We present a case of successful removal of late calcium deposition on the posterior surface of a silicone intraocular lens (IOL) optic in association with asteroid hyalosis using a surgical technique that included pars plana vitrectomy, a lighted pick, and a modified silicone-tipped cannula. The lighted pick provided the most efficient and complete removal of calcium deposits. Postoperatively, the dystrophic calcification was removed and the IOL optic was clear at 6 months follow-up. The patient's symptoms resolved and uncorrected distance visual acuity returned to 20/20. This method can be considered in patients with dystrophic calcification of a silicone IOL in association with asteroid hyalosis and might avoid the need for IOL exchange and its associated complications and uncertain refractive outcomes.

Aim: The aim of this study was to report outcomes following radiation therapy in patients with biopsy-proven extranodal marginal zone lymphoma of the ocular adnexa and uvea. Methods: Records from a single institution were retrospectively reviewed from January 1997 to December 2015. The mean follow-up duration was 38 months (range 0-194). Radiation therapy was administered to 77 eyes (60 patients); 57 of the 77 eyes (74%) were treated with radiation only (range 20-36 Gy, median 15 fractions). Radiation cataract, radiation retinopathy, and optic neuropathy assessments were performed on all eyes treated with radiation. Results: 100% of the 47 patients treated with radiation therapy only had local control with an average dose of 26.5 Gy (median 25.2 [range 20-36] Gy; 150-200 cGy per fraction). Four patients lost 2 lines or more of vision after radiation. The most common complication of radiation therapy was cataract formation/progression in 19 eyes (25%). Radiation retinopathy was observed only in 1 patient (1%). Conclusion: Our results confirm that radiation therapy (median 25 Gy) for extranodal marginal zone lymphoma of the ocular adnexa is associated with high local control and low risk of visually significant complications.

S. marcescens induces corneal inflammation by activation of TLR4/MD-2/MyD88 and the IL-1R1/MyD88 pathways, which are potential therapeutic targets for inhibition of S. marcescens-induced corneal inflammation.