Diabetes mellitus (DM) is one of the most prevalent non-communicable diseases worldwide and has attained pandemic proportions in India. According to the ICMR-INDIAB study, the prevalence of diabetes among Indian adults is estimated at 11.4%, with an additional 15.3% classified as prediabetic, placing India among the countries with the highest burden of diabetes globally [1]. Type 2 diabetes mellitus (T2DM) accounts for over 90% of cases and is associated with well-recognized microvascular complications such as retinopathy, nephropathy, and peripheral neuropathy.

In recent years, the cochlea has been increasingly recognized as a target organ for diabetic microangiopathy. The stria vascularis, spiral ligament, and organ of Corti are richly vascularized and metabolically active structures that are vulnerable to the same pathological processes—basement membrane thickening, endothelial dysfunction, and microthrombosis—that damage the retina and renal glomeruli [2,3]. Additionally, hyperglycemia-induced polyol pathway activation, advanced glycation end-product accumulation, and oxidative stress may cause neuropathy of the cochlear nerve, further contributing to sensorineural hearing loss (SNHL).

Several Indian studies have examined the auditory profile of diabetic patients. Kakarlapudi et al., in a study conducted in South India, reported a significantly higher prevalence of SNHL among diabetics compared to age-matched non-diabetic controls, with predominant involvement of higher frequencies [4]. Similarly, a study by Rajendran et al. from Tamil Nadu found that the degree of hearing loss correlated with the duration of diabetes and the presence of other microvascular complications such as retinopathy and neuropathy [5]. Sharma and colleagues, in a North Indian tertiary care setting, further demonstrated that poor glycemic control, as measured by HbA1c, was an independent predictor of audiometric threshold shifts, even after adjusting for age and duration of disease [6].

Glycated hemoglobin (HbA1c) is a validated marker of average blood glucose control over the preceding two to three months and is now recommended by both the American Diabetes Association and Indian guidelines as a diagnostic and monitoring tool for diabetes [7]. Unlike fasting or random blood glucose values, which reflect glycemic status only at a single point in time, HbA1c provides a more stable and reproducible index of chronic hyperglycemic exposure, making it a suitable parameter for correlation with cumulative end-organ damage such as SNHL.

Despite the growing body, the relationship between the degree of glycemic control and the severity of hearing impairment remains incompletely characterized, and audiometric screening is not yet a part of routine diabetic care protocols in most Indian institutions [8]. Early identification of subclinical hearing loss in diabetics could allow for timely audiological rehabilitation and reinforce the importance of strict glycemic control. This study was therefore undertaken to evaluate the association between HbA1c levels and sensorineural hearing loss in patients with type 2 diabetes mellitus attending a tertiary care hospital, and to determine whether the severity of hearing loss correlates with the degree of glycemic control.

 Objectives

• To evaluate the association between glycemic control (HbA1c) and sensorineural hearing loss in patients with type 2 diabetes mellitus, and to correlate HbA1c levels with the severity and pattern of hearing loss.

Study Design and Setting

This was a hospital-based, cross-sectional, analytical study conducted in the Department of Otorhinolaryngology in collaboration with the Department of General Medicine at a tertiary care teaching hospital, over a period of 12 months after approval from the Institutional Ethics Committee. Written informed consent was obtained from all participants prior to enrolment.

 Sample Size

Based on an expected prevalence of SNHL of approximately 45% among diabetics from previous research, with 95% confidence interval and 8% absolute precision, a minimum sample size of 144 was calculated; 150 patients were enrolled to account for attrition.

 Inclusion Criteria

• Patients aged 30-65 years with a confirmed diagnosis of type 2 diabetes mellitus (as per ADA criteria).
• Patients willing to give informed consent and undergo audiometric evaluation.

 Exclusion Criteria

• Type 1 diabetes mellitus or gestational diabetes.
• Pre-existing conductive hearing loss, chronic suppurative otitis media, or otosclerosis.
• History of noise exposure, ototoxic drug intake, head trauma, or familial/congenital hearing loss.
• Patients with chronic kidney disease on dialysis, hypothyroidism, or other conditions independently affecting hearing.

 Methodology

Detailed history including age, sex, duration of diabetes, treatment history, and presence of other complications (retinopathy, nephropathy, neuropathy) was recorded on a predesigned proforma. Otoscopic examination was performed to rule out conductive pathology. Venous blood samples were collected for estimation of HbA1c using high-performance liquid chromatography (HPLC), and fasting/postprandial blood glucose was measured by the glucose oxidase-peroxidase method. Patients were categorized into three groups based on glycemic control: Good control (HbA1c <7%), Fair control (HbA1c 7-9%), and Poor control (HbA1c >9%).

Pure tone audiometry (PTA) was performed in a sound-treated room using a calibrated diagnostic audiometer, assessing air and bone conduction thresholds at 250, 500, 1000, 2000, 4000, and 8000 Hz. Hearing loss was graded according to WHO criteria (normal ≤25 dB; mild 26-40 dB; moderate 41-60 dB; severe 61-80 dB; profound >80 dB), and the pattern (high-frequency, flat, or mixed) was noted.

 Statistical Analysis

Data were entered in Microsoft Excel and analyzed using SPSS software (version 26.0). 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 or ANOVA as appropriate. Correlation between HbA1c and audiometric thresholds was assessed using Pearson's correlation coefficient. A p-value <0.05 was considered statistically significant.

A total of 150 patients with type 2 diabetes mellitus were included in the study. The mean age of the study population was 54.6 ± 8.2 years, with a male-to-female ratio of 1.3:1. The mean duration of diabetes was 8.4 ± 5.1 years, and the mean HbA1c was 8.6 ± 1.9%.

Table 1: Demographic and Clinical Characteristics of Study Participants (n=150)

 Table 2: Prevalence and Severity of Sensorineural Hearing Loss (n=150)

Sensorineural hearing loss was bilateral in 82 of 96 affected patients (85.4%) and predominantly involved the high frequencies (4000-8000 Hz), consistent with a descending audiometric curve pattern in 78.1% of affected ears.

 Table 3: Association Between Glycemic Control (HbA1c) and Sensorineural Hearing Loss

χ² = 30.42, p < 0.001 (statistically significant)

 Table 4: Correlation of HbA1c with Mean Hearing Threshold and Duration of Diabetes

A statistically significant positive correlation was found between HbA1c and high-frequency hearing thresholds (r=0.612, p<0.001), indicating that poorer glycemic control was associated with greater hearing impairment. Duration of diabetes >10 years was also significantly associated with the presence of SNHL (p=0.002), and patients with coexisting diabetic retinopathy or peripheral neuropathy had a significantly higher prevalence of SNHL compared to those without these complications (p=0.014 and p=0.031, respectively).

The present study demonstrates a high prevalence (64.0%) of sensorineural hearing loss among patients with type 2 diabetes mellitus, with a clear and statistically significant gradient of increasing prevalence and severity across categories of worsening glycemic control. These findings are consistent with earlier Indian studies. Kakarlapudi et al. reported SNHL in nearly two-thirds of diabetic patients studied in a South Indian tertiary care center, with a similar predilection for high-frequency involvement ^[4], while Rajendran et al. observed that the severity of hearing loss increased progressively with longer duration of disease and poorer metabolic control, mirroring the correlation coefficients obtained in the present study ^[5].

The strong correlation between HbA1c and high-frequency hearing thresholds observed here (r=0.612, p<0.001) supports the hypothesis, proposed by Sharma et al., that chronic hyperglycemic exposure rather than isolated hyperglycemic episodes is the principal driver of cochlear microangiopathic damage ^[6]. This is biologically plausible given that the cochlea, particularly the stria vascularis, is highly sensitive to ischemia due to its high metabolic demand and limited collateral circulation. Chronic hyperglycemia promotes basement membrane thickening of the capillaries of the stria vascularis, reduces cochlear blood flow, and causes demyelination of the auditory nerve—mechanisms analogous to those implicated in diabetic retinopathy and nephropathy ^[2,3].

The predominance of high-frequency involvement in our cohort is consistent with the pattern described in most Indian and international studies and is attributed to the greater vulnerability of the basal turn of the cochlea, which is responsible for high-frequency sound perception, to ischemic and metabolic insults ^[4,9]. A community-based study by Bainbridge et al. using data from the U.S. National Health and Nutrition Examination Survey similarly reported that diabetic adults had significantly poorer hearing thresholds compared to non-diabetics, particularly in the high-frequency range, independent of age and noise exposure ^[10], lending further support to the association observed in our study population.

The significant association between duration of diabetes and SNHL noted in the present study corroborates the findings of Reddy and Kumar, who reported that patients with diabetes for more than 10 years had nearly three times higher odds of SNHL compared to those with a shorter disease duration ^[11]. Similarly, the higher prevalence of SNHL among patients with coexisting retinopathy and neuropathy in our cohort is in agreement with the concept of shared microvascular pathogenesis across multiple end-organs, a relationship also emphasized in a multicentric Indian study by Agarwal et al., which found retinopathy to be an independent predictor of audiometric abnormality in diabetics ^[12].

These findings collectively suggest that HbA1c, being an integrated marker of glycemic burden, could serve as a practical, low-cost tool to identify diabetic patients at higher risk of SNHL who may benefit from audiological screening. Incorporating pure tone audiometry into the routine complication-screening protocol for diabetic patients, especially those with long-standing disease and poor glycemic control, may facilitate early detection and timely rehabilitative intervention, an approach increasingly advocated in recent Indian consensus statements on diabetic complication screening ^[13].

 Limitations

The cross-sectional design precludes establishment of a definite causal relationship between HbA1c and SNHL Single-center hospital-based sampling may limit generalizability of the findings to the wider population. Other contributory factors such as dyslipidemia, hypertension duration, and genetic predisposition were not analyzed in detail. Longitudinal follow-up would be required to assess whether improvement in glycemic control halts or reverses progression of hearing loss.

This study demonstrates a significant association between poor glycemic control, as reflected by elevated HbA1c, and the presence and severity of sensorineural hearing loss in patients with type 2 diabetes mellitus, with predominant involvement of the high frequencies. The risk of SNHL increases with both the duration of diabetes and the degree of glycemic derangement. Given the high prevalence of asymptomatic hearing impairment in this population, routine audiometric screening should be considered an integral part of complication surveillance in diabetic patients, particularly those with long-standing or poorly controlled disease. Strict glycemic control may help in preventing or delaying the onset of diabetes-related cochlear damage, and further prospective, multicentric studies are warranted to establish causality and evaluate the impact of glycemic optimization on auditory outcomes.

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