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• W1529824891 abstract "To the Editor: Paraneoplastic retinopathies are uncommon manifestations of systemic malignancy that have diagnostic and clinical importance. The paraneoplastic retinopathies include carcinoma-associated retinopathy (CAR), melanoma-associated retinopathy, and diffuse uveal melanocyte proliferation. We describe a patient who developed acquired color blindness and progressive visual loss associated with recurrent prostate cancer. Clinical features and the electroretinogram (ERG) supported the diagnosis of carcinoma-associated cone dysfunction, a rare subset of CAR. Treatment of prostate cancer led to complete resolution of symptoms. Ocular manifestations of systemic malignancy have diagnostic and clinical significance. Symptoms and signs may be related to metastatic infiltration, compressive phenomena, or autoimmune, paraneoplastic syndromes. There are several well-described paraneoplastic retinopathies whose frequent presentation before the detection of a malignancy or before recurrence of a known malignancy heightens their importance.1 The paraneoplastic retinopathy syndromes include CAR, melanoma-associated retinopathy, and diffuse uveal melanocyte proliferation syndrome. Patients with CAR (most frequently associated with small-cell carcinoma of the lung and less frequently other malignancies) present with slowly progressive decline in rod and cone function manifesting as progressive loss of vision, photosensitivity, night blindness, impaired color vision, central or ring scotomas, constriction of visual fields, and marked attenuation of the ERG. The vast majority of CAR patients have circulating antibodies to retinal antigens: antirecoverin antibodies.2 These polyclonal antibodies are most commonly directed at 23 kDa antigen, a calcium-binding protein found in photoreceptor and bipolar cells of the retina. The carcinoma-associated cone dysfunction syndrome, part of the CAR spectrum, is a rare manifestation of a systemic malignancy, with only a few cases reported in the literature.3–5 Patients with carcinoma-associated cone dysfunction syndrome have antibodies primarily directed against cones and consequently have loss of color perception, central scotomas, and an ERG showing reduction in cone responses.6 In this report, we describe a patient who presented with acquired colored blindness and eventual marked decline in visual acuity. These findings preceded recurrence of metastatic prostate cancer. A literature review of the association between prostate cancer and paraneoplastic retinopathies revealed two previously described cases.3,4 One patient had clinical similarities to our patient, initially complaining of color vision loss before the diagnosis of recurrent prostate cancer.4 A 73-year-old Caucasian male noticed difficulty in interpreting traffic signals beginning in May 2000. The patient had diabetes mellitus, hypertension, Graves' disease (treated with radioactive iodine), and open-angle glaucoma. He had had a prostatectomy 12 years previously for prostate cancer. On ophthalmological examination, he was unable to identify any Ishihara charts. There were centrocecal scotomas using Humphrey visual fields and retinal pigmentary changes using funduscopy. Visual acuity was 20/40 in the right eye and 20/60 in the left eye, identical to readings obtained 12 months earlier. There was bilateral proptosis (Hertel 27/100–23/100) and mild periorbital edema. Initially, Graves' ophthalmopathy was believed to be responsible for the patient's symptoms. Corticosteroid treatment, prednisone 70 mg daily was started. He noted subjective improvement in color vision, although objective improvement was lacking. Gradual corticosteroid tapering resulted in subjective relapse of the patient's visual symptoms. The patient underwent orbital radiation therapy in December 2000, which resulted in minimal improvement of his color vision. Visual acuity declined in January 2001, to 20/100 and 20/200. A second course of radiation therapy was given in June 2001, but the patient's vision continued to deteriorate. A second opinion was requested, and age-related macular degeneration was suspected. Fluorescein and indocyanine green angiograms were performed. These studies demonstrated unusual pigment atrophy with primarily a peripapillary distribution as opposed to the parafoveal distribution typically seen in atrophic macular degeneration. A multifocal ERG revealed symmetrical central area flattening, diagnostic of greatly reduced activity in central cone response. CAR was considered. The patient's serum was sent to the University of California at Davis for antirecoverin antibody and ocular hypersensitivity testing (courtesy of Charles E. Thirkill, PhD). Antirecoverin antibody testing was negative, and ocular hypersensitivity revealed an abnormally elevated amount of antibody reactive with the retinal and optic nerve antigens. In November 2001, the patient presented with backache, lower extremity weakness, and numbness with a sensory level at T2. Visual acuity at this time was 20/400 and 20/400. Magnetic resonance imaging of his spine revealed a T2-T3 mass compressing the spinal cord and destruction of vertebral architecture (Figure 1). His prostate-specific antigen (PSA) level, which had been undetectable after surgery 12 years previously, was 1.9 ng/mL and rose to 5.5 ng/mL, supporting a metastatic recurrent prostate carcinoma. Computed tomography–guided biopsy of the vertebral mass was nondiagnostic. Imaging and evaluation for other possible primary malignancies were negative. In December 2001, he underwent radiation of the T1-T3 region that resulted in reduction of vertebral mass, with an improvement in his mobility and sensation. Goserelin acetate and bicalutamide were administered. With postradiation and hormonal therapy, the patient's color vision and visual acuity improved (20/100 and 20/100 in December 2002, 20/60 and 20/70 in September 2003, 20/40 and 20/60 in May 2004), and he has been able to return to his premorbid functional status. The patient's PSA remains undetectable. Magnetic resonance image of the thoracic spine demonstrating complete replacement of the T2 vertebral body with extension into the pedicle and lamina bilaterally and significant cord compression. This patient's initial presentation was acquired loss of color vision. Although he had many ophthalmological conditions that could have contributed to his visual symptoms, there is indirect and robust evidence for the diagnosis of a paraneoplastic retinopathy. Specifically, the lack of response to medical intervention directed against Graves' disease and resolution of the patient's disease, after radiation therapy to the spine and hormonal therapy, speak to a paraneoplastic retinopathy as the predominant process. The ERG findings and the results of ocular hypersensitivity testing provided further support for a variant of CAR, carcinoma-associated cone dysfunction syndrome. Without isolation of specific antibodies against cone-related epitopes, the diagnosis of carcinoma-associated cone dysfunction syndrome is speculative, but this patient would fulfill many of the proposed criteria. The patient's history of prostate cancer, which had been quiescent for the previous 12 years, is a noteworthy feature. His visual symptoms preceded the appearance of backache, lower extremity weakness, and vertebral mass. The concomitant and rapid rise in PSA supports the recurrence of prostate cancer. Also remarkable is the durable improvement in ocular and neurological symptoms after radiation therapy and antiandrogen therapy. One could suggest that this pronounced response may have occurred because of the autoimmune response to the patient's tumor. The removal of the antigenic source allowed the visual symptoms to improve. In conclusion, paraneoplastic retinopathies should be considered in the differential diagnosis of acquired color blindness and vision loss, especially with prior history of prostate carcinoma. Financial Disclosure: David Harper, Edward Arsura, Ravi Bobba, Chakradhar Reddy, and Amar Sawh have no financial support for research, consultantships, and speakers' forum and no company holdings (e.g., stocks) or patents in connection with this paper. David Harper performed the acquisition and manuscript preparation. Edward Arsura and Ravi Bobba performed the analysis and manuscript preparation. Chakradhar Reddy performed the manuscript preparation. Amar Sawh performed the acquisition of subjects. Sponsor's Role: None." @default.
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• W1529824891 date "2005-07-01" @default.
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• W1529824891 title "ACQUIRED COLOR BLINDNESS IN AN ELDERLY MALE PATIENT FROM RECURRENT METASTATIC PROSTATE CANCER" @default.
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• W1529824891 doi "https://doi.org/10.1111/j.1532-5415.2005.53384_6.x" @default.
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