gms | German Medical Science

Background: A rare but severe cause of pigment epithelium damage in humans is iodate intoxication. We saw three patients with extensive pigment epithelium alterations caused by iodate intoxication because of internal use of a certain PVP-iodine formulation in thoracic surgery.

Methods: Three patients with severe iodate induced pigment epithelium damage were examined including visual acuity, visual fields, fluorescein angiography, ICG angiography, electroretinograms and visual evoked potentials. Based on the clinical findings a pubmed research was performed.

Results: In the acute phase visual acuity was perception of handmovements to 20/200. Fundus examination showed only delicate alterations but fluorescein angiography revealed a massive early hyperfluorescence at the posterior pole without leakage. Over a period of one year, visual acuity recovered to approximately 20/20, at the fundus stippled RPE atrophy and proliferation developed. As a animal model for RPE-damage is based on iodate usage, parts of its mechanism is already understood.

Discussion: At retina toxic levels iodate interacts with melanin. This results in a peak of oxidative stress as oxidants appear and scanvangers are removed. As the findings are markedly restricted to the posterior pole, it is hypothesized that the underlying reactions are triggered by light. In the acute phase a breakdown of the retinal diffusion barrier develops and in the follow-up pigment epithelium cell death with atrophy and proliferation occurs. The appearance of the fundus at the follow-up visits has parallels to the phenotype of dry ARMD which in return implicates an involvement of oxidative stress in the pathogenesis of dry ARMD.