Effects of Type 2 Diabetes Mellitus on Cochlear Structure in Humans

Abstract

To evaluate the effects of type 2 diabetes mellitus on cochlear elements in humans. Design: Comparative study of the histopathologic characteristics of human temporal bones. Setting: Otopathology laboratory in a tertiary academic medical center. Patients: Temporal bones from 18 patients with type 2 diabetes mellitus were divided into 2 groups according to the method of management of diabetes: insulin in 11 patients (mean age, 51.9 years; age range, 44-65 years) and oral hypoglycemic agents in 7 patients (mean age, 54.4 years; age range, 45-64 years). The diabetic groups and 26 age-matched controls (mean age, 52.9 years) were examined using light microscopy, and the cochlear changes were compared between groups. Main Outcome Measures: Morphometric measurements of vessel wall thickness in the basilar membrane and stria vascularis were made in all turns of the cochlea at the midmodiolar level. Area measurements of the stria vascularis were made in all turns of the cochlea at the midmodiolar level. Cochlear reconstructions and standard cytocochleograms were prepared using an oil immersion objective. The number of spiral ganglion cells was determined for each segment of the cochlea. Comparisons were made in each segment between diabetic and control groups. Results: In the insulin group, walls of the vessels of the basilar membrane and stria vascularis in all turns were significantly thicker than those of controls. Walls of the vessels of the stria vascularis in the basal turn were also significantly thicker in the oral hypoglycemic group than in controls. Atrophy of the stria vascularis in most turns of the insulin group and the lower middle turn of the oral hypoglycemic group was significantly greater than in the controls. Loss of cochlear outer hair cells was significantly greater in the lower and upper basal turns in both diabetic groups. No significant difference was found in the number of spiral ganglion cells or inner hair cells between groups. Conclusion: This study demonstrates that cochlear microangiopathy and degeneration of the stria vascularis and cochlear outer hair cells are found in patients with type 2 diabetes mellitus.

The Association between Impaired Fasting Glucose and Noise‐induced Hearing Loss

“…The suggested pathogenesis includes cochlear microangiopathy, hyperglycemia of the cerebrospinal fluid or perilymph, auditory neuropathy and diabetic encephalopathy 8) . Fukushima et al described a diabetesassociated pathology in the cochlea that includes thickened vessels of the stria vascularis, atrophy of the stria vascularis and loss of outer hair cells 9) . Many other studies have reported that diabetes is a risk factor for hearing loss [10][11][12][13] .…”

A Comparative Study of Age Related Hearing Loss among Diabetic Patients

“…[5] However, there is not enough evidence to solidly define diabetes mellitus as a cause of hearing loss. [6] The two important factors seen in diabetics which affect hearing are: Diabetic angiopathy and neuropathy.Diabetes mellitus causes increased rate of triglyceride production due to insulin resistance. There is endothelial proliferation and accumulation of glycoproteins, with thickening of the capillary vessels in basement membranes.…”

Identifying Early Onset of Hearing Loss in Young Adults With Diabetes Mellitus Type 2 Using High Frequency Audiometry

“…But in HFA the type 2 diabetic individuals showed a significant bilateral mild or moderate degree symmetrical sloping hearing loss with high variability in thresholds. This can be accounted to the fact that atrophy and thickening of blood vessels of stria vascularis in basal turns of cochlea occurs in individuals with type 2 diabetic mellitus [3].…”

“…In type 2 DM, walls of blood vessels of stria vascularis were thicker in basal turns in subjects who took oral hypoglycemic agents, walls of blood vessels of stria vascularis and basilar membrane were thicker in basal turns in subjects who were on insulin therapy. Atrophy of stria vascularis of most turns in subjects who were on insulin therapy and the atrophy involved the lower turns in oral hypoglycemic agent subjects [3].…”