Elsevier

Metabolism

Volume 48, Issue 11, November 1999, Pages 1346-1350
Metabolism

Cochlear dysfunction in type 2 diabetes: A complication independent of neuropathy and acute hyperglycemia

https://doi.org/10.1016/S0026-0495(99)90141-5Get rights and content

Abstract

The effects of type 2 diabetes on evoked otoacoustic emissions (e-OAEs) elicited by clicks in subjects with normal hearing and the involvement of the central (CNS) and peripheral nervous system and acute hyperglycemia were investigated. In study 1, 110 type 2 diabetic patiens and 106 control subjects matched for age and gender were investigated by a-OAEs. Central and peripheral neuropathy were evaluated respectively by auditory brainstem responses (ABRs) and according to San Antonio Consensus Conference criteria. In study 2, 10 healthy and 10 type 2 diabetic men matched for age, all with normal e-OAEs, underwent a 5-hour hyperglycemic clamp study. e-OAE tests were performed before and during the hyperglycemic clamp. In study 1, e-OAEs were impaired in 51.8% (57 of 110) of the diabetic subjects, in comparison to 4.7% (five of 106) of the control group (P < .0001). Diabetics with impaired e-OAEs (e-OAEs−), in comparison to those with normal e-OAEs (e-OAEs+), were older (51.0 ± 5.8 v 45.1 ± 6.0 years, P < .001), had diabetes longer (11.5 ± 4.4 v 7.0 ± 3.9 years, P < .001), achieved poorer metabolic control as judged by hemoglobin A1c [HbA1c] 6.9% ± 0.4% v 6.5% ± 0.3%, P < .001), and had more peripheral neuropathy (46% v 23%, P < .02). No difference was observed between e-OAEs− and e-OAEs+ subjects for retinopathy or nephropathy. Nevertheless, when the duration of diabetes was corrected by multiple regression analysis, the correlation between sensorineural damage and peripheral neuropathy lost singificance (P = .12). Diabetic groups (e-OAEs+ and e-OAEs−) showed greater latency in waves I, III, and V and greater interwave latency for waves I to V than the control group, but there was no significant difference in ABRs between e-OAEs+ and e-OAEs− subjects. In study 2, there were no significant changes in e-OAE intesities compared with basal values during the entire hyperglycemic clamp in either type 2 diabetic or control subjects. No difference was observed between the two groups at each time of the clamp. Thus, type 2 diabetic subjects show a higher rate of compromised e-OAEs than healthy individuals. The e-OAE dysfunction does not associate with either an injury to the auditory nervous pathway of diabetic microvasculopathy. The apparent interference of peripheral neuropathy in e-OAEs loses significance when corrected for the duration of diabetes.

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