Plasma Glycated Albumin Levels Clearly Detect Hearing Loss and Atherosclerosis in Patients with Impaired Fasting Glucose

血浆糖化白蛋白水平可明确检测空腹血糖受损患者的听力损失和动脉粥样硬化

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Abstract

OBJECTIVE: To describe the relationship between atherosclerosis and hearing thresholds in prediabetic patients with impaired fasting glucose (IFG) and to determine the efficacy of glycated albumin in predicting carotid artery atherosclerosis in patients with isolated IFG. SUBJECTS AND METHODS: The study included 82 patients (aged 53.73-80 years) divided into two groups based on fasting glucose levels, the IFG group: 59 patients (32 females, 54.2%), and the normal fasting plasma glucose level group: 23 patients (12 females, 52.2%). Patients underwent audiological testing to determine hearing thresholds, and carotid intima-media thickness (CIMT) was measured using carotid artery Doppler sonography. Multivariate analyses were performed to determine whether or not the plasma glycated albumin levels could predict hearing loss and CIMT. RESULTS: Patients in the IFG group (mean age: 59.8 ± 9.5 years) had higher hearing thresholds and pure-tone average scores (PTA) than those in the group with normal glucose levels (mean age: 56.2 ± 10.1 years) (left ear: 27.65 ± 8.85 vs. 25.75 ± 21.96 dB, p = 0.021; right ear: 29.22 ± 8.51 vs. 22.39 ± 6.99 dB, p = 0.001). The CIMT was significantly higher in the IFG group than the control group (0.75 ± 0.26 vs. 0.56 ± 0.16 mm, p < 0.001 for the left and 0.74 ± 0.26 vs. 0.51 ± 0.19 mm, p < 0.001 for the right carotid arteries). Glycated albumin levels were independently related with increased CIMT (left CIMT: r = 0.32, p = 0.003; right CIMT: r = 0.42, p < 0.001), and serum glycated albumin levels were significantly associated with PTA (left ear: r = 0.28, p = 0.01; right ear: r = 0.30, p = 0.006). CONCLUSION: Sensorineural hearing loss was more common in patients with IFG. Plasma glycated albumin levels were strongly correlated with CIMT and carotid plaques as a marker of atherosclerosis and with hearing impairment thought to develop due to atherosclerosis in patients with IFG.

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