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

• Published in: Metabolism, clinical and experimental clinical and experimental, 1999-11, Vol.48 (11), p.1346-1350
• Main Authors: Sasso, Ferdinanco Carlo, Salvatore, Teresa, Tranchino, Gaetano, Cozzolino, Domenico, Caruso, Arturo Armone, Persico, Marcello, Gentile, Sandro, Torella, Daniele, Torella, Roberto
• Format: Article
• Language: English
• Subjects: Acute Disease; Adult; Associated diseases and complications; Biological and medical sciences; Case-Control Studies; Cochlear Diseases - blood; Cochlear Diseases - etiology; Cochlear Diseases - physiopathology; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic Neuropathies - physiopathology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Evoked Potentials, Auditory, Brain Stem; Female; Glucose Clamp Technique; Glycated Hemoglobin A - metabolism; Humans; Hyperglycemia - etiology; Hyperglycemia - physiopathology; Logistic Models; Male; Medical sciences; Middle Aged; Time Factors
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/S0026-0495(99)90141-5

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 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 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.