We performed vitrectomy on both eyes of a patient with bilateral vitreoretinal amyloidosis. In one eye, concurrent panretinal photocoagulation prevented recurrence.
In August 1991, a 52-year-old African American woman complained of floaters in both eyes. Visual acuity was 20/25 OD and 20/20 OS. Results of ophthalmic examination showed no abnormalities, except for acellular vitreous opacities, and no treatment was advised. By June 1992, visual acuity had decreased to 20/40 OU, consistent with increased vitreous opacities and the diagnosis of probable amyloidosis was made.
Pars plana vitrectomy was performed in the left eye in July 1992. Histopathologic stains were consistent with amyloidosis. The patient's postoperative visual acuity improved to 20/20 OS, but amyloidosis has a high recurrence rate.1 Vitrectomy in the right eye was performed in August 1992, with concomitant endolaser panretinal photocoagulation to destroy the possible site of production or secretion. In May 1993, the patient was symptom free with visual acuity of 20/20 OU; however, results of her ophthalmic examination showed asymmetric intraocular pressure of 16 mm Hg OD and 21 mm Hg OS, with a clear posterior segment in the right eye and opacities in the vitreous in the left eye. In June 1994, visual acuity had deteriorated to 20/25 OD and 20/80 OS, with intraocular pressure at 14 mm Hg OD and 57 mm Hg OS. The left eye showed an afferent pupillary defect, large recurrent vitreous opacities, optic nerve cupping, and marked visual field loss.
Maximum medical treatment did not sufficiently control intraocular pressure, and a mitomycin-augmented trabeculectomy failed after several months. In February 1995, the patient underwent pars plana vitrectomy with endolaser panretinal photocoagulation and placement of an Ahmed glaucoma drainage tube. The patient has done well since that time; the most recent ophthalmic examination in July 1997 showed a visual acuity of 20/30 OD and 20/40 OS consistent with mild cataract, intraocular pressure of 10 mm Hg OD and 13 mm Hg OS, and clear vitreous in both eyes. She has been diagnosed with cardiac, neurological, and gastrointestinal deposition of amyloid.
Amyloidosis is considered a complex of related diseases characterized by extracellular deposition of amyloid protein.2 Amyloid fibrils are composed of various proteins arranged in a β-pleated sheet configuration.3
Various protein abnormalities can cause amyloidosis. Genetically aberrant prealbumin is thought to be responsible for all cases of vitreoretinal amyloidosis in which the deposits have been chemically sequenced. Prealbumin has a high proportion of proteins in the β-pleated sheet structure, which may polymerize into the amyloid fibril. Prealbumin synthesis has been seen in retinal pigment epithelium,4 although the major source is considered to be the liver. Other research suggests that vitreoretinal amyloid has a retinal vascular origin.5
The mechanism by which laser panretinal photocoagulation led to resolution of vitreoretinal amyloidosis is unclear. A secondary effect on the retinal vasculature could have reduced secretion of amyloid formed elsewhere, eg, in the liver. Alternatively, destruction of retinal pigment epithelium could have destroyed the site of amyloid synthesis. In our patient, glaucoma was probably due to amyloid obstructing trabecular meshwork. The panretinal argon laser photocoagulation probably helped reduce the amount of amyloid deposited in the trabecular meshwork.
Panretinal argon laser photocoagulation prevented recurrence of amyloid deposits in the vitreous. The small number of individuals with ocular amyloidosis prevents investigating laser therapy with a clinical trial. We are optimistic, however, that our observations may prove useful in treating other patients with this condition.
Reprints: Michael D. Baum, MD, 8830 Cameron St, Silver Spring, MD 20910.
Baum MD, Weiss HS, Sanders RJ. Panretinal Photocoagulation in the Treatment of Vitreoretinal Amyloidosis. Arch Ophthalmol. 1998;116(11):1534. doi: