Limits...
Choroidal atrophy in a patient with paraneoplastic retinopathy and anti-TRPM1 antibody.

Ueno S, Ito Y, Maruko R, Kondo M, Terasaki H - Clin Ophthalmol (2014)

Bottom Line: The full-field electroretinograms were negative type, indicating ON bipolar cell dysfunction.We followed him for more than 2 years from the initial visit and his symptoms have not changed.However, consistent with the choroidal hypopigmentation of the fundus, spectral domain optical coherence tomography showed a decrease in choroidal thickness of about one third over a 2-year follow-up period.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

ABSTRACT
The purpose of this paper is to report choroidal atrophy in a patient with cancer-associated retinopathy who had autoantibodies against the transient receptor potential cation channel, subfamily M, member 1 (TRPM1). A 69-year-old man visited our clinic in July 2010 with complaints of blurred vision and night blindness in both eyes. The full-field electroretinograms were negative type, indicating ON bipolar cell dysfunction. General physical examination revealed small cell carcinoma of the lung, and Western blot of the patient's serum showed autoantibodies against TRPM1. We diagnosed this patient with cancer-associated retinopathy and retinal ON bipolar dysfunction due to anti-TRPM1 autoantibody. We followed him for more than 2 years from the initial visit and his symptoms have not changed. However, consistent with the choroidal hypopigmentation of the fundus, spectral domain optical coherence tomography showed a decrease in choroidal thickness of about one third over a 2-year follow-up period. We suggest that this case of gradually progressive choroidal atrophy was caused by the autoantibody against TRPM1 directly, because TRPM1 is expressed not only on ON bipolar cells but also on melanocytes. These findings indicate that we should be aware of choroidal thickness in patients with paraneoplastic retinopathy who have retinal ON bipolar dysfunction with the anti-TRPM1 antibody.

No MeSH data available.


Related in: MedlinePlus

Fundus photographs of a patient diagnosed with carcinoma-associated retinopathy who developed choroidal atrophy during a 2-year follow-up period. Fundus photographs of the right (A) and left (B) eyes taken at the initial examination in June 2010. Fundus photographs of the right (C) and left (D) eyes taken in October 2012.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3921079&req=5

f2-opth-8-369: Fundus photographs of a patient diagnosed with carcinoma-associated retinopathy who developed choroidal atrophy during a 2-year follow-up period. Fundus photographs of the right (A) and left (B) eyes taken at the initial examination in June 2010. Fundus photographs of the right (C) and left (D) eyes taken in October 2012.

Mentions: We have followed this patient ophthalmologically for more than 2 years since his initial visit and his symptoms have not changed. His best-corrected visual acuity decreased slightly to 0.8 in the right eye and 0.5 in the left eye due to progression of cataracts. His visual field has not constricted and his ERGs have not changed (see Figure 1). Rod responses were nonrecordable in 2010 and 2012. The amplitudes for a-wave of cone-rod mixed maximum response were 240 μV and 220 μV in 2010 and 2012, respectively, and those for b-wave were 150 μV and 120 μV, respectively. The amplitudes of cone response were about 25 μV for the a-wave and 50 μV for the b-wave at both times in 2010 and 2012. The amplitudes of the 30 Hz flicker ERGs were 14 μV in 2010 and 11 μV in 2012. The difference in the ERGs was most likely within the error of measurement and not due to differences in retinal function. However, fundus photographs taken in October 2012 showed diffuse choroidal hypopigmentation in both eyes (Figure 2). We also found that the choroidal vessels were more visible than those obtained at the initial examination (Figure 2).


Choroidal atrophy in a patient with paraneoplastic retinopathy and anti-TRPM1 antibody.

Ueno S, Ito Y, Maruko R, Kondo M, Terasaki H - Clin Ophthalmol (2014)

Fundus photographs of a patient diagnosed with carcinoma-associated retinopathy who developed choroidal atrophy during a 2-year follow-up period. Fundus photographs of the right (A) and left (B) eyes taken at the initial examination in June 2010. Fundus photographs of the right (C) and left (D) eyes taken in October 2012.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3921079&req=5

f2-opth-8-369: Fundus photographs of a patient diagnosed with carcinoma-associated retinopathy who developed choroidal atrophy during a 2-year follow-up period. Fundus photographs of the right (A) and left (B) eyes taken at the initial examination in June 2010. Fundus photographs of the right (C) and left (D) eyes taken in October 2012.
Mentions: We have followed this patient ophthalmologically for more than 2 years since his initial visit and his symptoms have not changed. His best-corrected visual acuity decreased slightly to 0.8 in the right eye and 0.5 in the left eye due to progression of cataracts. His visual field has not constricted and his ERGs have not changed (see Figure 1). Rod responses were nonrecordable in 2010 and 2012. The amplitudes for a-wave of cone-rod mixed maximum response were 240 μV and 220 μV in 2010 and 2012, respectively, and those for b-wave were 150 μV and 120 μV, respectively. The amplitudes of cone response were about 25 μV for the a-wave and 50 μV for the b-wave at both times in 2010 and 2012. The amplitudes of the 30 Hz flicker ERGs were 14 μV in 2010 and 11 μV in 2012. The difference in the ERGs was most likely within the error of measurement and not due to differences in retinal function. However, fundus photographs taken in October 2012 showed diffuse choroidal hypopigmentation in both eyes (Figure 2). We also found that the choroidal vessels were more visible than those obtained at the initial examination (Figure 2).

Bottom Line: The full-field electroretinograms were negative type, indicating ON bipolar cell dysfunction.We followed him for more than 2 years from the initial visit and his symptoms have not changed.However, consistent with the choroidal hypopigmentation of the fundus, spectral domain optical coherence tomography showed a decrease in choroidal thickness of about one third over a 2-year follow-up period.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

ABSTRACT
The purpose of this paper is to report choroidal atrophy in a patient with cancer-associated retinopathy who had autoantibodies against the transient receptor potential cation channel, subfamily M, member 1 (TRPM1). A 69-year-old man visited our clinic in July 2010 with complaints of blurred vision and night blindness in both eyes. The full-field electroretinograms were negative type, indicating ON bipolar cell dysfunction. General physical examination revealed small cell carcinoma of the lung, and Western blot of the patient's serum showed autoantibodies against TRPM1. We diagnosed this patient with cancer-associated retinopathy and retinal ON bipolar dysfunction due to anti-TRPM1 autoantibody. We followed him for more than 2 years from the initial visit and his symptoms have not changed. However, consistent with the choroidal hypopigmentation of the fundus, spectral domain optical coherence tomography showed a decrease in choroidal thickness of about one third over a 2-year follow-up period. We suggest that this case of gradually progressive choroidal atrophy was caused by the autoantibody against TRPM1 directly, because TRPM1 is expressed not only on ON bipolar cells but also on melanocytes. These findings indicate that we should be aware of choroidal thickness in patients with paraneoplastic retinopathy who have retinal ON bipolar dysfunction with the anti-TRPM1 antibody.

No MeSH data available.


Related in: MedlinePlus