Title : The protective role of neurotrophin-3 in patients with sensorineural hearing loss of autoimmune and ischemic origin
Sensorineural hearing loss is an urgent problem, it significantly reduces the quality of life of patients, the molecular mechanisms of its occurrence are not fully understood, and in fact there are no effective and safe methods of treatment that stop the progression of the process.
Aim: to study the dependence of the rate of SNHL progression of proven autoimmune and ischemic genesis on the level of neurotrophin-3 in the blood of patients.
Methods: We studied 24 patients with SNHL (17 men and 7 women) aged 63 ± 9 years. In 8 patients (5 women and 3 men), anticochlear antibodies (anti-68kD, hsp-70) were detected in the blood. In 16 patients (14 men and 2 women), hemodynamically significant pathology of the vertebral arteries was revealed. All patients were divided into 2 groups depending on the rate of SNHL progression: with slow (15) and fast (9) progression. The level of neurotrophin-3 in the blood of all patients was investigated. The control group consisted of 20 volunteers (15 men and 5 women) with normal hearing at the age of 58 to 67 years who did not have anticochlear antibodies and pathology of the vertebrobasilar arteries.
Results: In the group of patients with rapidly progressive SNHL, the level of neurotrophin-3 in the blood was reduced by almost 2.1 times compared with patients with slowly progressive SNHL (p≤0.05). In the control group were individuals with both normal and reduced levels of neurotrophin-3 in the blood. Interestingly, patients with the lowest levels of neurotrophin-3 in the blood were single people. And interestingly, 6 out of eight patients with anticochlear antibodies in childhood suffered from mumps.
Conclusions: A relatively high level of neurotrophin-3 in the blood slows down the rate of progression of SNHL of proven autoimmune and ischemic origin, and in patients with relatively low levels of neurotrophin-3, SNHL progresses rapidly. It is possible that SNHL of autoimmune origin is a long-term consequence of childhood mumps.
Audience Take Away:
• Relatively high levels of neurotrophin-3 in the blood slows down the progression rate of HCT of proven autoimmune and ischemic genesis; in patients with relatively low levels of neurotrophin-3, HCT progresses rapidly.This confirms the results of other researchers, and gives hope for the future development of effective drugs for the treatment of HCT.
• It is possible that HCT of autoimmune genesis is a remote consequence of childhood mumps, which requires further research.
• It is likely that living alone affects the level of neurotrophin-3 in the blood.