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Risk of developing sudden sensorineural hearing loss in patients with hepatitis B virus
infection: A population-based study

By Yao-Te Tsai, MD; Ku-Hao Fang, MD; Yao-Hsu Yang, MD, MSc; Meng-Hung Lin,
PhD; Pau-Chung Chen, MD, PhD; Ming-Shao Tsai, MD; Cheng-Ming Hsu, MD

Introduction

The U.S. National Institute on Deafness and Other Communication Disorders defines sudden
sensorineural hearing loss (SSNHL) as an idiopathic hearing loss of greater than 30 dB in at least
three contiguous audiometric frequencies, occurring over a period of 72 hours or less.1 SSNHL
accounts for 1% of all sensorineural hearing loss cases, with an overall slight male
preponderance,2 and its incidence has been reported to range from 5 to 20 new cases per 100,000
population per year.3,4 Despite detailed investigation, a specific etiology can be identified in less
than 10% of patients with SSNHL, and it is thought that most SSNHL is multifactorial in
etiology.

In recent years, a variety of diseases were identified to be associated with a higher risk of
SSNHL, including diabetes mellitus,5 systemic lupus erythematosus,6 chronic kidney disease,7
chronic otitis media,8 osteoporosis,9 psoriasis,10 iron deficiency anemia,11
hypercholesterolemia,12 human immunodeficiency virus infection, 13 and acquired and inherited
cardiovascular risk factors.14

Currently, the proposed pathogenesis includes viral infection, vascular insufficiency,

autoimmune disease, rupture of the inner ear membrane, and central nervous system
anomalies.15 Among these, there is considerable evidence to support viral infections in the
pathogenesis of SSNHL. In patients with SSNHL, there was a significantly higher incidence of
seroconversion to measles, mumps, rubella, rubeola, varicella-zoster, herpes simplex,
cytomegalovirus, and influenza viruses types A and B.

Some viruses also were directly identified in the inner ear by either perilymph culture or
immunofluorescent methods.16-22 Loss of cochlear neurons, hair cells, and supporting cells, as
well as atrophy of the tectorial membrane or stria vascularis, have been revealed to be the same
in patients with SSNHL and patients infected by mumps, measles, and rubella on the basis of
temporal bone histopathology findings.23 Yoon et al declared that loss of cochlear neurons was
the main histopathology finding in SSNHL of viral infection.24

Hepatitis B virus (HBV) infection is frequent, with about 400 million individuals infected
worldwide.25 Acute necroinflammatory liver disease caused by HBV infection can lead to
cirrhosis and liver cancer. The HBV is omnipresent in host liver, but at the same time it can
cause continuous infections in many other organs, including the hearing system.

A previous study described a higher prevalence of chronic sensorineural hearing loss in patients
with HBV infection,26 and several case reports also indicate that SSNHL might be the
complication of acute exacerbation of chronic HBV infection and HBV vaccination.27-30
Moreover, much histopathologic evidence, including middle/inner ear vasculitis, supports the
concept that HBV-associated polyarteritis nodosa can play a role in contributing to SSNHL. 31-34
The results of these cited studies inspired us to investigate the relationship between the HBV
infection and SSNHL.

To the best of our knowledge, there is no cohort study or case series that has investigated the risk
of SSNHL in patients with HBV infection. To identify the effect of HBV infection on the risk of
SSNHL, we did a population-based cohort study using data from a nationwide medical insurance
claims database in Taiwan. We also investigated whether, in addition to the HBV, the incidence
of SSNHL increases with the comorbidities of diabetes mellitus, coronary artery disease, chronic
renal disease, and hypertension.`

Patients and methods

Approval of this study was obtained from the Institutional Review Board of Chang Gung
Memorial Hospital.

Data source. In Taiwan, the National Health Insurance (NHI) program is a nationwide
healthcare system launched in 1995 that provides medical services for the country's 23.5 million
residents. It represents more than 99% of the population in Taiwan and records clinical diagnoses
in accordance with the International Classification of Diseases, Ninth Revision, Clinical
Modification (ICD-9-CM) codes.

All claims data are collected in the National Health Insurance research database (NHIRD), which
contains encrypted patient identification numbers, details of prescription drugs, codes for
diagnoses and clinical procedures, admission and discharge dates, and fundamental
sociodemographic information including sex and date of birth. Confidentiality assurances were
addressed by abiding by the data regulations of the bureaus of the NHI.35

All the data used in this study originated from the Longitudinal Health Insurance Database 2005,
which is a subset of the NHIRD that includes all the claims data (from 1997 to 2008) of 1 million
individuals who were randomly selected from the 2005 registry of beneficiaries (n = 23.72
million) of the NHI program, representing approximately 5% of all enrolled persons in Taiwan.
The NHIRD uses a multistage, stratified, systematic sampling design to eliminate all statistically
significant differences in age or sex between the sampled group and beneficiaries of the NHI
program.

Study design. This retrospective cohort study was conducted in two study groups: an HBV group
and a matched no-viral-hepatitis control group. The HBV group included patients with a
diagnosis of HBV infection (ICD-9-CM code 070.2, 070.3, and V02.61). Subjects without
medical claims for viral hepatitis but matched for sex, age, and index date were selected
randomly for the control group.

The index date for the HBV patients was the date of their first registration of having HBV
infection. The year of the HBV patient's index date also was used to create the index date for
each control subject. The A-code was also used to define the diseases because it was used in
Taiwan before the ICD-9 code.

We selected patients aged 18 years and older who had received a first-time diagnosis of SSNHL
(ICD-9-CM code 388.2) from an otolaryngologist. To increase diagnostic validity, we only
included patients who had at least two SSNHL diagnoses in ambulatory visits or one SSNHL
diagnosis while hospitalized. The inclusion criteria demanded at least two SSNHL diagnoses in
ambulatory care settings because the management of SSNHL always needed sequential visits
within the same episode in Taiwan. We defined the first ambulatory care visit or hospitalization
for the treatment of SSNHL as the index date for cases.

To identify the association between the occurrence of SSNHL and the disease progress of HBV,
only patients with newly diagnosed HBV from 2000 to 2008 were included. Patients diagnosed
with SSNHL before the index date of HBV infection were excluded.

Comorbidities developing before the index date were defined, including coronary artery disease
(ICD-9-CM code 410-414, A270, A279), diabetes mellitus (ICD-9-CM code 250.xx and A-code
A-181), chronic renal disease (ICD-9-CM code 582-588), and hypertension (ICD-9-CM code
401-405). Comorbidities were identified either through a diagnosis made during admission or
from three or more ambulatory care claims.

Both the HBV and control groups were selected from claims made during 2000 to 2008 and
followed up until the end of 2013, for a minimum of 5 years of follow-up, to determine the
incidence of SSNHL, or they were excluded due to death.

Statistical analysis. Descriptive statistical analyses with the Pearson chi-square test were
performed to compare the differences in demographic characteristics and comorbidities between
the HBV group and control group. The incidence rate was calculated as the number of SSNHL
cases diagnosed in the follow-up period, divided by the total person-years for each group by sex,
age, and number of follow-up years.

The risk of SSNHL was compared between the HBV group and the control group by estimating
the incidence rate ratio (IRR) with Poisson regression. The risk of developing SSNHL associated
with comorbidities-including coronary artery disease, diabetes mellitus, chronic renal disease,
and hypertension-was estimated using the Cox proportional hazard models. The Cox
proportional hazard regression analysis and Kaplan-Meier analysis were used to calculate the
cumulative incidence rates of SSNHL in the two cohorts. The log-rank test was used to analyze
the differences in the incidence curves between two groups.

All analyses were performed using the SAS version 9.4 (SAS Institute; Cary, N.C.), and the
statistical significance was set at two-sided, p < 0.05.
Results

Incidence of SSNHL by patient characteristics. Between the years 2000 and 2008, 33,234
patients aged 18 years or older with HBV met the eligibility criteria based on the claims data. An
additional 132,936 subjects aged 18 years or older without viral hepatitis were randomly selected
for the control group. The demographic characteristics for patients with HBV and the control
group were similar in sex, age distribution, urbanized level, and monthly income (table 1).

Table 1. Demographic characteristics and comorbidities of HBV patients and control

subjects

HBV (n = Controls (n =
Variable 33,234) n 132,936) n p Value
(%) (%)
Key: HBV = hepatitis B virus; SSNHL = sudden
sensorineural hearing loss; CAD = coronary artery disease;
DM = diabetes mellitus; CRD = chronic renal disease; HTN =
hypertension; NT = new Taiwan dollar.
Sex      
19,061
Male   76,244 (57.4) 1.000
(57.4)
14,173
Female   56,692 (42.6)  
(42.6)
Age (yr)      
9,968
18-34   39,872 (30.0) 1,000
(30.0)
12,616
35-49   50,464 (38.0)  
(38.0)
7,697
50-64   30,788 (23.2)  
(23.2)
≥65   2,953 (8.9) 11,812 (8.9)  
SSNHL      
Yes   279 (0.8) 845 (0.6) <0.0001
32,955 132,091
No    
(99.2) (99.4)
Baseline comorbidities      
CAD        
4,279
Yes     14,344 (10.8) <0.0001
(12.9)
28,955 118,592
No      
(87.1) (89.2)
DM        
5,389
Yes     17,368 (13.1) <0.0001
(16.2)
 HBV (n = Controls (n =
Variable 33,234) n 132,936) n p Value
(%) (%)
27,845 115,568
No      
(83.8) (86.9)
CRD        
Yes     2,593 (7.8) 7,199 (5.4) <0.0001
30,641 125,737
No      
(92.2) (94.6)
HTN        
9,259
Yes     34,184 (25.7) <0.0001
(27.9)
23,975
No     98,752 (74.3)  
(72.1)
Urbanized level      
9,703
1 (city)   38,812 (29.2) 1.000
(29.2)
16,352
2   65,408 (49.2)  
(49.2)
5,055
3   20,220 (15.2)  
(15.2)
4 (village)   2,124 (6.4) 8,496 (6.4)  
Monthly income      
4,172
NT   <15,840 16,688 (12.6) 1.000
(12.6)
9,809
NT 15,841-25,000   39,236 (29.5)  
(29.5)
13,320
NT ≥25,001   53,280 (40.1)  
(40.1)

There were significant baseline differences in the prevalence of comorbid coronary artery
disease, diabetes mellitus, chronic renal disease, and hypertension between the two groups as the
comorbidities were more frequent in the HBV group (all values of p < 0.0001).

The estimated risk of developing SSNHL based on age, sex, and the number of years of follow-
up between the HBV group and the control group was compared. By the end of the follow-up
period, the incidence of SSNHL was higher in the HBV group than in the control group (p <
0.0001; figure). The incidence of SSNHL was 1.33-fold higher in the HBV group than in the
control group (9.18 vs. 6.89 per 10,000 person-years; table 2).

Figure. Chart shows SSNHL incidence in the HBV group and the control group in Taiwan
(2000-2008).

Table 2. Risk of SSNHL for HBV patients and control subjects

  HBV Controls    
IRR
Person Person p
  n SSNHL Rate* n SSNHL Rate* (95%
years years Value
CI)
* Rate per
10,000
person-years;
incidence
rate ratio was
compared
using
Poisson
regression.

Key: HBV =
hepatitis B
virus;
SSNHL =
sudden
sensorineural
hearing loss;
IRR =
incidence
rate ratio;
CAD =
coronary
artery
disease; DM
= diabetes
mellitus;
CRD =
chronic renal
disease;
HTN =
hypertension.
1.33
1,225,622.
Overall 33,234 279 303,792.9 9.184 132,936 845 6.894 (1.16- <0.001
4
1.53)
Sex
1.38
Male   19,061 170 172,686.2 9.844 76,244 501 701,897.0 7.138 (1.16- <0.001
1.64)
1.27
Female   14,173 109 131,106.7 8.314 56,692 344 523,725.4 6.568 (1.02- 0.032
1.57)
Age (yr)
  HBV Controls    
IRR
Person Person p
  n SSNHL Rate* n SSNHL Rate* (95%
years years Value
CI)
1.61
18-34   9,968 55 94,810.7 5.801 39,872 134 372,792.4 3.594 (1.18- 0.003
2.21)
1.28
35-49   12,616 91 117,675.0 7.733 50,464 284 471,352.0 6.025 (1.01- 0.038
1.63)
1.41
50-64   7,697 103 68,358.0 15.068 30,788 302 283,001.0 10.671 (1.13- 0.003
1.77)
1.03
≥65   2,953 30 22,949.2 13.072 11,812 125 98,477.1 12.693 (0.69- 0.885
1.53)
Comorbidity
1.10
CAD   4,279 54 38,059.5 14.188 14,344 165 128,216.1 12.869 (0.81- 0.534
1.50)
1.05
DM   5,389 66 46,544.1 14.180 17,368 210 155,291.6 13.523 (0.80- 0.737
1.38)
1.53
CRD   2,593 40 22,312.9 17.927 7,199 74 63,129.4 11.722 (0.94- 0.3304
1.81)
1.13
HTN   9,259 103 81,563.8 12.628 34,184 345 309,447.1 11.149 (0.91- 0.2672
1.41)
Follow-up
(yr)
1.34
  <1 33,324 23 32,868.2 6.998 132,936 69 132,564.5 5.205 (0.83- 0.219
2.16)
1.34
1-3   32,658 60 64,728.2 9.270 132,151 181 262,511.3 6.895 (1.05- 0.047
1.80)
1.43
3-5   32,075 54 63,589.6 8.492 130,294 154 258,480.6 5.958 (1.13- 0.025
1,94)
1.29
  >5 31,146 142 142,607.0 9.957 128,029 441 572,066.0 7.709 (1.07- 0.008
1.56)
The incidence rates of SSNHL, as classified by age and follow-up years, were mostly higher in
the HBV group than in the control group. Significantly higher incidences of SSNHL were noted
in HBV patients aged 18 to 34, 35 to 49, and 50 to 64 (p = 0.003, 0.038, and 0.003, respectively)
compared to similarly aged patients in the control group (table 2). Notably, HBV patients in the
50 to 64 years of age subgroup showed the highest incidence of SSNHL and the highest adjusted
HR (HR = 2.351; 95% confidence interval [CI] = 1.935 to 2.855 (data available in table form
upon request from the corresponding author).

A stratified analysis of the duration of follow-up exhibited a significantly higher risk of

developing SSNHL in the HBV group compared with the control group when stratified by >1 to
3, >3 to 5, and >5 follow-up years (p = 0.047, 0.025, 0.008, respectively; table 2).

SSNHL and comorbidities. The multivariate Cox proportional hazard regression analysis with
sex, age, and comorbidities revealed an association with HBV and an adjusted SSNHL HR of
1.315 (95% CI = 1.142 to 1.498), where HR increased with age. Sex difference was found not to
be significant in the risk of SSNHL. Of the comorbidities, diabetes mellitus showed a significant
adjusted HR at 1.414 (95% CI = 1.209 to 1.645) during the follow-up period, and the HR was
less influenced by the time endpoints used.

To examine the effect of comorbidities, the IRRs were further calculated between the HBV
group and the control group for each comorbidity subgroup in table 2. The risk of SSNHL was
compared between the HBV group and the control group by estimating the IRR, which was not
significant in subgroup analysis for coronary artery disease, diabetes mellitus, chronic renal
disease, and hypertension (p = 0.534, 0.737, 0.330, and 0.267, respectively).

Discussion

Increased risk of developing SSNHL in HBV patients. The major finding in this study was that
patients with HBV diagnosed between the years 2000 and 2008 in Taiwan had a substantially
higher incidence of SSNHL compared with control subjects from the general population, with an
incidence rate ratio of 1.33 (95% CI = 1.16 to 1.53; table 2) and an adjusted HR of 1.315 (95%
CI = 1.142 to 1.498) calculated using a Cox proportional hazard regression model.

The patients with HBV infection in the 50 to 64 years of age subgroup had the highest incidence
of SSNHL and the highest adjusted HR. Several studies suggested that the incidence of SSNHL
was higher in the male subjects than in the female subjects.2,36 However, when sex was used as
a factor that resulted in SSNHL, we found it was not significant for HBV patients when
compared with control subjects.

Clinical implications. Our study points to meaningful diagnostic implications. By analyzing a

large-scale registry of 166,170 patients, a significant association between HBV infection and
subsequent occurrence of SSNHL was detected. After adjusting for covariables, the risk of
developing SSNHL was higher for HBV patients than individuals without viral hepatitis. We
suggest that clinicians should be aware of the increased risk of SSNHL in HBV patients,
especially in those more than 35 years old or diagnosed with HBV infection for more than 1
year.
It is important to counsel HBV patients to seek medical advice if there is any acute change in
their hearing for the early detection and timely treatment of SSNHL.

Association between HBV infection and hearing loss. The association between HBV infection
and SSNHL or chronic sensorineural hearing loss was not widely investigated in the literature. In
a case-control study of 192 patients, Nasab et al concluded that the incidence of chronic
sensorineural hearing loss was significantly higher in the HBV group than in controls.26 Also, it
has been reported that permanent or fluctuant sensorineural hearing loss developed rapidly after
hepatitis B vaccination, implying that HBV infection may contribute to acute and chronic
hearing impairment.27-30

Impact of underlying comorbidities. In this study, we observed that HBV infection was a risk of
developing SSNHL, but the underlying mechanism remains unclear because direct evidence is
lacking. However, we also found that comorbidities that could affect the microcirculation,
especially of the inner ear, were more frequent in HBV groups than in controls, which may
partially explain the increased risk of SSNHL in HBV patients. Shen et al proposed that HBV
infection with a high viral load, presence of liver cirrhosis, long duration of HBV, and alcoholic
steatosis are potential risk factors for the development of type 2 diabetes mellitus.37

Lin et al further demonstrated that diabetes mellitus was associated with an elevated risk of
SSNHL and the risk increased with the severity of diabetes. 5 Our study found that diabetes
mellitus is significantly more frequent in HBV patients, which may contribute to the increased
risk of developing SSNHL. Lin et al also proposed a significant association between chronic
kidney disease and an increased risk of SSNHL.7 Our study also demonstrated that chronic renal
disease is more frequent in HBV patients since glomerulonephritis is an important extrahepatic
manifestation of chronic HBV infection found in both adult and pediatric patients.38,39

Hypotheses regarding the correlation between HBV infection and SSNHL. The extrahepatic
manifestations of HBV that occur in up to 20% of the patients with both acute and chronic
infections may contribute to the development of SSNHL by circulatory inflammatory cytokines
or immune-mediated responses.

Interferon. In the published literature, most viral-hepatitis-associated SSNHL came from the use
of interferon (IFN) treatment in patients with chronic hepatitis C virus (HCV) infection; SSHNL
is encountered in approximately 1% of HCV patients receiving this therapy. 40 Görür et al
reported a similar finding, that administration of IFN-α led to sudden but reversible sensorineural
hearing loss in 9 of 27 patients with chronic HBV infection.41

Actually, host IFN-α secretion is a functionally distinct mechanism of CD8+ T cells that account
for control of HBV viral replication during infection.42 Both host immune and treatment-related
IFN might lead to SSNHL from direct ototoxicity, autoimmune response, or hematologic
changes with subsequent intracochlear hemorrhage. 43-45 Future studies may be conducted to
explore the association between the antiviral treatment and subsequent development of SSNHL
in patients with viral hepatitis.
Tumor necrosis factor. Tumor necrosis factor (TNF) is a cytokine involved in acute
inflammatory reactions. Several studies have indicated that the TNF-α system is activated in
patients with HBV as its level correlates with the histopathology index and can be used to assess
disease activity of HBV infection.46 TNF-α is also the primary upstream mediator in the cochlear
inflammatory response with well-documented ototoxicity.47,48

In an animal model, Scherer et al found that TNF-α markedly reduces cochlear blood flow via
activation of the vascular sphingosine-1-phosphate signaling.49 In a prospective, case-control
study of 43 patients with SSNHL, aged 35 to 67 years, Demirhan et al observed that patients
without treatment response showed significant higher values of TNF-α. 50 The level of plasma
TNF demonstrated diagnostic and prognostic value in SSNHL and immune-mediated
sensorineural hearing loss.51,52 These findings suggested that TNF may play a role between
HBV infection and the risk of SSNHL.

HBV-associated polyarteritis nodosa. Polyarteritis nodosa (PAN) is a systemic vasculitis

affecting the small and medium-sized arteries, and its pathogenesis has been attributed to the
immune-complex deposition with antigen excess.53 HBV-associated polyarteritis nodosa is a
typical form of PAN and has been considered to be the etiology in 36% of patients with PAN.54

SSNHL is one of the otologic manifestations of PAN, which may result from the immune-
complex deposition and activation of complement in the inner ear, or from vasculitis with
subsequent ischemia in the labyrinthine artery, based on histopathologic findings.31,32
Therefore, we assumed that HBV-associated PAN may be involved in the pathogenesis of
SSNHL in HBV patients.

Impact of disease duration on the risk of SSNHL. In our study, the incidence of SSNHL
increased with the duration of follow-up. Among the 279 patients with HBV who later developed
SSNHL, approximately half of the SSNHL events occurred later than 5 years after the HBV
infection (50.9%, n = 142). Only 8.2% of HBV patients developed SSNHL within the first
follow-up year. This finding indicates that clinicians should watch for the development of
SSNHL even 5 years after the initial diagnosis of HBV infection.

It is not clear why the association between HBV infection and SSNHL seems to be found mostly
in patients followed for more than 1 year. However, the duration between initial diagnosis and
subsequent development of SSNHL seemed to vary among different diseases. Lin et al reported
that 72.7% of patients with systemic lupus erythematosus developed SSNHL between 1 and 5
years of follow-up.6 In contrast, in patients with stroke, chronic kidney disease, chronic otitis
media, and diabetes mellitus, the risk of SSNHL significantly increased within the first year of
follow-up.5,7,8,55 These recent studies demonstrated that among different diseases, the risk of
SSNHL varied in terms of disease duration, suggesting the existence of differences in
pathogenesis.

Strengths and limitations of this study. The primary strength of this study is that it overcame the
difficulty of recruiting patients with a disease of low incidence, allowing us to investigate the
elevated risk of developing SSNHL in HBV patients in Taiwan. The advantages of this
population-based survey included its large sample size, minimal selection bias, and follow-up of
all cohort members. It also demonstrated increased statistical power with precise risk appraisal.

In Taiwan, the NHIRD has been reported to be a valid source for population-based research, with
regular examinations of the accuracy of medical coding and clinical records. 35 Nevertheless,
there are several limitations to our study.

First, the incidence of HBV could be underestimated because it was based on claims data.
However, it is also possible that the diagnosis of SSNHL was underestimated as patients with
HBV might have considered their hearing impairment to be age-related and hence did not
aggressively seek immediate evaluation.

Second, detailed information regarding the severity of hearing loss or other laboratory test
results, such as blood sugar levels and liver enzyme tests, were not available in the claims data.
Thus, the relationship between the severities and treatment outcomes of SSNHL and HBV
infection, as well as the level of disease control based on laboratory results among the study
subjects, cannot be evaluated.

Third, degrees of bias may occur because some suspected contributing risk factors for SSNHL
were not available from the insurance data, such as the use and dosages of potentially ototoxic
medications, personal history of alcohol and cigarette consumption, and preceding occupational
or recreational noise exposure. This resulted in a confounding covariate for which it is difficult to
adjust.

Finally, this population-based study is limited in exploring the underlying mechanism by which
HBV infection is associated with SSNHL. Although the results of our study reached statistical
significance and extend the spectrum in exploring the pathogenesis of SSNHL, we remind
readers to remember these limitations when interpreting the results of this study.

Conclusion

The current study determined that Taiwanese patients with HBV infection between 2000 and
2008 had a higher risk of developing SSNHL than did the matched control group, which could
serve as an early warning for acute hearing loss in HBV patients that might otherwise go
unrecognized. We also observed a sustained increase in the risk of SSNHL in patients older than
35 years or follow-up for more than 5 years.

Clinicians managing HBV patients should be aware of the potential risk of SSNHL and counsel
patients to seek medical advice if there is any acute change in their hearing ability.

Acknowledgment

The authors thank Professor I-Shun Huang for assistance in the study design and data
interpretation. We also would like to thank the Center of Excellence for Chang Gung Research
Datalink (CORPG6D0163) for comments on and assistance with data analysis.
 

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From the Department of Otorhinolaryngology-Head and Neck Surgery (Dr. Y-T Tsai, Dr. M-S
Tsai, and Dr. Hsu), the Department of Traditional Chinese Medicine (Dr. Yang), and the Center
of Excellence for Chang Gung Research Datalink (Dr. Lin), Chang Gung Memorial Hospital,
Chiayi, Taiwan; the Department of Otorhinolaryngology-Head and Neck Surgery, Chang Gung
Memorial Hospital, Linkou, Taiwan (Dr. Fang); and the Institute of Occupational Medicine and
Industrial Hygiene, National Taiwan University College of Public Health, Taipei, Taiwan (Dr.
Chen). The study described in this article was conducted at Chang Gung Memorial Hospital,
Chiayi, Taiwan.
Corresponding author: Cheng-Ming Hsu, MD, Department of Otolaryngology-Head and Neck
Surgery, Chang Gung Memorial Hospital, Chia-Yi, Taiwan: No. 6, W. Sec., Jiapu Rd., Puzi City,
Chiayi County 613, Taiwan, R.O.C. Email: kilikkilik121415@gmail.com
Ear Nose Throat J. 2018 October-November;97(10-11):E19

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