|Year : 2020 | Volume
| Issue : 3 | Page : 352-357
The relationship between rheumatoid arthritis disease and hearing loss
Marwa A El Reheem1, Tawfik A Elkholy2, Mohammed F Zidan2, Iman Eladawy2
1 Department of Internal Medicine, Faculty of Medicine for Girls, Al Azhar University, Cairo, Egypt
2 Department of Otorhinolaryngology, Faculty of Medicine for Girls, Al Azhar University, Cairo, Egypt
|Date of Submission||05-Mar-2020|
|Date of Decision||10-Mar-2020|
|Date of Acceptance||16-Mar-2020|
|Date of Web Publication||2-Oct-2020|
MD Iman Eladawy
Audio Vestibular Medicine, Lecturer of Audio Vestibular Medicine, Al-Azhar, Department of Otorhinolaryngology, Faculty of Medicine for Girls, Al Azhar University, Faculty of Medicine for Girls, Al-Azhar University, 6 Elkhabeer Street El-Zaytoun, Cairo, 11766
Source of Support: None, Conflict of Interest: None
Background Rheumatoid arthritis (RA) is one of the most common systemic autoimmune diseases, characterized by chronic persistent and progressive erosive polyarthritis, leading to irreversible joint disability and increased mortality. It is a disease that affects 1% of the population. The auditory system may be involved during the course of disease; however, the association of RA and hearing impairment (HI) has not been clearly defined.
Aim The aim of this work was to evaluate the pattern of HI in patients with RA and to examine the possible associations between RA and hearing loss.
Patients and methods A total of 55 patients with RA (mean age of 42.10±11.80 years; female sex: 100%) and 55 healthy controls (mean age of 40.92±8.70 years; female sex: 100%) were included in this study. The two groups were matched for age and sex (P>0.05). The mean RA duration is 88.10±27.39 months. Otoscopic examination was normal in all participants. HI was evaluated by pure tone audiometry and tympanometry including the static compliance and acoustic reflex threshold test. Complete medical history and thorough physical examination were taken along with full investigation (including rheumatoid factor, erythrocyte sedimentation rate, C-reactive protein, and the presence of anticyclic citrullinated peptide antibodies).
Results Both groups were comparable regarding age and sex. However, there was a significant increase of HI in the studied group when compared with control group (36.7 vs 3.3%, respectively). Audiometric tests revealed significant increase in the hearing threshold and increased air bone gap. The immitancemetry revealed decrease of static compliance and significant increase of average acoustic reflex in the study group when compared with the control group.
Conclusion Hearing loss is statistically increased in RA, and disease activity is usually associated with HI.
Keywords: hearing loss, pure tone audiometry, rheumatoid arthritis, tympanometry
|How to cite this article:|
El Reheem MA, Elkholy TA, Zidan MF, Eladawy I. The relationship between rheumatoid arthritis disease and hearing loss. Sci J Al-Azhar Med Fac Girls 2020;4:352-7
|How to cite this URL:|
El Reheem MA, Elkholy TA, Zidan MF, Eladawy I. The relationship between rheumatoid arthritis disease and hearing loss. Sci J Al-Azhar Med Fac Girls [serial online] 2020 [cited 2020 Oct 26];4:352-7. Available from: http://www.sjamf.eg.net/text.asp?2020/4/3/352/296934
| Introduction|| |
Rheumatoid arthritis (RA) is an autoimmune multisystemic disease characterized by the inflammation of synovial membrane of the diarthrodial joints which include two arthrodeses located in the middle ear, namely the incudomalleolar and incudostapedial joints, causing conductive hearing impairment (HI) in up to 1.9% of the cases . It has been suggested that when these joints are affected, there is stiffening of the ossicular system and patients present with conductive HI .
In addition, extra-articular involvement is a potential feature of patients with RA and may also affect the auditory system, although a different putative mechanism of damage has been proposed, targeting the inner ear and causing sensorineural HI in 22–43% of the patients ,. Despite the high incidence of impaired hearing among patients with RA, this aspect of the disease has received scant attention in the literature. Hearing loss (HL) may be sensorineural, conductive, or of the mixed type .
HI in RA is generally under diagnosed; symptoms are progressive and patients are not aware of the damage until it interferes with their usual activity . Despite the increasing number of research studies about this topic, there is no clear evidence indicating that RA per se might be a direct cause of HL as the physiopathology remains unclear ,. There is no consensus about when to screen for HI in patients with RA with audiometric and clinical methods, or usefulness of these methods. The nature and prevalence of HL in RA remain debated . Thus, each of the anatomical structures of the ear (internal, external, and middle) has been cited to be possibly affected by this chronic rheumatic disease ,.
In addition, RA, by way of vasculitis or neuropathy, could also cause sensorineural HL or labyrinthine dysfunction ,. Ototoxicity of RA medications used for the treatment of the disease has been also reported by previous data ,. Conductive hearing loss (CHL), occurring in association with an acute exacerbation of the disease and remitting on the institution of the corticosteroid therapy, has been reported . Other groups have reported a permanent, nonreversible conductive deficit with a minor or major sensorineural deficit ,.
Subsequent work supported the latter view , and in addition, a relationship was found between disease activity and auditory impairment. As always in a chronic disease like RA, the question must be asked whether the problem is owing to the disease or iatrogenesis .
The objective of this work was to evaluate the pattern of HL in patients with RA and also to examine the possible associations between HL and related RA features especially disease activity.
| Patients and methods|| |
This study was conducted on 55 patients with RA diagnosed according to revised American College of Rheumatism criteria (1987) and 55 apparently healthy participants as a control group. The patients were selected randomly from the Rheumatology Clinics of Al-Azhar University Hospitals. An informed consent was obtained from each participant participating in the study. The study was approved by the Local Ethics and Research Committee, Faculty of Medicine (Al-Azhar University). There were 55 (100%) females, and their ages ranged from 22 to 65 years, with mean age of 42.10±11.80 years. The control group was 55 (100%) females, with their ages ranged from 28 to 63 years, with mean age of 40.92±8.70 years. Moreover, the disease duration ranged from 64 to 216 months, and the mean disease duration was 88.10±27.39 months.
Otoscopic examination was normal in all participants. HI was evaluated by pure tone audiometry and tympanometry including the static compliance and acoustic reflex threshold test. A complete medical history and thorough physical examination were made, and the following patients were excluded from the study: those with a history of HL under 24 h; those who presented with barotrauma, head trauma, or acoustic trauma; and those diagnosed with Meniere’s disease, otosclerosis, chronic otitis media, presbycusis, exposure to ototoxic medication, chronic exposure to intense noise, cardiovascular disease, or chronic neurological disease.
Clinical and demographic characteristics and disease activity were taken, including how long they had been diagnosed with RA, treatment, and current dosage; number of inflamed, painful joints; visual analogue scale: speed of globular sedimentation; and rheumatoid factors: C-reactive protein and presence of anticyclic citrullinated peptide antibodies (anti-CCP antibodies).
The control group consisted of 55 volunteers with a similar age and sex distribution, who presented without pathology in the hearing examination, as normal during tympanometry and who were without occupational noise exposure, with no remarkable history of familial hearing disorder or exposure to ototoxic mediations.
- Pure-tone audiometry was done using two-channel audiometer Piano plus (Inventis, Pandova, Italy). This included air conduction (air conduction hearing thresholds were determined by frequency range between 0.250 and 8 kHz) and bone conduction (bone conduction hearing thresholds were determined by frequency range between 0.500 and 4 kHz). Hearing thresholds greater than 25 dB were considered as HL.
- Speech audiometry (speech reception threshold using Arabic spondee words and the word discrimination scores using Arabic phonetically balanced words).
- Immittancemetry using MAICO model M144 (MICO, Berlin, Germany). This included tympanometry and acoustic reflex threshold measurement.
Cervical vestibular evoked myogenic potentials
Testing of cervical vestibular evoked myogenic potentials (cVEMPs) was performed using an auditory evoked response apparatus (Eclipse/EP25; Interacoustics, Denimark). The skin was prepared, surface cup disc electrodes were symmetrically placed, over midpoint of the sternocleidomastoid muscle bilaterally, with active electrode on the ipsilateral muscle, reference electrode on the sternal notch and ground electrode on the contralateral sternomastoid muscle. The muscle must be contracted to elicit the response, so the participants were instructed to rotate their heads to the opposite side of the stimulated ear as much as possible. The response of the ipsilateral SCM muscle to monaural stimuli, 500 Hz tone-bursts, with 1 ms rise–fall time and 5 ms plateau time at 95 dBnHL was recorded. All stimuli were presented via insert phones at a repetition rate of 5.1 per second. The responses of 120 stimuli were recorded and averaged per trial. EMG signals were amplified and band-pass filtered from 10 to 1000 Hz. The first positive deflection was marked as p13 and the first negative deflection after p13 was marked as n23. The latencies and amplitudes of these waves were calculated and recorded. The cVEMPs asymmetry ratio was calculated according to the following formula:[INLINE 1]
Values are presented as mean±SD for numerical data and frequency and percentages for categorical data. Between-groups differences were estimated by independent-sample Student’s t-test (numerical variables), χ2-test, or Fisher’s exact test (categorical variables). All data analysis was done using Statistical Package for the Social Sciences program version 18.0 software (SPSS Inc., Chicago, Illinois, USA), considering a two-tailed level of P less than 0.05 statistically significant.
| Results|| |
A total of 55 patients with RA, with mean age of 42.10±11.80 years, representing all females (100%), and 55 healthy controls, with mean age of 40.92±8.70 years, representing all females (100%) were included in our study. The two groups were matched for age and sex (P>0.05), which shows that there was no statistical significant difference between both groups. Moreover the mean disease duration was 88.10±27.39 months. The disease activity score 28 (DAS28) score ranged from 1.10 to 4.90; the mean value was 2.68±1.17, and median score was 2.25 ([Table 1]).
|Table 1 Comparison between the studied group and control group as regard patient age and gender|
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In both right and left ears, the static compliance was significantly low, whereas average acoustic reflex threshold was significantly high in the study group when compared with the control group. In addition, air-bone gap was significantly increased in both right and left ears in study when compared with the control group ([Table 2]).
|Table 2 Comparison between the study and control groups regarding immitancemetry|
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HI regardless of its type was reported in 36.7% in study group and 5.45% in control group, with significant difference ([Table 3]). There was a highly significant difference in sensory neural hearing loss (SNHL) among both groups ([Table 4])
|Table 3 Hearing impairment (regardless of its type) in the studied populations|
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Latencies of p13 and n23 were significantly higher in patients with RA than controls ([Table 5]).
|Table 5 Comparison of the cervical vestibular evoked myogenic potentials parameters between the study and the control group|
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Disease activity index was significantly and proportionately correlated with average acoustic reflex of left ear and significantly and inversely correlated with air-bone gap on both right and left ears ([Table 6]).
| Discussion|| |
The present study found a high prevalence of HL in patients with RA when compared with their controls and showed that its nature could be conductive but also sensorineural and mixed. Where is this in this study, the HI in RA patients were subclinical comorbid state. As most of the patients are not aware of their hearing disorder and have no clinical complaints, it is important that physicians consider hearing damage in these patients .
In the present work, 36.7% of patients with RA developed HI. Pascual-Ramos et al.  in a previous report demonstrated that 24% of 113 patients with RA had HI. These values are lower than the present work, and this could be attributed to the fact that 13% of our patients with RA in their duration had short disease duration and low disease activity.
In this study, 29.09% of patients had SNHL and 1.8% of the patients complained of CHL, whereas mixed HL were detected in 5.45%. This agreed with Murdin and colleagues who reported that CHL is also present in patients with RA, but at a lower prevalence, between 0 and 13%. Moreover, El-Fatta and colleagues reported only five (11.11%) cases with CHL. In addition, Takatsu et al.  reported the frequency of sensorineural HI in patients with RA to be higher than normal controls (36.1 vs 13.9%). These results are comparable to that of the present work. On the contrary, this disagreed with the results found by Heyworth and Liyanage  who suggested that there was no evidence that suggests HI owing to rheumatoid involvement of the ossicular joints. Dikici reported that the conductive component may start later after the occurrence of sensorineural component that will result in mixed HL.
The pathogenesis of HL in RA has been a matter of debate for decades, and it is still poorly understood. Causes of HL have been described as multifactorial. Hearing damage is most frequently found in patients with RA, and it has been attributed to disease activity and extra-articular involvement such as vasculitis . Subclinical atherosclerosis and intima-media thickening of carotid arteries are other possible pathogenetic mechanisms for HI in RA, as it reduces the blood flow for the brain circulation and compromise the inner ear cells .
In addition, most drugs used in the treatment of RA such as nonsteroidal anti-inflammatory drugs and disease-modifying antirheumatic drugs, given to patients with more active disease, have also been recognized as potential contributors to HL . Thus, an association between disease activity and HI has not been not consistent ,.
Our present study does not consider medications used in RA as relevant factor as we narrowed our patient spectrum by restricting our inclusion criteria to include only first line drug treatment group, which could be less ototoxic with less severe RA disease.
In this study, latencies of p13 and n23 were significantly higher in patients with RA than controls tale . This agreed with the results reported by Macias-Reyes et al.  Moreover, this could be attributed to slow conduction along the vestibulospinal pathway that may occur in patients with RA and lead to elimination of VEMP response or increased latency.
On the contrary, there was an insignificant difference between patients with RA and controls regarding amplitude. The absolute amplitude is not considered as an important factor in the differential diagnosis owing to the large variation range that varies from 25 to 250 µv. In addition, the VEMP amplitude depends on sound intensity and contraction of sternocleidomastoid muscle.
In contradiction to the results of the present work, Murdin et al.  studied 54 patients with RA and reported HL in 29.6%, and they found no correlation between DAS28 score and HI. This could be attributed to different sample size and inclusion criteria. In addition, Yildirim et al.  failed to find a relationship between HL and disease activity.
On the contrary, Lasso de la Vega et al.  studied a series of 53 patients with RA and detected a prevalence of HL in 69.8% in very high frequencies that reduced to 43% in conventional audiometry. The impairment was bilateral and symmetric. This incidence is high than the present work. However, the impairment is bilateral and symmetric as in the present study.
| Conclusion|| |
HI showed statistically significant increase in number in patients with RA than controls, and disease activity is usually positively correlated with increased HI. However, no significant correlation had been found between duration of drug use and the HL type and severity.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Murdin I, Patel S, Walmsley J, Yeoh LH. Hearing difficulties are common in patients with rheumatoid arthritis. Clin Rheumatol 2008; 27:637–640.
Ozcan M, Karahuş MF, Gündüz OH, Tuncel U, Sahin H. Hearing loss and middle ear involvement in rheumatoid arthritis. Rheumatol Int 2002; 22:16–19.
Takatsu M, Higaki M, Kinoshita H, Mizushima Y, Koizuka I. Ear involvement in patients with rheumatoid arthritis. Otol Neutrotol 2005; 26:755–761.
Baradaranfar MH, Doosti A. A survey of relationship between rheumatoid arthritis and hearing disorders. Acta Med Iran 2010; 48:371–373.
Pascual-Ramos V, Contreras-Yánez I, Rivera-Hoyos P, Enriquez L, Ramirez-Anguiano J. Cumulative disease activity predicts incidental hearing impairment in patients with rheumatoid arthritis (RA). Clin Rheumatol 2014; 33:315–321.
Peters MJ, Symmons DP, McCarey D, Dijkmans BA, Nicola P, Kvien TK et al.
EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis 2010; 69:325–331.
Kastaniodakis I, Skevas A, Daniellidis V, Tsiakou E, Drosos AA, Moustopoulos MH. Inner ear involvement in rheumatoid arthritis: a prospective clinical study. J Laryngol Otol 1995; 109:713–718.
Emamifar A, Bjoerndal K, Hansen IM: Is hearing impairment associated with rheumatoid arthritis? A review. Open Rheumatol J 2016; 10:26–32.
Siamopoulou-Mavridou A, Skevas A, Moutsopoulos HM. Middle ear function in patients with juvenile chronic arthritis. Ann Rheum Dis 1990; 49:620–623.
Elwany S, El-Garf A, Kamel T. Hearing and middle ear function in rheumatoid arthritis. J Rheumatol 1986; 13:878–881.
Heyworth T, Liyange SP. A pilot survey of hearing loss in patients with rheumatoid arthritis. Scand J Rheumatol 1972; 1:81–83.
Magaro M, Zoli A, Altomonte L, Mirone L, Corvino G, Di Girolamo S et al.
Sensorineural hearing loss in rheumatoid arthritis. Clin Exp Rheumatol 1990; 8:487–490.
T Mijovic T, Zeitouni A, Colmegna I. Autoimmune sensorineural hearing loss: the otolgy-rheumatology interface. Rheumatology (Oxford) 2013; 52:780–789.
Goodwill CJ, Lord IJ, Knill RP. Hearing in rheumatoid arthritis. Ann Rheum Dis 1972; 31:170–173.
Doig JA, Whaley K, Dick WC, Nuki G, Williamson J, Buchanan WW. Otolaryngological aspects of Sjogren’s syndrome. Br Med J 1971; 4:460–463.
Silan F, Demirci L, Egeli A, Egeli E, Onder HI, Ozturk O et al.
Syndrome etiology in children at schools for the deaf in Turkey. Int J Pediatr Otorhinolaryngol 2004; 68:1399–1406.
Garcia Callejo FJ, Conill Tobias N, Munoz Fernández N, de Paula Vernetta C, Alonso Castaneira I, Marco Algarra J. Hearing impairment in patients with rheumatoid arthritis. Acta Otorrinolaringol Esp 2007; 58:232–238.
Macias-Reyes H, Duran-Barragan S, Cardenas-Contreras CR, Chavez-Martin CG, Gomez-Bañuelos E, Navarro-Hernandez RE et al.
Sensorineural hearing impairment and subclinical atherosclerosis in rheumatoid arthritis patients without traditional cardiovascular risk factors. Arch Rheumatol 2016; 31:208–214.
Jung TT, Rhee CK, Lee CS, Park YS, Choi DC. Ototoxicity of salicylate, nonsteroidal anti-inflammatory drugs and quinine. Otolaryngol Clin North Am 1993; 26:791–810.
Stevens G, Flaxman S, Brunskill E, Mascarenhas M, Mathers CD, Finucane M. Global and regional hearing impairment prevalence: an analysis of 42 studies in 29 countries. Eur J Public Health 2013; 23:146–152.
Gazeau P, Saraux A, Devauchelle-Pensec V, Cornec D. Long-term efficacy of infliximab in autoimmune sensorineural hearing loss associated with rheumatoid arthritis. Rheumatology (Oxford) 2014; 53:1715–1716.
Yildirim A, Surucu G, Dogan S. Relationship between disease activity and hearing impairment in patients with rheumatoid arthritis compared with controls. Clin Rheumatol 2015; 35:309–314.
Lasso de la Vega M, Villarreal IM, Lopez-Moya J. Examination of hearing in a rheumatoid arthritis population: role of extended-high-frequency audiometry in the diagnosis of subclinical involvement. Scientifica 2016; 2016:1–7.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]