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CLINICAL COURSE OF PARANEOPLASTIC RETINOPATHY WITH ANTI-TRPM1 AUTOANTIBODY IN JAPANESE COHORT

Ueno, Shinji, MD, PhD*; Inooka, Daiki, MD*; Nakanishi, Ayami, MD, PhD*; Okado, Satoshi, MD*; Yasuda, Shunsuke, MD, PhD*; Kominami, Taro, MD, PhD*; Sayo, Akira, MD*; Morimoto, Takeshi, , MD, PhD; Kondo, Mineo, MD, PhD; Katagiri, Satoshi, MD, PhD§; Hayashi, Takaaki, MD, PhD§; Terasaki, Hiroko, MD, PhD*

doi: 10.1097/IAE.0000000000002329
Original Study: PDF Only

Purpose: To report the clinical course of eyes with paraneoplastic retinopathy caused by an autoantibody against transient receptor potential cation channel, subfamily M, member 1 (TRPM1).

Methods: Ten paraneoplastic retinopathy patients with retinal ON-bipolar cell dysfunction, including six melanoma-associated retinopathy, from eight institutions in Japan were evaluated for the presence of an anti-TRPM1 antibody. The results of ophthalmic examinations and the presence of anti-TRPM1 antibody were analyzed.

Results: Five patients were positive for the anti-TRPM1 antibody. These patients had similar clinical findings in both eyes at the time of diagnosis; relatively preserved best-corrected visual acuity, absence of fundus and optical coherence tomography abnormalities, and specific abnormalities of the electroretinography (ERG); and negative-type ERGs with bright stimulus flashes. One patient whose retinal ON-bipolar cells remained dysfunctional for the entire testing period, although the anti-TRPM1 antibody had disappeared. On the other hand, the ERGs recovered in 2 cases within 2 years after the onset. One case progressed to additional impairment of the photoreceptors with deterioration of ERGs. One case died and the clinical course was unavailable.

Conclusion: Paraneoplastic retinopathy patients with retinal ON-bipolar cell dysfunction possess autoantibodies against TRPM1 at the onset of the disease process; however, the clinical course of these eyes can be different.

Patients with paraneoplastic retinopathy with ON-bipolar cell dysfunction occasionally have autoantibodies against TRPM1 at the onset of the disease process; however, the clinical course of these eyes can be different.

*Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan;

Department of Ophthalmology, Osaka University Graduate School of Medicine, Suita City, Osaka, Japan;

Department of Ophthalmology, Mie University Graduate School of Medicine, Tsu City, Mie, Japan; and

§Department of Ophthalmology, The Jikei University School of Medicine, Tokyo, Japan.

Reprint requests: Shinji Ueno, MD, PhD, Department of Ophthalmology, Nagoya University Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan; e-mail: ueno@med.nagoya-u.ac.jp

Grant-in-Aid for Scientific Research C (No. 16K11320 to SU) from the Ministry of Education, Culture, Sports, Science and Technology of Japan (http://www.jsps.go.jp/).

None of the authors has any financial/conflicting interests to disclose.

© 2018 by Ophthalmic Communications Society, Inc.