - eye finding

 85% of cases are X-linked, with some dominant and

(29)

Neurofibromatosis Type 2

 Affects 1 in 40,000

 Hallmark feature is vestibular schwannoma - tumor on

8th nerve

 Symptoms include tinnitis, hearing loss, balance

problems, occasional facial palsy

 Other features include tumors on brain or spinal cord,

early cataracts

(30)

Usher Syndrome

 Prevalence of 3.5 per 100,000 population; 1 in 70 carrier frequency  Autosomal recessive – 11 loci, 2

 Association of hearing loss with retinitis pigmentosa  At least 11 loci

 2 identified

 Progressive vision loss - night blindness and loss of peripheral vision

noted in second decade

 Electroretinography can identify abnormalities in younger children

 - Three subtypes

 Type 1: congenital bilateral profound HL and abnormal vestibular

function

 Type 2: moderate HL and normal vestibular function

(31)

Pendred Syndrome

 ~1/7500  Congenital severe-profound SNHL  Enlarged vestibular aqueduct or Mondini dysplasia on temporal bone CT

 Thyroid goiter - develops

in adolescence or adulthood

 Autosomal recessive  SLC26A4 gene

 Mutations in this gene may

cause up to 5-10% of congenital hearing loss

(32)

Jervell and Lange-Nielsen Syndrome

3

6

fainting sudden death

long QT JLN

 Profound SNHL and

syncopal episodes resulting from cardiac conduction defect

 ECG reveals large T waves

and prolonged QT interval

 Can result in sudden death

 ECG should be done on all

children with uncertain etiology of hearing loss

 Autosomal recessive

(33)

 Family history

 Three generation family

history

 Age onset hearing loss

 Description of hearing loss  Heritable / non-heritable  Conductive / neurosensory / mixed  Unilateral / bilateral  Symmetric / asymmetric  Congenital / acquired  Progressive / stable / fluctuant  Isolated / syndromic

(34)

Evaluation for Syndromic Hearing Loss

 Visual anomalies :

 heterochromia, retinitis pigmentosa, myopia, retinal detachment, early cataracts,

night blindness

 Dysmorphology:

 preauricular pits, ear anomalies, cleft lip/palate, dental anomalies, pits, lumps or

fistulae on the neck

 Endocrine work up:

 thyroid disorders and diabetes

 Cardiac work up:

 syncope, sudden death, prolonged QT interval, fainting spells, CHD

 Renal abnormalities

 hematuria, proteinuria, structural defects

 Skin abnormalities

 abnormal pigmentation, premature graying, white forelock, dry skin/keratoderma

 Bone:

(35)

Medical Genetic Evaluation of Hearing Loss

Smith et al 1998

 Stage 1 o Medical Genetics o Audiology o Otolaryngology  Stage 2 o Vestibular o Ophthalmology o CT of temporal bones o Urinalysis/serum creatinine o Serology  Stage 3

o Perchlorate discharge (if CT abnormal) o DNA

(36)

Genetic counseling for hearing loss

 "In contrast to the medical model which considers

deafness to be a pathologic condition, many deaf people do not consider themselves to be

handicapped but define themselves as being part of a distinct cultural group with its own language,

(37)

References

 Medical genetic evaluation for the etiology of hearing loss in children. Smith SD, Kimberling WJ, Schaefer GB, Horton MB, Tinley ST. J Commun Disord. 1998 Sep-Oct;31(5):371-88; quiz 388-9. Review.

 Genetics Evaluation Guidelines for the Etiologic Diagnosis of Congenital Hearing Loss. Genetic Evaluation of Congenital Hearing Loss Expert Panel. ACMG statement. ACMG.Genet Med. 2002 May-Jun;4(3):162-71.  Genetests.org

 A prospective, longitudinal study of the impact of GJB2/GJB6 genetic testing on the beliefs and attitudes of parents of deaf and hard-of-hearing infants. Palmer CG, Martinez A, Fox M, Zhou J, Shapiro N, Sininger Y, Grody WW,

Schimmenti LA. Am J Med Genet A. 2009 Jun;149A(6):1169-82.

 Genetic counseling of the deaf. Medical and cultural considerations.Arnos KS, Israel J, Cunningham M. Ann N Y Acad Sci. 1991;630:212-22.

 Deaf adults' reasons for genetic testing depend on cultural affiliation: results from a prospective, longitudinal genetic counseling and testing study. Boudreault P, Baldwin EE, Fox M, Dutton L, Tullis L, Linden J, Kobayashi Y, Zhou J, Sinsheimer JS, Sininger Y, Grody WW, Palmer CG. Deaf Stud Deaf Educ. 2010 Summer;15(3):209-27. Epub 2010 May 20.

 Attitudes of deaf adults toward genetic testing for hereditary deafness. Middleton A, Hewison J, Mueller RF. Am J Hum Genet. 1998 Oct;63(4):1175-80.

 Slide acknowledgementt

 1. Dr.Bradley Schaefer, Geneticist, UAMS, KUSM-W

References

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