The mental foramen (MF) is one of the most consistently Allergic rhinitis (AR) is one of the most common chronic disorders encountered in clinical practice, characterised by an IgE-mediated inflammatory response of the nasal mucosa to inhaled allergens, manifesting as sneezing, nasal obstruction, rhinorrhoea, and itching. It is estimated to affect between 10% and 40% of the population globally, with a rising trend attributed to urbanisation, pollution, and changing lifestyle patterns. Sharma et al¹ reported a prevalence of allergic rhinitis of nearly 20–30% among the Indian population attending otorhinolaryngology outpatient departments, while Prasad et al² observed that allergic rhinitis was one of the leading causes of chronic upper respiratory morbidity in North Indian patients.

The nasal cavity, paranasal sinuses, nasopharynx, and the middle ear cleft share a common respiratory mucosal lining and are connected functionally through the eustachian tube. Inflammatory mediators released during an allergic reaction — histamine, leukotrienes, and cytokines — are not confined to the nasal mucosa alone and may extend to the eustachian tube, resulting in tubal dysfunction, negative middle ear pressure, and secondary middle ear effusion. Kumar and Singh³ demonstrated eustachian tube dysfunction in a significant proportion of allergic rhinitis patients using tympanometry, supporting the concept of a unified allergic airway. Beyond conductive pathology, several authors have proposed that circulating inflammatory mediators and immune complexes may also affect the cochlea and inner ear structures directly, producing sensorineural hearing loss through cochlear microvascular changes, endolymphatic hydrops-like changes, or immune-mediated inner ear damage.

The concept of allergy-related inner ear disease is not new. Derebery⁴ and other Western authors described the association between allergic disease and Meniere's disease as well as sudden sensorineural hearing loss, hypothesising a common immune-mediated pathway. In the Indian context, Bhatia et al⁵ studied auditory function in patients with chronic rhinosinusitis and allergic rhinitis and found a higher incidence of subclinical sensorineural hearing loss on pure tone audiometry compared to normal controls, particularly in the higher frequency range. Similarly, Reddy et al⁶ observed that patients with long-standing allergic rhinitis of more than five years' duration had significantly poorer hearing thresholds at 4000 Hz and 8000 Hz than those with shorter disease duration.

Despite this growing body of evidence, sensorineural hearing loss remains an underrecognised and underreported complication of allergic rhinitis, often overshadowed by the more obvious nasal and conductive middle-ear manifestations of the disease. Most patients with allergic rhinitis are managed by physicians or otolaryngologists focusing on nasal symptoms alone, and audiometric evaluation is not routinely performed unless the patient specifically complains of hearing difficulty. This may result in delayed diagnosis of an insidious, progressive sensorineural hearing impairment.

With this background, the present study was undertaken to determine the incidence of sensorineural hearing loss among patients with allergic rhinitis attending a tertiary care hospital, and to study its correlation with the severity and duration of the disease, so as to emphasise the importance of audiological screening in this common clinical entity.

 AIMS AND OBJECTIVES

1. To determine the incidence of sensorineural hearing loss in patients with allergic rhinitis.
2. To compare pure tone audiometric thresholds between allergic rhinitis patients and healthy age- and sex-matched controls.
3. To correlate the severity (ARIA classification) of allergic rhinitis with the occurrence and degree of sensorineural hearing loss.
4. To study the relationship between duration of allergic rhinitis and severity of hearing loss.

Study design: A hospital-based prospective observational case–control study.

Study setting: Department of Otorhinolaryngology, in association with the Department of Audiology, of a tertiary care teaching hospital.

 Study period: Eighteen months, after obtaining clearance from the Institutional Ethics Committee.

 Sample size: 100 diagnosed cases of allergic rhinitis and 100 age- and sex-matched healthy controls, selected by purposive sampling, based on an expected incidence of SNHL of approximately 15–20% from previous literature, with 95% confidence interval and 5% absolute precision.

 Inclusion Criteria

• Patients aged 15–55 years, of either sex, clinically diagnosed as allergic rhinitis according to ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines.
• Patients willing to give informed written consent and to undergo audiological evaluation.

Exclusion Criteria

• Pre-existing conductive hearing loss due to causes other than allergic rhinitis (e.g., chronic suppurative otitis media, otosclerosis, wax impaction).
• History of ototoxic drug intake, noise exposure, head injury, or ear surgery.
• Congenital hearing loss or family history of hereditary hearing loss.
• Diabetes mellitus, hypertension, or other systemic illness known to affect hearing.
• Patients with acute upper respiratory tract infection at the time of examination.

 Methodology

After obtaining informed consent, all subjects underwent a detailed clinical history including duration of nasal symptoms, seasonal or perennial pattern, associated symptoms of ear discomfort, aural fullness, tinnitus, or hearing difficulty, followed by a thorough ENT examination comprising anterior rhinoscopy, oral cavity examination, and diagnostic nasal endoscopy where indicated. Allergic rhinitis was classified according to ARIA guidelines into intermittent/persistent and mild/moderate–severe categories based on symptom duration and impact on quality of life. The Total Nasal Symptom Score (TNSS) was recorded for each patient.

All subjects then underwent otoscopic examination followed by pure tone audiometry (PTA) performed in a sound-treated room using a calibrated diagnostic audiometer, testing air conduction thresholds at 250, 500, 1000, 2000, 4000, and 8000 Hz, and bone conduction thresholds at 500–4000 Hz. Tympanometry was performed to rule out middle ear effusion and conductive pathology. Hearing loss was graded according to the World Health Organisation (WHO) classification as normal (≤25 dB), mild (26–40 dB), moderate (41–60 dB), severe (61–80 dB), and profound (>80 dB). Sensorineural hearing loss was defined as an air-bone gap of less than 10 dB with elevated air and bone conduction thresholds above 25 dB in one or both ears.

Data collected were tabulated and analysed using SPSS software version 22.0. Categorical variables were expressed as frequencies and percentages and compared using the Chi-square test; continuous variables were expressed as mean ± standard deviation and compared using Student's t-test. A p-value of less than 0.05 was considered statistically significant.

A total of 100 patients with allergic rhinitis (cases) and 100 age- and sex-matched healthy individuals (controls) were studied. The findings are summarised below.

Table 1: Age and Sex Distribution of Study Population

The mean age of cases was 32.4 ± 9.6 years and of controls was 31.8 ± 9.1 years (p=0.62, not significant). Male to female ratio was comparable between the two groups (p=0.78).

 Table 2: Duration of Allergic Rhinitis in Cases

 Table 3: ARIA Classification of Allergic Rhinitis among Cases

Table 4: Type of Hearing Loss Observed among Cases and Controls

The difference in incidence of sensorineural hearing loss between cases and controls was statistically significant (χ²=11.48, p<0.001).

Table 5: Degree of Sensorineural Hearing Loss among Affected Cases (n=19)

 Table 6: Mean Pure Tone Audiometric Thresholds (dB) at Different Frequencies

A statistically significant elevation of hearing thresholds was noted in the higher frequencies (2000–8000 Hz) among cases as compared to controls, suggesting a high-frequency pattern of sensorineural hearing loss associated with allergic rhinitis.

Table 7: Association between Severity (ARIA Category) of Allergic Rhinitis and Incidence of SNHL

A statistically significant association was found between increasing severity of allergic rhinitis and incidence of sensorineural hearing loss (χ²=14.62, p=0.002).

 Table 8: Association between Duration of Allergic Rhinitis and Incidence of SNHL

Patients with disease duration greater than 5 years had a significantly higher incidence of SNHL compared to those with shorter duration (χ²=8.94, p=0.01).

 Table 9: Distribution of Associated Otological Symptoms among Cases with SNHL (n=19)

Nearly one-third of patients with sensorineural hearing loss were entirely asymptomatic and were detected only on routine audiometric screening, highlighting the subclinical nature of this association.

rhinitis and an equal number of matched controls, found sensorineural hearing loss in 19% of allergic rhinitis patients compared to 4% of controls, a difference that was highly statistically significant. This is comparable to the observations of Bhatia et al5, who reported subclinical SNHL in approximately 18% of chronic allergic rhinitis and rhinosinusitis patients on pure tone audiometry, and to Reddy et al6, who noted a similar high-frequency pattern of hearing loss in patients with long-standing disease.

The predominance of high-frequency (4000–8000 Hz) threshold elevation observed in our study is consistent with the pattern described by Derebery4 in Western literature on allergy-related inner ear disease, where the basal turn of the cochlea, responsible for perception of higher frequencies, was postulated to be more susceptible to immune-mediated microvascular insult due to its relatively end-arterial blood supply. Kumar and Singh3 similarly demonstrated eustachian tube dysfunction in allergic rhinitis patients using tympanometric studies, which supports the broader concept of a 'unified airway' extending inflammatory effects from the nose to the middle and inner ear.

A statistically significant correlation was found in our study between the severity of allergic rhinitis, as graded by the ARIA classification, and the incidence of sensorineural hearing loss — patients with moderate–severe persistent disease had nearly six times the incidence of SNHL compared to those with mild intermittent disease. This finding is in agreement with Sharma et al1, who observed that the severity and chronicity of nasal allergic inflammation correlated with the degree of associated otological morbidity in Indian patients. Similarly, Prasad et al2 reported that patients with persistent allergic rhinitis had a higher burden of associated middle ear and, to a lesser extent, inner ear pathology compared to those with intermittent disease.

Duration of disease also emerged as a significant factor in our study, with patients suffering from allergic rhinitis for more than five years showing a markedly higher incidence of SNHL (30.6%) compared to those with disease of less than one year's duration (5.6%). This trend supports the hypothesis of a cumulative, progressive inflammatory insult to the cochlea over time, rather than an acute, reversible phenomenon, and is in keeping with the long-term follow-up observations of Reddy et al6.

Notably, nearly one-third of the patients found to have sensorineural hearing loss in our study were entirely asymptomatic with respect to their hearing, and the impairment was detected only on routine audiometric screening. This underscores the insidious and often clinically silent nature of allergy-associated SNHL, and highlights the importance of incorporating audiological assessment into the routine work-up of patients with chronic or severe allergic rhinitis, rather than reserving it only for those who volunteer otological complaints.

The precise pathophysiological mechanism linking allergic rhinitis to sensorineural hearing loss remains incompletely understood, but proposed mechanisms include: (i) circulating immune complexes and cytokines causing microvascular changes in the stria vascularis and cochlear microcirculation; (ii) IgE-mediated mast cell degranulation within the inner ear itself, given the presence of mast cells in the endolymphatic sac; (iii) chronic eustachian tube dysfunction leading to recurrent negative middle ear pressure with secondary effects on the round and oval window membranes; and (iv) a shared systemic atopic diathesis affecting both the respiratory and inner ear mucosa simultaneously. Further molecular and histopathological studies are required to clarify the exact mechanism.

This study was limited by its relatively modest sample size, single-centre design, and comparatively short follow-up period, which precluded assessment of the reversibility of hearing loss with treatment of the underlying allergic rhinitis. Larger, multicentric, longitudinal studies with serial audiometric follow-up before and after anti-allergic therapy would help establish causality more firmly and determine whether early treatment of allergic rhinitis can prevent or reverse the associated sensorineural hearing impairment.

The present study demonstrates a statistically significant association between allergic rhinitis and sensorineural hearing loss, with an overall incidence of 19% among affected patients as compared to 4% in healthy controls. The hearing loss was predominantly mild in degree, affected the higher frequencies preferentially, and correlated significantly with both the severity and duration of the underlying allergic rhinitis. A considerable proportion of affected patients were asymptomatic, emphasising the subclinical nature of this complication.

These findings support the recommendation that patients with moderate–severe or long-standing allergic rhinitis should undergo periodic audiological evaluation, even in the absence of overt otological symptoms, to allow early detection and appropriate management of sensorineural hearing impairment. Increased clinical awareness of this association among otolaryngologists, allergists, and primary care physicians may help reduce the burden of undiagnosed hearing loss in this common patient population.

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