The Clinical Details of MYH9-Related Disease and DFNA17 in a Large Japanese Hearing Loss Cohort
<b>Background/Objectives</b>: <i>MYH9</i> gene variants cause <i>MYH9</i>-related disease (<i>MYH9</i>-RD), which is also known as Epstein syndrome, Fechtner syndrome, May-Hegglin anomaly, and Sebastian syndrome. <i>MYH9</i>-RD is characterized by sensorineural hearing loss, macrothrombocytopenia, thrombocytopenia, hematuria/proteinuria, glomerulonephritis, cataracts purpura, and mucosal bleeding. In addition, the <i>MYH9</i> gene is also known to be causative of autosomal dominant non-syndromic hearing loss (DFNA17). <i>MYH9</i>-RD is a relatively rare disorder, and the detailed clinical features and mutational spectra remain unclear. <b>Methods</b>: In this study, we performed next-generation sequencing analysis for 15,684 hearing loss patients and identified <i>MYH9</i>-associated hearing loss patients. Detailed clinical information was collected for these patients and summarized. <b>Results</b>: In this study, we identified 24 patients from 18 families with <i>MYH9</i>-associated hearing loss. We clarified the details of hearing deterioration observed in patients based on collected serial audiogram data. Some cases showed rapid hearing deterioration that worsened by about 50 dB within 5 years. Hearing loss is more likely to progress in patients with myosin head domain variants than in patients with myosin tail domain variants, but hearing loss in each set of patients finally deteriorates to bilateral profound hearing loss. <b>Conclusions</b>: In this study, we were able to clarify the detailed characteristics of <i>MYH9</i>-RD- and DFNA17-related hearing loss in a relatively large number of patients, particularly in some cases that showed rapid and asymmetrical hearing deterioration progressing to bilateral profound hearing loss. Our data will be useful for providing more appropriate treatment and follow-up for <i>MYH9</i>-associated hearing loss.
Authors
- Kotaro Ishikawa (ORCID: https://orcid.org/0000-0002-6832-5923)
- Akira Sasaki (ORCID: https://orcid.org/0000-0002-1346-5312)
- Kazuma Sugahara (ORCID: https://orcid.org/0000-0003-0612-8323)
- Chihiro Morimoto (ORCID: https://orcid.org/0000-0001-5406-901X)
- Tadashi Nakamura (ORCID: https://orcid.org/0000-0002-0508-7876)
- Chikako Shinkawa
- Hiroshi Nakanishi (ORCID: https://orcid.org/0000-0003-2610-3203)
- Natsumi Uehara (ORCID: https://orcid.org/0000-0002-6620-4546)
- Kozo Kumakawa (ORCID: https://orcid.org/0000-0001-5802-7386)
- Kiyoshi Oda
- Tetsuro Wada
- S. Usami
- Nobuhiro Nishiyama
- Shinichi Goto
- Taku Ito
- Shin-ichiro Oka
- Tetsuo Ikezono
- Marina Kobayshi
- Testuya Okazaki
- Naoko Sakuma
- Shin-ya Nishio
Institutions
- Yamagata University (JP)
- University of Miyazaki (JP)
- Shinshu University (JP)
- University of Tsukuba (JP)
- Hirosaki University (JP)
- Tokyo Medical University (JP)
- Yamaguchi University (JP)
- Hamamatsu University School of Medicine (JP)
- Tokyo Institute of Psychiatry (JP)
- Tohoku University Hospital (JP)
- Nagasaki Rousai Hospital (JP)
- Saitama Medical University Hospital (JP)
- Mita Hospital (JP)
- National Rehabilitation Center for Persons with Disabilities (JP)
- Toranomon Hospital (JP)
- Tottori University (JP)
- Nara Medical University (JP)
- Kobe University (JP)
- Nippon Medical School (JP)
- Saitama Medical University (JP)
Publication Details
- Journal
- Genes
- Published
- 2026-01-29
- DOI
- https://doi.org/10.3390/genes17020154
- Primary Topic
- Skin and Cellular Biology Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00