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

The effects of type 2 diabetes on evoked otoacoustic emissions (e-OAEs) eli cited by clicks in subjects with normal hearing and the involvement of the central (CNS) and peripheral nervous system and acute hyperglycemia were in vestigated. In study 1, 110 type 2 diabetic patients and 106 control subjec ts matched for age and gender were investigated by e-OAEs. Central and peri pheral neuropathy were evaluated respectively by auditory brainstem respons es (ABRs) and according to San Antonio Consensus Conference criteria. In st udy 2, 10 healthy and 10 type 2 diabetic men matched for age, all with norm al 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 wer e 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 impaire d e-OAEs (e-OAEs-), in comparison to those with normal e-OAEs (e-OAEs+), we re older (51.0 +/- 5.8 v 45.1 +/- 6.0 years, P < .001), had diabetes longer (11.5 +/- 4.4 v 7.0 rt 3.9 years, P < .001), achieved poorer metabolic con trol as judged by hemoglobin A(1c) ([HbA(1c)] 6.9% +/- 0.4% v 6.5% +/- 0.3% , P < .001), and had more peripheral neuropathy (46% v 23%, P < .02). No di fference was observed between e-OAEs- and e-OAEs+ subjects for retinopathy or nephropathy. Nevertheless, when the duration of diabetes was corrected b y multiple regression analysis, the correlation between sensorineural damag e and peripheral neuropathy lost significance (P = .12). Diabetic groups (e -OAEs+ and e-OAEs-) showed greater latency in waves 1, III, and V and great er 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 intensities compared w ith basal values during the entire hyperglycemic clamp in either type 2 dia betic or control subjects. No difference was observed between the two group s at each time of the clamp. Thus, type 2 diabetic subjects show a higher r ate of compromised e-OAEs than healthy individuals. The e-OAE dysfunction d oes not associate with either an injury to the auditory nervous pathway or diabetic microvasculopathy The apparent interference of peripheral neuropat hy in e-OAEs loses significance when corrected for the duration of diabetes . Copyright (C) 1999 by W.B. Saunders Company.