|Year : 2018 | Volume
| Issue : 3 | Page : 199-203
Vestibular dysfunction and glycemic control in diabetes mellitus: Is there a correlation?
Chetana S Naik, Raviraj Tilloo
Departments of Otorhinolaryngology and HNS, Smt Kashibai Navale Medical College and General Hospital, Pune, Maharashtra, India
|Date of Web Publication||11-Jan-2019|
Prof. Chetana S Naik
Department of Otorhinolaryngology and HNS, Smt Kashibai Navale Medical College and General Hospital, Pune - 411 041, Maharashtra
Source of Support: None, Conflict of Interest: None
Objectives: The aim of this study is to evaluate and find the proportion of patients with Type-II diabetes mellitus (DM) with sensorineural hearing loss (SNHL) and vestibular dysfunction (VD) and association with glycemic control. Materials and Methods: An observational cross-sectional study was carried out in 100 patients (age group: 30–60 years) diagnosed with Type-II DM coming to the outpatient department of our Rural Tertiary Care Teaching Hospital, fulfilling the inclusion criteria. Prior approval of the Institutional Ethics Committee and written informed consent was obtained. All patients were subjected to investigations to assess their diabetes control, hearing, and vestibular function. The findings were subjected to statistical analysis. Results: Out of 100 patients, 62 were male and 38 were female between the age group of 30 and 60 years. The mean hemoglobin A1c (HbA1c) level was 9.16 ± 2.4. The patients were divided into three groups depending on HbA1c level, to denote control, good (≤7%), moderate (>7, ≤12%), and poor (>12%). There were a total of 69 patients with SNHL and 70 patients with VD. SNHL was present in 57.6% of good control group, 66.1% of moderate control group, and 100% of poor control group. Analysis with Chi-square test for correlation between glycemic control and SNHL was statistically significant. Out of the 70 patients with VD, 51.4% had right vestibulopathy, 41.4% had left vestibulopathy, and 7.2% had a bilateral vestibulopathy. Twenty-two patients had benign paroxysmal positional vertigo. VD was present in 42.3% of good control group, 74.5% of moderate control group, and 100% of poor control group. Chi-square test was statistically significant. Conclusion: There is a significant association between Type II DM, and SNHL and VD, especially with worsening of glycemic control. Screening for these debilities should be a part of the routine workup of a diabetic patient. VD is a potential cause for imbalance and vertigo in DM.
Keywords: Diabetes mellitus, hearing loss, vestibular dysfunction
|How to cite this article:|
Naik CS, Tilloo R. Vestibular dysfunction and glycemic control in diabetes mellitus: Is there a correlation?. Indian J Otol 2018;24:199-203
| Introduction|| |
Diabetes mellitus (DM) is a multisystemic disease with variety of manifestations. The “International Diabetes Federation” estimates that the total number of diabetics in India is around 40.9 million, expected to rise to 69.9 million by 2025. A variety of molecular mechanisms play a role in the pathogenesis of the complications in DM, like the formation of advanced glycation end-products, polyol formation, increased activity of protein kinase C, increased production of extracellular matrix proteins, and glycosaminoglycans. All this ultimately leads to microvascular damage termed as “Microangiopathy.” Makishima and Tanaka, found microangiopathy to be a significant cause of sensorineural hearing loss (SNHL) in diabetics. A similar correlation has also been established between diabetic SNHL and acoustic neuropathy,, the latter commonly being a late complication.
All these findings led us to extrapolate similar mechanisms for vestibular dysfunction (VD) in DM. The current data regarding in diabetes are limited, especially in India and studies conducted along these lines have not associated VD with glycemic control in DM. The need to consider DM as a potential cause for SNHL and VD is important, so that timely rehabilitation of hearing and balance disorders can be performed along with management of DM. The study focuses on Type-II DM, and its association with SNHL and VD. We have used hemoglobin A1c (HbA1c), which is a sensitive parameter for the assessment of diabetic control, which has not been used in many studies.
Aims and objectives
(1) To evaluate the patients of Type-II DM for SNHL and VD. (2) To find the proportion of Type-II DM patients suffering from SNHL and VD. (3) To grade the SNHL and VD and associate it with the glycemic control in the patients.
| Materials and Methods|| |
Study design: An observational cross-sectional study. Study population: Patients of Type-II Diabetes diagnosed with per diagnostic criteria of the American Diabetes Association (ADA) attending the outpatient department of our Rural Tertiary Care Teaching Hospital. Sample size: 100. Inclusion criteria: (1) Patients diagnosed with Type-II DM, (2) Age: 30–60 years. Exclusion criteria: (1) Type-I DM, (2) Pregnancy, (3) Ototoxic drug intake, (4) Ear discharge, (5) History of head injury, (6) Noise exposure, (7) Family history of deafness, (8) History of hypertension, meningitis/encephalitis, ear surgery, Meniere's disease, migraine, or metabolic disorder, (9) Patients not giving consent. The Institutional Ethics Committee approval was taken. A written informed consent was obtained. Patients fulfilling the selection criteria underwent a detailed history and oto-neurological examination. Patients were evaluated with the dizziness handicap inventory (DHI) and underwent the aforementioned investigations. Investigations for diabetes included; blood sugar level–fasting and postprandial after 2 h, HbA1c levels, lipid profile, serum ketones, serum creatinine, urine sugar, and albumin. Audio-vestibular investigations included; pure-tone audiometry including Short Increment Sensitivity Index and tone decay tests, otoacoustic emissions, videonystagmography with caloric tests and subjective visual vertical.
Patients were evaluated for glycemic control status as per the criteria of ADA. The criteria for ideal glycemic control are as follows: (1) HbA1c <7.0% (2) Preprandial capillary plasma glucose should be 80–130 mg/dl (3) Peak postprandial capillary plasma glucose should be <180 mg/dl. The major parameter used by us was HbA1c, to classify the patients into groups to denote their glycemic control status. The patients were divided into three groups depending on HbA1c, to denote control, good (≤7%), moderate (>7, ≤12%), and poor (>12%). Statistical analysis was performed with Microsoft Excel and SPSS software version 22, IBM, Chicago, USA.
| Observations and Results|| |
Out of 100 patients, 62 were male and 38 were female between 30 and 60 years of age. Eighteen patients were between 31 and 40 years, 34 (41–50 years), and 48 (51–60 years). The mean fasting blood glucose level was 140.5 ± 70 mg/dl, and the mean postprandial blood glucose (2 h) was 231 ± 70 mg/dl. The mean HbA1c level was 9.16 ± 2.4. There were 26 patients with good control, 59 patients with moderate, and 15 patients with poor control [Figure 1]. SNHL was found in 69 patients and VD in 70 patients. Out of 69 patients with SNHL, 46.3% had slight SNHL (16–25 dB), 7.2% had mild SNHL (26–40 dB), 27.5% had moderate SNHL (41–55 dB), 14.4% had moderately severe SNHL (56–70 dB), and 4.6% had severe (71–90 dB) SNHL [Figure 2]. Out of 69 patients with SNHL based on recruitment and the tone decay tests, 24.7% had SNHL, 55.1% had sensory type and 20.2% had a neural type. Selective high-frequency SNHL (≥4000 Hz) was seen in 18.8%. There were 5 (33.33%) high-frequency SNHL cases in the good control group, 7 (17.9%) cases in the moderate control group and 1 (6.25%) case in the poor control group. Seventy-one patients had abnormal otoacoustic emissions (OAEs). Abnormal OAEs were found in 46.1% of good control, 74.5% of moderate control, and 100% of the poor control group [Figure 3]. All 100 patients were evaluated with DHI score. Out of 100 patients, 50 patients had an insignificant score, 25 had mild handicap, 16 had moderate handicap, and 9 patients, severe handicap, as per the DHI grading. Out of the 100 patients, 70 had evidence of VD. Out of these, 51.4% had right vestibulopathy, 41.4% had left vestibulopathy, and 7.2% had a bilateral vestibulopathy [Figure 4]. In addition, 22 patients were found to have benign paroxysmal positional vertigo (BPPV) on positional testing. SNHL was present in 15 (57.6%) in good control group, 39 (66.1%) in moderate control group, and 15 (100%) in poor control group [Figure 5]. Results of Chi-square test were statistically significant (χ2 = 8.525, degrees of freedom = 2, P = 0.01409 with 95% confidence limit). VD was present in 11 (42.3%) in good control group, 44 (74.5%) in moderate control group, and 15 (100%) in poor control group [Figure 6]. Results of Chi-square test were statistically significant (χ2 = 16.51, degrees of freedom = 2, P = 0.0002598 with 95% confidence limit). Out of 100 patients, 62 were male and 38 were female. Thirty-nine (62.9%) males and 30 (78.9%) females had SNHL. Results of Chi-square for sex versus SNHL: χ2 = 6.204, degrees of freedom = 1 and P = 0.01275. SNHL was found to be comparatively more in females than males, and this was statistically significant. Forty-three (69.3%) males and 27 (71%) females had VD. Results of Chi-square for sex versus VD were: χ2 = 0.06119, degrees of freedom = 1 and P = 0.8046. Sex-wise distribution of VD showed the only slight difference and this was not statistically significant.
|Figure 1: Distribution of patients with diabetes mellitus as per hemoglobin A1c levels (glycemic control groups)|
Click here to view
|Figure 2: Distribution of grades of sensorineural hearing loss among glycemic control groups|
Click here to view
|Figure 3: Distribution of patients with abnormal otoacoustic emissions in various glycemic control groups|
Click here to view
|Figure 4: Distribution of patients with various vestibular dysfunctions in different glycemic control groups|
Click here to view
|Figure 5: Correlation of sensorineural hearing loss with glycemic control (X-axis: Number of patients, Y-axis: Glycemic control group)|
Click here to view
|Figure 6: Correlation of vestibular dysfunction with glycemic control (X-axis: Number of patients, Y-axis: Glycemic control group)|
Click here to view
| Discussion|| |
DM is a systemic disease affecting multiple organs. DM is being linked with inner ear diseases since the 19th century. Knowing that DM causes peripheral neuropathy, researchers hypothesized SNHL to be linked to it. Friedman et al. in 1975 evaluated 20 DM patients with peripheral neuropathy and showed that hearing thresholds were elevated in these patients. Most studies have evaluated SNHL by pure tone audiometry., Other modalities have also been used to assess inner ear dysfunction like OAE,, and auditory brainstem response (ABR)., Parving et al. found that ABR results were abnormal in 40% of patients, with long-standing DM history. Histopathological studies of temporal bone have also been performed in DM patients, for evidence of cochlear microangiopathy, to establish it as a cause for diabetic SNHL. Type-I and Type-II DM have been evaluated separately as well as together in different studies., Many studies support the association between the two, the majority of which show a significant association,, which also includes the recent meta-analyses., However, certain inconsistency is reflected from the fact, that some of them only show a weak association, whereas some of them do not show it.,
Studies have tried to find a relationship between VD and diabetes. Klagenberg et al. found a significant association between Type-I DM and VD. Detection of VD in people with diabetes often gets delayed, and patients are only referred for dizziness and instability, which is subjective and can be due to multiple causes in DM. Studies for assessing VD and SNHL have been performed, to associate them with multiple metabolic disorders together,, without specifically focusing on Type-II DM, which is more prevalent than others. Overall consensus for DM and VD is that certain studies do not support this correlation, some suggest only a weak association, whereas few other studies show a strong positive relationship between the two., None of the studies are done in India. The study consisted of a total of 100 patients of Type-II DM, of which 62 were male and 38 were female. These patients had a mean fasting blood glucose level was 140.5 ± 70 mg/dl, and the mean postprandial blood glucose (2 h) was 231 ± 70 mg/dl. The mean HbA1c levels were 9.16% ±2.4%. After dividing patients based on HbA1c levels in 3 groups, good (≤7%), moderate (>7, ≤12%), poor (>12%) as an index of their glycemic control, we found 26 patients with good control, 59 patients with moderate control, and 15 with poor control. Out of total 100 patients, 69 patients had SNHL and 70 had VD, i.e., 69% and 70% was the prevalence rate, respectively. SNHL was seen in 15 (57.6%) of the good control group, 39 (66.1%) of the moderate control group and 15 (100%) of poor control group, thus showing an increasing trend with decline of glycemic control. Similarly, VD as present in 11 (42.3%) of good control group, 44 (74.5%) of moderate control group, and 15 (100%) of poor control group, again displaying an increasing trend with decline of glycemic control.
The prevalence of SNHL was found to be almost similar to one other previous study. However other studies, especially which have been carried with a larger sample size have found a comparatively lower prevalence rate., Kakarlapudi et al. reported a prevalence of only 13.1%. Although this study was carried on a bigger scale, they screened patients of SNHL for DM, which is opposite to our methodology. For VD, the prevalence rate is similar to what other researchers have found. Chávez-Delgado et al. have reported 89% prevalence in their study of 385 patients. The difference seen in the two rates could be due to the inclusion of other risk factors such as dyslipidemia and hypertension. Comparing the SNHL levels with glycemic control of the patients, we found that the relationship between the two was statistically significant, with 95% confidence limit (P = 0.01409). Similarly, for VD and glycemic control also, the relationship was statistically significant with 95% confidence limit (P = 0.0002598).
Majority of the cases had slight or mild SNHL in our study. Our study also differentiated between the types of SNHL, showing that the majority of the patients had a sensory type of SNHL, indicating a cochlear pathology. This was also supported by abnormal OAE results pointing to outer hair cell dysfunction which showed an increasing trend with decrease in the quality of diabetic control. This reinforces the hypothesis put by studies that cochlear microangiopathy is a major cause of diabetic SNHL., Furthermore, neural type of hearing less which is due to acoustic neuropathy, was mainly seen in poor control group and in patients of higher age group. This correlates to the finding that acoustic neuropathy is usually a late complication. Previous studies have said that DM is known to cause high-frequency SNHL, especially in the early stages, this finding is similarly depicted in our study.
Majority of our patients had insignificant score with DHI, which could be attributed to the varied presentation of vertigo and subclinical vestibulopathy. As DM is a systemic disease, bilateral VD might be expected to be more common. However, we found that unilateral dysfunction was far more common than bilateral disease which was similar to one of other study. BPPV which is found to be associated with diabetes was found in 22% of our cases. This may be related to the ischemic insult to otoliths resulting from microangiopathy associated with DM. In our study, SNHL was more common in females than males with DM. Age largely influenced the presence of VD or SNHL, along with the quality of glycemic control. This might be because aging itself can worsen diabetic control and thus make the patient more prone to VD or SNHL.
| Conclusion|| |
There is a significant association between Type II DM, and SNHL and VD. Furthermore, both are more likely to occur, with worsening of glycemic control. Cochleopathy is more common in DM than the neuropathy, but neuropathy is more likely in a patient with poor glycemic control. It is important to recognize vestibulopathy as a potential cause for imbalance and vertigo in patients with diabetes and should be considered if a patient of DM presents with dizziness. Early detection would prevent falls and morbidity. Thus, screening for SNHL and VD should be part of the routine workup of a diabetic patient. Better diabetes control would prevent these complications thus assuring a better lifestyle for these patients.
This study was funded by the Indian Council of Medical Research for short-term student project. Authors declare no conflicts of interests. Authors would like to acknowledge the support of the Dr. K.J Shinde, head of the Department of ENT, Dr. S.M. Bhat, head of Department of Medicine and Mr. Bedake, Audiology and Speech Therapy.
Financial support and sponsorship
The study was approved and funded by the Indian Council of Medical research (ICMR) as a part of short-term student project.
Conflicts of interest
There are no conflicts of interest.
| References|| |
Sicree R, Shaw J, Zimmet P. Diabetes and Impaired Glucose Tolerance. Diabetes Atlas. 3rd
ed. Belgium: International Diabetes Federation; 2006. p. 15-103.
Wada R, Yagihashi S. Role of advanced glycation end products and their receptors in development of diabetic neuropathy. Ann N Y Acad Sci 2005;1043:598-604.
Makishima K, Tanaka K. Pathological changes of the inner ear and central auditory pathway in diabetics. Ann Otol Rhinol Laryngol 1971;80:218-28.
Friedman SA, Schulman RH, Weiss S. Hearing and diabetic neuropathy. Arch Intern Med 1975;135:573-6.
Naufal PM, Schuknecht HF. Vestibular, facial, and oculomotor neuropathy in diabetes mellitus. Arch Otolaryngol 1972;96:468-74.
Jacobson GP, Newman CW. The development of the dizziness handicap inventory. Arch Otolaryngol Head Neck Surg 1990;116:424-7.
American Diabetes Association. Glycemic targets. Section 6. In standards of medical care in diabetes-2015. Diabetes Care 2015;38 Suppl 1:S33-40.
Wang C, Crapo LM. The epidemiology of thyroid disease and implications for screening. Endocrinol Metab Clin North Am 1997;26:189-218.
Sieger A, White NH, Skinner MW, Spector GJ. Auditory function in children with diabetes mellitus. Ann Otol Rhinol Laryngol 1983;92:237-41.
Kurien M, Thomas K, Bhanu TS. Hearing threshold in patients with diabetes mellitus. J Laryngol Otol 1989;103:164-8.
Lisowska G, Namysłowski G, Morawski K, Strojek K. Cochlear dysfunction and diabetic microangiopathy. Scand Audiol Suppl 2001;30:199-203.
Ottaviani F, Dozio N, Neglia CB, Riccio S, Scavini M. Absence of otoacoustic emissions in insulin-dependent diabetic patients: Is there evidence for diabetic cochleopathy? J Diabetes Complications 2002;16:338-43.
Parving A, Elberling C, Balle V, Parbo J, Dejgaard A, Parving HH, et al.
Hearing disorders in patients with insulin-dependent diabetes mellitus. Audiology 1990;29:113-21.
Zhang MH, Zhang L. A study on the diagnostic value of brainstem auditory evoked potentials in diabetic deafness. J Clin Intern Med 2005;22:563.
Wackym PA, Linthicum FH Jr. Diabetes mellitus and hearing loss: Clinical and histopathologic relationships. Am J Otol 1986;7:176-82.
Kakarlapudi V, Sawyer R, Staecker H. The effect of diabetes on sensorineural hearing loss. Otol Neurotol 2003;24:382-6.
Lisowska G, Namysłowski G, Morawski K, Strojek K. Early identification of hearing impairment in patients with type 1 diabetes mellitus. Otol Neurotol 2001;22:316-20.
Weng SF, Chen YS, Hsu CJ, Tseng FY. Clinical features of sudden sensorineural hearing loss in diabetic patients. Laryngoscope 2005;115:1676-80.
Agarwal A, Pujary K, Ganapathy K, Balakrishnan R, Nayak D, Hasan F. Pure tone audiometry and otoacoustic emissions for the assessment of hearing loss in diabetic patients. Indian J Otol 2013;19:13. [Full text]
Horikawa C, Kodama S, Tanaka S, Fujihara K, Hirasawa R, Yachi Y, et al.
Diabetes and risk of hearing impairment in adults: A meta-analysis. J Clin Endocrinol Metab 2013;98:51-8.
Akinpelu OV, Mujica-Mota M, Daniel SJ. Is type 2 diabetes mellitus associated with alterations in hearing? A systematic review and meta-analysis. Laryngoscope 2014;124:767-76.
Dalton DS, Cruickshanks KJ, Klein R, Klein BE, Wiley TL. Association of NIDDM and hearing loss. Diabetes Care 1998;21:1540-4.
Cullen JR, Cinnamond MJ. Hearing loss in diabetics. J Laryngol Otol 1993;107:179-82.
Harner SG. Hearing in adult-onset diabetes mellitus. Otolaryngol Head Neck Surg 1981;89:322-7.
Klagenberg KF, Zeigelboim BS, Jurkiewicz AL, Martins-Bassetto J. Vestibulocochlear manifestations in patients with type I diabetes mellitus. Braz J Otorhinolaryngol 2007;73:353-8.
Chávez-Delgado ME, Vázquez-Granados I, Rosales-Cortés M, Velasco-Rodríguez V. Cochleovestibular dysfunction in patients with diabetes mellitus, hypertension and dyslipidemia. Acta Otorrinolaringol Esp 2012;63:93-101.
Santos MD, Bittar RS. Vertigo and metabolic disorders. Int Tinnitus J 2012;17:16-20.
Kim SK, Lee KJ, Hahm JR, Lee SM, Jung TS, Jung JH, et al.
Clinical significance of the presence of autonomic and vestibular dysfunction in diabetic patients with peripheral neuropathy. Diabetes Metab J 2012;36:64-9.
Gawron W, Pospiech L, Orendorz-Fraczkowska K, Noczynska A. Are there any disturbances in vestibular organ of children and young adults with type I diabetes? Diabetologia 2002;45:728-34.
Tyler HR, Samuels MA. Neurologic disorders associated with endocrine and metabolic disorders. In: Farmer TW, editor. Practice of Medicine: Disease of the Nervous System. Vol. 10. Philadelphia: JP Lippincott Co.; 1978. p. 18-21.
Taylor IG, Irwin J. Some audiological aspects of diabetes mellitus. J Laryngol Otol 1978;92:99-113.
Cohen HS, Kimball KT, Stewart MG. Benign paroxysmal positional vertigo and comorbid conditions. ORL J Otorhinolaryngol Relat Spec 2004;66:11-5.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]